Cardiology Lectures 1 4 DR - Deduyo PDF

Medicine II
CARDIOLOGY Worldwide the level of BP control is far from ideal

Finals Coverage – Dr. Deduyo
AMS 204 Note: If the hypertension level is 140/90 and higher, below 140/90
BP is said to be a controlled level except for the diabetic
Coverage of Final Examination: population. In the diabetic population, the BP of 130/80 or higher is
I. Hypertension already considered to be hypertension. If the person has already
II. Atherosclerosis and CAD achieved the goal, it doesn’t mean that the treatment should be
III. Acute Coronary Syndrome stopped.
IV. Congestive Heart Failure
V. Venous Thromboembolism and Pulmonary Hypertension management comparison, developing versus
Hypertension – Dr. O. Deduyo developed countries
Note: The data is almost the same for both.

HYPERTENSION
Hypertension profile in the Philippines
- Terms:
Hypertension is the leading cause of death globally,
o Prevalence – incidence
especially in Asia.
o Treated – patients taking the medication
o Compliant – patients are following the dosage
Note: It is not the hypertension that is the cause of death but its
prescribed by the physician
complications. Smoking and second-hand smoke is the second
o Controlled – because of compliance,
leading cause of death. Factors: Diets low in fruits, high BMI, high
controlled level is achieved
blood glucose (diabetes), physical inactivity or low physical activity,
high dietary salt, etc.
Profile of anti-hypertension treatment
- No medication = 44%
CVD risk doubles with each 20/10 mmHg BP increment
- Medication = 56%
Note: For every increment of 20 systolic BP and 10 diastolic BP,
Treatment Compliance
the CVD (Stroke, heart attack, heart failure) risk doubles
- Mostly
- Sometimes
Example:
- Rarely
115/75mmHg (relative risk = 1)
- Never
135/85mmHg (RR = 2)
155/95mmHg (RR = 4)
175/105mmHg (RR = 8) Treatment compliance versus BP control
- The compliant are 66% controlled and 55% uncontrolled
o The problem could have been the drug itself or
The higher the BP, the higher the risk of developing CVD
the dosage
- The non-compliant are 34% controlled and 46%
BP is strongly and directly related to vascular mortality
without any evidence of threshold down to at least uncontrolled
115/75mmHg
Number of anti-hypertensive drug used
- Type of medications:
Note: Vascular à cerebral artery, coronary artery, and also the
o Beta blocker – cheapest
peripheral vascular diseases.
o Calcium channel blockers
o ARBs
Stroke and Ischemic heart disease mortality linked to SBP
o ACE inhibitors
levels
o Centrally acting drug (Clonidine)
- Number of hypertensive drug used
Note: The leading cause of death is stroke and ischemic heart
o Monotherapy – majority
disease (complications of hypertension). As the BP increases, the
higher is the mortality both for stroke and ischemic heart disease. o 2 drugs – 11%
o 3-4 drugs – 0.4%
Hypertension prevalence does not discriminate by gender,
Note: When we first determine and recognize the presence of
geography, or income level
hypertension, we try to categorize whether it is Grade 1 or Grade
Prevalence of hypertension in developing countries from 2. If the BP is more than 160/100mmHg it cannot be managed by
only one drug, it should be 2 or more. But if the BP is 140/90mmHg
National Surveys
to 159/99mmHg then 1 drug can be given.
Note: The prevalence in both developing and developed countries
is the same.
Prevalence of hypertension in adults >18 years old
Note: The nationwide registry showed that from 11% in 1992 à

25% à rapid rise to 28% in 2013 (Presyon 1 to Presyon 3)
1 | J K C P V i l l a r a m a
BP control versus Drug Combination Note: There are several types of BP, not only Stage 1 and Stage 2
- Drug combination gives a better control than a single (by ACC and AHA) or Grade 1, Grade 2, Grade 3 (by European
drug Society of Cardiology), there are also:
- The number of anti-hypertensive drugs would tell - Excessive BP variability
whether a control level would be achieved - White coat hypertension
- Masked hypertension
The many causes of uncontrolled BP - Non-dipper/Reverse dipper
o BP is more elevated during nighttime than
Diverse pathogenesis and etiology during the day
- RAAS
- Salt-sensitive, volume of body - Morning surge
fluid
- Sympathetic nerve activity Besides staging, we must also know these by doing 24h
- Sleep apnea syndrome ambulatory BP monitoring. According to the latest ESC, all
- Secondary forms
hypertensive patients are advised to undergo 24h ambulatory BP
UN
monitoring to be able to determine the type of BP.
Important therapeutic regimens C Poor Adherence to anti-
- Low renin activity O hypertensive medications Measurement of the BP can be done in the office or the clinic, and
- Lifestyle (sodium intake) N
T
- Reduced self CV the out-of-the-office which is the home of the patient.
- Interfering substances R perception
- Fail to adjust drug species or O - forget
dosage timely L - Adverse drug reaction 2013 Europe hypertension guidelines: ESH/ESC emphasize
L - Poor therapeutic effects out of office BP measurement
E
D
BP The task force for the management of arterial hypertension of the
European society of hypertension and cardiology tells us about the
BP Types emphasis in the out-of-office BP measurement.
- Excessive BP variability
o White coat and masked Values:
hypertension
o Non-dipper/reversed dipper - Separating from medical environment better reflects true
(nighttime) hypertension BP condition than office BP
o Morning surge - Use out of office BP for risk stratification
- Patients with high office BP but normal out-of-office BP is
Note: There are many causes of uncontrolled BP. There is diverse termed as white coat hypertension
pathogenesis and etiology. - Those with white coat hypertension have a lower
- There is a need to determine the diverse pathogenesis cardiovascular risk than patients whose BP is elevated at
and the etiology of the elevation of the blood pressure. home but normal or low in the clinic or in the hospital.
o RAAS activation à give anti RAAS This is called as masked hypertension. It is frequently
o Excess volume or body fluid à give diuretics associated with cardiovascular risk factors and has
o Increased sympathetic nerve activity à give increased risk of cardiovascular events.
beta blockers
o Sleep apnea syndrome is different. In the time Lower CV Risk à White coat hypertension
of apnea, there is irregularity in breathing and it Higher CV Risk à Masked hypertension
can be monitored in the sleep center.
o It can also be secondary: pheochromocytoma, - There is a close association with hypertension induced
renal artery stenosis, because it is not organ damage especially left ventricular hypertrophy
controlled it can lead to uncontrolled BP or among patients with masked hypertension more than the
hypertension. white coat hypertension.
- Proper therapeutic regimen - There is a better prediction of CV morbidity and mortality
o Is there low renin activity? than the office BP thus the emphasis of out of office BP
§ Try to determine what is the level of measurement.
renin
o Lifestyle (Sodium intake) Poor compliance is a global problem
o Interfering substances - 1/3 of patients will discontinue the initial therapy within 6
§ Frequent use of NSAIDs interfere months after treatment and only ½ of patients will
with the drug continue treatment after 1 year
o Fail to adjust drug species or dosage timely - Self-monitoring of BP is an important means of
- Poor adherence to the anti-hypertensive therapy is very improving adherence
common o Disadvantage: Patient takes medication only
o Reduced self CV perception – very common when the BP is elevated. The anti-hypertensive
especially in the young adults drug is treating the atherosclerotic problem that
o Forget – long acting preparation should be is going on in a patient with hypertension. It is
given important that the patient is educated.
o Adverse drug reaction – usual side effects
should be disclosed to the patient Comprehensive BP management
o Poor therapeutic effect - Focusing on patients and confining doctors as well as
communities
- Self-monitoring of BP is a key component of Clinical Indications for Out-of-office BP Measurements for
comprehensive BP management Diagnostic Purposes
Definitions of HPN by Office and Out-of-office BP levels
Note: There are different values! We say that there is hypertension

in the office if the BP is = or > 140/90mmHg. In an ambulatory BP,
it is divided into daytime BP (awake period) and nighttime BP
(asleep period). The average of the two is taken (24h BP).
HPN definitions
- White coat HPN
o A discrepancy of >20/10 mmHg between the
clinic and average daytime ambulatory BP
monitoring (ABPM) or average home BP Note: Clinical indications for HBPM (Home BP Monitoring) or
monitoring at the time of diagnosis ABPM (Ambulatory BP Monitoring). BP variability – every time the
BP is taken it is different. There is a significant difference in the
§ Example: If the average daytime
level of the BP.
ambulatory BP is 130/80 and 160/90
in the clinics Risk of Mortality with Isolated and/or Combined Elevated
- Masked HPN – with higher cardiovascular risk Office, Home and Ambulatory BP — PAMELA study
o The converse of white-coat hypertension. A - The analysis of the Presyon done in Italy compared the
subject with masked hypertension has normal office, home, and ambulatory BP values between 1990
BP measurements in office or clinic but w/ and 1993 with cardiovascular and non-cardiovascular
episodes of elevated BP outside of the death:
clinical environment o 69 Cardiovascular
o 233 All cause death
Note: For people identified as having white coat hypertension and
- The increase in home BP shows a greater risk of
masked hypertension, consider day time ambulatory BP monitoring
cardiovascular mortality
or home BP monitoring as an adjunct to the clinic BP
measurement to monitor the response to the treatment. o Increase home and 24 hour BP had the greater
risk of cardiovascular and all cause death than
The normal circadian rhythm of BP has a nocturnal decrease of the increase in office BP
15% to 25% in BP compared with the awake BP values. This is - The risk of mortality is higher w/ a combination
called as the dipping pattern.
BP Dipping Status Predicts CV events
- Non dipping - CV events are higher in reverse dippers as compared
o Defined arbitrarily as BP reduction during with non-dippers, dippers and extreme dippers
sleep is <10% compared to the BP during o Reverse dippers – very high BP during
awake period nighttime
o Non-dippers – 10% reduction in the nighttime
o Occurs in about 25-40% of patients w/ HPN
BP compared to daytime BP
- Reverse dipping o Dippers – Normal
o Significant increase in BP when asleep or o Extreme dippers – very low BP during
when in supine position compared to the BP nighttime
while awake.
o Also called a riser pattern Blood Pressure Variability
§ Example: 170/110mmHg at night and - BP normally fluctuates during the day and can vary from
140/90mmHg during daytime day-to-day in response to environmental challenges
(stress, activities, etc.)
- Pronounced fluctuations in BP can occur over a short
term and long term observation period
o BPV has been observed over a 24hour period
ABPM, showing hour-by-hour variability
o There can also be a visit-to-visit variability Note: Subclinical organ damage – the organ damage of patients
either short term or long term with hypertension without clinical event
- Episodic HPN is common - Heart – LVH
o In a cohort of patients with previous TIA, only - Arteries – Atherosclerosis
12% has stable HPN while 69% has episodic o Can be determined by carotid duplex scan
HPN - Kidneys – proteinuria in urinalysis but with normal
creatinine
§ some systolic BP of less than or
equal to 140mmHg and some with
There is organ damage but is subclinical. For it to be clinical, LVH
greater or equal to 140mmHg
à angina pectoris, ischemic heart disease, or the patient is in
- BP variability is difficult to measure in routine clinical failure. Carotid atherosclerosis à Intima media thickness is
practice and there is no clearly defined or widely adapted greater than 1cm affecting the lumen of the carotid artery which is
diagnostic definition or treatment goal a gateway towards the brain
o BPV is best determined through ABPM
- ABPM can identify patients with the so-called “morning Note: BP Variability can also lead to a clinical event and it is quite
surge” and predicts CV events better than the office BP increased especially when there is decreased arterial compliance.
level Decreased adherence to AHT is the worst. To summarize BP
- High blood pressure measurement is a good alternative variability, there could be increased risk subclinical organ damage
to a 24h ABPM and variability has been correlated with but there is also an increased risk for a clinical event which is a
target organ damage, CV outcome and stroke mortality patient in failure that goes into mortality, CVA that goes into fatal
- Standard deviation and co-efficient of variation of BP condition, or a patient having albuminuria which leads to ESRD.
measurements are commonly used as parameters
- Variation independent of the mean is a transformation of
the standard deviation uncorrelated with the mean blood
pressure
BP Variability over different time periods has been evaluated

in several clinical trials
Note: Different trials have been conducted and they have proven
that BP variability indeed exists especially among patients who had
undergone 24h ABPM.
Mean Determinants of Increase in BPV

- Short term monitoring
o Hour-to-hour
- Day-to-day home BP monitoring
- 24 h monitoring
- Visit-to-visit monitoring
Determinants and Prognostic Relevance of BPV
Pronounced fluctuations in BP can occur over short-and-long Morning BP surge
term observation periods - Morning BP surge is associated with increased risk of
- There is a well-established morbidity and mortality stroke by 22%
associated with BP variability whether it is short term or
long term monitoring. Which class of anti-hypertensive drug is best suited to treat
- Increased 24 hour BP variability has been associated the morning BP surge?
with cardiovascular damage. - The long-acting preparation is preferred.
- Rate and severity of target organ damage o Take effect for the whole 24 hours or beyond
- mild to moderate hypertension o Examples:
- increased awake systolic BP variability correlates with § Calcium channel blockers
subclinical target organ damage • 34 - 36hours
- Day to day BP variability is an independent predictor of • Drugs:
cardiovascular event and stroke mortality after o Amlodipine
adjustment from BP and other confounders than in o Nifedipine
Japan among Japanese residents § ARBs
- The visit to visit increase in BP and BP variability • 36 hours
increases cerebrovascular risk in 683 non-dependent • Drugs:
subjects whose age is more than 65 years of age. o Telmisartan
- The difference in BP and uncontrolled BP will predict that
there will be an increase cardiovascular mortality. Note: Beta blockers have 4-6 hour peaks. Beta blockers only
- Comparing visit to visit variability: 3 drugs decrease the heart rate and it has nothing to do with endothelial
o Chlorthalidone (Diuretics) function. But there are vasodilating beta blockers like carvedilol
o Amlodipine (CCB) and nevibolol which has an anti-oxidant effect and improves
o Lisinopril (ACE inhibitor) endothelial function. ACE inhibitors are good anti-hypertensive
drugs but with cough as side effect.
Note: ACE inhibitor is the best drug for hypertension. Side effect:
cough Summary
- The guidelines continue to recommend the office BP for
Example of 24hr BP screening and diagnosis of hypertension and it is
- 6pm à midnight à 6am à noontime recommended that the diagnosis of hypertension be
- When a patient is about to sleep the systolic BP goes based on at least 2 BP measurements on separate visits
down and then increases at midnight to the awake - Out-of-office BP should be considered to confirm the
period. This is called as the morning surge diagnosis of hypertension
- Identify the type of hypertension and detect hypertensive
Morning BP surge
episodes and maximize prediction of cardiovascular risk
- Morning BP surge is defined as the morning BP (average
of 2 hours after arising) minus the nighttime lowest BP - For out-of-office BP measurement, ambulatory BP
(average of the 3 BPs nighttime) monitoring, home blood pressure monitoring may be
- Finding: patients with sleep-trough surge of >55mmHg considered depending on indication, availability, ease,
were classified as a morning BP surge cost of use, and if appropriate, the patient’s preference.
- Reducing morning hypertension may also prevent - There is increasing evidence that high morning BP is
cardiovascular outcome. associated with increased stroke risk, damage to the
- Reducing the morning BP surge as well as the mean BP heart, atherosclerosis and organ damage
in hypertensive patients has been suggested as a - High morning BP is increasingly being recognized as an
potential therapeutic target to prevent vascular outcome important aspect in managing hypertension
particularly acute coronary syndrome, cardiac - Studies have been conducted to investigate the
arrhythmias, and sudden cardiac death on all cause determinants of high morning BP and how control rates
mortality. differ between the clinical population.
- Meta analysis of randomized studies established the
prognostic value of the morning BP surge in the general
Note: Differential effect of CCB compared with other agents like
population.
ACE, Beta blockers for BP variability may account for the disparity
in observed efficacy in reducing the risk of stroke. It is not only
Example: If there is a rise in BP during the morning, the drug is
CCB but also ARBs especially Telmisartan which has the longest
administered before going to sleep knowing the peak plasma level.
half life
An exaggerated morning BP surge, exceeding the 90th percentile
of the population, is an independent risk factor for mortality and CV
and cardiac events, especially in smokers.
The rapid rise of BP in the morning is one of the critical risk

variables for CV events
- BP form of untreated hypertension patient
- Incidences of MI and stroke at different time intervals
have demonstrated that there is a rapid rise of BP early
in the morning.
Case # 1 Case # 2
Mr. S, a 36 year old male salesman who reported to a doctor’s Mr. MDC, a 75 year old male known hypertensive for the last
clinic for a problem of hypertension which was detected about a 10 years with poor compliance to medication. (The patient
month ago. He thought that the elevated BP was due to his work knows that he is hypertensive but he does not take it regularly.
for he is emotionally stressed (increased sympathetic aNS This is a very common scenario). He took his antihypertensive
activity) because he cannot achieve the sales quota set by his medication only when he thought his BP is elevated. About 3
employer. However he is also afraid because his father died of months prior to admission in the hospital, he began to suffer from
CVA secondary to hypertension at the age of 56 and his only easy fatigability but no chest pain. Such symptoms he attributed
brother died of a heart attack at the age of 46. His mother also to his age.
died at the age of 56 due to heart failure secondary to
hypertension (Strong family history). Smokes half-pack of Note: Nape pain has nothing to do with the BP, it is not
cigarette for the last 10 years and drinks beer on occasion. related. Hypertension is without symptoms unless there
Complains of palpitations especially when stress and after is clinical organ damage. If there is subclinical organ
drinking coffee and soda (both contains caffeine which causes an damage, the patient is still asymptomatic. When
increase in heart rate). symptoms begin to appear, this is because of the target
organ complications. Any pain can elevate the systolic
PE showed: BP due to increase in sympathetic drive. The expression
BP – 160/92 mmHg, sitting on both arms. of fatigability is due to a low cardiac output.
If seeing the patient for the first time, take it on both However about 3 weeks prior to admission he had episodes of
arms. A difference of greater than 10 mmHg in systolic paroxysmal nocturnal dyspnea and orthopnea (awaken at night
blood pressure, there could be a vascular problem; ask if because of difficulty in breathing and stays in a sitting position
the patient is taking BP at home to r/o white coat overnight) He felt very weak and walking for a minute or two
hypertension; this is a candidate for ABPM makes him very tired. Meantime he noticed bilateral pedal edema
and he spends the night sleeping using 3-4 pillows to support his
HR – 110 bpm back. Thus he decided to consult at the emergency room.
RR – 18 cpm
BMI – 26 PE showed:
Fundoscopy - did not reveal retinal exudates or other signs of BP – 160/96 mmHg
retinopathy. HR – 120 bpm and regular, no arrhythmia
RR – 26cpm
Note: Evidence of atherosclerosis can be seen through (+) Jugular venous engorgement at 60 degrees position
fundoscopy (+) Hepatojugular reflux
(+) Bilateral crackles occupying (1/2) on both lung fields.
Eyes are the window of the Heart: check for retinopathy Bilateral crackles is not pneumonia, that is usually heart failure
or a hypertensive fundus, presence of atherosclerotic
plaques Heart: Apical beat is visible and palpable at the 5th ICS LAAL
and sustained. (There is obvious displacement of the apical beat)
Auscultation of the carotid arteries did not reveal any bruit on Heart sounds revealed tachycardia at 120bpm but normal rhythm.
both sides. Increased S1, Normal S2, (+) S3 gallop noted at the left ventricle.
Note: If there is bruit (like amurmur because of a Note: This patient has a very big heart because his
turbulence) it means to say that the carotid artery is apical beat is already displaced.
>50% occluded. If it is totally occluded, there is no bruit
heard. Always check for bruit because it is a sign of Abdomen: Unremarkable
turbulence. If there is more than 50% stenosis in the Extremities: Cold with bilateral pedal edema extending up to
carotid artery, there will be bruit. below the knee. (diminished COà diminished peripheral perfusion)
Heart: Apex beat is palpable on the 5th ICS LMCL and is Note: This is a description of a patient with organ
sustained with regular rhythm. HR is 110bpm with increased S1, damage. The heart is enlarged and it is symptomatic of
normal S2, no gallop and murmur present. He has good peripheral heart failure.
pulses.
Note: S1 and S2 loudness can be affected by the heart

rate. It can also be affected by the presence of valvular
diseases, arrhythmia, etc.
ECG: reveals an axis of -30 degrees with borderline voltage

criteria for left ventricular hypertrophy
Note: There is already evidence of subclinical organ

damage.
Pathophysiology of Hypertension - Alterations in adrenergic receptors that influence heart
rate, inotropic properties of the heart, and vascular tone;
and altered cellular ion transport.
Note: Atherosclerosis is a disease of the blood vessel wall and not

of the lumen.
What factors would affect endothelial dysfunction?

- Environmental stress
- Genetic
- Angiotensinogen, etc.
- CNS à sympathetic activation
- Cardiac à diminished cardiac output
- Renal à sodium retention
- GI à Obesity
- Endocrine à insulin
- Age Note: The determinants of the blood pressure would be the
cardiac output and the total peripheral resistance. If there is
Note: All of these causes malfunctioning of the endothelium. When increase in the TPR (Total Peripheral Resistance) or SVR
nitric oxide is diminished, there is increased substance P, CGRP (Systemic Vascular Resistance) even in the presence of a normal
and natriuretic peptide. cardiac output, there would be hypertension.
- Increased sympathetic nervous system activity causes Difference between the two major kinds of hypertension
an elevation of the BP (targeted by beta blockers, to
reduce heart rate)
- Heightened exposure or response to psychosocial stress
- Overproduction of sodium retaining hormones and
vasoconstriction
- Long-term high sodium intake
- Inadequate dietary intake of potassium and calcium
- Increased or inappropriate renin secretion with resultant
increased production of angiotensin II and aldosterone
o Because of a decrease in cardiac output, there
would be diminished renal blood flow that
would stimulate renin release
o The end result would be angiotensin II and
aldosterone and anti-diuretic hormone
o This explains the presence of edema in the
patient
- Deficiencies of vasodilators such as prostacyclin, nitric
oxide, the natriuretic peptides and a variety of other
vasodilator peptides inducing angiotensin (1-7) peptide,
calcitonin gene-related peptide (CGRP), substance P,
and adrenomedullin
- Alterations in expression of the kallikrein-kinin system
(part of RAAS) that affect vascular tone and renal salt
handling (targeted by ACE and ARBs)
Note:
- Abnormalities of resistance vessels, including selective - Primary or essential hypertension – majority of
lesions in the renal microvasculature (targeted by patients presenting in clinics
vasodilators like CCBs) - Secondary hypertension – there is a known medical
- Diabetes mellitus condition that causes the elevation of the BP. This is only
- Insulin resistance considered when the patient has been given four anti-
- Obesity hypertensive drugs but the BP is still elevated.
- Increased activity of vascular growth factors
The Natural History of Untreated Hypertension

Low moderate, high, and very high risk refers to 10 years risk of a
CV fatal or non-fatal event. The term “added” indicates that in all
categories risk is greater than average
Note: There is subclinical target organ damage (LVH, etc.) at first Note: Risk factors include family history of the patient, age, DM,
but these can be determined through examination and diagnostic dyslipidemia, sedentary lifestyle, excessive alcohol intake, etc. If
tests. Then after some time, the patient would be clinically relevant the BP is 120/80 to 129/84, it is considered by the ESC as normal.
(stroke, MI, etc) which can lead to death. When patients are seen If with comorbidities, even at low BP there is already moderate
at this point, we want to at least prevent them to go into the clinical added risk so the BP must already be managed at this point
event. together with the metabolic syndrome especially in patients with
very high added risk.
The Benefits of Antihypertensive Treatment
- Effective antihypertensive treatment can reduce stroke
and CAD
- For both systolic & diastolic hypertension and isolated
systolic hypertension: stroke and all other cardiovascular
diseases can be controlled as long as the blood pressure
is controlled.
Note: As for fatal and non-fatal events and mortality, it can reduce
stroke by 42% and coronary heart disease by 40%; mortality all
causes 14% cardiovascular 21% non cardiovascular. For isolated
systolic increase, fatal and non fatal events and mortality, stroke
can be reduced by 30%; 23% all cause mortality, cardiovascular
event and non-cardiovascular event.
Note: Hypertensive treatment strategy: there should be a broad

range of anti-hypertensive drugs that should be used.
Choice of antihypertensive therapy: ESH/ESC 2007

- Main benefit are due to BP lowering
- Specific drug classes may differ in their effects
- Drugs are not equal in adverse event profiles
- Major drug classes are suitable for initiation and
maintenance of therapy
- Choice of drug will be influenced by patient experience
and preference, concomitant conditions and cost and risk
profiles
- Long-acting drugs that provide once-daily, 24 – hour
efficacy are preferable (CCBs: Amplodipine and
Nifedipine: 36 hours, ARBs: Telmisartan)
The goals of antihypertensive treatment
- In hypertensive patients, the primary goal of treatment is
the maximum reduction in long-term total risk of
cardiovascular disease requiring:
o A reduction in raised blood pressure
o Treatment of all associated reversible risk
factors (obesity, smoking, and High salt intake)
Note: Diabetes and Dyslipidemia are not included because they

are not reversible but controlled.
The projected mortality

- As the BP goes up, there is a high mortality risk
- Raised BP has a high global mortality and it is the
leading CV mortality
- 7.1 million Asians die because of hypertension each year
- Asians are more prone to fatal and non-fatal coronary
artery disease compared with the Caucasians.
Note: When we treat hypertension, always tell the patient that we

can prevent MI by 20 to 25% and stroke by 30 to 35% and CKD by
47%. Other risk factors should also be treated.
ISCHEMIC HEART DISEASE protected and also the growing children from atherosclerotic
(Coronary Artery Disease and Atherosclerosis) changes.
- There would be smooth muscle migration, foam cell formation,
Note: There are two things to consider in IHD: coronary artery and activation of the T cell, adherence of the platelet, the
myocardium. The coronary artery is the blood supply of the heart aggregation of the platelet, as well as the aggregation of the
specifically the myocardium and the structures inside the chambers of the many leukocytes.
heart.
Advanced Plaque
Definition: - There is accumulation of macrophage, formation of a necrotic
- Coronary Artery Disease core, and fibrous cap formation which is a thin fibrous cap (a
o refers to the atherosclerosis of the coronary arteries vulnerable plaque because the cap is very thin and can be
that may result in significant obstruction to the subjected to rupture)
coronary blood supply leading to myocardial
ischemia Atherosclerosis: a generalized and progressive process
- It is a progressive course
Note: It refers to the presence of atherosclerosis. Hypertension is a risk - From the 1st decade of life, you can see that there is a
for the development of atherosclerosis because of impulses beginning. On the 2nd decade of life onwards, atherosclerosis
malfunctioning of the endothelium. There is endothelial dysfunction in can set in.
atherosclerosis. This is the reason why we need to control the elevation of
the blood pressure to prevent further damage and malfunctioning of the Atherosclerosis can set in the 2nd or 3rd decade
endothelium. - Unstable angina
- MI
- Myocardial ischemia - Ischemic stroke/ TIA
o Refers to a condition in which there is an imbalance - Critical leg ischemia
between the oxygen supply (carried by the coronary - Cardiovascular death
artery) and oxygen demand of the myocardium
usually due to a severe fixed or dynamic obstruction Note:
of the myocardial blood supply, or an increase in - When there is thrombus formation because of plaque rupture,
myocardial oxygen requirements, or both. there will be an acute coronary syndrome in the form of:
o Unstable angina
Note: One of the reasons why there is an increase in myocardial oxygen o MI
requirement by the heart is the presence of hypertrophy which is a o STEMI
consequence of a chronic uncontrolled hypertension. A concentric left o NSTEMI
ventricular hypertrophy and may exceed the concentric form into an - It does not only affect the heart when there is rupture of the
eccentric form becoming bigger, heavier, with a very thick myocardial plaque.
segment. The bigger the muscle, the bigger will be the requirement. o It can circulate and gain entrance into the brain
causing ischemic stroke or TIA, or
Coronary Arteries o In the peripheral vascular system causing critical leg
- Two main coronary arteries: ischemia especially among those whose comorbity
o Left coronary artery is DM on top of hypertension.
§ Divides into: o The usual death of patients is the presence of
• Circumflex coronary artery arrhythmia in the form of ventricular fibrillation
• Left anterior descending - At first there is stable angina in the heart. In the peripheral
coronary artery vascular system, there is intermittent claudication.
o Most often o Stable angina in the coronary artery in the
damaged myocardium where the chest discomfort is
o When there is a precipitated by effort which further increases the
clot or thrombus myocardial oxygen demand. There is a chest
that will be discomfort which is relieved by rest.
released because o Intermittent claudication is pain in the leg muscles.
of a rupture of the (gastrocnemius muscles become painful upon
atherosclerotic walking). Upon resting or sitting, there will be a
plaque, it finds its decrease in the demand and the symptom will be
way more into the relieved.
left side (LADCA)
o Right coronary artery Pathophysiology of MI
§ Supplies the right side of the heart and
the posterior portion of the heart. Oxygen requirement Oxygen supply
Pathogenesis of Atherosclerotic Plaque: endothelial dysfunction and Ischemia

inflammation
- Leukocyte migration Lactic acidosis ST segment change âcontractility Angina
- Increase adhesion of the endothelium
- Platelet aggregation
Note: It is something that increases the oxygen requirement in the heart
Note: These happen in the wall of the artery. There is presence of plaque. (LVH, increased HR, etc). The oxygen supply is the status of the coronary
artery. When there is an imbalance between the requirement and supply,
Fatty streak there will be ischemia of the myocardium. When there is ischemia, the
- First lesion muscle will suffer and there will be lactic acidosis. There will be reduction
- Fatty streaks have been seen even in the infants born from in the contractility, changes in the ST segment of the ECG. If there is
parents with family history of hypertension. Babies are not severe injury, ST segment elevates. In ischemia, there will be depression
of the ST segment. This is clinically significant because of the presence of
angina pectoris.
o It could also be a musculoskeletal pain
Spectrum of CA disease - Constant pain lasting for several days
- Very brief episodes of pain lasting and few seconds
Asymptomatic CAD o It could also be caused by anxiety
- Pain radiation to the lower extremities
Stable angina pectoris o It could also be neuropathy in the presence of DM
Unstable AP Physical Exam in Chronic CAD

- Many patients with CAD have normal physical findings
Non-STEMI - General: corneal arcus (in a young individual), xanthomas
and xanthelasma (these are cholesterol deposits that suggests
STEMI that the cholesterol level is elevated), retinal arteriolar
changes (atherosclerotic changes seen in the retinal lateral
Sudden death vessels during fundoscopic exam), elevated BP (considered as
a risk factor), diagonal earlobe crease (prone to heart
Note: Asymptomatic CAD à there is already a coronary atherosclerosis attacks), diminished arterial pulses and bruits (by
but there is still a balance between oxygen supply and myocardial auscultating the carotids, abdomen in the renal arteries which
demand. Until the time when there is imbalance, there is stable angina will suggest that there is a concomitant atherosclerosis or
pectoris or stable ischemic heart disease where the symptoms are felt aneurysm).
during activity because it further increases the demand and is relieved by - Cardiac examination: during an episode of angina pectoris, one
rest. Chest pains that are not relieved by rest are unstable angina, may detect an S3 paradoxical splitting of S2, transient systolic
NSTEMI, and STEMI which are all very symptomatic. Stable angina lasts murmurs, and pulmonary rates. A displaced left ventricular
for 5-10 minutes then disappears. Unstable anginas are felt even at rest. impulse suggests ventricular dysfunction.
This lasts for about 30 minutes. Chest pain of NSTEMI is continuous and
progressive with cold sweats. Note: When you examine a patient, usually there is a normal physical
examination finding. There are some clues to the presence of
Acute CAD versus Chronic CAD atherosclerosis such as those stated above.
- Acute – event is sudden - Cardiac findings:
- Chronic – event is gradual o S3 gallop
§ Suggests that there is a LV systolic
Clinical Manifestations of Chronic CAD malfunctioning
- Symptoms § Hallmark to diagnose the presence of a
- PE heart failure
- Biochemical tests o Paradoxical splitting of S2
- ECG o Transient systolic murmur or crackles due to the
- Other ancillary tests diminished LV function
o Displaced LV impulse which means that the heart is
Note: Chronic CAD is also called as chronic stable ischemic heart enlarged
disease or stable ischemic heart disease
Biochemical tests in chronic CAD
Angina Pectoris - Lipid profile
- AP is a discomfort of the chest or adjacent areas caused by o Total cholesterol >190mg
myocardial ischemia o LDL >70mg
- Usually brought on by exertion or stress o HDL â<50 in male; <40 in female
- Described as constricting, crushing, heavy (on the sternum), o Triglycerides >150mg/dL
squeezing in character
- Retrosternal in location but may radiate to other areas of the Note: In atherosclerosis, when there is endothelial
chest, ulnar surface of the arms, more commonly the left arm, dysfunction where the endothelium becomes permeable,
epigastrium, and mandible. the LDL is able to enter and penetrate the endothelium.
- It begins gradually and reaches its maximum over a few The macrophages will engulf the LDL transforming it into
minutes before it dissipates. foam cells and then continuous smooth muscle cell
- It may be associated with dyspnea, vagueness, easy fatigue, migration and the end result is the fibrous plaque. The
and ____ because of the stress and anxiety why the symptoms presence of a low HDL and high triglycerides usually is
appeared but is not related to the condition. usually suspicious of a patient with DM.
Note: There is no pain felt because there is no inflammation. If there is - Fasting Blood Glucose
inflammation, there will be pain which is persistent for several days o Normal <100mg/dL
(costochondritis, myosiitis). It is precipitated by exertion. o Impaired fasting glucose 100 -125mg/dL
§ Indicative of insulin resistance
Symptoms NOT suggestive of AP § Equivalent to pre-diabetes
- Pleuritic pain, brought on by respiratory movement or cough o Level suggestive of DM >126mg/dL
o Always try to differentiate if it is cardiac or - Other biochemical markers
pulmonary o Lipoprotein Lp(a)
§ Pulmonary – related to a pulmonary o Homocysteine level
symptom (most common: cough) o High sensitivity C-reactive protein
§ Cardiac – related to cardiac symptoms § Indicative for the presence of
(most common: chest discomfort) atherosclerosis
- Pain located in the middle or lower abdomen § In other words, maybe a person is not
o if it is located on the right or left and aggravated by diabetic, no increase in the level of
deep breathing or coughing, it is a pleuritic chest cholesterol or even the LDL, but there is
pain a high sensitivity C-reactive protein =
- Pain localized in one finger atherosclerosis
- Pain reproduced by movement or palpation of the chest wall
ECG in Chronic CAD
- Resting ECG is normal in 50% of patients with chronic stable Stress Testing
angina pectoris - Treadmill exercise test
- Most common ECG findings in chronic CAD are non-specific - Bicycle ergometer
ST-T wave changes with or without Q waves.
o “medyo bumaba pero hindi ganun kababa and Abnormal Stress ECG
without significan Q wave and T wave medyo - Horizontal downsloping of ST segment
bumaliktad pero mababaw” - very significant lowering of ST segment
- Various arrhythmia, especially ventricular primitive beats may
be seen Other forms of non-invasive stress testing
o It is not common but it may be seen - Those patient with nonspecific changes in ECG but
symptomatic and you want to prove there is a CAD
Note: In any patients complaining of chest pain especially when there is a
suspicion of risk factors, always request for ECG. Note: If the exercise tests did not show any abnormalities, do other forms
of non- invasive stress testing.
ECG tracing
- Our attention should be on the ST segment Nuclear cardiology techniques
- Stress myocardial perfusion imaging
o Uses either thallium, Tc99 sestamibi, or Tc99
tetrofosmin
- Pharmacologic nuclear stress testing
o For patients unable to exercise adequately
§ Ex. Stroke patients with chest discomfort;
advanced age who can’t do physical
tests such as treadmill
o May use dipyridamole, adenosine, or dobutamine
to “Stress” the heart
§ These increase the contractility of the
heart. There would be an increase in the
myocardial oxygen demand using these
drugs.
- Positron emission tomography
- Map the myocardial segments: o Useful to detect myocardial viability of the injured
o I, AVL, V5, V6 – lateral portion of the heart heart (myocardium)
§ If there is something wrong or if there is o expensive
less perfusion of that portion of the
myocardium, there will be changes in the Stress Echocardiography
ECG - Exercise echocardiography
o II, III, AVF – inferior portion of the heart - Looks at wall motion
o V1, V2, V3, V4 – anterior and septum portion of the - Pharmacologic stress echocardiography
heart
Note: Echo done during rest and will look at the wall motion, during
Note: There could also be a combination because there could be two or exercise, and post exercise. Look for abnormalities in the contraction of
more vessels affected so more changes in the ECG. the heart.
Non-invasive Stress Testing Nuclear Gamma Camera

- Provides useful information to establish the diagnosis and
estimate the prognosis in patients with chronic stable angina Radionuclide Myocardial Perfusion Imaging
- Most helpful in patients considered to have a moderate - Looks at the perfusion of the myocardium.
probability of CAD based on clinical symptoms, normal ECG, - If there is less perfusion, refer the patient for angiogram.
and risk factors. o If positive in angiogram, you can immediately do
o A normal ECG will not rule out the possibility of dilatation of the artery by inserting a stent.
CAD.
Stress Echocardiography (wall motion and diminished contractility)
Note: If the patient has normal ECG but is symptomatic and presents with - Exercise echography
the risk factors seen in the biochemical tests and PE, subject the patient to - Pharmacologic stress echography
non-invasive stress testing. - Abnormality in wall motion
- Thin à cannot contract effectively
Exercise ECG
- Most widely used test to diagnose CAD Note: There is an abnormality in the wall motion and thinning wherein it
- Usually performed on a treadmill or bicycle ergometer (two cannot contract effectively.
equipments used)
- Gives information not only the presence or absence of ECG Newer non-invasive imaging technologies for CAD diagnosis
evidence of ischemia but also on exercise capacity, BP and HR - Computed Tomography (CT Scan)
responses to exercise o Electron beam CT coronary calcium scoring
- ECG findings of horizontal or downsloping ST segment § Looks at the coronary calcium scoring
depression is indicative of myocardial ischemia (>2mm small § Calcium is needed for the contractility of
square) the muscle (ex. Striated muscles of the
o “bumabagsak yung ST segment” heart)
- Accuracy of ECG diagnosis may be limited in patients with o Multi-slice CT coronary angiography
abnormal baseline ECG (right bundle heart block configuration) - Magnetic resonance imaging
o “Meron namang abnormal pero yung mga normal
have to undergo further testing”
- Statins (HMG CoA reductase inhibitors) are drug of choice
Invasive Testing in CAD o Atorvastatin – good statin for CAD. There is
- Cardiac catheterization and coronary angiography superior reduction with high dose atorvastatin.
o Definitive diagnosis of CAD
o Precise assessment of anatomical severity of It lowers LDL and cholesterol
CAD The most important effect is stabilization of plaque.
o Assessment of LV function It will not rupture which may release thrombus that my occlude the arteries
o Requires the insertion of a catheter in a peripheral In patients with CAD in high risk category, high intensity lipid control is
artery (radial artery is used because it is shorter needed meaning the highest dose of statins should be maintained to
compared to the femoral artery) which is advanced control dyslipidemia and stabilized the plaque.
intravascularly to the heart under fluoroscopic
guidance. Extra-cardiac factors which may provoke angina
- IVUS (Intravascular ultrasonography) - Fever (increase HR)
o Myocardium is seen - Hypertension (LVH)
- Anemia(increase HR)
Note: The hallmark on the diagnosis of coronary artery disease leading to
ischemic myocardium is seen with cardiac catheterization and coronary - Hypoxia ( decrease O2)
angiography. Cadiac catheterization (for coronary arteries) and IVUS (for - Tachyarrhythmias
myocardium) are done simultaneously - Thyrotoxicosis
- Illicit drug use - direct injury to the myocardium
IVUS
- The wall of the coronary artery and the presence of Pharmacologic Therapy of CAD
atherosclerotic plaque can be seen in IVUS - Anti-platelet agents
o Aspirin – drug of choice; cheapest
Management of CAD § can cause gastric irritation to the gastric
- Lifestyle modification mucosa specially aspirin à use PPI:
- Control coronary risk factors Pantoprazole
o DM, hypertension, hyperlipidemia, etc. § The use of omeprazole decrease the
- Management of extracardiac contributing factors efficiency of clopidogrel by 50%
- Pharmacologic therapy o Clopidogrel (Plavix)
- Coronary revascularization o Ticlopidine (Ticlid)
o Significant test but not an ultimate therapy - Anti-ischemic drugs – diminishes oxygen demand by
because you cannot control atherosclerosis decreasing the end-diastolic volume
o Tries to enhance coronary blood supply but o Nitrates – In the acute stage, this is given
atherosclerosis remains to be present sublingually and maintain an oral long-acting
§ The patient should be under medication preparation of Isosorbide mononitrate for prevention
indefinitely § More on venous dilatation to decrease
return to the RA and RV. Dimished return
Non-pharmacologic measures in the management of CAD to the left side à lessen end diastolic
- Lifestyle modification volume (from 80%-50%) à lessen the
o Maintain ideal BMI myocardial work load
§ BMI = weight (kg)/height(m2) § Form of Isosorbide that is rapid in action
§ Regular aerobic exercise (to improve is dinitrate. Dinatrate is given for acute
blood flow) minimum 30-45 minutes four attacks – short-acting
times a week (30mins of walking 4x a o Beta blockers
week) § Decrease HR àdecrease oxygen
o Healthy heart diet - low salt, low fat, high fiber demand à decrease cardiac workload
o Smoking cessation § No effect on vessels. It has no effect on
o Control coronary risk factors endothelial function.
- Hypertension § Side effects: asthma – provoke the
o Goal is to maintain BP < or = 130/80 attack
o In patients with CAD, beta blockers, CCB (calcium • What can be given is
antagonists), or ACE inhibitors preferred. diltiazem or isoptin verapamil
§ Beta blockers, ACE or ARBs are more but these two have (-)
preferred inotropic effect in the heart.
§ Calcium antagonists: dihydropyridine and § Vasodilator beta blockers: carvedilol
non-dihydropyridine and nebivolol. (Included in studies
• Non-dihydropyridine which regarding heart failure and not in CAD)
has a similar effect as beta • Carvedilol - with alpha
blocker: verapamil and blocker as vasodilator
diltiazem
• Nebivolol – has nitric oxide
- DM
which is a powerful
o Maintain normal fasting and post-prandial glucose
vasodilator and enhances
and glycosylated hemoglobin; ACE or ARB
endothelial function.
inhibitors preferred
o CCB
§ Glycosylated hemoglobin tells us the
§ Verapamil and diltiazem
control of diabetes.
§ (-) inotropic effect
- Dyslipidemia
o ACE inhibitors
o Goals are more stringent in patients with CAD
§ Total cholesterol = <200%
§ LDL = <70mg
§ HDL = >45
§ Tg = <150mg
Pharmacologic therapy of ischemic heart disease: antiplatelet agents Pharmacologic Therapy of CAD: Anti-ischemic agents
Agent Action Usual dose Side effects Agent Indication Dosage A/E or C/I
Aspirin Inhibits GI irritation Diltiazem Diltiazem is Angina pectoris The most
cyclooxygenase 80-325mg od indicated for – initially commonly
Ticlopidine Inhibits ADP Neutropenia unstable angina 120mg/day in observed side
(Ticlid) – mediated platelet 250mg BID pectoris including equally divided effects were
not activation withdrawn from angina die to doses. Optimum edema,
available in the market coronary artery dose range: 180- asthenia,
the market spasm, or 360 mg/day in flushing, sinus
Clopidogrel Same same following MI. It is divided doses bradycardia,
(plavix) 75mg OD also indicated for first degree AV
chronic stable Hypertension – block,
angina, Initially 12-240 headache,
Note: To prevent GI irritation, what can be given are PPIs like hypertension, and mg/day in nausea, rash,
Pantoprazole which does not affect the strength of the Clopidogrel. for the prevention divided doses. joint swelling,
Omeprazole decreases the effect of Clopidogrel by 50%. of graft failure Usual dose fatigue and
following kidney range: 240-360 dizziness.
Effect of anti-ischemic drugs transplantation mg/day in divided
doses
Agent HR Contractility BP LV Coronary Collate
vol. blood rals Kidney
flow transplantation
Nitrates á NC â ââ á á – initially 120
Beta ââ â â NC NC NC mg/day in two
blockers or equally divided
á doses. Optimum
CCB áâ â or NC â NC á NC dose range 180-
(Non-D) 300 mg/day in 3
equally divided
Pharmacologic Therapy of CAD: Anti-ischemic agents doses
Verapamil Treatment of Verapamil 40-80 Edema,
Agent Indication Dosage A/E or C/I coronary artery mg q 6-8h asthma,
Nitroglycerines Ischemic, SL: 0.4mg Headache, disease including flushing, sinus
(Isosorbide) hypertension ISDN: 5-10mg TID âBP, crescendo angina bradycardia,
(because it (short-acting/rapid) hypoxemia, pectoris at rest, first degree AV
decreases the ISMN: 30-60mg BID caution with vasospastic angina block,
BP), CHF (long-acting - for RV infarct or Prinzmetal headache,
(which is d/t prevention of chest angina, and post-Mi nausea, joint
IHD) discomfort) infarction angina in swelling, rash,
NTG patch: 5-10mg patients with heart fatigue,
OD (applied over the failure if beta dizziness
chest for 12h and blockers cannot be
then remove then given
reapply to prevent
nitrate tolerance)
Metoprolol: Anti-ischemic, IV not available Bradycardia, Pharmacologic therapy of IHD: ACE Inhibitors
other beta anti- PO: 25-50mg q6h, AV block,
blockers hypertensive, then 50-100 mg BID CHF, asthma Agent Indication Dosage A/E or C/I
anti-arrythmic Captopril LV dysfunction 6.25mg initially; Renal failure,
Diltiazem: Ischemia not Diltiazem CHF, with CHF titrate to 50mg low BP, cough
verapamil responsive to 30-90 mg q6-8hrs LVEF<40%; TID
beta blockers, AV block; Enalapril Same 6.25mg initially Same
(N-d CCBs rapid AF Verapamil 40-80 mg low BP, titrate to 10-20
NOT Nifedipine without CHF q6-8hrs avoid mg BID
and Amlodipine nifedipine Lisinopril Same 6.5mg initially Same
which are D titrate to 10-20
CCBs) Not given in mg OD
patients with
HF with an Metabolic approaches to MI
ejection - Preconditioning (nicorandil)
fraction - Sinus node inhibition (Ivabradine)
<40% o This has a study in heart failure by inhibiting the
because it sinus node and therefore decreasing the heart rate
has a (-) without the side effect of beta blockers, ACE
inotropic inhibitors, or non-dihydropyridine CCBs.
effect - Late sodium current inhibition (ranolazine)
o In myocardial ischemia, there is inhibition in the
action potential (late sodium current). With inhibition
of the late sodium current, there is an increase in
the calcium that would promote more contractility
and stiffness of the myocardial segment. There is
LV diastolic dysfunction. If this is given, calcium will
be blocked and so there will be more expansion
during the period of diastole.
o People with LV diastolic dysfunction have a low
cardiac output and low stroke volume but ejection
fraction is normal. Because of the low cardiac output
and low stroke volume, the patients will feel easy
fatigability.
o The symptom of easy fatigability is controlled with
this ranolazine
- Metabolic modulations (trimetazidine)
o Increasing oxygenation of the myocardium
Non-pharmacologic therapy of IHD

- Percutaneous transluminal coronary angioplasty (PTCA)
with or without coronary stent implantation (to maintain the
patency)
- Coronary artery bypass grafting (CABG)
o Even in a stable IHD, this is the treatment of choice.
o This is done when the patient have been
bombarded with all the different drugs but the
patient remains to be symptomatic and ECG shows
ST segment depression with concomitant T wave
inversion seen from V1 to V6 à carotid
angiography is done to see how severe the
obstruction of the coronary artery is and a
consequent angioplasty.
Post MI Risk Assessment

- Treadmill stress test
- ECG
- Radionuclide ventriculography
- Holter monitoring; signal averaged
o For 24h ECG monitoring
- Dipyridamole or adenosine thallium testing
- Coronary angiography
o If the patient is positive, another coronary
angiograpy is warranted.
Secondary prevention of MI
- Aspirin – indefinitely
o Counterpart is Clopidogrel
- Beta blockers – 2 years to indefinitely
- Converting enzyme inhibitors – all patients with or without LV
dysfunction; indefinitely
- Diet and lipid lowering therapy – statins; indefinitely
- Exercise and rehabilitation
- Smoking cessation
Note: If the patient survives the attack and the patient responded to the
optimum medical therapy or the patient had undergone more invasive
procedures such as angioplasty and bypass procedure, indefinite
prevention must be followed. It is a lifetime disease and a lifetime intake of
medications. Patient education is a must!
ACUTE CORONARY SYNDROME - There are two types of plaque:
- Severe form of ischemic heart disease o Stable plaque
§ The fibrous cap is thick with a lipid core
ATHEROTHROMBOSIS o Disrupted plaque
- Acute thrombosis occurring in the presence or pre-existing § Plaque having a narrower cap containing
atherosclerosis produces acute ischemic strokes, acute the lipid core
ischemic syndromes of peripheral arteries (called peripheral § There is a site of rupture
arterial disease or peripheral arterial occlusive disease) and § Thrombus or blood clot
acute coronary syndrome including unstable angina,
myocardial infarction (NSTEMI and STEMI based on Pathologic and Clinical Presentation of Acute Coronary Syndromes
electrocardiogram) and sudden death
Burden of Acute Coronary Syndrome

- Significant public health problem both in industrialized and
developing countries
ACUTE CORONARY SYNDROME

- Unstable angina is a non-ST elevation MI
o There are 1.43 million hospitalizations in the US
- ST Elevation Myocardial Infarction (STEMI)
o 1,680,000 hospitalization for ACS in 2001
o 30% of ACS patients have STEMI
o 500,000 STEMI events per year in USA
ATHEROSCLEROSIS TIMELINE
Case: Patient has ischemic discomfort (discomfort in the region of the

chest). It is described as heaviness, squeezing, or something that
compresses the region of the chest. There is no pain because it is just a
very uncomfortable feeling. The working diagnosis is acute coronary
syndrome.
Note: The kind of ACS depends upon electrocardiogram and the

biochemical markers to be able to reach the final diagnosis.
- We look at the ECG and look for the ST segment if there is
elevation or not.
o If it is not elevated à NSTEMI or unstable angina
o If it is elevated à STEMI
Note: It starts during the first decade of life and the artery is still well- - STEMI and NSTEMI are formerly referred to as:
dilated. There are already beginning atherosclerotic changes in the form of o Non Q MI
a fatty streak which is the early stage of atherosclerosis. On the second o Q wave MI
decade, it becomes bigger. On the third decade, it also becomes bigger
and thicker and the artery becomes narrower. In the later part of the third CARDIAC BIOMARKERS - UNSTABLE ANGINA vs NSTEMI
decade there will be an atheroma or the plaque is already formed. On the
fourth decade, a fibrous plaque is well-formed and the artery is narrow
and there is a rupture of the plaque. When it ruptures, a lot of thrombus
or clot will circulate. It depends upon where it will land and how big is the
clot when an event happens. When it goes to the brain into the cerebral
artery it will produce stroke in the form of an infarct. Similar to this, when it
lands to the heart into the coronary artery it will produce. The more
arteries affected, the more segments affected. It is a thrombus that
basically semi-occluded or occluded therefore diminishes or stops blood
flow to that myocardial segment à necrosis à fibrinoid degeneration.
It will affect the overall function of the heart which is pumping blood in
order to perfuse the peripheral arteries.
Atherosclerosis to atherothrombosis
Note: To differentiate between the two, it is based on the biochemical

cardiac markers.
- Unstable angina and NSTEMI
o Both do not present with ST elevation
- It can be a non-occlusive thrombus or there is a vasospasm on
top of a non-occlusive thrombus. When the artery becomes
spastic it becomes narrow even if the thrombus is not occlusive
(not occluding completely the artery that has been affected) it
will be similar to a complete or partial occlusion of a coronary Note: On the first several days, the site of necrosis does not extend on the
artery. whole extent of the myocardial segment. After several weeks or months,
o If it is a non-occlusive thrombus there will be less there will be fibrinoid degeneration. Some subendocardial muscle will die
severe ischemia and less myocardial damage à but the lesion does not extend throughout the entire myocardial segment
Unstable angina or the wall.
o Non-occlusive + vasospasm: there would be
severe ischemia and more myocardial damage à ECG
NSTEMI
- When there is myocardial damage, there will be necrosis
followed by fibrinoid degeneration. During necrosis, the
cardiac myocytes will release troponins (troponins located in
the thin filaments: Troponin T, Troponin I, Troponin C). It
serves as a clue to the severity of the damage. Tropinin is the
one that would differentiate NSTEMI from Unstable angina.
History:
- severe localized chest or arm pain at rest or on minimal
exertion > 20mins crescendo pattern
Physical exam:
- pulmonary edema new or worsening MR, S3, new or worsening Note: The point that we are looking for is the ST segment.
rales
- First several days
Note: sometimes there will be crackles due to pulmonary edema, apical o Some subendocardial muscle dies (necrosis,
systolic murmur, or S3 gallop on auscultation decrease perfusion, not enough blood in
myocardium), lesion does not extend through the
ECG: entire heart wall
- transient ST segment changes (>0.05mv), new bundle branch o In terms of electrocardiogram, what we can see are:
block, sustained ventricular tachycardia § R wave persists but may diminish
somewhat
Note: The ECG shows some ST segment changes but is only 0.05mV. § Q wave not significant—significant if it is ¼
For it to be significant, it must be 2 or more mV. Both have the same of the height of R wave.; necrosis
presentation and what would separate the two would be the cardiac § ST segment often returns to baseline
markers. § T-wave inversion may occur
- After several weeks or months
Cardiac Markers o Lesion heals. Some subendocardial fibrosis may
Unstable angina NSTEMI occur but does not involve the entire thickness of
Shows no elevation of Troponin I, Troponin T, CKMB (creatinine heart wall so the heart can still contract.
Troponin. There could kinase and myoglobin are also released by the § Q wave not significant
be troponin up to 50 cardiac myocytes in response to the presence § ST segment and T wave may or may not
nanogram per deciliter. of necrosis but this is not used nowadays return to normal. T wave is upright.
because it does not last long). In early
necrosis, myoglobin is elevated but it lasts for
only a few minutes to hours. CKMB will be
elevated on the 2nd day. Troponin I and
Troponin T are elevated during the 1st day.
- CKMB lasts for 24 hours
- Trop I lasts for 6-7 days
- Trop T lasts for 10 days
Note: Troponins further increases in the presence of necriosis. They have
longer stay in the plasma as a manifestation that there is a myocardial
damage. The presentation of unstable angina and NSTEMI is the same
but what differs is the level of Trop I and Trop T. Note:
- There are other markers called high sensitive Troponin T and Location ECG leads Blood supply
high sensitive Troponin I Inferior wall lead II, III, AVF RCA/LCX
Lateral wall lead I, AVL, V5 and V6 LAD/LCX
PATHOLOGIC and ECG changes in NSTEMI
Anterior wall V3 and V4 LAD
Anteroseptal V1 and V2 LAD
- Posterior wall is represented by reciprocal changes
What do we look for in the ECG?

- ST segment: elevated, depressed, or at the baseline (normal)
- T wave: inverted or upright
- Q wave: can be deep or ¼ of the size of the R wave or wide
more than 0.4seconds
Note: ECG
- When we refer to the timing, it is horizontal.
- When we refer to the voltage, it is vertical.
ECG changes in Unstable Angina/NSTEMI Note: These are the reasons why the troponins are markedly elevated
- ST segment depression (30%) signifying the severity of damage in the myocardium. Refer the patient
- T-wave inversion (20%) immediately to the cardiac cath lab for emergency angiogram and a
- Transient ST-segment elevation (5%) possibility of bypass operation due to widespread damage.
PATHOLOGIC and ECG changes in STEMI
- ST segment depression at V4, V5, V6

- T wave inversion at Lead I, AVL It affects the whole or entire segment of the myocardium because of total
occlusion à necrosis (black). Because there is necrosis:
Note: In II, III, AVF involvement, 2 out of 3 or all of the three must be - First and second days
present to consider an inferior wall involvement. In I and AVL, both must o Transmural infarction nearly complete. Some
be present to consider a lateral wall involvement. ischemia and injury may be present at borders
o R wave gone or nearly gone
o Significant Q wave
o ST elevation may decrease
o T wave inversion beginning
- After 2 or 3 days
o Transmural infarction complete
o No R wave
o Deep T wave inversion
o Marked Q wave
o ST may be at baseline
- After several weeks or months
o Infracted tissue replaced by fibrous scar, sometimes
bulging (ventricular aneurysm)
§ There is fibrinoid degeneration or
fibrosis
- Significant T wave inversion – deep and symmetrical at V2, o Some R wave may return (but is not tall)
V3, V4, V5, and V6 o T wave often less inverted (smaller)
- No ST segment elevation or depression o Significant Q wave usually persists
- With small Q wave (the elevation should be >2mv) o ST elevation
Note: V2 – V6 changes = anteroseptal wall and lateral wall involvement STEMI ECG findings
à diffuse myocardial ischemia
ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

- There is total occlusion
- Clinical Diagnosis
o History
§ Accelerating Angina and rest pain
(>30mins)
§ Constricting, crushing, compressing,
heaviness, choking
§ Retrosternal radiating to ulnar aspect of left
arm
§ Atypical presentation
- Physical exam
o Soft S1, S3, S4, Mitral regurgitation due to papillary
- At least 2mm ST segment elevation in two or more precordial
muscle dysfunction, pericardial friction rub
leads
o Hypotension, tachycardia, bradycardia
- ST segment elevation of at least 1 mm in two or more leads
- ECG
o ST Segment Elevation, Q waves (signifies necrosis)
Note:
- Cardiac Markers
- 2mm ST segment elevation in V2, V3, and V4 à there is
o Troponins (cTnT, cTnI), CK-MB mass, Myoglobin
occlusion of the left anterior descending coronary artery. If it is
- Pathological Diagnosis
the only one occluded and angiogram and immediate
There is total occlusion
angioplasty is done, the patient will recover.
o Prolonged ischemia
- ST elevation in II, III, AVF + depression in I and AVL à which
o Myocyte Death
is significant? à Inferior changes are more significant and in
o Coagulation Necrosis
the leads opposite the site there are depressions and these
o Myocytolysis
are called reciprocal changes.
Myocardial Ischemia, Injury and Infarction ST Segment changes in infarct
- ST segment elevation indicative of injury

- Disturbance in current flow across the membrane
Note: This is a typical ST segment elevation because there is an acute

injury to the myocardium. There is a disturbance in the current flow across
- Zones: the membrane. The Q is not significant so it means that this is a recent
o Infarction infarction (4-6 hours). At this point, thrombolysis can still be done because
o Injury there is an acute injury with significant elevated ST segment.
o Ischemia
PRIMARY AND RECIPROCAL ST CHANGES IN ACUTE PHASE
INFARCTION
Myocardial ischemia T wave inversion
Before Infarct In acute phase infarction
Myocardial injury Elevation of the ST segment
(Injury)
Infarction Significant Q wave appears Lead facing infarct zone ST elevation à typical primary
ST segment elevation change
Q wave persist s, ST goes back to normal Lead opposite infarct zone ST depression à Typical
reciprocal change
Note: If you see an ST elevation + the patient has chest discomfort à
thrombolysis (best thrombolytic agent is rtPA) can still be done to Note: If you see a ST elevation, it is the one that is significant. If you see a
dissolve the thrombus. If there is already occlusion and the presence of Q depression, it is the reciprocal change.
wave à don’t do thrombolysis.
T wave changes in Myocardial Infarction
Reciprocal effect on the opposite side of the infarct - Deep symmetrical T wave inversion
- Since there is elevation in one side, there is depression on the - “Symmetry” refers to the equality of the angles of downstroke
opposite side because the QRS axis is moving to the opposite and upstroke of the T wave
side away from the site of injury.
o If there is elevation, the reciprocal change is a Evolution of ECG changes in Acute STEMI
depression.
QRS Complexes in Infarction

- Normal QRS progression
- Height of R wave is related to thickness of viable myocardium
o If there is a small R wave, this means that there is a
site of injury. In echo, there is thinning of the
myocardial segment because there is a site of
injury.
- Full thickness infarction show abnormal Q waves and QS
complexes
o If there is a negative wave immediately after the P, it
is the Q wave
o If there is a negative wave after the R wave, it is the
S wave. - Normal
o No contraction - In hours à ST elevation
- Extent of wall thickness involved in infarction determines R o In about 4-6 hours
wave voltage and abnormal Q waves. o Thrombolysis can be done (within golden period)
- In days à Q waves, Small R, ST elevation
Abnormal Q waves o Thrombolysis cannot be done anymore because of
the presence of Q wave
- In weeks à Q waves, Small R, ST isoelectric, Deep T
inversion
- In months à Q waves, small R, ST isoelectric, T wave upright
Note: Q wave signifies that there is already a fibrosis (lifetime)
- Duration: >0.04sec
o The duration is more than one square moving
horizontally
- Depth: >25% of the height of R wave
o The depth is more than ¼ of the height of R wave
INFARCT, LOCATION AND ECG LEAD INVOLVEMENT
Location of infarction Leads showing primary

changes
Anterior Infarction
Anteroseptal V1, V2, V3
Anterior V1-V3, V4-V6
Anterolateral V4-V6, I and AVL, possibly II
Extensive Anterior V1- V6, I and AVL
High Lateral AVL (plus high precordial leads)
Inferior infarction
Inferior II, III,AVF
Inferolateral-Apical II, III, AVF, V5, V6 and
sometimes also I and AVL Occlusion of the right coronary artery, where is the significant lesion?
Inferoseptal II, III, AVF, V1-V3 - Reciprocal change in V1, V2, V3, V4
Other changes - No significant elevation of the ST segment
Posterior infarction V1, V2( inverse of usual changes - II, III, and AVF – QS wave (inferior wall)
elsewhere) - Injury in the posterior wall
Subendocardial Infarction Any lead (usually multiple leads)
Early intervention + medical management should be given!
Note: The posterior portion of the heart is supplied by the right coronary
artery, including the inferior. Since we know that in V1 and V2 are CASE 1: 55 year old male bank executive experienced severe constricting
negative waves (P wave, small R, S, upright T), the wave of depolarization chest pain radiating to the back after a heated discussion. 3 hours later
is moving away from it moving to the left. Therefore, we use the reciprocal was brought to the ER because of persistent chest pain
changes. In V1 and V2 there is inversion as the usual change elsewhere.
There is a tall R and ST depression and T wave inversion. Reciprocal
change seen in V1 and V2, (and sometimes V3), it is a reciprocal change
of an infarction affecting the posterior portion of the heart supplied by the
right coronary artery.
Subendocardial à symmetrical T wave inversion (diffuse ischemia)
Anteroseptal Wall STEMI
There is occlusion of a branch of the left anterior descending coronary

artery, where is the significant lesion?
- ST elevation V1, V2, and V3
(+) Q wave – thrombolysis cannot be done anymore
CASE 2: 65 year old female obese diabetic was awakened early in the
morning becayse of severe epigastric pain radiating to the anterior chest
There is occlusion of the left anterior descending coronary artery, where is

the significant lesion?
- Q wave in I and AVL
- V2, V3, V4, V5
Occlusion of the right posterior descending coronary artery, where is the dDx: GERD, Acid peptic disease, cholelithiasis
lesion? (+) risk factors for atherosclerosis – age, obese, diabetic
- II, III, and AVF ECG: ST elevation in II, III, AVF; reciprocal changes in I and AVL
- Reciprocal changes in I and AVL (-) Q wave – can still perform thrombolysis
CASE 3: 53 year old female diabetic, meat vendor complained of on and Note: Aspirin should be chewed and absorbed under the tongue for
off chest pain for the last 3 days. Persistence of pain prompted to consult immediate effect. During the acute attack/rupture, there would be platelet
cardiologist where an ECG was done. adhesion and aggregation that contribute to the size of the thrombus.
Aspirin is the anti-platelet drug of choice. Aspirin + 4 tablets of Clopidogrel
swallowed.
PCI (percutaneous coronary intervention) with possible angioplasty or

bypass
Further tests include treadmill or stress echo or nuclear imaging. Echo
looks at the wall motion and nuclear looks at the myocardial perfusion and
angiogram looks at the lumen of the coronary artery (coronary angiogram
+ intravascular ultrasound done to look into the wall of the heart)
Results should be correlated clinically
Acute coronary syndrome/ acute myocardial infarction Algorith

(PHA council on CardioPulmonary Resuscitation)
ACUTE CORONARY SYNDROME

- Most common proximate cause of sudden cardiac death
(+) Risk factors: age, diabetic, possible dyslipidemia due to occupation - Manifested as a chest pain
ECG: peaking of T wave, symmetrical T wave inversion, (+) Q wave - With ECG changes
(days) [recent is ST elevation] - Cardiac markers
Dx: Inferior wall myopcardial infarction
Tall T wave of hyperkalemia, stress, etc Treatment objective
- Reduce myocardial necrosis
CASE 4: 45 year old male surgeon, smoker complains of retrosternal - Prevent major adverse cardiac events
chest pain with choking sensation lasting for 30 minutes. o ACS à
§ fatal arrhythmias – sudden cause of death
§ goes into heart failure
§ aneurysm
§ cardiogenic shock
• Manifestation of cardiogenic shock to
differ it with circulatory or neurogenic
is progressive lowering of blood
pressure, urine output, and
confused.
• Stage 1 to 4
o 1 – responds to
treatment
o 2 – chest pain but able
to tolerate it
o 3 – pulmonary edema
o 4 – cardiogenic shock
Risk factors – male, age, stress
- Treat life threatening complications (pulmonary edema or
ECG: No ST elevation, ST depression in V4, V5, and V6 (significant/true)
cardiogenic shock)
Dx: To consider Unstable angina or NSTEMI, lateral wall (request for
cardiac markers to confirm) ST segment
MANAGEMENT
Infarct – ST elevation
Ischemia – ST depression
Unstable angina
Note: End result of these is that the myocardium becomes ischemic or

necrotic
CASE the workload and cannot dilate the
- 55y/o man damaged coronary artery. Vasodilating
- Hypertensive, diabetic, smoker effect is on the venous and in the normal
- High cholesterol coronary artery but not in the damaged
- Severe substernal chest heaviness> 30 minutes, “crushing”, coronary artery. It can promote collateral
“squeezing” circulation (Isosorbide + Beta blocker)
o Clopidogrel
What do you do? o Heparin (UFH or LMWH)
a. Assess ABCs § To prevent coagulation
b. Insert IV line § Promote reduction of the symptoms of the
c. Give oxygen per nasal canula patient
d. Get a 12 lead ECG o ACE inhibitors (or ARB)
§ Choice
Chest pain (Suggestive of ischemia) à § Within the 24 hours onset + HMG CoA
A. Immediate assessment 80mg Atorvastatin can be given
- Vital sign, O2 saturation
- IV access If there is a ST depression and dynamic T wave inversion, management is
- 12 lead ECG the same!
- Brief history and PE
- Cardiac Markers STEMI or NSTEMI or unstable
- Electrolytes, coagulation and portable CXR - select reperfusion strategy
- Begin fibrinolytic checklist in order to determine if thrombolysis - -be aware of reperfusion goals
can be done or not (if there is tendency for bleeding) o Door to balloon inflation(PCI) goal of 90 min
o Door to needle (fibrinolysis) goal of 30 mins
B. Immediate general treatment o Continue adjunctive therapies and HMGCoA
- Oxygen 4LPM reductase inhibitor(statin)
- ASA 160-325mg § Statin of choice is Atorvastatin
- Nitroglycerin SL or spray
o Isosorbide dinitrate Time onset of symptoms
- Morphine - >12 hours
o Best given for the relief of the discomfort o Monitor the patient in the emergency room and
assess risk status
MONA - Morphine, Oxygen, NTG, ASA - <12 hours
- Cardiac cath lab unit or notify receiving hospital o Select reperfusion strategy
C. Assess initial 12L ECG If there is cardiogenic shock or contraindications to fibrinolysis, reperfusion
(surgical) is needed. PCI is the treatment of choice. If PCI is not available,
A. Assess the Initial ECG use fibrinolytics.
12L ECG is central to triage of ACS in the ER. Classify patients
as being 1 to 3 symptoms within 10 minutes of arrival Fibrinolytic therapy selected
a. STEMI - Altapase
§ ST-segment elevation - Streptokinase
§ Or new or presumably new LBBB - APSAC
b. High risk unstable (NSTEMI) - Recombinant tissue plasminogen activator
§ ST-segment depression o Best
§ Dynamic T-wave inversion
c. Intermediate/ low risk unstable angina Absolute contraindications to beta blockers
§ Non-diagnostic ECG - heavy failure
§ ST depression 0.5-1mm - pulmonary edema
§ T-wave inversion or flattening or flattening - bradycardia (HR <60)
in leads with dominant R waves - Hypotensive
o Systolic BP <100
Note: Before we do other tests, do cardiac markers. If normal, do other - Signs of poor peripheral perfusion
tests. Flattening of ST segments is suspicious so treadmill tests are - Presence of a 2nd or 3rd degree heart block
usually done.
Fibrinolytic
Q: Small R wave, widened QRS, V5 and V6 - Contraindications:
A: LBBB – manifestation of ST elevation MI o Very high blood pressure
- Even though it is a manifestation of STEMI with increase in o Recent surgery
Troponins, we cannot do thrombolysis because there is no o Bleeding tendency
elevation. There is no clue whether the infarct is recent or not
(within the 4-6 hours after the rupture of plaque). No
Dynamic T wave inversion
thrombolysis for LBBB! RBBB is usually insignificant and is not
included in STEMI.
High risk group
A. ST elevation or new LBBB/ ST elevation AMI - Ischemic chest discomfort (recurrent)
- Treatment - V-tach – prelude to ventricular fibrillation
o Start Adjunctive Treatment (within 24hrs of onset/ - Hemodynamic instability
stable) - Heart failure
o B-blockers - Early invasive strategy
§ Decreases the heart rate/workload similar to o Cardiac catheterization and revascularization within
the effect of nitroglycerine that decreases 48h of MI
Main Objective is
Treatment for STEMI and NSTEMI is the same! - to reduce necrosis that affects the myocardium
- prevent major cardiac event and ventricular aneurysm, cardiac
In general, treat these patients with anti-thrombin, heparin, and anti- arrhythmia, rupture of chorda tendinae and most common
platelet agents complication (Heart failure) and most common cause of death
(Cardiac arrhythmia)
Persistent symptoms, recurrent ischemia, diffuse or widespread ECG
abnormalities, depressed LV function, heart failure, serum cardiac Start adjunct tx:
markers à needs reperfusion therapy - NTG
- Betablocker
Who stays in the ICU? - Clopidogrel-less expensive, for three months
- No persistent symptoms - Heparin
- Symptoms disappear - Glycoprotein IIb/IIIa
Optimum medical management can be given: High risk subgroup:

- refractory ischemic chest pain
- Anti-platelet
- recurrent/persistent ST deviation
- Clopidogrel
- Hemodynamic instability
- ACE or ARBs
- Pump failure
- Beta blockers
- Nitrates or Isosorbide dinitrate
Early invasive strategy includes cathetherization and
- Glyc IIb/IIIa inhibitor revascularization.
EXTRA NOTES: Prevention:
- Clopidogrel and Aspirin - within 90mins of thrombus formation - Clopidogrel-less expensive,( FOR LIFE)
- New antiplatelet: PRASUGREL AND BRELINTA
Why do we give beta blockers? - Statin therapy high dose(FOR LIFE)
- It decreases the HR - ACE/ARB(FOR LIFE)
- increased HR àmore oxygen consumption needed
Contraindications of Beta blocker :

- pulmonary edema
- heavy failure
- bradycardia
- hypotensive
- complete heart block
Contraindications of Fibrinolytic therapy (streptokinase, Tissue

plasminogen activator)
- (+) bleeding episode
- CVA hemorrhage
In short the patient needs to undergo REVASCULARIZATION
Primary PCI selected

- Experienced operators
- High volume centers
- Cardiac surgical capability
Fibrinolytic therapy selected

- Altapase
- Streptokinase
- APSAC
B. ST depression/ dynamic T-wave inversion (High risk UA/ non-

STEMI)/ ST elevation or new LBBB/ ST-elevation AMI
C. Non-diagnostic ECG
- ST depression 0.5-1mm
- T wave inversion or flattening in leads with dominant R waves
- Intermediate/low risk unstable angina
Absolute contraindications to beta blocker therapy

- Severe LV failure and pulmonary edema
- Bradycardia(heart rate < 60bpm)
- Hypotension( SBP < 100mm Hg)
- Signs of poor peripheral perfusion
- Second or third-degree heart block
If there is ST elevation, initiate Ischemic therapy and non dx ECG.

Combine ECG and serum markers
CONGESTIVE HEART FAILURE
Note: The determinants of blood pressure are cardiac output and

peripheral resistance. When there is an increase in the CO which is
determined by the HR and SV (SV is determined by the amount of
Note: The common risk factors to develop atherosclerosis are preload which is affected by renal sodium retention – genetic or intake
hypertension, dyslipidemia, high BP, DM, etc. where patients can have of excess sodium which is not only taken from the common table salt but
subclinical organ damage such as LVH. If there would be a plaque also other sources such as processed and preserved foods so patients
rupture, this will lead to CAD in the form of chronic stable angina or acute are advised for low salt diet and more on fresh vegetables and fruits). This
coronary syndrome such as unstable angina, NSTEMI, or STEMI. The renal sodium retention leads to an increase in fluid volume à
most common cause of death in ACS is cardiac arrhythmia because of increase preload à increase CO. Sympathetic nervous system
the loss of the muscle on account that it became necrotic and fibrotic and activity can be increased by anxiety, stress, apprehension, and intake of
only a very few percentage of normal muscle is contracting so this could caffeine. The increase in this activity can lead to an increase in heart rate
be fatal. If there would be ventricular remodeling (ventricle becomes and contractility à increase CO à increase BP. It does not only
dilated in order to improve the cardiac output), in the long run the patient increase the HR, but also stimulates the RAAS releasing Angiotensin II
goes into heart failure where the hemodynamic abnormality is a reduction (potent vasoconstrictor agent), aldosterone, ADH (increases fluid
in the cardiac output and this is regarded as the end-stage of heart volume). Sympathetic stimulation also is a potent vasoconstrictor that
disease. can increase peripheral vascular resistance. In the choice of anti-
hypertensive treatment, we need to determine what is wrong in the
PROGRESSION FROM HPN TO HF patient. Hypertension is not only classified according to its level of BP:
Common Comorbid Risk Factors
- LVH Recall:
- DM
- Insulin resistance JNC
- Hyperlipidemia - Normal below 120/80
- Renal dysfunction - Pre-hypertension 120/80
o when the creatinine is beginning to elevate we call it - Stage 1 140/90 – 150/99
prerenal azotemia - Stage 2 160/100 or more
- Obesity
- Cigarette consumption European
- Grade 1
Note: Hypertension leads to heart failure. Given a patient with heart failure - Grade 2
symptoms, the most common underlying cause or etiology of heart failure - Grade 3 180/110
is hypertension. It is aggravated by the presence of a previous LVH.
What causes the hypertrophy is a chronic uncontrolled hypertension Isolated systolic hypertension 140 or higher/90 or below
coupled with the presence of DM, pre-diabetes in the form of insulin o Even if it is only the systolic, there is increased rate
resistance, presence of dyslipidemia – increase in the total cholesterol, of strokes and cardiac mortality
LDL, TG, or reduction in HDL. In the presence of these problems, we can
say that there is a mix dyslipdemia in a patient. There could be a renal Classification of BP
dysfunction, obesity, and smoking which could be a risk for further - Masked HTN, white coat HTN, non-dippers, reverse dippers,
atherosclerosis which can cause a chronic uncontrolled hypertension. morning surge, BP variability
- Shows what time of day or night is BP elevated
- Home BP monitoring and ambulatory BP monitoring to see BP
variability
- At high risk to move to a stage of heart failure
Note: How does hypertension link to a major cause of HF?
- Since the basic pathology in coronary artery disease is
atherosclerosis, and hypertension causes atherosclerosis
through endothelial dysfunction, therefore when there is
hypertension, it is very common that we expect that CAD will
also be present. Hypertension leads to LVH
- In CAD, you either have a chronic stable angina, unstable
angina, NSTEMI, and STEMI basing on the ECG
- When there is LVH, there would be further dilatation. MI if not
treated will be allowed to progress to necrosis and fibrinoid
degeneration and only small parts of the myocardium contract
depending on how many arteries are damaged. Fibrosis is
irreversible.
- There would be damage to the LV à CO impaired because it
will not contract effectively due to muscle weakness so the
output is affected.
- In a patient with LVH, at first, the malfunctioning could either be
a diastolic malfunctioning or a diastolic failure and later on a
systolic failure.
o Diastolic is the LV filling. When there is hypertrophy,
Note: The effect of hypertension: it serves to be injurious to the the part of the LV that is thickened are the septum,
endothelium. In the choice of anti-hypertensive agents, we should select a lateral wall, inferior wall, posterior wall, and anterior
drug that is proven to be beneficial to the endothelium to improve wall. It is a muscle with a cavity. If there is
endothelial function such as CCBs, ARBs, ACE inhibitors, and thickening of the wall, the cavity becomes smaller. If
vasodilating beta blockers but the traditional beta blockers only reduces there is normal ventricular filling and systolic
the heart rate without any effect on the peripheral vascular resistance and ejection
is not included in the improvement in the function of the endothelium. It is
prone to endothelial injury because it changes the redox status and
increase the free radicals which can stimulate deoxidation of LDL which
will be engulfed by the macrophages and transform to foam cells then
fibrous plaque formation. There would be a change in lipid metabolism,
there would be dyslipidemia, increase in the total cholesterol, LDL and
decrease in HDL
Recall:
- Statins are good for HDL production but no drugs have been
proven whose intention is to improve the HDL
- CETP inhibitors (Torcetrapib) – it increases the HDL but is not Note: There would be early filling of the ventricle. This can easily be filled
allowed by the FDA to be recommended because the BP also up which is the reason why in patients with hypertension the LA becomes
increases The adverse effect is more than the therapeutic enlarged. Because of chronic hypertension, the blood remains inside the
effect atrium and only some amount of blood can enter through an effective atrial
- Sildenafil – vasodilating agent; intended originally as anti- contractility called as the atrial gallop. In the bedside, an S4 gallop is
hypertensive agent; BP was not significantly lowered but is heard (+) S4. If the volume is low and the myocardium contracts there will
good for erectile dysfunction; do not use this together with a be no problem because it is very strong and there is increased force of
vasodilator because it can promote hypotension contractility.
Endothelial injury will cause a change in the gene expression, cytokines, Recall:
growth factors, adhesion molecules à atherosclerosis. Hypertension - The normal CO is 5.7 L
begets atherosclerosis through an endothelial malfunctioning and injuring o CO = HR x SV
the vessel wall thickness à atherosclerosis. § Normal HR – 60-100bpm
§ Normal SV – 70cc or 80cc
• End-diastolic volume
o If the HR 100 and the SV is 80cc à 8L
In this case, we have a problem with diastole. We have a diastolic

dysfunction. There is a very small capacity so it will not be able to carry
80cc which is the normal value. The volume would also be low. The
normal SV or end diastolic volume is 80cc so it can go down to 40cc in
this case. If the stroke volume is low, the CO is decreased. There will be a
reduction in the CO and reduction in SV.
Diastolic failure or malfunctioning will be symptomatic although there is a

good systolic function. In this kind of condition, there is LV stiffness
because it could not expand. There will be symptoms because the CO is
low. There would be decreased peripheral perfusion, decreased perfusion
of the diaphragm à breathing abnormalities and easy fatigability as a
manifestation. Diastolic dysfunction or relaxation abnormality is a very
serious problem and treatment should be given upon diagnosis.
Atrium becomes bigger: Frank Starling mechanism states that in the

presence of a reduction in the CO, there would be stretching of the
myocardial fibers. When it is being stretched, the cavity becomes bigger
so there would be greater stroke volume and a greater CO. This is the
compensatory state in the presence of a diastolic malfunctioning. Frank § left side of the heart à pulmonary due to
Starling will be mobilized. If there is further stretching, this will lead to reverse flow (backward failure theory). It
thinning of the ventricular wall so the ejection capacity will become lesser goes back to the atrium then back to the
so there will be systolic dysfunction. pulmonary. When there is LV failure, the
right side of the heart is normal and can
In a patient with systolic malfunctioning aggravated by MI or others which contract effectively and supply blood to
have a direct injury to the myocardium (CAD, chronically ischemic the pulmonary. Backflow to the
cardiomyopathy, uremic patients on dialysis à uremic pulmonary à dyspnea, orthopnea,
cardiomyopathy, apparently healthy with attack of viral condition à easy crackles bilateral. Reduction in CO
fatigability, DOB, etc à viral cardiomyopathy, drug abuse which are causes these.
directly injurious to the myocardium à drug-induced cardiomyopathy, o The patient is also cold due to diminished perfusion,
alcohol-induced cardiomyopathy, etc. There are a lot of dilated vasoconstriction, pale, etc.
cardiomyopathy rather than hypertrophic obstructive cardiomyopathy and
should be differentiated. Adrenergic has an effect on the heart and vasculature
- On the heart there is tachycardia and increased myocardial
Patient is very symptomatic because of the decrease in tissue perfusion. oxygen consumption. There is cardiac remodeling,
Because they are very symptomatic, there would be an indication for hypertrophy, and apoptosis worsening of the heart failure.
hospitalization. - On the vasculature, there would be decreased renal blood flow
which is a signal for renin angiotensin aldosterone system
activation. The end result is fluid retention, fluid in the lungs,
peripheral edema worsening of the heart failure
- There is vasoconstriction, increase in the afterload causing
more blood goes back to the right side of the heart and throws
it into the pulmonary. In the vasculature, there is adverse
metabolic effect and worsening of the risk profile and
worsening of heart failure.
Note: Aside from Frank Starling’s, there is a neurohormonal mechanism

where there is an adrenergic system activation and a renin-angiotensin
activation wherein when one is activated, the other is also activated. A
signal for the activation of the adrenergic system or the sympathetic
nervous system and a signal for the activation of the Renin-angiotensin
system is the reduction in the CO. When the CO becomes low, these
hormonal mechanisms where hormones will become mobilized.
There is adrenergic system activation because of the presence of an

increased HR and increased contractility. This will increase myocardial Note: Part of the treatment would be to block the adrenergic. Blocking the
oxygen demand so if the etiology is an ischemic heart disease, there adrenergic would mean using the beta blockers.
would be more imbalance because of the oxygen demand so there would
be further damage to the myocytes which is expressed in the increase in Survival Rates compared with CHF
cardiac markers or cardiac troponins. This serves as a clue of the cause of 1 year 2 years 3 years
the heart failure à myocyte damage due to troponin release and would Breast CA 88 80 72
further decrease myocardial contractility. Prostate CA 75 64 55
Colon CA 56 48 42
Direct cardiotoxicity – alcohol CHF 67 41 24
Decrease in the myocardial contractility causing a decrease in CO causing Note: The survival rate of patients with heart failure was compared to
activation of adrenergic system. So it is a vicious cycle. patients with cancer. With this, it has a worse prognosis than cancer.
Renin-Angiotensin system activation Concepts on the pathogenesis of CHF

- The hormone that is released is angiotensin II which causes - 1970s – contractile performance (digitalis, unloaders)
vasoconstriction. The hormone that causes volume overload o More people are dying from heart failure because
are aldosterone and ADH. drugs only improves contractility (digitalis – old and
- There would be an increase in the wall stretch leading to reliable drug that is still in use up to now; it has a
hypertrophy, increase in the myocardial oxygen demand, positive inotropic effect and anti-arrhythmic effect
decrease myocardial contractility, and the cycle repeats. It is especially for AF)
indeed a vicious cycle. o Unloaders - unload the work load of the heart
- At the bedside, it is recognized by: - 1980s – hemodynamic concept (nitrates, vasodilators,
o Patient is tachycardic hydralazine - which is a good peripheral vasodilator agent but
o Volume overload
with side effects and now only used in patients with eclampsia
– generalized vasoconstriction)
o Unloaders - unload the work load of the heart
o It decreases the end diastolic volume or the
myocardial workload
- 1990s – neuroendocrine model (B blockers, ACE, or ARBs)
o Neuroendocrine model fully understood
o Sympathetic nervous system activation and RAAS
activation
o These drugs have shown good results in HF
patients.
Note: In the pathogenesis of CHF, there is an improvement in the

concept.
Note: The presence of Ang II which is the end result of RAAS stimulation
and NEP which is the hormone secreted with activation of the adrenergic
system or the sympathetic nervous system. This can explain why there is
hypertrophy, apoptosis, ischemia, arrhythmia, remodeling, and fibrosis. Note:
- First assess the LV function by means of ECG.
Pharmacotherapy of CHF o For example, in CAD the best diagnostic modality
would be a coronary angiogram and not the
toponins because these are just markers which can
also be seen in patients with renal dysfunction.
o To assess the overall function of the contractility of
the heart, the echocardiogram is the gold standard
to diagnose or the radionuclide ventriculogram or
nuclear using thalium or sestamibi. This is used
together with stress echo or drug-induced.
- An ejection fraction of less than or equal to 40% is positive.
o The normal ejection fraction is 55% to 77%.
- Signs and symptoms of fluid retention à only diuretics can be
used or digitalis depending on how fast the heart rate is and
titrate to a dry state.
o Crackles, edema, orthopnea, tachycardia à give
diuretic (furosemide and not the slow-acting like
hydrochlorothiazide) à can cause a reduction in
- (+) inotropic agents renal perfusion à AKI
o Na-K ATPase inhibitors o Prerenal azotemia can happen when there is a
§ Digitalis decrease in renal perfusion and renal flow,
o Beta adrenergic agonists creatinine increases. If creatinine is significantly high
o PDE inhibitor and there is no output, emergency hemodialysis
- Vasodilators should be done because it may cause cardio-renal
o Nitrovasodilators failure. As long as the kidney is still functioning, the
o Hydralazine patient can still urinate an appropriate amount of
o Flosequinan urine it is good. During the dry state, then start ACE
- Neurohumoral blockers or ARBs or beta blockers.
o ACE inhibitors
o Angiotensin II antagonist
o Beta blockers
o Endothelin antagonists
§ Potent vasoconstrictor Remember
- Diuretics ü Get the patient to dry weight before treatment
o Loop diuretics ü Keep the patient at dry weight during treatment (continue the
o Thiazides diuretics) spinirolactone
o Aldosterone antagonist
Adverse reactions
Note: Nitrovasodilators are still used for patients with ischemic heart ü Vasodilatory reactions (hypotension)
disease. Those without ischemic heart disease, ACE inhibitors and beta ü Fluid retention and worsening heart failure
blockers are used. ü Bradycardia and heart block(especially when using B-blockers)
How do we approach patients with heart failure? Note: Note for hypotension because diuretics can cause hypotension
which can worsen the heart condition because low BP diminishes
perfusion of the myocardium. Abrupt decrease from high BP to low BP will
cause more stress to the heart. The worst thing that could happen is
complete heart block where there is a need for an emergency pace maker.
o If you are in doubt whether the patient is in failure or
not, use BNP as basis for hospitalization.
THE CHALLENGE TO PHYSICIANS o This is not a gold standard. It is just a marker
- 80-85% of patients with heart failure due to LV systolic o Endothelin and TNF not usually done.
dysfunction should be receiving a B-Blocker
- On top of an ACE or ARB since ACE causes cough, ARBs are LV Ejection fraction
used more. • This is a powerful independent prognostic factor in CHF
- Less than 5% of patients with heart failure are receiving a B- • Those with advanced CHF have an EF of <20% and further
Blocker decrements do not add significant prognostic value
Two year Mortality of CHF patients treated with ACE inhibitors Note: Further decrease will not add to the poor prognosis.
New York Heart Association Classification
Determinants of Prognosis
NYHA CLASS % MORTALITY • Several studies showed that diastolic dysfunction as
determined by Doppler echo have prognostic value
I 10 • A “restrictive” transmitral Doppler pattern (increase E/A,
II 20 decrease deceleration time of E, short isovolumic relaxation
III 30-40 time) was associated with worse prognosis.
o Seen in echo
IV 40-50
Symptoms of CHF
Note: The basis is the presence of cardiovascular symptoms of chest • None: truly asymptomatic or asymptomatic because of
pain, palptation, fatigability, and dyspnea. sedentary lifestyle
o We cannot evaluate patients who are bed ridden
• Dyspnea on exertion
• Decrease exercise tolerance
• Orthopnea( common symptom and most important)
• Paroxysmal nocturnal dyspnea (common symptom and most
important)
• Fatigue or easy fatigability (minor only)
• Edema (minor only)
o Peripheral edema
• Abdominal Pain (minor only)
• Palpitations (minor only)
• Syncope or presyncope
Poor Prognostic factors in Systolic Dysfunction • Embolic events (CNS, Peripheral vascular disease)
• ISCHEMIC CAUSES - CAD • None of the symptoms are specific for systolic ventricular
• ADVANCED AGE - elderly dysfunction
• DURATION OF SYMPTOMS • Dyspnea on exertion and fatigue are early but very nonspecific
• EJECTION FRACTION - low symptoms
• LV < 25% o Because these are also seen in diastolic failure
• RV <35% • Pulmonary disease, obesity, deconditioning and old age
• Hemodynamics: o They easily get tired which could not be heart failure
o Low cardiac index, stroke work index • Paroxsymal nocturnal dyspnea and true orthopnea are
§ Compute for the cardiac index; can be more specific for heart failure but are relatively insensitive
done using echo symptoms.
o High PCWP (pulmonary capillary wedge pressure), o because the clinician may fail to establish it through
PASP (pulmonary artery systolic pressure) interview
o Restrictive filling pattern on 2D echo doppler
Physical findings of CHF
Functional class: • The PE findings are not sensitive and many are nonspecific
- NYHA Class III and IV have bad prognosis • Patients with significant systolic dysfunction may not have any
- Decreased exercise duration of the physical findings and cannot be used to exclude the
- Peak oxygen consumption <14ml/kg presence of systolic ventricular dysfunction.
- 6 minute walking distance <350m
Note: One of our bases for the improvement of cardiac function is a 6- Physical Findings:
minute walk test. The maximum is 30-minute walk every day at least 5 • Hepatomegaly (+) or (-)
days a week would be a good cardiac exercise with improvement of the • Muscle wasting (+) or (-)
cardiac output. • Blood pressure (+) or (-)
High levels of neurohormonal Function

- NEP FRAMINGHAM CRITERIA FOR THE DIAGNOSIS OF CHF
- Plasma renin activity Similar to Jones criteria for the diagnosis of RHF
- Aldosterone Major Criteria
- Angiotensin II 1. PND or orthopnea
- Atrial or brain atrial natriuretic factors 2. Neck vein distention
o Available 3. Crackles (bilateral)
o Similar to troponins 4. Cardiomegaly
o It is just a marker of heart failure 5. Acute pulmonary edema (crackles all over)
o Marker whether a person with difficulty breathing 6. S3 gallop
has to be admitted in the hospital. 7. Increase jugular venous pressure >16cmH2O
8. Circulation time >25s - Atenolol and propranolol are not given. Only those that are
9. Hepatojugular reflex included in the trial can be given.
- Achievement of target dose
Note: When you see a neck vein distended, push the liver and see if it
further distends à positive hepatojugular reflex ACE inhibitors
- Any ACE inhibitors can be given
Minor Criteria ARBs
1. Ankle edema - There are two ARBs that are involved in the trial that can
2. Night cough improve mortality and decrease rate of hospitalizations
3. Dyspnea on exertion o Candesartan
4. Hepatomegaly o Valsartan
5. Pleural effusion - Others are not involved in trials for HF but are involved in HTN
6. Vital capacity decrease 1/3 from the maximum such as losartan
7. Tachycardia (Heart rate >120bpm)
MAJOR OR MINOR CRITERIA

o Weight loss > 4.5kg in 5 days in response to treatment
Note: It could be because of diuretics
DEFINITE CHF
o 2 Major criteria or
o 1 Major 2 Minor criteria
CLINICAL PRESENTATION OF CHF
When heart failure is suspected, the physician should provide an

estimation of the functional class based on the assessment of the patient’s
activity and the limitations imposed on the patient’s symptoms of heart
failure.
CLASS I
o Patients with heart disease but with resulting limitation of
physical activity
o Cardiomegaly, MR, AR but can do ordinary physical
activity without limitation
o Ordinary physical activity does not cause undue fatigue,
palpitation, dyspnea or anginal pain
CLASS II
o Patients with heart disease resulting in slight limitations of
physical activity
o They are comfortable with rest
o Ordinary activity results in fatigue, palpitation, dyspnea and
anginal pain
CLASS III
o Patients with heart disease resulting in marked limitations of
physical activity
o They are comfortable at rest
o Less than ordinary physical activity result in fatigue, palpitation,
dyspnea and anginal pain
CLASS IV
o Patients with heart disease who are unable to carry on any
physical activity without discomfort
o Symptoms of cardiac insufficiency or of angina are present at
rest
Beta blockers in CHF

- This effect becomes apparent in 3-6 months and on average,
patients who receive beta blockers have an increase of about
5% in their EF.
- Improvement in diastolic function may also occur after
treatment with beta blockers.
Trials
Beta blockers
- There is a deficient effect on mortality
SAMPLEX 16. Laboratory Test to prove the cause of patient’s HF
à Troponin
1. 36 yo,with hx of hypertension, BP 150/100 sitting,refused to take 17. what to request to know prognosis of patient in
meds heart failure à Nt pro BNP
2. Apex beat is at 5th ICS LAAL, HR 110,with incr s1 =, positive in s4 18. Most common etiology for this px: (case)
gallop A. Valvular
1stchoice of meds beta blocker B. Chronic uncontrolled
3. 50 y/o female, admitted d/t dizziness. 5 yearshypertensive and C. Cad only
diabetic. PE: bruit on the neck. What important diagnostic test will D. Cad and hpn
you request? 19. The best treatment to relieve the dyspnea?
A. Brain CT Scan àfurosemide
B. ECG 20. Which drug will relieve the symptoms of Heart
C. Carotid Duplex Scan Failure but will not prolong patient's life
D. 2D echo Doppler A. Digitalis & Diuretics
4. 64 y/o female, chronic uncontrolled HPN for 10years, taking 3 B. ACEI
antiHPN drugs,bilateral palpable kidneys C. ARB's
A. Renal artery stenosis D. BB
B. Polycystic kidney disease 21. Diagnostic test of HF?-
C. Pheochromocytoma a. 2D ECHO
D. Abdominal aorta aneurysm b. NTPROBNP
5. A 28 year old hypertensive male with complaintof palpitation. He 22. Diagnostic test to confirm ACS
has history of asthma since childhood. Whatmedication will you Coronary Angiogram
give? 23. What is the treatment for px with dvt? Case based
A. Beta blocker a. comaudin+ warfarin *
B. VD beta blocker b.low molecular weight heparin
C. Non-DHP Channel blocker 25. Best treatment for acute coronary syndrome:
D. ACE A.LMWH
6.52yrs old, with htn , comb therapy with three antihypertensive B. Clopidogrel
drugs, + bruit in renal artery C. Statin
Secondary hypertension D. Revascularization
7. Left sided hemiplegia,+ cerebral hemorrhage 26. Case. 40 y/o male, businessman, no previous
Htn Emergency illness, complains of heaviness in the legs,
8.40 years old with sudden LOC, Bp: 210/130, with papilledema relieved temporarily by elevating the legs and
Malignant htn walking. After going somewhere, complains of
9. patient was admitted due to BP of 200/120, HR:68bpm, AB located bilateral swelling in thigh, was brought to er. Left
at the 5th ICS anterior axillaryline, increased s2 , +s4, no murmurs, lower extremities: ankle-21cm; calf-38cm; thigh-
noarrhythmia, patient is asymptomatic 50cm
A. hpn urgency Right lower extremities: ankle-24; calf-42; thigh-
B. hpn emergency 56cm. Ongoing impression: DVT. What test will
C. malignant hpn you do?
D. secondary hpn A. D-dimer
10. 45 yrs old, female, severe DOB, BP: 210/110 ;HR: 110, + B. CT-Scan with contract of LE
cardiomegaly, + bilateral crackles C. MRI
A. hpn urgency D. Venous duplex scan of LE
B. hpn emergency E. Venography
C. malignant hpn 28. Working dx : pulmonary embolism. What will be
D. secondary hpn the non invasive diagnosis?
11. Patient with DM, HPN BP of 180/110 with STElevation at AVL, v3- A. Cxr
v6 and a reciprocal change atII, III and AVF. Troponin ( - ) B. v/q scan
A. CSAP C. MRI with contrast
B. Unstable AP D. Spiral ct with contrast
C. STEMI 30. In virchows triad, which medical condition is due tovenous
D. NSTEMI stasis?
12. Si patient nag Jo-Jogging à + Chest pain. A. Vasculitis
Relieved by rest: B. sepsis
A. CSAP C. Cancer
B. Unstable AP D. Hyperviscocity
C. STEMI E. Estrogen use
D. NSTEMI
14. Sudden onset, 46 yo meat vendor. Deep t wave
inversion, elev v1-6, avL, I
A. Stable
B. Unstable
C. Stemi
D. Nstemi
15. + T Wave Inversion, ( - ) Trop I
A. CSAPI
B. Unstable AP
C. STEMI
D. NSTEMI
SAMPLEX
12. 61 y/o male with orthopnea, fatigue and dyspnea, diabetic with
1. Best antihypertensive with 30 year old patient with asthma and insulin treatment. With dilated ischemic cardiomyopathy.
heart rate of 110-120 bpm a. Stage A
a. ND CCB b. Stage B
b. D CCB c. Stage C
c. B Blocker d. Stage D
d. ACEI 13. Gold standard for the diagnosis of heart failure
2. Female hypertensive, bilateral kidney palpable, abdominal bruit a. ECG
a. Renal artery stenosis b. CXR
b. Polycystic kidney disease c. 2D echo Doppler
c. Hyperaldosteronism d. Pro BNP
d. Pheochromocytoma 14. NC 30 y/o, call center agent, with no previous medical illness
3. The patient had ECG and cardiac biomarkers, what other test complained of daily bilateral leg heaviness while at work.
the patient need immediately to detect CAD? Elevating the legs or walking would temporarily relieve the
a. 2D echo symptoms. While playing basketball, he tripped and fell landing
b. Coronary angiography on his leg. He was brought to the hospital for treatment. The
c. Chest X-ray leg X-ray was negative for fracture. He was sent home with
d. ____ NSAIDs. 3 days later the patient noticed the entire left leg is
4. A 28 year old female is hypertensive with a bp of 140/100- swollen. He was brought to ER for evaluation and treatment.
160/100. The hypertension had been diagnosed 4 years ago. On measurement, the right ankle is 21 cm, calf is 38 cm and
Which antihypertensive drug is best for a 28 year old fertile thigh is 50 cm. on the left lower extremity the ankle measures
female? 25 cm, calf is 44 cm, thigh is 54 cm. Wells score is 4. Your
a. CCB working impression is DVT. What initial test will you do next?
b. B blocker a. Venograph
c. ACEI b. D-dimer
d. ARBs c. Venous duplex scan of LE
5. 36 y/o male, non HPN, 5cm ST elevation at lead I,AVL, (sorry d. CT scan of LE
di ko maalala masyado) troponin of 150ug/L 15. Non invasive procedure to rule in pulmonary embolism
a. Stable angina Answer: VQ scan
b. Unstable angina 16. Confirmed pulmonary embolism in left lung, what is the best
c. NSTEMI treatment of choice?
d. STEMI a. Direct catheter thrombolytics
6. A 62 y/o male was admitted due to severe progressive chest b. Systemic thrombolytics
pain. He is hypertensive with COPD because of chronic c. --------
smoking. BP is 160/100. ECG revealed sinus tachycardia with d. LMWH and dabigatran
tall and peaked T wave. Troponin T is negative.
a. Chronic stable angina pectoris
b. Unstable angina pectoris 1. Endocarditis prophylaxis is indicated in the following:
c. NSTEMI a. Prosthetic heart valves
d. STEMI b. Previous infective endocarditis
7. A 60y/o patient complained of severe progressive chest pain. c. VSD
BP is 180/110mmHg. ECG revealed LBBB, (+) Troponin T. d. HOCM
a. Chronic stable angina e. All of the above
b. Unstable angina 2. Most common site of metastasis in the heart
c. NSTEMI a. Pericardium
d. STEMI b. Myocardium
8. 70 y/o male, (+) DM, (+) HPN, continuous? Severe chest pain, c. Endocardium
ST depression at lead II, III, V3, V4, V5, AVL?, (+) Troponin d.
after 6 hours. 3. Treatment of choice for ACS
a. Stable angina Answer: CABG
b. Unstable angina
c. NSTEMI
d. STEMI
9. Which is a contraindication for a thrombolytic therapy in ACS?
a. CVA hemorrhage
b. 180/100mmHg
c. ST elevation ……..
d. ST elevation ……..
10. This is the common cause of death in acute coronary
syndrome.
a. Heart failure
b. Pneumonia
c. Ventricular Fibrillation
d. Sinus tachycardia
11. A 40 y/o male, athletic, hypertensive, but can do regular gym
activities without any cardiac symptoms
a. Stage A
b. Stage B
c. Stage C
d. Stage D

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Medicine II

CARDIOLOGY Worldwide the level of BP control is far from ideal

Note: The data is almost the same for both.

Prevalence of hypertension in adults >18 years old

Note: The nationwide registry showed that from 11% in 1992 à

Definitions of HPN by Office and Out-of-office BP levels

Note: There are different values! We say that there is hypertension

BP Variability over different time periods has been evaluated

Mean Determinants of Increase in BPV

Determinants and Prognostic Relevance of BPV

The rapid rise of BP in the morning is one of the critical risk

Note: S1 and S2 loudness can be affected by the heart

ECG: reveals an axis of -30 degrees with borderline voltage

Note: There is already evidence of subclinical organ

Note: Atherosclerosis is a disease of the blood vessel wall and not

What factors would affect endothelial dysfunction?

Note: Hypertensive treatment strategy: there should be a broad

Choice of antihypertensive therapy: ESH/ESC 2007

Note: Diabetes and Dyslipidemia are not included because they

The projected mortality

Note: When we treat hypertension, always tell the patient that we

Pathogenesis of Atherosclerotic Plaque: endothelial dysfunction and Ischemia

Unstable AP Physical Exam in Chronic CAD

Non-invasive Stress Testing Nuclear Gamma Camera

Non-pharmacologic therapy of IHD

Post MI Risk Assessment

Burden of Acute Coronary Syndrome

ACUTE CORONARY SYNDROME

Case: Patient has ischemic discomfort (discomfort in the region of the

Note: The kind of ACS depends upon electrocardiogram and the

Note: To differentiate between the two, it is based on the biochemical

- Posterior wall is represented by reciprocal changes

What do we look for in the ECG?

PATHOLOGIC and ECG changes in STEMI

- ST segment depression at V4, V5, V6

ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

- ST segment elevation indicative of injury

Note: This is a typical ST segment elevation because there is an acute

QRS Complexes in Infarction

Note: Q wave signifies that there is already a fibrosis (lifetime)

Location of infarction Leads showing primary

Subendocardial à symmetrical T wave inversion (diffuse ischemia)

Anteroseptal Wall STEMI

There is occlusion of a branch of the left anterior descending coronary

(+) Q wave – thrombolysis cannot be done anymore

There is occlusion of the left anterior descending coronary artery, where is

PCI (percutaneous coronary intervention) with possible angioplasty or

Results should be correlated clinically

Acute coronary syndrome/ acute myocardial infarction Algorith

ACUTE CORONARY SYNDROME

Note: End result of these is that the myocardium becomes ischemic or

Optimum medical management can be given: High risk subgroup:

Contraindications of Beta blocker :

Contraindications of Fibrinolytic therapy (streptokinase, Tissue

In short the patient needs to undergo REVASCULARIZATION

Primary PCI selected

Fibrinolytic therapy selected

B. ST depression/ dynamic T-wave inversion (High risk UA/ non-

Absolute contraindications to beta blocker therapy