Cardiology

Ischemic heart disease

It's an imbalance between demands and supply. Most common cause of decrease
supply is atherosclerosis. Other causes are thrombosis, embolism, spasm, arteritis and
coronary artery dissection

Atheroma is insidious and its precursor is fatty streak.

Risk factors
 Modified risk factor
o Hypercholerstrolemia (increase LDL and decrease HDL to level
<40mg/dl
o Tobaco smokers are 2 times higher than non smoker to develop IHD.
Secondhand or passive smoking are at higher risk to develop IHD. The
risk returns to level of non-smoker after 2 year cessation of smoking
o HTN increase risk even at level above 110/90
o DM.
o Obesity: increase risk of IHD via increasing BP, cholesterol and
triglycerides with decreasing HDL
o Physical activity: it increases HDL and control DM as well as decrease
BP
o Stress lifestyle. It's thought it increases likelihood to become smoker
and less active

One is diabetic hypertensive and has hypercholesterolemia. The risk of IHD is

3X3X3= 27 times more to develop IHD than normal patient !!

There is compelling evidence that tight control of BP, blood glucose and cholesterol
will decrease morbidity significantly !!

 Non modified risk factor

o Age
 Male >55
 Female>65
o Family history, first degree relative
 Male <45
 Female<55
o Sex: men >women, because endogenous estrogen has protective effect.

Most common risk factor is HTN. Worst risk factor is DM (even if it's controlled).
Rapid improvement after solving it is smoking (return to non smoker after 2 years of
cessation).
Ischemia can lead to

 Ischemic symptom (pain, SOB, sweating, nausea and vomiting)

 ECG changes
 Reduce uptake during myocardial scanning
 LV regional or diffuse dyskinesia (on echo)

Stable angina
It's chronic coronary syndrome. Angina means chest pain, typically characterized via

 Pain suggesting ischemia

 Exaggerated by exercise
 Relief by rest or nitroglycerine

If only 2/3 atypical angina.

Note, esophageal spasm improves with nitroglycerine and GERD deteriorates with
nitrates. So, response to nitroglycerine by itself is not enough for diagnosis of
coronary disease

Do not forget that diabetic can manifest in angina pain just diffuse weakness+
breathlessness.

What does stable mean?

Stable angina (lasts5-15 minutes) means that angina does not occur at rest. It does
occur once we do fixed level of exercise or due to increase level of demand due to
other causes (anemia, hypovolemia, thyrotoxicosis and infection). So, it's demand
ischemia. However, in ACS, it's supply ischemia mainly (however both are
present).

ECG  ST depression during attacks. ST elevation in prinzemetal angina and

unstable angina. ST elevation means transmural MI, while ST depression means
ischemia

Stress test (traedamill test) for confirmation stable angina, determine severity and
assess treatment of IHD. +Ve if becomes blood pressure decrease more than 10
mmHg or ST depression >2 mm or both present. ST elevation development  stop it
at once. The earlier of ECG changes or decrease in BP more likely to be significant
decrease likelihood to be false +ve. However, it has high false +ve and false –ve
result. False +ve occurs mainly in young or stenosis <50%. So, it increases accuracy
with increasing likelihood to have IHD.

After determining the severity, if it was sever enough  do PCI increase blood
supply to heart increase functioning of heart  increase quality of life.
It can also be used to assess the effectiveness of treatment after surgery for example.

If patient can not run  give dobutamine (increase HR) or adenosine/ dipyridamole
(due to steal phenomenon)

It can be used after ACS but at low level of exercise just to know the functional
capacity and knows ECG changing during exercise. However, it's less commonly used
and we go in ACS toward PCI.

Stress test is CI in case

 There is jeopardy to patient like in case of post ACS (unstable angina-

STEMI), severely uncontrolled HTN, aortic stenosis and HOCM and aortic
dissection.
 There is an abnormality in baseline of ECG like LBBB, LV hypertrophy and
apply pacemaker. In this case, stress test is difficult to interrupt, so use nuclear
stress test (has higher sensitivity and specificity, in which we give nuclear
injection prior and after exercise, if area uptakes only prior exercise 
ischemia during exercise. If not uptake even prior exercise dead tissue.
 Patient on B blocker (blunt tachycharida during exercise) or digioxin (it causes
ST depression). These drugs must withheld 5 days prior stress test.

We can do Echo with stress test to see ventricular dyskinesia during exercise.

Indication for cardiac catheter

 CI to stress test
 Non invasive test are inadequate for diagnosis
 To determine after stress test to do PCI or bypass surgery. Do bypass surgery
in case
o Left main coronary artery involvement
o 3 vessels or mores occluded
o 2 vessels but diabetic (DM increase risk of stent stenosis)
o More beneficial although more risky in case of low ejection fraction

Most of stable angina do not need PCI or cardiac bypass (used once function of heart
is markedly decrease). However, PCI most commonly used in ACS
Acute coronary syndrome ACS
It's a syndrome ranges from unstable angina to ST elevation MI. Some says that
sudden cardiac death is part of ACS. It's one of most common cause of emergent
admission to emergency department.

MI means presence of cardiac biomarker + evidence of ischemia

What are the evidences of ischemia ??

 Pain suggesting ischemia (squeezing or burning pain from umbilicus to left

jaw)
 ECG changes ST elevation or depression, new LBBB and new Q waves
 Echo finding like dyskinesa wall

So characteristic of unstable angina is

 New onset. If lasted stable for 6 monthsbecomes stable

 Develops at rest or worsening
 Does not respond to nitroglycerine

Pathogenesis of ACS

The cornerstone of ACS is rupture of atheroma

Atheroma occurs due to LDL deposition subendothelialy. It consists of lipid and

inflammatory cells with fibrous cap.

There are two type of plaques:

Rich of Ca stable (low risk for rupture or laceration)

Rich of lipid vulnerable atheroma risk of rupture.

Rupture, ulceration or fissuring of atheroma  exposing of subendothelial to blood

 activates platelet  release thrombaxane A2(vasospasm), glycoprotein IIa/IIIb and
ADPaggregation of platelet.

If thrombus occludes vessels totally  STEMI. It's rich of fibrin, so thrombolytic can
solve it. If partially  unstable angina or NSTEMI (thrombus is rich of platelet, so no
useful to give thrombolytics

STEMI on ECG any one of the following

 ST elevation >2mm in at least 2 chest lead (V1-V6)

 ST elevation >1 mm in at least 2 limb lead (I,II,III, avF, avL and avR)
 New LBBB
U do not need to wait increase cardiac biomarker for diagnosis of STEMI

Unstable angina (also called crescendo or preinfarction angina) and NSTEMI

differentiated by absence of cardiac biomarker in forward and presence in latter
after 12-24 hours after onset of symptoms.

NSEMIsubenodthelial MI. STEMI transmural MI

1/3 of unstable angina has thrombosis. 50% of cases in absence of treatment

progress to MI.

NSTEMI  ST depression >0.5mm or T wave inversion >2mm. However, 50% has

normal ECG

Unstable angina or NSTEMI can be high risk or low risk

High risk features

 Hemodynamic unstable
 LV ejection fraction <40% or syncope
 Prior PCI or CABAG
 Elevated cardiac biomarker
 Chronic renal failure
 DM
 Sustained ventricular tachycardia
 Repetitive chest pain

Other causes for ACS

 Coronary spasm like variant angina (in men, associated with atherosclerosis,
while in women are not) and cocaine abuse. They cause ST elevation
 Coronary embolus from atrial or ventricle thrombus and atrial myxoma
 Vasculitis like Kawasaki, polyarteritis nodosa and SLE
 Hyper-coagubility state either
o Congenital like
 factor V leidan mutation
 Protein C or S deficiency
 Anti-thrombin mutation
o Acquired like anti-phsopholipid anti-body
 Polycythmia

Note, in variant angina, spasm is triggered via ergonovine. If does  confirm

diagnosis. As a doctor, we see ST elevation MI, we can not know wheter it's variant
angina or STEMI. However, we treat it as STEMI. We know it was not after doing
coronary angiography.Variant angina treated via Ca channel blocker like amplodipine
and nifedipine. B blocker is CI.

Complication of ACS
 Electrical complication
o Premature beat either atrial or ventricular. No need for management
o Bradycardia: sinus/ atrioventricular junction and idioventricular.
Treated with atropine
o Tachyarrhythmia either
 Supra-ventricular: like atrial tachycardia and atrial fibrillation
 Ventricular like ventricular tachycardia and ventricular
fibrillation.
 Pump dysfunction
o Contractile weakness either in LV and RV
o Mechansical disruption like MR or ventricular wall rupture
o Electromechanical dissociation
 Post-infarction angina after thrombolytics treated with cardiac bypass
surgery
 Preicarditis (called dresseler's syndrome)  NSAID, if failed  steroid.
 Thromboembolism either from Atrial fibrillation or prolonged immobilization
 Sudden cardiac death due to ventricular fibrillation (most commonly) or
ventricular tachycardia

History
Most common presentation is chest pain mainly retrosternal and squeezing in nature.
Most common associated symptom is sweating. Can be associated with SOB and
nervousness especially in case STEMI. In inferior MI, there is nausea, vomiting,
diarrhea and hypotension due to vagal irritation

MI pain lasts more than 20 minutes and can last for few days + does not respond to
nitroglycerin.

Ask about DM,HTN hyperlipidemia and renal disease.

Do not forget that elderly with DM can present with only SOB and nausea without
chest pain.

Chest pain tearing in nature and radiate to the back  aortic dissection

Pleuratic chest pain  PE, pneumonia, Pneumothorax and pericarditis

Vague chest pain with flu like symptom  Heart failure, think of myocarditis mainly
coxsacke virus.
Physical examination
No specific signs for ACS

Do vital signs. BP in both arms, if difference >20 mmHg  think of aortic dissection.
Fever  think of esophageal rupture or infection. Hypotension  cardiac shock or
large PE

Look for cause (signs of hyperlipidemia, which is corneal arcus <55 year old, if above
senile arcus and xanthelassma)

General appearance

Rule out other causes

 Chest wall tenderness costchondritis or teitz syndrome (in latter there is

other joint involved)
 Aortic dissection 50% develops AR
 Inferior MI rupture of papillary muscle MR with bradycardia
 Look for paradoxical split (P2 prior A2)  either LBBB or severly weakened
LV
 Chest auscultation for pneumothorax and pneumonia
 Check lower limb for edema and calf tenderness

Investigation
For confirmation

ECG within 5-10 minutes. Do your best to get older ECG to compare. If u can not 
consider everything is new.

 Inferior MI: II, III and avF. It's due to right coronary artery involvement
 Anterior MI : V2-V4: It's due to left anterior descending artery
 Lateral MI in I, avL, V4-V6 due to LAD
 Posterior MI in V1-V2 due to posterior descending artery.

Note, peaked T wave and ST elevation appears immediately and last for 24 hours and
6 weeks respectively. However, long Q wave>0.4 seconds appears after several days
and lasts for year (sometimes for life). T wave inversion occurs within 6-24 hours and
lasts for months up to years.

Cardiac biomarker (do not wait in case ST elevation or new LBBB)

 Ask For troponin I (Troponin T elevates in renal failure and polymyositis or

Dermatomyositis). Peaks within 24 hours and lasts for 2 weeks.
 Ask for creatin kinase (CK-MB) only in case of re-infarction within 2 weeks
because it returns to normal after 3-4 days (peak is 12-24 hours). It's found in
 skeletal muscle, brain, kidney and lung. If troponin is +ve and –ve CK-MB 
minimal infarction.
 First things arise is myoglobin. It has high –ve predictive value if –ve after 4
hours.

Note, elevation of cardiac enzyme can not detect infarction size

Elevation of troponin with normal CK-MB  minor re-infarction.

Echo

For detection risk factor

Fasting blood sugar

Lipid profile mainly HDL and LDL

Kidney function test (can be cause, affect management like drug excretion and
evaluation prior contrast)

For complication

Echo, CXR and cardiac catheter

Treatment
 Aspirin 300mg plane (not coated, for rapid absorption) and chewed (absorbed
from bucal mucosa). 75-325 mg is anti-platelt. If >350 mg  anti-
inflammatory effect)
 Clopidegrol (300 mg , give 600mg if u would like to do percutenous coronary
intervention). Other options like ticagrelor or prasugrel Avoid Clopidegrol in
case u would like to do emergent cardiac bypass surgery. Must be stopped 5
days prior cardiac bypass surgery
 Pain relieving medication (morphine +nitroglycerine CI in hypotension and
stops once develops hypotension, inferior MI and RV failure- characterized
via clear lung with raised JVP and hypotension)
 Anti-thrombin medication like unfractioned heparin 60IU/kg or subcutenous
enoxparin (LMWH). We aim INR to be 1.5-2
 We use Glycoprotein IIb/IIIa inhibitor like abciximab, tirofibian or eptifibatide
in case we would like to do invasive strategy (like PCI or bypass cardiac
surgery). They cause immune mediated thrombocytopenia, so monitor platelet
 after 24 hours of Gp IIb/IIIa admission . They are better than combination of
aspirin and heparin. If we use it with giving fibrinolytic  risk of bleeding.
 Statin High dose even in no history of hyperlipidemia
 B blocker / Ace inhibitor within 24 hours

Specific for Unstable angina or NSTEMI

In case of presence of high risk  do coronary angiography within 48 hours and do
PCI or CABAG depending on case. If it was low risk  do stress test (submaximal
after 4-7 days and maximal after 4-6 weeks of infarction) and myocardial perfusion
scan to know residual ischemia.

Specific ST elevation MI
 Thrombolytic within 30 minutes once enter emergency. How do we know that
thrombolytic acts ??. within 90 minutes, there should be
o Decrease pain
o Decrease ST elevation via 50%
o Idioventricular rhythm
 PCI within 90 minutes

Note thrombolytic or PCI should be done within 12 hours from starting presentation,
if after 12 hours  do not except there is hemodynamic instability.

We always go forward PCI if it's present (better outcome and less death due to MI). If
it was not  give thrombolytics (t-PA or streptokinase) in case of absence of
thrombolytics. Most common used is t-PA, because streptokinase(from bacteria can
induce antibody formation against it decrease its efficacy in next time).

The earlier of treatment  better outcome, especially earlier than 12 hours from onset
of symptoms.

CI for thrombolytic

 Absolute CI
o History of intracranial hemorrhage
o Within 3 month history of ischemic stroke
o Significant closed head trauma within 3 months
o History of bleeding diathesis. Or active bleeding right now
o Suspected aortic dissection
 Relative CI
o Major surgery within 3 weeks
o Within 4 weeks internal hemorrhage
o Active peptic ulcer
 o Prolonged cardio-pulmonary resuscitation
o History of ischemic stroke more than 3 months ago
o Severely uncontrolled HTN

We precede to cardiac bypass surgery (It decreases mortality in ACS) if

 PCI is failed to relieve pain or still hemodynamic unstable called post

infarction angina.
 Recurrent ACS even with medication

There are other types of coronary interventions

 Rescue PCI, done in case of failure of thrombolytic. Question, if thrombolytic

fails after 90 minutes, can we save muscle ??
o Pain means viable tissue
o Thrombolytic cause recanalization of thrombus. If failed, it does not
mean that it's totally failed (some opening occurs)
o However, there is risk to loss muscle
 Facilitated PCI, give half dose of thrombolytic and transfer to unit has ability
to do PCI.

Long term medication

Aspirin, clopidegrol, nitrate ,B- blocker, Ace inhibitor, statin (even with normal lipid
profile, but not given if ACS is not due to atheroma rupture) and warfarin in case of
atrial fibrillation to avoid thrombus formation. Drugs in red decrease mortality in
ACS

Do not forget to tell them to avoid sedentary life style, smoking and drinking alcohol
if they present.

Indication of clopidegrol (plavix)

 Intolerance to aspirin
 Given in ACS with aspirin
 Post fibrinolytic for a month or post PCI with aspirin for 9-12 months.
Congestive heart failure
It's an impair of cardiac muscle performance either in systolic or diastolic leads to
neuroendocrine stimulation as a compensatory mechanism secondary to decrease
cardiac output (volume ejected by blood per minutes, CO= SV X HR). 70% of cases
due to IHD.

It's divided clinically into

 Systolic (decrease ability of pump to contract, so low ejection fraction <52%)

Vs diastolic ( inability of muscle to relax, so increased EDD).
 Right sided heart failure (lower limb edema, hepatomegaly, cyanosis and
raised JVP) Vs left sided heart failure (pulmonary edema , paroxysmal
nocturnal dyspnea, orthopnea and fatigue).
 Acute (progressive within 2 weeks in patient with free history of heart failure)
Vs Chronic (a known case of heart failure)
 High cardiac output, which is hyperdyanmic circulation characterized with
wide pulse pressure (>25 mmHg) occurs in anemia, thyrotoxicosis, PDA and
AV shunt. Low cardiac output.
 CHF means there is biventricular failure.
 Compensated Heart failure is heart failure with decreased EF or increased
EDD but asymptomatic. Once becomes symptomatic  decompensated HF.
Decompensated also means worsening of baseline. Usually in decompensated
heart failure, there is a precipitating factor place additional burden to cardiac
muscle like anemia, infection (especially pulmonary infection), arrhythmia
(especially atrial fibrillation), excessive dietary salt intake, thyrotoxicosis and
uncontrolled HTN

Pathophysiology
The key sentence is decrease cardiac output  sympathetic and rennin-angiontensin –
aldestrone activation (angiotensin II has vasoconstrictor  increase after load and
causes aldesterone release Na and water retention increase preload. The end
result is remodeling.

In sympathetic B1 increase HR and contractility and conduction. Via alpha I

vasoconstriction.

So, giving B-blocker (bisoprolol, metaprolol and carvidolol) or hydralazine 

decrease remodeling.

In RAA system, there is vasoconstriction and increase volume. So, giving ACE
inhibitor, angiotensin receptor blocker or spirnolactone  decrease remodeling.
These compensatory mechanism causes remodeling.

CHF causes tachycardia. If patient has bradycardia, what does it mean?? It means
either

 Patient takes B blocker. If not,

 Pre-cardiac arrest stage

Etiology
Systolic heart failure

 Myocardial disease like IHD( 70% of cases), inflammatory like myocarditis

and inherited dilated cardiomyopathy. IHD abnormal angiography, while
inherited cardiomyopathy has normal angiography. X-syndrome IHD with
normal angiography occurs in elderly mainly in women.
 Valvular disease mainly regurgitation like AR and MR. late stage of untreated
AS can cause Systolic failure. MS is a protective factor for LV.
 Drugs like alcohol and chemotherapy. This is why patient who is described
chemotherapy must do echo.
 Endocrine like hyperthyroidism and anemia

Diastolic heart failure

 Valvular or obstructive lesion like HOCM and AS

 Pericardial effusion (involving temponade) and pericardial fibrosis
 DM and HTN
 Infiltrative disease like sarcoidosis, amylodosis and hemochromatosis

We need echo for diagnosis and to classify heart failure (either systolic or diastolic)

History
Try to know whether left, right or CHF.

Try to know the severity (NYHA classification for CHF)

 I no limitation in daily activity

 II, minimal limitation in daily activity
 III, sever limitation in daily activity but no symptoms at rest
 IV  symptoms present at rest.

Rule out other causes for dyspnea

Examination
Look for sign of CHF like crepitation, raised JVP, hepatomegaly and lower limb
edema with cyanosis.

Look for causes like murmur or systemic involvement like amylodosis and sarcodosis

Look for complication like hypotension or irregular pulses or cyanosis. Decrease

urine output is also a complication.

Investigation
Investigation for confirmation:

First step  CXR

 Cardiomegaly
 Pulmonary edema
 Kerly B line
 Pleural effusion

If u do not see cardiomegaly does not rule out HF because it occurs in acute HF

Causes of acute HF  ischemic MR, HTN and myocarditis

Second step  echo for confirmation and to know is it systolic/diastolic (both same
presentation but differ in etiology and management). Moreover, look for cause
(valvular lesion or inflammation in which we see global dyskinesia) and complication
(dilation or thickness of ventricular wall)

Brain natriuretic peptide (BNP) a test rarely used. We use it when we are not sure
whether symptoms are secondary HF or other causes mainly respiratory origin. If it
was low  for sure not heart disease.

Investigation to know the cause like

CBC for anemia, infection and platelet count (affect management)

Cardiac enzyme and fasting blood sugar

ECG (hypertrophy, arrhythmia and conduction problem) and serum electrolyte

TSH, KFT (can be cause, complication and affect management) and LFT(albumin and
PT). PTT is not part of LFT

Echo and ECG for complication.

Management
Non-pharmacolgic intervention like increase controlled exercise, stop smoking and
alcohol intake, limit Na and fluid intake(1.5-2 L) and decrease weight.

Pharmacological management

In diastolic, no drug improves survival rate, just to improve quality of life like
diuretics, B blocker or Ca channel blocker. Digoxin is not used in pure diastolic
failure. Excessive diuretic and vasodilator worsen diastolic failure.

In systolic, there are medication that improves survival like

 B-blocker (metorpolol, bisoprolol and carvidolol)

 Ace-inhibitor (enalapril, captoapril and lisinopril)
 ARB like valsartan, losartan and candesartan
 Aldesterone antagonist like: spironolactone (has estrogen and androgen
effectgynecomastia) and epleronone (no estrogen or androgen activity, so no
gynecomastia). Both causes hyperkalemia
 Hydralazine (reverse vasoconstriction of alpha 1 activation) and nitrates
(given combined)

First line drug is Ace inhibitor/ B blocker . Preferred to be combined in absence of CI

CI for ACE inhibitor

 Renal failure
 Bilateral renal artery stenosis (because it decreases GFR via dilation of
efferent)
 Angioedema

CI for B blocker

 Cardiac conduction problem

 Bradycardia
 Hypotension

In renal failure use Nitroglycerine +hydralyzine

If patient symptomatic add loop diuretic like furosemide

If still symptomatic  add spirnolactone/eplerenone CI in renal or hepatic

impairment. They reduce by 30% hospitalization and death. If u use it, u should
monitor K level

If still symptomatic + HF class is III or IV or associated with atrial fibrillation 

give digoxin (does not improve survival rate, just increase quality of life and decrease
hospitalization)
If patient has dilated cardiomyopathy with EF <35%  apply implanted cardioverter
defibrillator (ICD). It does not improve quality of life, it just prevent arrhythmia
because most common cause of death in CHF is arrhythmia.

If still symptomatic or has QRS >120mSeconds apply cardiac resynchronization

therapy-defibrallator(CRT –D), which act as a pacemaker, prevent arrhythmia. It
improves failure symptom in case of failure of anti-CHF medication. . It has 3 leads in
RA, RV and LV. CRT also called bi-ventricular pacemaker without defibrillation
(CRT-D is much more expensive than CRT)

Indication of CRT-D

 Failure of anti-failure with EF<35

 LBBB (long QRS complex>120m Seconds

Failure of CRT-D occurs only 30% of cases (70% responds well to CRT-D). If
failed consider cardiac transplant if meet the criteria (most important point is
that it's provided to young patient)

Do not forget that NSAID decrease renal flow fluid retention and exacerbates CHF.

In dilated cardiomyopathy with EF<35%  (ICD). If QRS >120mSecond  bi-

ventricular pacing (CRT without defibrillator)

Some side effect

 Ace inhibitor
o Non-productive cough (solved by giving ARB)
o Rash
o Angioedema (stop it and ARB can not used too)
o Protinuria
o Taste disturbance
o Renal failure
 Nitroglycerine
o Headache
o Postural hypotension
o Methemoglobinemia
 Hydralazine
o Drug inducing SLE, especially in person with slow acetylation process
o Rash and fever

Some diuretics action and side effect

 Thiazide like chlorothiazide and hydrochlorothiazide, in which they inhibit

NaCl co-transport in distal tubule. They cause hyponatermia, hypokalemia,
 hyperuricemia and hypercalcemia. Allergy, agrnulocytosis, leukopenia and
metabolic alkalosis may develops
 Loop diuretics like furosemide, bumetanide and ethacrynic acid, in which they
inhibit Na/K 2Cl co-transport in thick ascending loop of henle. They cause
hyponatermia, hypokalemia, hyperuricemia and hypocalcemia. Moreover,
they has oto-toxicity and risk of interstitial nephritis. Leukopenia and
metabolic alkalosis can develop
 Potassium sparing diuretics like spirnolactone and eplerenone via inhibiting
aldersterone. They cause hyperkalemia.

Digoxin mechanism of action is inhibition of Na/K pump increase intracellular Na

and decrease exchange of Ca with extracellular Na  increase Ca intra-cellular 
increase force and velocity of contraction. Do not forget that digoxin competes K to
bind Na/K pump, so in case of hyperkalemia  decrease its efficiency, while in hypo-
kalemia  increase risk of digoxin toxicity.

Indication of digoxin

 Atrial fibrillation
 SVT
 CHF in III-IV stage

Factors increase digoxin toxicity

 Renal failure
 Hypercalcemia, hypokalemia or hypomagensia
 Advanced age
 AV block
 Hypothyrodism

Digoxin toxicity manifests

 Blurred vision
 Yellow halo around object
 Nausea and vomiting
 Arrhythmia mainly paroxysmal atrial tachycardia with AV block

Treated with stopping medication and giving phenyton and lidocaine (for arrhythmia).
In case of acute ingestion of high dose digibind (Ab binds digoxin  prevents
toxicity).

In case we have pulmonary edema secondary to cardiac cause, what should we do?

Do ECG to know if arrhythmia is the cause or not. Then give

 Oxygen
 Morphine and nitroglycerine
  Sitting upright position
 Diuretics mainly loop one
 Digoxin in case of atrial fibrillation

Infective endocarditis (IE)

It's an infection of endocardium by deposition of vegetans (platelet + fibrin
+colonization of micro-organism) mainly in valves and less commonly in mural
surface of endocardium like less pressure side of cardiac defect

Infection of shunt is called infective endoarteritis like PDA or AV shunt

Risk factors
 Prosthetic valve
 Previous IE
 Cardiac transplant+ valvulopathy (so, aortic valve and Mitral valve disease are
high risk, so no need for prophylaxis)
 Indwelling cardiac catheter
 IV abuser
 Cyanotic heart disease if unrepaired/ first 6 month after repairing or repairing
with retaining shunt (not VSD, PDA or AV shunt!!).

Pathogenesis
Endothelium is resistant to thrombus or infection if it's intact. Once it's injured 
thrombus and fibrin deposition. At this level, it's called non-bacterial endocarditis
(NBE). It acts as site for bacterial attachement in case of bacteremia to become
vegetation. NBE can develops with intact endothelium (called marantic) such in case
of hyper-coagubility state like Malignancy and chronic systemic disease. NBE in case
of anti-phospholipid syndrome (called limban sack endocarditis). Moreover, S.aureus
can adhere directly to intact endothelium secondary to have fibronectin binding
protein This is why S.aureus is a major cause of IE in previous normal valve.

Organism founds deeply in vegetation  metabolically inactive, so it's resistant to

medication, while organism on surface of vegetation  are active and shedding
continuously.

Classification
It can be classified based on temporal evolution of disease, causative agent and site of
infection.

 Left Vs right valves involved. Left sided valve involved > right sided valve.
Aortic > mitral. Right sided (mainly tricuspid) more commonly in IV abuser ,
 indwelling catheter, apply central line and cardiac device. They develops even
with intact native valve because most common causative organism is S.aureus.
Right or left sided classification is important to expect organism in giving
empiric therapy.
 Acute Vs subacute endocarditis :
o Acute is characterized via hectically fever, damages cardiac structure
within weeks, hematogenously seeds and if untreated death. This is
due to highly virulent causative organism like S.aureus. Usually
develops in native normal (healthy) valve. It can invade myocardium
 abscess formation.
o Subacute is indolent disease that rarely damages cardiac structure (if
does, it's slow process), rarely seeds hematogenously unless embolism
of mycotic aneurysm is occurred. Usually develops in prosthetic valve.
 Native valve Vs prosthetic valve
o Native: usually develops acute because they are infected with virulent
organism
o Prosthetic, less virulent organism.
 Early within 2 months  nosocomial either contamination
intra-operatively or post operative bacetermia. Most commonly
is S.epidermidis
 Late >2 months  most commonly is Strep viridians
 Nosocomial Vs community acquired. Nosocomial has atypical causative
agents like gram –ve (pseudomonas). Community most commonly due to
Strep.viridan

Typical organisms

 Entry from oral cavity Strep.viridans Most common cause of IE in

community acquired.
 Entry from skin is S.aureus and S.epidermidis.
 Entry from upper respiratory tract  HACEK organisms
o Hemophilus
o Actinobacillus
o Cardiobacterium
o Eiknella
o Kingella
 S.bovis originates from GI tract, if +ve in IE  rule out colon cancer.
 Enterococci enters from genitourinary tract.

Clinical manifestation
It ranges from acute-subacute manifestation.

 Cardiac manifestation
 o Endocarditis  85% of cases there is rupture of chordiae tendinee 
new mumur.
o 30% causes CHF due to new sudden valvular lesion. However, CHF in
minor cases due to endocarditis associated with myocarditis
o There is risk of extension of abscess beyond valve leaflets
perivalvular abscess  fistula can reach pericardium pericarditis+
murmur or to upper part of interventricular septum  disrupt heart
conduction
o Emboli of abscess to coronary artery  ischemia
 Non cardiac manifestation
o Fever and constitutional symptoms like decrease appetite, decrease
weight and generalized fatigue.
o Imunogenic phenomenon like osler node (raised tender nodule on
palmar side of fingers. Other immunogenic phenomenon is
glomerulonephritis causing low C3 and hematuria.
o Vascular accident(secondary to septic emboli) like janway lesion
(macule non tender not painful skin lesion on palms, which is brown in
color) and splinter hemorrhage (dark vertical hemorrhage in nail).
Others like roth's spot (retinal hemorrhage in fundoscope) and
subconjunctival hemorrhage. They occur especially if cause is S.aureus
and vegetation>10mm and affected valve is mitral.

Diagnosis
 Based on duke's criteria (clinically)
o Major criteria
 Echo findings like regurgitation, peri-valvular abscess,
dehiscence and vegetation
 At least 2 positive blood culture for typical organisms. 1
positive blood culture for coxiella burnetii (Q fever) or titer
for coxille >1:800
o Minor criteria
 Blood culture does not meet major criteria
 Echo does not meet major criteria (except 1 positive for
S.epidermidis or non-common cause of IE)
 Has predisposing factor (high risk)
 Fever >/=38
 Vascular phenomenon
 Immunogenic phenomenon
o Diagnosis made in case of presence 2 major/ 1 major+3 minor or 5
minor.
o 3 minor /1 major+2 minor  possible IE.
 o Rejected IE, if other disease can explain manifestation or improved
within 4 days from starting treatment (needs 1 week to start to
improve)
 Based on pathology, autopsy of vegetation or septic emboli shows
organism.

Approach to this patient

History

Chief complains either chronic low grade fever (in subacute) or new onset of acute
fever associated with generalized weakness(in acute). Moreover, they can present
with stroke or CHF (stroke in young  disease, so do carotid and cardiac echo). He
has +ve risk factor like prosthetic valve, IV abuser, indwelling catheter or central
venous line, heart transplan with valvulopathy and cyanotic heart disease. Ask about
recent oral procedure/ bronchoscopy with mucosal invasion.

Physical examination

Check vital signs mainly tempreture

General looking  in acute endocarditis, he looks severely ill.

Look for IE stigmata:

o Janway lesion
o Osler nodes
o Splinter hemorrhage
o Roth's spot
o Subconjunctival hemorrhage

Clubbing is present, but not a stigmata.

Check oral hygiene and recent procedure

Then moves to examine cardiovascular for new murmur.

Investigation

o To confirm diagnosis
o Blood culture: 3 blood sample, separated and each from different site.
Each sample sends for aerobic and anerobic culture.
 Separation is half an hour/ hour or 12 hours depending on
clinical presentation. Severely ill every half an hour. If stable
do every 12 hours
 
It's important to write rule out IE because some bacteria has
slow growth
 Blood culture takes one week, so after taking blood sample
give anti-biotic in both acute and subacute endocarditis
o Echo (transesophageal echo has higher sensitivity than transthoracic
echo), can see new valve disease (usually regurgitation), valve
dehiscence (infectionweakness of suture between valvular ring and
annulus), perivalvular abscess, fistula and vegetation.
o Why does patient has IE
o CBC, anemia, WBC (for infection) and platelet (low in anti-
phospholipid)
o CXR, source of IE is pneumonia
o Complication
o ECG, risk of heart block or pericarditis due to abscess invasion and
making fistula
o Kidney function (for CHF) and urineanalysis (for hematuria)
o C3-C4 level (low in IE induce membrnoproliferative disease). D/Dx
for low C3-C4 is SLE, membranoproliferative kidney disease,
cryglobulinemia and post-streptococcal glomerulonephritis.

D/Dx for IE with –ve blood culture

 Fungal cause
 Fastidious bacteria
 Taking incomplete anti-biotic course
 Libman sack

Treatment

Basic:

Drug must be bacterocidial and prolonged and given parentally. Empiric given in
acute and subacute. Classification here is helpful to know the best guess in empiric
therapy.

IV abuser or indwelling catheter S.aureus /S.epidermidis

Prosthetic valve within 2 monthS.epidermidis

NVE or late prosthetic most commonly S.viridans

 Strep viridian or Strep bovis  IV penicillin for 4 weeks or IV penicillin+

gentamicin for 2 weeks. If there is penicillin allergy (not anaphylaxis)  IV
ceftriaxone for 4 weeks or ceftriaxone+gentamicin for 2 weeks. In case of
 penicillin induce anaphylaxis  IV vancomycin for 4 weeks. If streptococcus
resistant IV vancomycin for 4 weeks
 Enterococci  Penicillin+gentamicin for 4-6 weeks. Other option is
vancomycin+gentamycin for 4-6 weeks Cephalosporin never cover
enterococci.
 HACEK give ceftriaxone 4 weeks

 Staphylococcus aureus infection depends whether it's native or prosthetic

valve
o Methicillin susceptible
 Native valve: amoxicillin/oxacillin for 4-6 weeks OR cefazolin
for 4-6 weeks
 Prosthetic valve amoxicillin/oxacillin for 6-8weeks +
gentamicin for 6-8weeks+ rifampin PO for 6-8 weeks
o Methicillin resistant
 Native valve: Vancomycin for 4-6 weeks
 Prosthetic valve: vancomycin+ gentamicin+ rifampin for 6-8
weeks

Prophylaxis is just amoxicillin .5-1 hour prior oral surgery or bronchoscopy involve
invasion of mucosa.
Pericardial disease
Introduction
It's a double layer separated by ultra-filtrate plasma (15-50ml) and has the following
function of pericardium

 Restrict sudden dilatation f heart chamber mainly R side in case of increase

preload like exercise or increase blood volume.
 Fixation of heart sight and prevent kinking of great vessels
 Delay of infection spread from lung and pleural cavity to heart
 Decrease friction of heart with surrounding structures.

Absence of pericardium either congenital or acquired has no clinical significance.

However, partial loss of left part of pericardium congenitally has risk of left atrium to
herniat and strangulated sudden cardiac death(very rare)

Cardiac temponade
Accumulation of fluid in pericardium space that impairs filling of R side of heart with
blood. It's fatal if not treated at once. It's characterized by beck's triad (hypotension,
raised JVP and absent or fainted heart sound). It's also characterized by paradoxical
pulse , which is decrease more than 10mmHg of systole while u inspire. Clinically,
pulse paradoxus detected by absence or massive decrease of pulse volume during
inspiration.

Pathogenesis of pulsus paradoxus is during inspiration, there is increase in Venous

return to Right side. So, increase RV size under fluid tension  will compress LV
and reduces its size decrease amount pumped. However, it's not pathognomic to
cardiac temponade, it can occur in constrictive pericarditis and sever obstructive
respiratory system like status asthmatics.

The most 3 causes for cardiac temponade is renal failure, neoplasm and idiopathic
pericarditis

It does not depend on amount of fluid in pericardial space. It depends on how quickly
fluid accumulates. If rapid accumulation cardiac temponade occurs in small
pericardial effusion 200ml. If it was slowly, it will occur if volume >2000ml

Due to pericardial effusion  QRS low voltage and alternas in ECG

Most D/Dx for cardiac temponade is RV infarction and constrictive pericarditis.

RV infarction has no pericardial effusion (no QRS alternas and no low QRS
amplitude)

Precardiac temponade state is called low pressure temponade, in which there is mild
increase intra-pericardial pressure, that causing mild increase central venous pressure
(increase JVP- sometimes stays normal) with no pulsus paradoxus or hypotension.
They complain of fatigue and mild dyspnea.

Type of pericardial effusion:

 Transudate: CHF, nephrotic syndrome and myxedema
 Exudate (applies modified light criteria like fluid/plasma protein is >.5. or
LDH ratio >.6 or LDH level >2/3 of normal upper limit in serum): Infectious
and rheumatic fever. There is dominance of neutrophills and low glucose level
in pericardial effusion in bacterial cause.
 Milky  involvement of lymphatic system. It's called chylopericardium
 Bloody
o Iatrogenic, most common cause in developed countries like trauma,
post-invasive cardiac procedure and anti-coagulants
o Malignancy mainly from lung and breast  increase monocyte counts.
Detected with cytology (if -ve does not rule out cancer). If –ve  do
tumor marker.
o Complication of infarction like ventricular rupture or ventricular
aneurysm rupture. In this case, we have increased BNP in pericardial
fluid.
o TB elevates ADA in pericardial effusion. Definitive is detection
tubercle bacilli in pericardial effusion.
o Pericarditis associated with renal failure or dialysis
o HIV, it's secondary to either TB or neoplasm like lymphoma
o Idiopathic

Diagnosis
By echo, we find

 Increase velocity of blood flow through pulmonic and tricuspid valve, but
decrease velocity through pulmonary vein, mitral and aortic valve.
 Late diastolic RV collapse (moves inward decrease chamber diameter)

Sometimes, we need to do trans-esophageal echo to know the cause, when we suspect

hemorrhagic effusion or loculated effusion
Pericardiocentesis is treatment and diagnostic

If u suspect infection  3 culture each for aerobe and anaerobe with blood culture

If bloody  ADA/ PCR for TB / cytology and cancer marker for cancer and BNP or
echo for post-infarction complication.

Treatment
Hospitalization+ pericardiocentesis. In recurrent temponade surgical drainage like
subxiphoid thoractomy We should analyze pericardial fluid

The most common pathological even of pericardium is acute pericarditis

Pericarditis
It's an inflammation of pericardium. It can be classified based on clinical and etiology.

Clinical classification

 Acute pericarditis <6 weeks. It can be

o Fibrinous
o Effusive
 Subacute 6weeks-6months
o Effusive
o Constrictive
 Chronic >6 months
o Effusive
o Constrictive
o Adhesive

Etiology:

 Infectious
o Viral mainly coxsackivirus A and B. Others like echovirus, influenza
and adenovirs can cause it. However, most of cases, we can not isolate
virus, this is why it's called idiopathic pericarditis.
o Pyogenic organism like streptococcus pneumonia, Neisseria and
Legionella. They occur post cardio-thoracic surgery via extension
infection from pleural cavity to pericardium or via esophageal rupture.
Key point is chills and high grade fever.
o TB
 o Fungal like candidiasis and histoplasmosis (Rare)
o Others like syphilis (rare)
 Non-infectious
o Acute MI
o Uremia or dialysis (differentiated without/with history of dialysis)
o Neoplasm either
 Primary either benign or malignant mesothelioma
 Secondary mainly lung, breast and lymphoma
o Trauma either penetrating or non penetrating chest wall
o Post-irradiation
o Hypersensitivity cause (they cause recurrent pericarditis)
 SLE
 RA
 Rheumatic fever
 Post cardiac injury (develops after 1-4 weeks from event
secondary to hypersensitivity to Ag from injured myocardium
or pericardium) like
 Post MI (dresseler syndrome)
 Post-pericardiotomy (incision of pericardium)
 Post cardiac trauma
 Post chest blow
 Drug induce like hydralazine and procainamide

Presentation
 Chest pain, presents in case the etiology is infectious or hypersensitivity cause
(autoimmune+ post-cardiac injury). So, absent in slow process like uremic, TB
, neoplasm and post irradiation patient. It's pleurtic increased with coughing
and inspiration. However sometimes it can mimic angina pain and complexed
with raising cardiac enzyme (increase due to concomitant myositis). However,
pericarditis pain it exaggerated with lying supine and decrease by leaning
forward. Other way for differentiating between MI and pericarditis is that
fever co-exist with chest pain in pericarditis while fever occurs after chest
pain. The definitive way for differentiation is coronary angiography.
 Pericardial friction rub, audible in 85% of cases. Best heard in left lower
sternal, while patient leans forward
 Pericardial effusion, rapid development  risk of cardiac temponade. Appear
as cardiac enlargement on CXR , however, heart sound is fainter.

Complication is pericardial effusion that can develop into cardiac temponade,

constrictive pericarditis and peri-myocarditis.

Investigation
For confirmation

 ECG changes: it has stages

o Stage I, widespread ST elevation. Can be associated with PR
depression in leads that have ST elevation
o Stage II after days, ST elevation becomes normal, but T becomes
inverted later on (in MI occurs simultaneously with ST elevation)
o Stage III, after weeks T waves return to normal
 CXR to rule out other causes pleurtic chest pain like pneumothorax and
pneumonia

Why does he have it ?

 CXR also pneumonia as a source of infection

 CBC, KFT, blood culture and pericardiocentesis
 anti-streptolysin o and anti-DNAase
 Anti- DNA anti-body and RF
 Chest CT in suspicion of malignancy

Complication

 Echo for pericardial effusion

 CT or MRI for pericardia thickening (seen in chronic pericarditis)

Treatment

 NSAID for 2 weeks, best are ibuprofen /naproxene. If pericaridits secondary

to MI  give aspirin in high dose (because ibuprofen and others delay cardiac
healing)
 Colchicines for 8 weeks
 Steroid after ruling out that the cause is not pyogenic (bacterial) if
o the cause is connective tissue disease or uremia.
o Failure of NSAID and colchicines
 If recurrence can not be controlled by colchicines or steroid for 2 years do
pericardioectomy

Chronic constrictive pericarditis

It's due to healing of pericarditis via obliteration of pericardial cavity with formation a
scar, which can calcify encasing the heart and interfering with Right side filling.
Early phase of diastolic is normal, while in late phase it's abruptly disturbed due to
limited elastic fiber. However, in cardiac temponade, filling is disturbed in whole
diastole. In both conditions, ventricular end-diastolic and stroke volumes are reduced
and the end-diastolic pressures in both ventricles and the mean pressures in the atria,
pulmonary veins, and systemic veins are all elevated to similar levels
In chronic constrictive pericarditis, there is risk that fibrosis process reaches
myocardium diastolic heart failure.

What differentiates constrictive pericarditis from cardiac temponade?

In constrictive pericarditis, there is prominent y wave, which is absent in cardiac

temponade. Normally, y denotes early phase of diastole. So, in cardiac temponade,
there will be no descent because impeding is at the beginning of diastole. Other ways,
Kusmall sign (fail to decrease JVP during inspiration) is present in constrictive
pericarditis (also in tricuspid stenosis, RV infarction and restrictive cardiomyopathy)
but not in cardiac temponade.

Constrictive pericarditis is differentiated from restrictive cardiomyopathy (same

pathophysiology, in which late diastole is disturbed) by

 Echo: thickened ventricular wall in restrictive cardiomyopathy.

 CT calcification of pericardium in case of constrictive pericariditis.

The definitive treatment for constrictive pericarditis is pericardiotomy.

Pulmonary embolism
Definition
It's an obstruction of pulmonary artery or one of its branch via material like embolism,
air, amniotic fluid and fat that originates elsewhere of body. If material was lodged in
bifurication of main pulmonary trunk, it's called saddle PE.

PE can be acute, in which signs and symptoms appear directly after obstruction or
chronic, in which symptoms appear slowly and progressive over year secondary to
pulmonary HTN.

Acute PE can be classified to

 Massive PE, causing hemodynamic unstable (systolic <90mmHg or drop more

than 40 mmHg from baseline at least 15 minutes). We fear from acute RV
failure and death. Major D/Dx for massive acute PE is RV infarction, cardiac
temponade, tension pneumothorax and new arrhythmia.
 Submassive  no hemodynamic instability.

In saddle PE, most cases are submassive, however, it can be massive

If it's untreated 30% risk of death secondary to recurrent embolism.

Pathophysiology
Most common origin of thrombus is lower extremity mainly ileofemoral vein. Other
origin like pelvic, renal and upper extremity vein. Thrombus in ileiac, femoral and
popliteal vein arise below popliteal vein and arise upward to reach these vein 80% and
20% arise from themselves. However, only 20% of below popliteal vein extends to
ileiofemoral vein and 80% resolves spontaneously.

If large thrombus, it will lodge in bifurication of pulmonary trunk or lobar branch of

pulmonary artery  hemodynamic unstable. If small  moves to distal branches to
reach parietal layer of pleura  initiates inflammatory response  pleuritic chest
pain Most pulmonary emboli are multiple.
Venous mechanical obstruction via thrombus and inflammatory mediators and
hypoxia  vasoconstriction  increase afterload  decrease LV preload  RV
failure and hypotension. This occurs once obstruction reaches 75% of pulmonary
artery.

Gas exchange mismatch occurs not only from mechanical obstruction of vascular bed,
but also due to release of inflammatory mediators surfactant dysfunction and
atelectasis

Risk factor

What increase DVT, increases risk of PE. Risk factor is virchow's triad :

 Stasis like immobility, paresis, paralysis and surgery within last 3 months
 Endothelial injury like obesity, HTN and smoking
 Hyper-coagubility state
o Congenital like protein C&S deficiency, anti-thrombin III deficiency
and factor V leiden mutation
o Acquired like nephrotic syndrome, anti-phospholipid anti-body
syndrome, polycythemia and medication

Presentation

Most common symptom is SOB. Most common sign is tachypnea.

 Symptoms dyspnea within seconds> pleurtic chest pain>thigh pain> cough

 Symptoms of DVT are common in 50% of cases like swelling, pain and
erythema+ tenderness
 Signs like tachypnea> tachycardia> rales and loud P2
 Circulatory collapse rarely occur just 8% of cases

Factors that affect prognosis

 Development RV dysfunction secondary to PE increases mortality by 2 to 3

fold from baseline
 Brain natriuteric peptide (BNP), increase BNP  RV dysfunction. Usually it
occurs in large thrombus and associated with increase troponin I or T.
 RV thrombus  PE increase mortality by two fold.

History
SOB within seconds-minutes associated with pleurtic chest pain. Ask about previous
similar attack, risk factor (work, surgery, smoking, HTN and family history of
coagulopathy)
Physical exam
Vital signs (mainly RR, HR, O2 sat and BP)

General, if he is cyanosed, conscious or looks ill

Respiratory and cardiovascular system: raised JVP, wide split (A2 P2 due to RBBB)
and decrease breath sound can occur with PE

After history and physical, we should be able to do modified Wells criteria

 Clinical symptoms of DVT (3 points)

 Other diagnoses less likely than PE (3 points)
 Heart rate >100 (1.5 points)
 Immobilization ≥3 days or surgery in previous four weeks (1.5 points)
 Previous DVT/PE (1.5 points)
 Hemoptysis (1 point)
 Malignancy (1 point)

If 0-3  low risk.

If 4-10  intermediate

If>10  high risk

Investigation
For confirmation

 ECG to rule out ischemia and arrhythmia and confirm diagnosis (tachycardia,
RBBB and S1Q3T3).
 CXR to rule out other causes of pleurtic chest pain (pneumothorax and
pneumonia). In PE, most of cases is free. However, we can see wedge shape
necrosis in case of massive PE and oligemia (decrease pulmonary vasculature)
or pleural effusion
 ABG (respiratory alkalosis with low PaO2). In case of circulatory collapse,
there will be hypercapnia and metabolic acidosis
  D-dimer if low risk (geneva <4) ,used as a –ve predicitive value. If it was high
 spiral CT angio(do not use in pregnancy, because it's normally
increased).
 If geneva score >4 Spiral CT angiograph. If –ve  pulmonary
angiography.
 V/Q mismatch scan (rarely used, if spiral CT angio or pulmonary angiography
like renal failure, allergy to contrast and prenancy), in which its accuracy
increase once it's combined with clinical picture (well's score). If scan and
clinical picture strongly indicates PE 95% has PE.

Why does he have it ?

 CBC for polycythemia and platelet count

 Protein/ creatinine ratio for nephrotic syndrome
 Anti-phospholipid Ab like anti-cardiolipin, anti- B glycoprotein and lupus
anti-coagulant.

For complication

 ECG to detect factors associated with poor prognosis

o RBBB
o Atrial arrhythmia
o T inversion in pricordial lead with ST elevation
 CXR for pleural effusion
 Troponin I and BNP associated with increase mortality
 Echo for RV assessment and to detect RV thrombus if present

Treatment
In case of suspicion  give heparin in case of absence of CI :

 Sever thrombocytopenia
 Uncontrolled active heparin bleeding
 Give low dose if u can not monitor INR

Then if u confirm diagnosis  complete heparin and start to introduce warfarin. If

hemodynamic unstable  give thrombolytic with heparin in case of absence of CI to
thrombolytic (if present surgical embolectomy). If PE is ruled out  stop heparin

In case, there is CI for heparin and confirm PE was diagnosis  inferior vena cava
filter and surgical embolectomy. PE is ruled out  no heparin used.
If it was first attack and provoked  treatment is for 3 months. If recurrent  3
month then reassess either life long or stop it.

If PE was not provoked  first attack, give for 3 months then reassess. If recurrent in
unprovoked case life long warfarin.