CARDIOLOGY

CLINICAL MEDICINE
SUMMARY

Done by: Juman Rezqalla

 Lecture 1: Basic Principles in Cardiac Arrhythmias
Diagnosing the Arrhythmia
1. QRS Complexes
a. Rate: Normal= 60-100
b. Regularity: R-R Interval is the same
c. Normal vs. Wide: Wide= ventricular tachycardia
2. P-waves
a. Normal Sinus Rhythm (normal p-wave before every QRS)
b. Intervals are normal (PR interval= 0.12 à 0.21 secs; QT interval= <0.4 secs)
c. Every p-wave is followed by QRS

Diagnosing the Arrhythmia

1. If hemodynamically STABLE:
a. Bradycardia: Atropine
b. Supreventricular tachycardia: ABCD (adenosine – BB – CCB – Digoxin)
c. Ventricular tachycardia: LAPS (Lidocaine – Amiodarone – Procainamide – Sotalol)
2. If hemodynamically UNSTABLE:
a. Bradycardia: Pacemaker
b. Tachycardia: DC shock

Sinus Tachycardia
• Normal p-wave followed by QRS
• Regular (regular R-R interval)
• Narrow QRS
• >100 bpm
• Camel lump (P merge with T)
• Treatment by treatment of underlying cause

Supraventricular Tachycardia: arising above the level of the Bundle of His. Narrow QRS.
Paroxysmal SVT - Atrial Fibrillation - Atrial Flutter

Paroxysmal SVT
• In young patients with no structural heart disease
• Abrupt onset and offset
• Seen with re-entry tachycardia
• 2 types:
o AVRT (Atrioventricular)
§ Anatomical reentry; accessory pathway (extra piece of conducting tissue
between atria and ventricles)
§ ex: WPW syndrome
o AVNRT (AV node)
§ Functional reentry within AV node (fast & slow pathways in AV node)
• On ECG:
o Regular, 250bpm (fast)
o Narrow QRS
o P-wave sometimes hidden in QRS (because it’s very fast)
o ST depression
• Treatment:
o Termination by acutely blocking AV nodal conduction
§ 1st line à IV adenosine & vagal maneuver
§ 2nd line à IV BB, Dilatizem, Verapamil
o Preferred to cure: Ablation of accessory pathway
Atrial Fibrillation
• Irregularly irregular
• No p-waves (only fine oscillations)
• Narrow QRS
• Most feared complication: embolism + stroke
• Can progress to V. Fib
• Can be fast or slow depending on AV node conduction
• Treatment:
o If less than 48 hours à Conversion to Sinus (Rhythm control)
§ Electrical
§ Drugs (Amiodarone, Flecainide, Propafenone)
o If more than 48 hours à Control Ventricular Response (Rate Control)
§ BBs, CCBs, Digoxin
o Anticoagulation to prevent embolic events

Atrial Flutter
• No p-waves; saw-toothed flutter waves
• Always some degree of AV block (2:1, 3:1, 4:1)
• Often occurs with A. Fib
• Associated with underlying heart disease/COPD/hyperthyroidism
• Treatment:
o Initial: cardioversion (restore sinus rhythm)
o Anticoagulation
o Drugs:
§ Rate control: BBs, CCBs
§ Rhythm control: Cathetar ablation, Amiodarone, Flecainide, Propafenone

Ventricular Tachycardia: arising above the level of the Bundle of His. Wide QRS
• 3 or more premature ventricular beats
• Sustained if >30 secs; non-sustained if < 30 secs
• Regular
• Wide aberrant bizarre-shaped QRS
• Capture beats & Fusion beats
• Dizziness, syncope, SOB, chest pain, palpitations, sudden death
• Causes:
o IHD
o Cardiomyopathy (hypertrophic/dilated
• Treatment:
o Cardioversion (from 100J)
o Lidocaine,, Amiodarone, Procainamide, Sotalol
o Correction of reversible causes (hypokalemia, ischemia, HF, hypotension`0

Torsades de Pointes
• Polymorphic ventricular tachycardia (twisting of the axis)
• Beat to beat variation in QRS shape
• Treatment: Magnesium Sulfate

Sinus Bradycardia
• Normal p-wave followed by QRS
• Regular (regular R-R interval)
• <60 bpm
• Treatment: could be normal/ stop offending agent (BB, CCB)/ Atropine
AV Blocks
• 1st Degree à AV conduction excessively slowed (but all conducted) ; constant PR
• 2nd Degree à AV conduction occasionally blocked
o Mobitz I: PR increases progressively until beat dropped
o Mobitz II: PR is constant
• 3 Degree (Complete Heart Block) à AV conduction is completely blocked
rd

o P-waves marching through

o QRSs without correlating p-waves
• Treatment:
o Atropine
o Pacemaker

Lecture 2: Clinical Concepts in Heart Failure

Cardinal Symptoms of Heart Failure:
• Shortness of breath
• Dyspnea on exertion
• Orthopnea
• PND (paroxysmal nocturnal dyspnea)
• Pitting peripheral edema
• Pulmonary edema
• Fatigue

NYHA Classification of Heart Failure

1. Class I: no symptoms with ordinary physical activity
2. Class II: slight limitation of physical activity. Symptoms with ordinary physical activity
3. Class III: marked limitation of physical activity. Symptoms with less than ordinary physical
activity
4. Class IV: unable to perform any physical activity. Symptoms at rest.

HF – REF HF – PEF
Systolic; contraction impaired Diastolic; relaxation impaired

EF is LOW (<45%) EF is = or more than 50%

Not dilated; Normal LV volume but high LV

Dilated; High LV volume
EDP

S3 sound S4 sound

Causes: MI (CAD), HTN, Valvular Heart

Causes: Left Ventricular Hypertrophy, HTN
Disease, Dilated Cardiomyopathy, Myocarditis

No large scale trails. Can only treat underlying

Has effective therapies. The lower the EF, the
cause, control heart rate to prolong diastole,
poorer the survival.
and diurese the patient
Management of HF - REF:

1. Improve Survival:
a. ACE I/ ARB – decrease risk of death
b. B-Blockers – increase survival
c. Mineralocorticoid antagonists (Spironolactone/Epleronone)
• If EF < or = 40%: BB + ACE I/ARB
• If EF < or = 35% & Symptoms persist despite BB + ACE I/ARB à give Mineralocorticoid
antagonists (decrease risk of death by 30% in severe heart failure on standard therapy

2. Improve Symptoms:
a. Diuretics
b. Digitalis

3. Device Therapy
a. ICD (implantable cardioverter-defibrillator)
b. CRT (cardiac resynchronization therapy)

4. Surgery
a. Coronary Revascularization (if the cause is CAD)
• To prevent further ischemia & promote recovery of function à improve symptoms and
survival
b. Valve repair/replacement (if the cause is Valvular Heart Disease)
c. Cardiac transplantation in end-stage HF

Diagnosis of HF:
(after history and physical examination)

1. Echocardiogram – SINGLE MOST IMPORTANT DIAGNOSTIC TEST

• HF – REF vs HF – PEF
• Underlying cause (wall motion abnormality, valvular disease)
• Severity of LV dysfunction
• Follow up effect of treatment

2. ECG
• HF – REF à evidence of CAD & Old MI
• HF – PEF à evidence of left ventricular hypertrophy

3. Chest X-Ray
• Cardiomegaly
• Dilated upper lobe veins due to congestion
• Pulmonary edema (bat wing appearance)
• Kerly lines due to interstitial edema
• Pleural effusion

4. Blood chemistry & thyroid function

5. CBC (anemia can precipitate symptoms)

 Lecture 3: Clinical Aspects of Hypertension
• Each stage of hypertension +20 systolic & +10 diastolic
o Stage 1 Hypertension: ≥140/≥90
o Stage 2 Hypertension: ≥160/≥100
o Stage 3 Hypertension: ≥180/≥110
• Goal of treatment is to lower below 140/90
• Most common, readily identifiable and reversible risk factor for CV diseases
• Risk of CV death doubles with every 20 increase in systolic and 10 increase in diastolic

Main Complications of Hypertension:

• Stroke
• Hypertensive encephalopathy
• Aortic aneurysms/dissection
• Hypertensive retinopathy (hemorrhages/exudate/papilledema)
• AF, LVH, MI, HF
• Hypertensive nephropathy (à chronic renal failure)
• Peripheral artery disease

Types of Hypertension:
1. Primary – no direct cause
2. Secondary – has a secondary treatable cause
a. Renal disease
b. Endocrine diseases (Cushing syndrome, Aldosteronism, Pheochromocytoma, hypo-
or hyperthyroidism, hyperparathyroidism)
c. Vascular diseases
d. Coarctation of the Aorta
e. Sleep apnea
f. Pregnancy
g. Drugs (contraceptive pills, steroids, NSAIDs, antidepressants, ginseng, licorice,
cocaine, methamphetamine)

Aims of Diagnostic Evaluation:

1. BP measurement à confirm diagnosis of hypertension
2. Detect secondary causes
3. Assess global risk (i.e. CV risk, Organ Damage, & concomitant disease)

Choice of treatment modality depending on total CV risk

Factors other that the BP # influence treatment and prognosis (BP level, risk factors,
asymptomatic organ damage, & established CV or renal disease)
• If the BP is very high (Grade 3 HTN), the patient is at high risk. Regardless of presence of risk
factors/organ damage/CV & renal disease or not, patient always gets drug treatment to lower
BP under 140/90
• If there is symptomatic kidney/CV disease, or diabetes with organ damage or risk factors, the
patient is at high risk (regardless if Grade 1, 2, or 3 HTN), and must get drug treatment to lower
BP under 140/90
• All must undergo lifestyle changes (salt restriction – moderate alcohol – 5 servings of
fruits/vegetables – weight reduction – physical exercise – smoking cessation)
Drugs Used in the Treatment of Hypertension:
1. Thiazide Diuretics:
a. Contraindications: Gout
b. Side Effects: Hypokalemia
2. Beta Blockers
a. Contraindications: Asthma – Grade 2 or 3 AV block
3. Calcium Channel Blockers
• Dihydropyridines:
a. Contraindications: Tachyarrhythmia – Heart failure
b. Side Effects: Leg swelling/edema
• Non-Dihydropyridines
a. Contraindications: Heart failure – Grade 2 or 3 AV block – Severe LV dysfunction
4. ACE Inhibitors
a. Contraindications: Angioneurotic edema – Pregnancy – Hyperkalemia – Bilateral renal
artery stenosis
b. Side Effects: Cough – Renal Impairment
5. ARB
a. Contraindications: Pregnancy – Hyperkalemia – Bilateral renal artery stenosis
b. Side Effects: Renal Impairment

Combination Therapy
• Preferred:
o Thiazide + ACE I
o Thiazide + CCB
o Thiazide + ARB
o ACE I + CCB
o ARB + CCB
• Useful:
o Thiazide + BB (but may increase onset of DM in susceptible patients)
• Not Recommended:
o ACE I + ARB (increased risk of renal damage)
• All others are possible
 Lectures 4 & 5:
Principles of Clinical Diagnosis and Management of Acute
Coronary Syndromes & Medical Perspectives of Chronic
Myocardial Ischemia
1. Stable Angina:
• Stable coronary artery disease
• Gradual/slow plaque progression à gradual supply/demand mismatch
• Slow progression from risk factors to atherosclerosis
• Stabilized plaque – Thick fibrous cap – Small lipid pool
• Minimal lumen reduction; <70% stenosis
• Predictable with exertion/emotional distress/cold/heavy meal
• Substernal chest pain due to transient myocardial ischemia (ischemic pain)
• Pain lasts for 1 to 5 minutes only
• Relieved by rest & nitrates

Acute Coronary Syndrome

ü Abrupt occlusion due to platelet rupture à acute supply/demand mismatch
ü Vulnerable plaque: thin fibrous cap – large lipid pool – many inflammatory cells
ü Fast progression from risk factors to atherosclerosis
ü Includes unstable angina and myocardial infarction (STEMI & NSTEMI).

2. Unstable Angina:
• Platelet thrombus (platelet aggregation & adhesion)
• Can be defined as:
o Angina of new onset (<2 months) with minimal exertion
o Crescendo angina superimposed on preexisting stable exertion angina
o Angina at rest
• ECG changes may be present; has prognostic significance (Patients with ST-segment
deviation have worse prognosis than those with normal ECG)
• No myocardial necrosis
• Ischemic pain for less than 30 minutes

3. Myocardial Infarction
• Rise and fall in troponin (released within 4-6 hours àelevated for 2 weeks) with at least one
of:
o Symptoms of ischemia
o ECG: new ST-T changes or new LBBB
o ECG: pathological Q-wave
o On imaging: new loss of viable myocardium or new wall motion abnormalities
o Angiography/autopsy: intracoronary thrombus
• Ischemic pain for > 30 minutes
• STEMI:
o ST elevation MI
o If 2+ leads have STEMI and others have NSTEMI it’s STEMI
o Clot fully occludes lumen
• NSTEMI
o Non ST elevation MI
o Could be normal, ST depression, or T-wave inversion
o Clot does not fully occlude lumen
 • Complications:
o Tachyarrhythmia or bradyarrhythmia
o Pericarditis
o Heart failure
o Cardiogenic shock
o Rupture of papillary muscle
o Rupture of IVS or free wall
o LV aneurysm
o LV thrombus

Ischemic Pain
• Central (points with whole fist)
• Heaviness/constriction/compressing + could be burning
• Located retrosternally
• Radiation:
o Left arm (ulnar) o Back
o Jaw o Epigastrium
o Neck
• Associated Symptoms:
o Nausea o Dizziness/fainting
o Vomiting o Palpitations
o Cold sweat o Anxiety
o Breathlessness o Feeling of impending doom
o Weakness
• Time = Muscle. After 30 minutes of plaque rupture & clot formation the tissue beyond the
clot dies.
o Stable Angina duration: 1-5 minutes
o Unstable Angina duration: <30 minutes
o MI duration: >30 minutes

Other Causes of Chest Pain

• MSK à most common, side, localized, tender, worse with breathing & coughing
• Acute Pericarditis à pleuritic, sharp, knife, characteristic radiation to trapezius,
positional relieving factor (sitting forward), worse with breathing & coughing
• Aortic Stenosis & Hypertrophic Cardiomyopathy à ischemic pain + syncope + murmur
• Aortic dissection à sudden, severe, chest to upper back, tearing/ripping, weak pulse in 1
arm, SOB, loss of consciousness, sudden difficulty speaking, loss of vision, paralysis of 1 side
• PE à pleuritic, breathlessness, tachycardia
• Pneumothorax à sudden, sharp, severe, on the side, breathlessness
• Pneumonia à sharp, on the side, worse with breathing, fever, cough, sputum
• Esophageal à epigastric/retrosternal, burning, no radiation, recumbent position, relief by
GTN
• Biliary Colic à right upper quadrant, colicky, nausea, vomiting, radiation to right shoulder

Diagnosis & Assessment

1. Clinical Evaluation (conditions associated with higher risk – check notes)
2. Ventricular Function – LVEF is the strongest predictor of long-term survival; LVEF <50%:
high risk for CV death.
3. Response to stress testing
a. Standard exercise ECG testing
b. Myocardial Perfusion Scan
c. Stress echocardiography
 4. Anatomical testing
a. CT Coronary angiography
b. Catheterization & Coronary angiography

Treatment
1. Typical/Stable Angina
• Improving Prognosis:
o Aspirin
o Statins
o BB (after MI)
o ACE I (if HTN, DM, HF)
• Relief of angina symptoms
o Nitrates
o BBs
o CCBs
2. Myocardial Infarction
• 1st – Dual Antiplatelet (aspirin + P2Y12 inhibitor ex: Clopidogrel) & Heparin IMMEDIATE
• 2nd –
o STEMI – immediate revascularization (primary PCI or fibrinolytic therapy) –
LIFESAVING
o NSTEMI – coronary angiography later
• Pain relief by nitrates/morphia
• Oral BBs
• ACE I/ARB especially in anterior STEMI, HF, or EF <40%
• Statins

Lecture 6: Clinical Concepts & Imaging in Valvular Heart

Disease
Regurgitation = Volume Overload
Stenosis = Pressure Overload
Echocardiogram is the most important test

Mitral Regurgitation
• Most common causes:
o Prolapse (myxomatous degeneration of leaflets)
o Rheumatic fever
o LV dilatation
o Ischemia (papillary muscle dysfunction)
• Volume overload and dilatation of left atrium & left ventricle
• Eventually increased left atrial pressure can lead to pulmonary congestion and edema
• Acute: normal sized LA, symptoms develop quickly
• Chronic: Dilated LA, symptoms develop over long time
• Diagnosis:
o hyperdynamic apex
o Soft S1
o Pansystolic murmur
o S3 (rapid LV filling)
o May lead to Atrial fibrillation, Pulmonary HTN, CHF
o High Cardiothoracic ratio, Dilated LA
o Left atrial enlargement and LVH
Mitral Stenosis
• Almost All (99%) Mitral Stenosis is Due to Rheumatic Fever à thickening & fusion of
commissures & chordal shortening & fusion à cusp immobility & orifice narrowing
• Increased diastolic mitral gradient pressure (stenotic valve has resistance to flow)
• May à Pulmonary edema, pulmonary HTN, Chest infections, Heart Failure: JVP, heave,
ascites, edema
• Rate of progression of MS varies across geographical areas
o Developed: Asymptomatic for 15-20 years. Symptoms appear age 45 to 65 years.
o Developing (India/Egypt): Much more rapid; Symptoms can present in children & teens.
• Diagnosis:
o Tapping apex beat that is not displaced
o Loud S1
o Opening snap low-pitched “rumbling” mid diastolic murmur
o Bifid P wave, RVH, AF on ECG
o Dilated LA
• Treatment may use Trans-septal balloon valvotomy with strict criteria

Aortic Regurgitation
• LV dilatation (high LV volume)
• Hyperdynamic circulation
• Can be acute or chronic (like mitral regurgitation)
• Causes:
o Disease of aortic valve leaflets or wall of aortic root
o Cystic medial necrosis (Marfan’s)
o Ankylosing spondylitis
o Syphilitic aortitis
• Diagnosis:
o Prominent (dancing) carotid pulse
o Apex is displaced and hyperdynamic
o High pitched early diastolic murmur
o Collapsing pulse and wide pulse pressure
o Cardiomegaly

Aortic Stenosis
• LV pressure overload à LV concentric hypertrophy (hallmark of AS)
• Causes:
o Age-related calcific degeneration (if it’s a bicuspid valve: more prone)
§ Risk factors same as those for vascular atherosclerosis
§ Bicuspid valve: most common genetic cardiac anomaly
o Rheumatic fever à adhesion and fusion of cusps with retraction & stiffening (valve is
regurgitant as well as stenotis)
o Therefore AS in 30s= rheumatic, in 50s=bicuspid, in 80s=tricuspid
• Symptoms: angina pectoris, syncope/dizziness, exertional dyspnea, HF
• Diagnosis:
o Slow-rising, late-peaking, low-amplitude carotid pulse
o Systolic thrill; Ejection systolic murmur radiates to carotid (maybe faint)
o Absent second aortic sound
o LV hypertrophy on ECG:
§ Deepest S in V1 or V2 & Highest R inV5 or V6 (together > 35mm)
§ Strain pattern (ST depression, T-wave inversion)
• Higher mean pressure gradient à more severe AS
• AV replacement by TAVI for high surgical risk patients
 Mitral Stenosis Mitral Regurgitation Aortic Stenosis Aortic Regurgitation
Primary MR (structural)
• Rheumatic heart disease
• IE • Rheumatic heart
• Rheumatic heart disease
• Valve prolapse disease
• IE
Rheumatic heart disease • Papillary muscle rupture • Calcified bicuspid valve
Etiology • HTN
(99%) (e.g. post MI ) (age 50-60)
• Marfan’s
• Marfan’s • Calcified tricuspid
• SLE valve (age 70+)
Secondary MR (functional)
• LV dilation
1. SOB &fatigue
1. SOB & fatigue 1. SOB
2. Pulmonary edema 1.SOB & fatigue
Presentation 2. Other LVF (orthopnea , 2. Syncope
/hemoptysis
PND) 3. Angina
3. RHF(late)
o Ejection systolic
o PANsystolic murmur o Early diastolic murmur
murmur
o MID-diastolic murmur o 3rd heart sound o 3rd heart sound
o 4th heart sound
Features o Opening snap o Audible “click” in valve o Displaced apex
o Slow raising pulse
o Loud 1st heart sound prolapse o Collapsing pulse
o Narrow pulse
o Displaced apex o Wide pulse pressure
pressure
o AF common
ECG AF common LVH strain pattern --
o P-mitrale (bifid wave)
Chest X-Ray o Enlarged left atrium Cardiomegaly -- Cardiomegaly
Adapted from “Essential Examination – 3rd Edition” by Ruthven
Special Thanks to Shamayel Al-Haqqan
 Lecture 7: Primary & Secondary Prevention of Cardiovascular
Diseases
• Primary prevention à preventing CVD before it occurs.
• Secondary prevention à preventing additional attacks of CVD after the first attack has
occurred.
• Ten-year ASCVD risk à risk of a first atherosclerotic cardiovascular disease (ASCVD) event
among people free from ASCVD at the beginning of the period
o Nonfatal myocardial infarction
o Nonfatal stroke
o Coronary heart disease death
o Fatal stroke
• Established ASCVD à TIA, MI, Stroke, PAD

Aspirin
• No primary prevention (increases bleeding risk)
• Secondary prevention for all established ASCVD

Statins
• Primary prevention if:
o LDL-C is > or = 5 mmol
o Diabetic
o 40-75 years + LDL-C 1.8 – 4.9 mmol/L+ estimated 10-year ASCVD risk of ≥ 7.5%
• Secondary prevention for all established ASCVD

BBs
• Secondary for all MI if not contraindicated

ACE I
• Secondary for STEMI with:
o Anterior infarction or
o EF < or = 40% or
o HF

Aldosterone Antagonists
• Secondary for STEMI already taking ACE I & BB with:
o EF < or = 40% and
o Symptomatic HF or
o DM

Implantable Cardioverter Defibrillators (ICD) for sudden cardiac death prevention

• Primary Prevention - LVEF ≤ 35%
o Due to prior MI (at least 40 days post-MI and NYHA Class II or III)
o Nonischemic DCM and NYHA Class II or III
• Secondary Prevention
o Survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after
excluding any completely reversible causes (ex: severe hypokalemia)

Good Luck! J