Cardiology Flashcards

Question

What are common symptoms of atrial fibrillation?

Answer 1

* Palpitations * Fatigue * Dyspnea * Syncope * May precipitate or worsen heart failure

Answer 2

* Myocardial infarction (MI) * Mitral stenosis * Hypertension (HTN)

Answer 3

* Thyrotoxicosis * Pulmonary embolism * Alcohol * Hypokalemia

Answer 4

Obtain an ECG

Answer 5

Perform an echo to assess cardiac function and rule out underlying structural cardiac disease (MS)

Answer 6

Use a Holter monitor

Answer 7

DC cardioversion

Answer 8

Rate control (to decrease heart rate) ## Footnote Medications include BB, CCB, and Digoxin.

Answer 9

Electrical (DC cardioversion) and pharmacological options ## Footnote Amiodarone if structural heart disease; flecainide or propafenone if no heart disease.

Answer 10

To prevent thromboembolism

Answer 11

Risk of thromboembolism in A. fib patients

Answer 12

No prophylaxis

Answer 13

Warfarin or NOAC

Answer 14

Age ≥ 75, Vascular disease, Female ## Footnote Each component contributes to the total score.

Answer 15

Treatment of underlying cause

Answer 16

No p-waves; saw-toothed flutter waves. ## Footnote Always some degree of AV block (2:1, 3:1, 4:1).

Answer 17

150 bpm, 2:1. After vagal maneuver goes to exactly 75 bpm (characteristic).

Answer 18

Underlying heart disease, cardiomyopathy, COPD, hyperthyroidism, hypertension.

Answer 19

In inferior leads (II, III, aVF).

Answer 20

Electrical cardioversion. ## Footnote Examples include hypotension, CHF, angina.

Answer 21

B-blocker, diltiazem, verapamil, or digoxin.

Answer 22

Sotalol, amiodarone, type I antiarrhythmics.

Answer 23

Same as for patients with atrial fibrillation.

Answer 24

Antiarrhythmics (Amiodarone, Flecainide, Propafenone) and radiofrequency (RF) or catheter ablation.

Answer 25

A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.

Answer 26

Patients with severe COPD or congestive heart failure.

Answer 27

Right axis deviation, tall R wave in V1, and deep S wave in V6 (due to right ventricular hypertrophy - cor pulmonale).

Answer 28

Usually 100-150 bpm; may be as high as 250 bpm.

Answer 29

Irregularly irregular rhythm with varying PP, PR, and RR intervals. No flutter waves.

Answer 30

At least 3 distinct P-wave morphologies in the same lead.

Answer 31

It resolves.

Answer 32

Considered a poor prognostic sign (→ increased mortality due to the underlying illness).

Answer 33

Arising below the level of the Bundle of His, characterized by wide QRS complexes and 3 or more consecutive premature ventricular beats.

Answer 34

Regular; Rate > 100 (usually 140-200).

Answer 35

Sustained if >30 secs; non-sustained < 30 secs.

Answer 36

Wide aberrant bizarre-shaped QRS.

Answer 37

Dizziness, syncope, SOB, chest pain, palpitations, sudden death.

Answer 38

Ischemic heart disease (IHD), cardiomyopathy (hypertrophic/dilated).

Answer 39

Monomorphic (more common) vs polymorphic (torsades).

Answer 40

Electrical cardioversion (from 100J).

Answer 41

Electrical cardioversion, amiodarone, Type I agents (procainamide, quinidine).

Answer 42

Correction of reversible causes (hypokalemia, ischemia, HF, hypotension).

Answer 43

Polymorphic ventricular tachycardia with twisting of the axis and beat to beat variation in QRS shape.

Answer 44

Congenital Long QT Syndrome, drugs (class IA and III), electrolyte disturbances (hypokalemia, hypomagnesemia).

Answer 45

IV Magnesium Sulfate and correction of the underlying cause of prolonged QT.

Answer 46

A very rapid and irregular ventricular activation with no mechanical effect and therefore no cardiac output.

Answer 47

The patient is pulseless, becomes rapidly unconscious, and respiration ceases (cardiac arrest).

Answer 48

Immediate defibrillation.

Answer 49

Survivors are at high risk of sudden death and treatment is with an ICD.

Answer 50

Shock in synchrony with QRS complex. ## Footnote Used for A. Fib, Atrial flutter, SVT, VT with pulse.

Answer 51

Has a pulse but hemodynamically unstable. ## Footnote Energy levels: 50-200 Joules. Elective, patient awake & frequently sedated.

Answer 52

Shock NOT in synchrony with QRS complex. ## Footnote Indicated for V. Fib, VT without pulse.

Answer 53

Patient is pulseless. ## Footnote Energy levels: 200-360 Joules. Emergency, patient is unconscious.

Answer 54

<60 bpm. Normal p-wave followed by QRS. Regular (regular R-R interval). ## Footnote Causes include normal conditions (sleep, athletes) and extrinsic factors (BB intake, hypothyroidism, hypothermia).

Answer 55

Could be normal/stop offending agent (BB, CCB)/atropine. ## Footnote Patients with persistent symptomatic bradycardia are treated with a permanent cardiac pacemaker.

Answer 56

Failure of sinus node to depolarize (sinus arrest) or failure of the sinus impulse to propagate to the atria (sinoatrial block) → BRADYCARDIA. ## Footnote This can cause ectopic pacemaker activity and tachyarrhythmias (tachy-brady syndrome).

Answer 57

Severe sinus bradycardia or intermittent long pauses between consecutive P waves. ## Footnote Treatment includes permanent pacemaker insertion & anti-coagulation.

Answer 58

AV conduction is excessively slowed but all conducted; constant PR.

Answer 59

AV conduction is occasionally blocked.

Answer 60

PR increases progressively until a beat is dropped.

Answer 61

PR is constant and then a beat drops.

Answer 62

AV conduction is completely blocked; P-waves march through with QRSs without correlating P-waves.

Answer 63

Atropine then percutaneous pacing.

Answer 64

Pacemaker.

Answer 65

Wide QRS, broad R with prolonged upstroke in lateral leads (I, aVL, V5, V6), ST depression and T-wave inversion, reciprocal changes in V1 and V2.

Answer 66

Wide QRS, RSR' in V1 and V2 (rabbit ears), ST depression and T-wave inversion, reciprocal changes in lateral leads (I, aVL, V5, V6).

Answer 67

No Body Knows Cardiology

Answer 68

Na channel blockers ## Footnote Examples: 1 AP - quinidine procainamide, 1 AP - lidocaine, Same AP - flecainide

Answer 69

Beta blockers ## Footnote Examples: propranolol, atenolol, bisoprolol. SE: bradycardia, intermittent claudication, low glucose tolerance.

Answer 70

K channel blockers ## Footnote Examples: Amiodarone, sotalol. SE: hypo/hyperthyroidism, skin, liver toxicity, corneal micro-deposits.

Answer 71

Ca channel blockers ## Footnote Non-dihydro: verapamil, diltiazem.

Answer 72

ABCD (adenosine - BB - CCB - Digoxin)

Answer 73

LAPS (Lidocaine - Amiodarone - Procainamide - Sotalol)

Answer 74

A chronic, progressive condition in which the heart muscle is unable to pump enough blood to meet demand, leading to insufficient oxygen delivery to tissues and fluid accumulation in the lungs.

Answer 75

Symptoms include dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, wheezing, and easy fatigability.

Answer 76

Symptoms include peripheral edema, ascites, raised JVP, and hepatomegaly.

Answer 77

A condition where the ejection fraction is low (<45%), characterized by systolic dysfunction and dilation of the heart.

Answer 78

Main causes include myocardial infarction (CAD), valvular heart disease, and dilated cardiomyopathy.

Answer 79

A condition where the ejection fraction is 50% or more, characterized by diastolic dysfunction and normal left ventricular volume but high left ventricular end-diastolic pressure.

Answer 80

Main causes include hypertension and other conditions that may lead to systolic dysfunction over time.

Answer 81

The lower the ejection fraction, the poorer the survival.

Answer 82

Treatment focuses on managing the underlying cause, controlling heart rate to prolong diastole, and diuresing the patient.

Answer 83

No symptoms with ordinary physical activity.

Answer 84

Mild limitation of physical activity. Symptoms with ordinary physical activity.

Answer 85

Marked limitation of physical activity. Symptoms with less than ordinary physical activity.

Answer 86

Unable to perform any physical activity. Symptoms at rest.

Answer 87

Echocardiogram.

Answer 88

Transthoracic echo.

Answer 89

Ejection fraction: HF - REF vs HF - PEF (systolic vs diastolic dysfunction).

Answer 90

Chamber dilation or hypertrophy, underlying cause (wall motion abnormality, valvular disease, cardiomyopathy), severity of LV dysfunction, and follow up effect of treatment.

Answer 91

Arrhythmias (ex: heart block, A. fib).

Answer 92

Evidence of CAD & old MI.

Answer 93

Evidence of left ventricular hypertrophy.

Answer 94

Holter monitor.

Answer 95

Cardiomegaly, dilated upper lobe veins due to congestion, pulmonary edema (bat wing appearance), Kerly lines due to interstitial edema, and pleural effusion.

Answer 96

CBC (to look for anemia), renal and liver profile, BNP (normal BNP excludes CHF), and thyroid function.

Answer 97

Excludes CHF; used to determine etiology of acute dyspnea: cardiac vs respiratory.

Answer 98

To determine precise valve diameters, septal defects, diagnosis of ischemic HF, and revascularization.

Answer 99

Improve Survival.

Answer 100

ACE inhibitors (ACE I) or Angiotensin Receptor Blockers (ARB).

Answer 101

Metoprolol, Bisoprolol, Carvedilol (mnemonic: MBC).

Answer 102

They are anti-ischemic, antiarrhythmic, and decrease heart rate. ## Footnote Not given in acute treatment but improve survival in maintenance treatment.

Answer 103

In more advanced stages of heart failure (class III and IV).

Answer 104

Hyperkalemia and gynecomastia (less with eplerenone).

Answer 105

As vasodilator therapy if an ACE I/ARB can't be used.

Answer 106

A combination of valsartan (ARB) and sacubitril (neprilysin inhibitor).

Answer 107

They are started from initial therapy, primarily loop diuretics (e.g., furosemide).

Answer 108

Controversial; used to control symptoms in symptomatic patients on both ACE I and beta-blockers.

Answer 109

To reduce sudden death from ventricular arrhythmias.

Answer 110

EF < 30% on optimal medical therapy, previous cardiac arrest due to VT/VF, previous MI with non-sustained VT on 24 h monitoring & EF < 35%, long QT syndrome, Brugada syndrome, HOCM.

Answer 111

Cardiac resynchronization therapy, also known as biventricular pacemaker.

Answer 112

Coronary revascularization for CAD, valve repair/replacement for valvular heart disease, and cardiac transplantation in end-stage heart failure.

Answer 113

Insufficient perfusion of the coronary arteries due to decreased supply or increased demand.

Answer 114

Mechanical factors include atheroma, thrombosis, spasm, embolus, and arteritis. Decreased blood flow can be due to anemia, carboxy Hb, or hypotension.

Answer 115

Increased cardiac output from hypertension (HTN) or hypertrophy from aortic stenosis (AS) or HTN.

Answer 116

Obstruction due to coronary atherosclerosis.

Answer 117

Initial endothelial injury/dysfunction due to mechanical shear stress, biochemical factors (e.g., high LDL, diabetes mellitus), immunological factors, inflammation, and genetic alteration.

Answer 118

Increased permeability to oxidized lipoproteins leads to accumulation and uptake by macrophages, forming lipid-laden foam cells.

Answer 119

It progresses from intracellular lipids to transitional plaque, with accumulation of macrophages and smooth muscle cell migration, leading to plaque formation.

Answer 120

A plaque consists of a lipid core (fat deposits, foam cells, lymphocytes, phagocytes, smooth muscle cells) and a fibrous cap (smooth muscle & collagen).

Answer 121

Thrombus may be adherent to plaque or extending into the lumen due to endothelial injury or plaque fissuring.

Answer 122

A luminal cross-sectional area of approximately 70%.

Answer 123

1. Stable Angina 2. Acute Coronary Syndrome: Unstable angina, Non-ST-elevation MI, ST-elevation MI.

Answer 124

1. Age (above 45 in men and above 55 in women) 2. Male gender 3. Family history of premature CAD (1st degree FH in male<55yo or female<65yo) 4. Diabetes mellitus 5. Hyperlipidemia (esp. T LDL) 6. Hypertension 7. Smoking 8. Obesity, sedentary lifestyle 9. Hypercoagulability (1 fibrinogen, factor VII) 10. Homocysteinemia 11. Drugs (OCP, COX-2 inhibitors) 12. Heavy alcohol consumption, cocaine use

Answer 125

Intermittent claudication is associated with a 2-4 times increased risk of CAD, CVA, and HF.

Answer 126

MI is associated with a 3-6 times increased risk of CVA and HF.

Answer 127

CVA is associated with a 2-4 times increased risk of MI and HF.

Answer 128

Angina is defined as central/substernal heavy/tight/gripping chest pain that may radiate to jaw/arms caused by myocardial ischemia due to an imbalance between blood supply and oxygen demand.

Answer 129

1. Chest pain on exertion/emotion/stress 2. Tight squeezing chest pain lasting 5-15 mins, gradual in onset 3. No pain at rest 4. Occurs when oxygen demand exceeds perfusion (Demand > supply) 5. Constant; same effort/duration 6. Relieved by rest or GTN within minutes

Answer 130

1. Chest pain at rest 2. Crescendo/deterioration in previously stable angina 3. Angina of recent onset (<24 h) 4. Due to reduced resting coronary blood flow, not due to demand 5. Usually >15 mins, not relieved by rest 6. No ST elevation, normal cardiac enzymes 7. Part of Acute Coronary Syndrome: Ruptured atherosclerotic plaque leading to coronary occlusion

Answer 131

CBC, coagulation profile, lipid profile, fasting glucose, HbA1c, TFT, RFT, troponin (to exclude MI), and chest x-ray.

Answer 132

Usually normal; may show ST depression and T-wave inversion during an attack, normal between attacks.

Answer 133

To detect silent ischemia, particularly in diabetics and the elderly.

Answer 134

If the ECG is normal; must stabilize unstable angina with medical treatment before stress testing.

Answer 135

ST segment depression.

Answer 136

Severe angina or ischemic changes, ST depression >1mm at low workload within 6 minutes, or paradoxical fall in BP with exercise.

Answer 137

Perform a myocardial perfusion scan with IV administration of thallium/technetium.

Answer 138

Wall motion abnormalities.

Answer 139

Beta-blockers (BB) to reduce contractility, heart rate, and oxygen demand.

Answer 140

For immediate angina relief (e.g., GTN).

Answer 141

Calcium channel blockers (CCB).

Answer 142

Aspirin and statins.

Answer 143

Smoking cessation, blood pressure control, weight control, exercise, and optimal diabetes management.

Answer 144

If there is low EF, LAD/Left main/3-vessel disease, or severe angina despite maximum medical therapy.

Answer 145

Admit patient, oxygen (if <94), morphine and nitrates, dual antiplatelets (aspirin + clopidogrel), beta blockers, LMWH (enoxaparin) for 48 hours, electrolyte replacement (K+ and Mg++), revascularization (if no improvement after 48 hours, hemodynamically unstable, or new murmur).

Answer 146

Continue aspirin + clopidogrel for 6-9 months, then aspirin for life, beta blockers, nitrates (GTN), statins (regardless of LDL level), risk factor control.

Answer 147

Spontaneous episodes of angina with transient ischemic ST changes on ECG due to severe spasm of an epicardial coronary artery, usually near an atherosclerotic lesion.

Answer 148

Chronic pattern of episodes of angina, predominantly at rest, usually at night, and typically occurs in young smokers.

Answer 149

ECG shows ischemic ST-segment changes during the episode, normal in between; diagnostic coronary angiography to exclude fixed obstructive coronary artery disease; acetylcholine provocation test to induce spasm.

Answer 150

Calcium channel blockers to reduce spasm, lifestyle modification (smoking cessation & lipid control), sublingual nitroglycerin to abort episodes of angina.

Answer 151

ACE inhibitors and beta blockers have no benefit; nonselective beta blockers should be avoided.

Answer 152

Necrosis of myocardium due to occlusion of a coronary artery (usually by thrombus following atherosclerotic plaque rupture) → interruption of blood supply.

Answer 153

Plaque rupture with subsequent platelet adhesion, aggregation, and thrombus formation + vasoconstriction triggered by thromboxane A2.

Answer 154

MI → LV systolic dysfunction → increased blood in the LV → increased LV end-diastolic pressure → back pressures lead to increased LAP → increased PCWP exceeding oncotic pressure of plasma → leakage of fluid into the interstitium → dyspnea.

Answer 155

Intense sub-sternal chest pain (described as crushing/elephant standing on chest), radiates to neck/jaw/left arm/back, not relieved by rest/nitroglycerin. Diaphoresis, dyspnea, nausea & vomiting, sense of impending doom, syncope. May be asymptomatic in elderly/diabetics/post-op pts.

Answer 156

S4 (ischemia is associated with non-compliance of LV).

Answer 157

STEMI: Transmural involving entire wall thickness (ST-elevation). NSTEMI: Subendocardial involving inner 1/3 (ST-depression).

Answer 158

ECG (peaked T waves, Q waves, T-wave inversion, ST-elevation/depression). Cardiac enzymes (Gold standard): Troponin I and T and CK-MB.

Answer 159

Location is known from the leads showing ST changes: II, III, aVF: inferior (right coronary artery); I, aVL, V5, V6: lateral (left circumflex artery); V1, V2: septal; V3, V4: anterior; V1, V2, V3, V4: anteroseptal (left anterior descending artery); V1 to V5/V6: anterolateral; V1 to V6, I, aVL: extensive anterior MI.

Answer 160

Troponin: more sensitive & specific; may be falsely elevated (ex: vasculitis, drug abuse, myocarditis, pulmonary embolism, sepsis, renal failure).

Answer 161

CK-MB is useful for detecting recurrent infarctions because it returns to normal levels within 48-72 hours.

Answer 162

Necrosis of myocardium due to occlusion of a coronary artery (usually by thrombus following atherosclerotic plaque rupture) → interruption of blood supply.

Answer 163

Plaque rupture with subsequent platelet adhesion, aggregation, and thrombus formation + vasoconstriction triggered by thromboxane A2.

Answer 164

MI → LV systolic dysfunction → increased blood in the LV → increased LV end-diastolic pressure → back pressures lead to increased LAP → increased PCWP exceeding oncotic pressure of plasma → leakage of fluid into the interstitium → dyspnea.

Answer 165

Intense sub-sternal chest pain (described as crushing/elephant standing on chest), radiates to neck/jaw/left arm/back, not relieved by rest/nitroglycerin. Diaphoresis, dyspnea, nausea & vomiting, sense of impending doom, syncope. May be asymptomatic in elderly/diabetics/post-op pts.

Answer 166

S4 (ischemia is associated with non-compliance of LV).

Answer 167

STEMI: Transmural involving entire wall thickness (ST-elevation). NSTEMI: Subendocardial involving inner 1/3 (ST-depression).

Answer 168

ECG (peaked T waves, Q waves, T-wave inversion, ST-elevation/depression). Cardiac enzymes (Gold standard): Troponin I and T and CK-MB.

Answer 169

Location is known from the leads showing ST changes: II, III, aVF: inferior (right coronary artery); I, aVL, V5, V6: lateral (left circumflex artery); V1, V2: septal; V3, V4: anterior; V1, V2, V3, V4: anteroseptal (left anterior descending artery); V1 to V5/V6: anterolateral; V1 to V6, I, aVL: extensive anterior MI.

Answer 170

Troponin: more sensitive & specific; may be falsely elevated (ex: vasculitis, drug abuse, myocarditis, pulmonary embolism, sepsis, renal failure).

Answer 171

CK-MB is useful for detecting recurrent infarctions because it returns to normal levels within 48-72 hours.

Answer 172

Admit to the CCU & establish IV access. Oxygen if O2 is <94%.

Answer 173

Aspirin + clopidogrel. Dual antiplatelets are given for the first 6 months, then aspirin for life.

Answer 174

Morphine, Heparin (usually after revascularization/PCI), Beta blocker, Nitrate, Statin.

Answer 175

PCI (door to balloon < 90 minutes) is superior to tPA if available.

Answer 176

Door to needle < 30 minutes, within 12 hours, preferably 6 hours.

Answer 177

Revascularization is not necessary immediately; initial treatment may include LMW heparin or GPIIb/IIIa inhibitors + angioplasty & stenting.

Answer 178

Heart failure, Arrhythmias, Recurrent MI, Mechanical complications.

Answer 179

Heart failure.

Answer 180

Arrhythmias, specifically ventricular arrhythmias.

Answer 181

Free wall rupture, Interventricular septum rupture, Papillary muscle rupture, Ventricular pseudoaneurysm/aneurysm.

Answer 182

A triad of fever, pericarditis + pleuritis, leukocytosis, treated with aspirin/ibuprofen. Develops after 2 weeks.

Answer 183

May be associated with right ventricular infarction, 3rd degree heart block, hypotension, and raised JVP with clear lung fields.

Answer 184

High volume fluid replacement. Nitrates are contraindicated.

Answer 185

Multiple infarcts, Acute MR, Recurrent infarcts, Rupture → VSD, Large infarcts, Pump failure → cardiogenic shock.

Answer 186

1. Propped up positioning 2. Oxygen 3. IV furosemide 4. Morphine 5. IV nitrate 6. Inotropic support if poor LV function 7. Intra-aortic balloon pump as a bridge prior to surgery.

Answer 187

Admit to the CCU & establish IV access. Oxygen if O2 is <94%.

Answer 188

Aspirin + clopidogrel. Dual antiplatelets are given for the first 6 months, then aspirin for life.

Answer 189

Morphine, Heparin (usually after revascularization/PCI), Beta blocker, Nitrate, Statin.

Answer 190

PCI (door to balloon < 90 minutes) is superior to tPA if available.

Answer 191

Door to needle < 30 minutes, within 12 hours, preferably 6 hours.

Answer 192

Revascularization is not necessary immediately; initial treatment may include LMW heparin or GPIIb/IIIa inhibitors + angioplasty & stenting.

Answer 193

Heart failure, Arrhythmias, Recurrent MI, Mechanical complications.

Answer 194

Heart failure.

Answer 195

Arrhythmias, specifically ventricular arrhythmias.

Answer 196

Free wall rupture, Interventricular septum rupture, Papillary muscle rupture, Ventricular pseudoaneurysm/aneurysm.

Answer 197

A triad of fever, pericarditis + pleuritis, leukocytosis, treated with aspirin/ibuprofen. Develops after 2 weeks.

Answer 198

May be associated with right ventricular infarction, 3rd degree heart block, hypotension, and raised JVP with clear lung fields.

Answer 199

High volume fluid replacement. Nitrates are contraindicated.

Answer 200

Multiple infarcts, Acute MR, Recurrent infarcts, Rupture → VSD, Large infarcts, Pump failure → cardiogenic shock.

Answer 201

1. Propped up positioning 2. Oxygen 3. IV furosemide 4. Morphine 5. IV nitrate 6. Inotropic support if poor LV function 7. Intra-aortic balloon pump as a bridge prior to surgery.

Answer 202

Infection with Group A Streptococcus Pyogens (GAS) leading to an autoimmune reaction. Develops 2-3 weeks after sore throat onset.

Answer 203

Chronic valvular abnormalities secondary to acute rheumatic fever, mostly mitral stenosis (MS).

Answer 204

Pathological findings seen in the heart during rheumatic fever.

Answer 205

Mnemonic: Jones (JeNES) - Joints (polyarthritis), Cardiac (murmurs, CHF, pericarditis), Subcutaneous nodules, Erythema marginatum, Sydenham's chorea.

Answer 206

Fever, elevated ESR or CRP or leukocytosis, prior history of rheumatic fever or heart disease, prolonged PR interval on ECG, arthralgia.

Answer 207

2 major criteria OR 1 major and 2 minor + throat culture growing GAS OR elevated anti-streptolysin O titers.

Answer 208

Complete bed rest, high-dose aspirin, penicillin, treatment monitored with CRP, prednisolone if cardiac involvement, treat valvular pathology.

Answer 209

Penicillin (erythromycin if allergic) in case of streptococcal pharyngitis.

Answer 210

10 years or until age 40, whichever is longer.

Answer 211

10 years or until age 21, whichever is longer.

Answer 212

5 years or until age 21, whichever is longer.

Answer 213

Infection of the endocardium or the vascular endothelium of the heart.

Answer 214

1. Acute: Mostly by S. aureus, normal valve, fatal in <6 weeks if untreated. 2. Subacute: More common, Streptococcus viridians or Enterococcus, damaged valve, takes >6 weeks to cause death.

Answer 215

Staphylococcus aureus.

Answer 216

Streptococcus viridians.

Answer 217

Staphylococcus epidermidis (acquired in perioperative period).

Answer 218

Streptococci (follows bacteremia).

Answer 219

S. aureus mostly, others are Enterococci, Streptococci, fungi (Candida), and gram-negative rods (Pseudomonas), usually affecting right-sided valves.

Answer 220

Coxiella burnetti, Bartonella, Chlamydia, and Legionella.

Answer 221

Fever, weight loss, anemia, and slight splenomegaly (important finding).

Answer 222

New heart murmur + fever → must rule out infective endocarditis.

Answer 223

Murmurs due to valve destruction (vegetations made up of fibrin, platelets, and infectious organisms destroying the valve).

Answer 224

Painless vascular phenomena associated with infective endocarditis.

Answer 225

Brain, kidney, spleen, and, if right-sided, lungs.

Answer 226

Small, linear, red or brown streaks in the nail bed associated with infective endocarditis.

Answer 227

Retinal findings associated with infective endocarditis.

Answer 228

Painful lesions associated with infective endocarditis.

Answer 229

1. Blood cultures (3 sets taken over 24 hours before antibiotics). 2. Serological tests for unusual organisms. 3. CBC: normocytic normochromic anemia, leukocytosis, raised ESR. 4. Echocardiography: Transesophageal is more sensitive than transthoracic for prosthetic valves. 5. CXR: Heart failure or evidence of embolization to lung if right-sided. 6. ECG: MI if embolization to coronary arteries, or conduction defect. 7. Urinalysis: hematuria. 8. Raised serum Ig and low complement due to immune complex deposition.

Answer 230

2 Major Criteria OR 1 Major and 3 Minor OR 5 Minor OR only direct evidence of infective endocarditis (e.g., vegetation histology or culture).

Answer 231

1 Major and 1 Minor OR 3 Minor.

Answer 232

• 2 positive blood cultures for an organism known to cause IE OR persistent bacteremia (2 +ve 12 hours apart or 3 of 4 +ve drawn over 1 hour) • ECHO evidence (oscillating mass on valve or supporting structures, abscess, new valvular regurgitation, or partial dehiscence of prosthetic valve).

Answer 233

• Predisposing factor (cardiac lesion, IV drug use) • Fever > 38°C • Evidence of emboli or vasculitis • Immunological features (Osler node, nephritis) • Echo of uncertain significance • Serology for Q fever or Chlamydial infection • Single +ve blood culture of uncertain etiology.

Answer 234

IV bactericidal antibiotics for 2 weeks, then oral for 2-4 weeks.

Answer 235

Benzylpenicillin + gentamicin generally, unless staphylococci are suspected, then vancomycin + gentamicin.

Answer 236

• Severe heart failure • Worsening renal failure • Extensive damage to the valve • Prosthetic valve.

Answer 237

NOT INDICATED for patients when they are diagnosed; taken if patient has BOTH a qualifying cardiac indication AND a qualifying procedure.

Answer 238

Use amoxicillin. If allergic to penicillin, use clindamycin/azithromycin.

Answer 239

• Prosthetic heart valve • Hx of IE • Transplanted heart with valvular disease • Unrepaired cyanotic congenital heart disease • Repaired congenital heart disease (CHD) with prosthetic material, during the first 6 months after procedure • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device.

Answer 240

• Dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa • Invasive respiratory tract procedures that involve incision or biopsy of the respiratory mucosa • Surgical procedure that involves infected skin, skin structure, or musculoskeletal tissue.

Answer 241

No prophylaxis for genitourinary or gastrointestinal tract procedures.

Answer 242

Rheumatic heart disease (99%) and congenital or carcinoid (1%)

Answer 243

Increased left atrial (LA) pressure leading to LA dilation and backup of blood into the pulmonary vasculature.

Answer 244

On exertion, increased heart rate (THR) and cardiac output (CO) reduce ventricular diastolic filling time, leading to more blood in the left atrium and increased LA pressure.

Answer 245

PCWP becomes higher than the oncotic pressure of plasma, leading to exudation of fluid into the interstitium, causing stiff lungs and symptoms of dyspnea.

Answer 246

Rupture of pulmonary capillaries and bronchial venous anastomosis.

Answer 247

Atrial fibrillation due to stagnation of blood in the left atrium can lead to thrombus formation and thromboembolism to the brain.

Answer 248

Warfarin and heparin until INR=2, then continue warfarin only.

Answer 249

A-wave on JVP, S4, and presystolic accentuation disappear.

Answer 250

Shortness of breath (SOB), fatigue, hemoptysis, hoarseness, and dysphagia.

Answer 251

Loud S1, normal S2, opening snap after S2, rumbling mid-diastolic murmur, presystolic accentuation, and mitral facies.

Answer 252

Atrial fibrillation is common with a low volume pulse.

Answer 253

Tapping apex that is not displaced.

Answer 254

• Soft S1 • Longer duration of the murmur • Shorter S2 - opening snap interval • Disappearance of the opening snap • Indirect signs: signs of pulmonary hypertension and RHF

Answer 255

• Straightening of left heart border (mitralization) • Widened carina (>70) • Double density shadow • +/- Signs of pulmonary edema • LV is normal size (no cardiomegaly)

Answer 256

• A. Fibrillation • P. mitrale (bifid p-wave) • May develop Pul. HTN → P. pulmonale (Right atrial hypertrophy) • Possibly RVH (right axis deviation, tall R waves in V1)

Answer 257

• EF = normal • Pathology: commissural fusion, leaflet thickening, calcified nodules, shortened chordae, fish-mouth orifice (hockey stick appearance) ## Footnote Signs of severity on echo: MV area = < 1cm2 [N = 4-6cm2], MV index < 0.6cm²/m², Mean pressure gradient across MV = severe > 10 [N = 0].

Answer 258

The presence of symptoms.

Answer 259

• Beta blockers for heart rate control • Loop diuretics for fluid overload + salt restriction • A. Fib → lifelong warfarin • Don't give ACE inhibitors

Answer 260

Percutaneous transseptal balloon valvotomy (TSBV) is the treatment of choice if severely symptomatic or if pulmonary hypertension develops. ## Footnote If there is an LA thrombus, MR, or a heavily calcified mitral valve, TSBV CANNOT be done → mitral valve replacement.

Answer 261

• Pulmonary hypertension • Right sided HF (high JVP, dependent edema, tender hepatomegaly, ascites) • Congestive heart failure • Acute pulmonary edema • Atrial fibrillation → sudden deterioration & systemic embolization

Answer 262

IHD leading to papillary muscle rupture/dysfunction, MVP causing ruptured chordae, and IE or RHD resulting in ruptured chordae or cuspal perforation.

Answer 263

Acute MR causes a sudden rise in left atrial pressure with normal LA size, leading to backflow into the lungs and increased pulmonary venous pressure. There is no time for compensation, presenting with pulmonary edema or cardiogenic shock.

Answer 264

MVP due to myxomatous degeneration (e.g., Marfan syndrome) and Dilated Cardiomyopathy (CM) causing annular dilatation.

Answer 265

Long-standing regurgitation leads to gradually increased LA pressure, accommodated by LA dilation and increased LA compliance. LV dilation results in LV dysfunction, and chronic backflow into pulmonary vessels causes pulmonary hypertension.

Answer 266

Volume overload of LA and LV leads to dilatation and hypertrophy as compensation, resulting in early palpitations, especially with exertion.

Answer 267

With time, compensation fails, leading to increased pressure and symptoms of left heart failure (LHF) such as dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), and fatigue.

Answer 268

Soft S1, normal S2, S3 added sound (ventricular gallop), pansystolic murmur radiating to axilla, and if MVP is the cause, a mid-systolic click followed by a late systolic murmur.

Answer 269

Hyperdynamic apex, added short mid-diastolic flow murmur, systolic thrill (grade 4), wide split S2 (early closure of A2), and signs of pulmonary hypertension.

Answer 270

Cardiomegaly and pulmonary edema.

Answer 271

May develop A. Fib.

Answer 272

Dilated left atrium (LA) and left ventricle (LV), decreased LV function.

Answer 273

Severity of regurgitation.

Answer 274

Follow-up echo and clinical examination.

Answer 275

ACE inhibitors to decrease afterload and diuretics for symptomatic relief.

Answer 276

Lifelong warfarin.

Answer 277

Emergency surgery: valve replacement.

Answer 278

Repair is better than replacement.

Answer 279

Severe with EF > 30% and end-diastolic diameter < 55mm.

Answer 280

End systolic dimension > 45mm and/or EF < 60%, preserved EF with A. Fib or pulmonary hypertension.

Answer 281

Myxomatous degeneration caused by Marfan syndrome.

Answer 282

One of the mitral valve leaflets prolapses back into the LA causing mitral regurgitation in some cases.

Answer 283

Atypical chest pain and palpitations.

Answer 284

Mid-systolic click followed by a later systolic murmur.

Answer 285

Murmur will decrease in intensity and click will increase.

Answer 286

Murmur will increase in intensity and click will decrease.

Answer 287

Echocardiogram.

Answer 288

Beta-blockers.

Answer 289

To prevent thromboembolism.

Answer 290

Aortic stenosis is a condition characterized by the narrowing of the aortic valve, leading to obstruction of blood flow from the left ventricle to the aorta.

Answer 291

Causes include calcification of a bicuspid valve in younger patients and a tricuspid valve in elderly patients, as well as rheumatic heart disease.

Answer 292

Stenotic valve leads to left ventricular (LV) outflow obstruction, resulting in LV hypertrophy (LVH). A smaller valve causes cardiac output (CO) to fail to increase on exertion, leading to angina.

Answer 293

Patients are often asymptomatic for years, then develop a triad of symptoms: angina, exertional syncope, and dyspnea. Symptoms of heart failure may also be present, indicating poor prognosis.

Answer 294

Normal S1, soft muffled S2, added S4 sound, and a systolic ejection murmur (harsh crescendo-decrescendo) best heard at the right upper sternal border, radiating to the carotids.

Answer 295

'Parvus et tardus' refers to a low volume, slow rising carotid pulse often seen in patients with aortic stenosis.

Answer 296

Signs include symptomatic dyspnea, soft S2, paradoxical splitting of S2, added S4, systolic thrill at the aortic area, parvus et tardus pulse, and a heaving apex.

Answer 297

Chest X-ray (CXR) may show calcified aortic valve, post-stenotic aortic dilatation, and pulmonary edema. ECG may show LV strain pattern and LVH.

Answer 298

Echocardiography with Doppler shows a mean pressure gradient > 40 mmHg.

Answer 299

Treatment typically involves aortic valve replacement. If open surgery is unsuitable, transcatheter aortic valve replacement (TAVR) may be performed.

Answer 300

Aortic regurgitation is a condition characterized by the inadequate closure of the aortic valve, leading to the reflux of blood from the aorta into the left ventricle during diastole.

Answer 301

Acute causes include infective endocarditis, acute rheumatic fever, aortic dissection, failed prosthetic heart valve, and myocardial infarction.

Answer 302

Chronic causes include rheumatic heart disease, bicuspid aortic valve, Marfan syndrome, Ehlers-Danlos syndrome, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, systemic lupus erythematosus, syphilis, and osteogenesis imperfecta.

Answer 303

Inadequate closure of the aortic valve leads to reflux of blood into the left ventricle during diastole, increasing left ventricular volume, causing dilatation, increased stroke volume, and pulse pressure, eventually leading to left ventricular failure.

Answer 304

Symptoms include being asymptomatic for years, signs of left ventricular failure (dyspnea, orthopnea), and in acute cases, cyanosis and shock.

Answer 305

Signs include widened pulse pressure, collapsing water-hammer pulse (Corrigan pulse), possible S3 added sound, and early diastolic murmur (increased when sitting forward and holding breath in expiration).

Answer 306

Signs of severe AR include Quincke pulse (pulsation in nailbed), head bobbing, and Hill sign (popliteal systolic BP > brachial systolic BP by 60mmHg or more).

Answer 307

Diagnosis can be made using chest X-ray (showing LVH and dilated aorta), ECG (showing LVH), and echocardiogram (to assess LV size and function and look for dilated aortic root).

Answer 308

Acute AR is a medical emergency requiring emergent aortic valve replacement. Symptomatic relief can be provided with nifedipine and ACE inhibitors, while definitive treatment is aortic valve replacement.

Answer 309

Tricuspid stenosis is almost always the result of rheumatic fever and is frequently associated with mitral and aortic valve disease.

Answer 310

Pulmonary hypertension, which can occur due to mitral stenosis leading to left heart failure, then pulmonary hypertension, right heart failure, and dilatation of the right ventricle.

Answer 311

Post myocardial infarction, congenital conditions (such as Ebstein anomaly), right-sided heart failure related to drug abuse, dilated cardiomyopathy, rheumatic heart disease, and carcinoid syndrome.

Answer 312

A pan systolic murmur located at the left lower sternal border, high in intensity with inspiration.

Answer 313

A prominent V-wave with S1 due to increased atrial filling in systole caused by regurgitation of blood back into the atrium.

Answer 314

Pulsatile tender hepatomegaly, severe peripheral edema, and ascites.

Answer 315

Mostly congenital conditions such as Tetralogy of Fallot and Noonan syndrome, with a minority being acquired.

Answer 316

Asymptomatic at first, but may later present with fatigue, syncope, and right ventricular failure.

Answer 317

A parasternal heave and a systolic thrill in the pulmonary area, along with a prominent a-wave in JVP.

Answer 318

A harsh ejection systolic murmur (usually grade 4) best heard at the pulmonary area during inspiration.

Answer 319

Post-stenotic dilatation and oligemic lung fields.

Answer 320

Valvuloplasty or surgery.

Answer 321

Pulmonary hypertension and dilatation of the valve ring, which may also result from endocarditis, particularly in IV drug abusers.

Answer 322

An early diastolic murmur heard at the upper left sternal edge, known as the Graham Steell murmur.

Answer 323

Usually asymptomatic, and treatment is rarely required.

Answer 324

Atrial contraction (before carotid pulse)

Answer 325

TS, PS, pulmonary HTN, RVH

Answer 326

Complete heart block, ventricular tachycardia

Answer 327

Atrial fibrillation

Answer 328

Atrial filling (with carotid pulse)

Answer 329

Alternating strong & weak beats ## Footnote Associated with heart failure and poor prognosis.

Answer 330

Aortic waveform with 2 peaks ## Footnote Seen in hypertrophic cardiomyopathy (jerky pulse), mixed AR + AS.

Answer 331

Weak pulse in inspiration & strong pulse in expiration ## Footnote Associated with cardiac tamponade.

Answer 332

Groups of 2 beats separated by a longer interval ## Footnote Indicates premature ventricular/ectopic heart beats.

Answer 333

Significant rise, late peak, low amplitude, anacrotic notch

Answer 334

Very rare, only felt in pure isolated MS and represents palpable S1

Answer 335

Hypertrophic pressure overload ## Footnote Associated with AS, HOCM, systemic HTN, coarctation of aorta.

Answer 336

Felt as multiple intercostal spaces (big area) ## Footnote High amplitude and goes down fast; associated with AR, MR, PDA, VSD.

Answer 337

Felt down and out (dilated = displaced)

Answer 338

S3 is a ventricular gallop caused by rapid ventricular filling in early diastole. It occurs during passive filling of an overly compliant left ventricle. ## Footnote May be normal in children, pregnant women, and athletes; may be pathological due to HF-REF, acute pulmonary edema, AR, MR, or dilated cardiomyopathy.

Answer 339

S4 is an atrial gallop that occurs just before S1, caused by atrial contraction against a stiff non-compliant ventricle. It is always pathological. ## Footnote Associated with HF-PEF, AS, HOCM, and systemic hypertension.

Answer 340

Inspiration makes right-sided murmurs louder, while expiration makes left-sided murmurs louder. ## Footnote Examples include MS and MR increasing with AS and AR.

Answer 341

Murmurs decrease with standing and Valsalva, while HOCM and MVP murmurs increase with standing and Valsalva. ## Footnote MVP murmur increases with standing and Valsalva, decreases with leg raise.

Answer 342

The MVP click increases with squatting and decreases with standing. ## Footnote In mitral valve prolapse, the murmur increases when standing and decreases when squatting.

Answer 343

A group of diseases of the myocardium affecting its mechanical or electrical functions.

Answer 344

Marked ventricular hypertrophy in the absence of abnormal loading conditions.

Answer 345

The hypertrophic ventricle.

Answer 346

Hypertrophic cardiomyopathy.

Answer 347

Asymptomatic, breathlessness, angina, syncope, jerky pulse, ejection systolic murmur, pansystolic murmur, bisferious pulse, double apical pulsation.

Answer 348

They increase the intensity of these murmurs.

Answer 349

Sudden death, thromboembolism, arrhythmias, infective endocarditis, heart failure.

Answer 350

Signs of LVH: Deep S in V1 V2, tall R in V5 V6, both together > 35 mm.

Answer 351

Septum 1.5 times the thickness of the posterior wall.

Answer 352

Amiodarone, ICD, beta blockers, verapamil.

Answer 353

Vasodilators, as they aggravate ventricular outflow obstruction.

Answer 354

Catheter ablation of the septum, surgical myomectomy.

Answer 355

Most common type of cardiomyopathy resulting from a dilated, weak, poorly contracting ventricle. ## Footnote Clinical features include shortness of breath, arrhythmias, embolism, and heart failure.

Answer 356

50% are idiopathic; other causes include CAD, toxic factors (alcohol, doxorubicin), metabolic issues (uremia, hypophosphatemia), thyroid disorders, familial factors, infections (viral, Chagas, HIV, Lyme), peripartum, haemochromatosis, collagen vascular diseases, and catecholamines (pheochromocytoma, cocaine).

Answer 357

ECG shows arrhythmias and T wave flattening; CXR shows cardiac enlargement; Echo shows global hypokinesia and dilated ventricle. ## Footnote Other methods include coronary angiography and viral/autoimmune screening.

Answer 358

Remove offending agents; use digoxin, vasodilators, and diuretics; consider anticoagulants.

Answer 359

Infiltration of the myocardium results in a rigid ventricle leading to impaired diastolic filling.

Answer 360

Causes include amyloidosis, sarcoidosis, haemochromatosis, scleroderma, carcinoid syndrome, and chemotherapy/radiation.

Answer 361

ECG, CXR, and Echo show abnormal and nonspecific features; diagnosis is made by cardiac catheterization showing pressure changes, and biopsy may be taken for histological diagnosis.

Answer 362

No specific treatment; prognosis is poor, but diuretics and vasodilators may be used for symptomatic relief.

Answer 363

Inflammation of the pericardial sac.

Answer 364

Idiopathic (post viral), infectious (viral, bacterial, fungal), acute MI (1st 24 hours), uremia, collagen vascular diseases, neoplasms, amyloidosis, radiation, trauma, and after surgery.

Answer 365

Chest pain (retrosternal, radiates to neck and back), fever, leukocytosis, and friction rub.

Answer 366

Aggravated by coughing, inspiration, and lying supine; relieved by leaning forward.

Answer 367

Pericardial effusion and cardiac tamponade.

Answer 368

ECG shows diffuse ST elevation and PR depression; ECHO often normal unless there is pericardial effusion.

Answer 369

Aspirin or ibuprofen + colchicine & bedrest are the mainstay of therapy; glucocorticoids if no response.

Answer 370

A condition where the heart is enclosed by a rigid fibrous pericardial sac, reducing diastolic filling of ventricles.

Answer 371

Idiopathic; any cause of pericarditis can lead to calcification and fibrosis.

Answer 372

Resembles right heart failure (peripheral edema, distended JVP, ascites, hepatomegaly), Kussmaul sign, pulsus paradoxus, atrial fibrillation, and pericardial knock.

Answer 373

Chest X-ray shows normal heart size with pericardial calcifications; CT/MRI shows pericardial thickening and calcification.

Answer 374

Diuretics to relieve edema and organomegaly; surgical excision of pericardium.

Answer 375

Exudation of fluid into the pericardial space.

Answer 376

Acute pericarditis, salt and water retention conditions (e.g., CHF, cirrhosis, nephrotic syndrome), or trauma.

Answer 377

Up to 2 liters over weeks to months.

Answer 378

Muffled heart sounds and dullness at the left lung base.

Answer 379

Echocardiogram (Echo).

Answer 380

Cardiomegaly without pulmonary vascular congestion and a flask shape appearance.

Answer 381

Most resolve spontaneously; if not, pericardiocentesis is performed.

Answer 382

Rapid accumulation of fluid in the pericardial space that prevents the heart from compensating, leading to acute impairment of ventricular filling.

Answer 383

Decrease in pulse (carotid/femoral) during inspiration and increase during expiration (decrease >10mmHg of BP during inspiration).

Answer 384

Tachypnea, tachycardia, hypotension, elevated JVP, clear lungs, and Beck's triad (muffled heart sounds, jugular vein distension, hypotension).

Answer 385

Penetrating trauma, iatrogenic causes (e.g., central line placement, pericardiocentesis), pericarditis, and post-myocardial infarction.

Answer 386

Echocardiogram (Echo).

Answer 387

Enlargement of the cardiac silhouette.

Answer 388

Perform pericardiocentesis.

Answer 389

Emergent surgery.

Answer 390

Do NOT use diuretics as they worsen the collapse.

Answer 391

Inflammation of the myocardium; typical patients are young males.

Answer 392

Viruses (HHV6, coxsackie, parvovirus B19), bacteria (group A beta hemolytic strept, Lyme disease, mycoplasma), SLE, and medications (sulfonamides, adriamycin).

Answer 393

Fatigue, chest pain, pericarditis, arrhythmias, CHF, or may be asymptomatic.

Answer 394

ECG (sinus tachycardia, low voltage, electrical alternans, ST elevation), cardiac enzyme levels (elevated), increased ESR, serum viral titers, chest X-ray (cardiomegaly), echo (may have decreased EF), biopsy (most accurate test).

Answer 395

Bed rest and treatment of heart failure (if low EF) with beta blockers and ACE inhibitors. NSAIDs and steroids are contraindicated.

Answer 396

Congenital narrowing of the aorta distal to the insertion of the ductus arteriosus, causing hypertension due to marked reduction in kidney perfusion.

Answer 397

Chest pain, murmur, hypertension in a young patient, radio-femoral delay, mid-late systolic murmur.

Answer 398

Rib notching due to collateral arteries eroding the undersurface of the ribs.

Answer 399

Normal pulmonary artery pressure (PAP) is 10-14 mmHg.

Answer 400

In pulmonary hypertension, there is an increase in PAP to more than 25 mmHg at rest, leading to right heart failure (RHF).

Answer 401

Pulmonary hypertension is due to an increase in pulmonary vascular resistance and an increase in pulmonary blood flow.

Answer 402

Common presentations include exertional dyspnea, lethargy and fatigue, loud pulmonary S2 sound, right parasternal heave, and signs of RHF (peripheral edema, hepatomegaly, distended JVP, prominent V wave).

Answer 403

Diagnosis is made through right heart catheterization to determine pulmonary wedge pressure (PWP) and confirm increased PAP, along with CXR, ECG, and echo to identify the underlying cause.

Answer 404

Treatment includes oxygen, warfarin, diuretics, oral CCB, and addressing the underlying cause.

Answer 405

Left to right shunt (e.g., VSD, ASD, PDA) presents with plethoric lung fields, QP:QS > 2:1, frequent severe chest infections, cardiac overactivity, and signs of cardiomegaly.

Answer 406

Causes of pulmonary artery prominence include pulmonary hypertension, left heart disease, Eisenmenger syndrome, chronic lung disease, recurrent pulmonary thromboembolism, CT disease (SLE, scleroderma), and peripheral pulmonary artery stenosis.

Answer 407

On examination, findings may include loud P2, left parasternal heave (right ventricular hypertrophy), Graham steel murmur (early diastolic), PR and TR murmurs, and prominent JVP.

Answer 408

Pulmonary stenosis presents with an oligemic lung field, is often congenital, and starts acyanotic before potentially becoming a right-to-left shunt.

Answer 409

On examination, findings may include heave, systolic thrill, prominent a wave in JVP, ejection systolic murmur best at inspiration, soft P2, and delayed P2.

Answer 410

Blood pressure above 140/90 based on 2 readings on separate occasions, unless severe hypertension (systolic ≥180 or diastolic ≥110) or evidence of end-organ damage.

Answer 411

Hypertension is a major cause of premature vascular disease leading to cerebrovascular events, ischemic heart disease, and peripheral vascular disease.

Answer 412

Mortality increases with increasing blood pressure.

Answer 413

Increased activity of the sympathetic nervous system, RAAS overactivation, sodium overload, vascular remodeling, endothelial cell dysfunction, and hyperinsulinemia.

Answer 414

80-90% of patients with hypertension have no known underlying cause.

Answer 415

Renal parenchymal disease, renal artery stenosis, high salt intake, metabolic syndrome, low birth weight, excess alcohol intake, Cushing's syndrome, pheochromocytoma, acromegaly, coarctation of the aorta, and certain drugs.

Answer 416

NSAIDs, combined oral contraceptives (especially high in estrogen), antidepressants (SNRI), acetaminophen, sympathomimetics, and steroids.

Answer 417

Screening may be opportunistic or community-based, indicated for ages 18 or above or patients with cardiovascular disease.

Answer 418

If blood pressure is normal, check every 5 years; if diabetic, check annually.

Answer 419

Cuff size should be 80% of arm height and 40% width. Measure in a quiet room with the patient seated quietly for 5 minutes.

Answer 420

Blood pressure should be repeated after 1 minute of standing if a reduction in systolic BP ≥ 20 mmHg is suspected.

Answer 421

No, a diagnosis cannot be made from a single reading unless it is very high (≥ 180 or ≥ 110).

Answer 422

140/90 to 180/120 mmHg

Answer 423

1. Ambulatory Blood Pressure Monitoring (ABPM): 2 measurements per hour, at least 14 during waking hours. 2. Home Blood Pressure Measurement (HBPM): 2 measurements per day for 4-7 days, recording the lowest reading.

Answer 424

Clinic BP ≥ 140/90 or Ambulatory/Home BP measurements ≥ 135/85

Answer 425

1. Prehypertension: Systolic 120-139 or Diastolic 80-89 2. Stage 1: Clinic Systolic 140-159 or Diastolic 90-99 & daytime average ABPM/HBPM ≥ 135/85 3. Stage 2: Clinic Systolic ≥ 160 or Diastolic ≥ 100 & daytime average ABPM/HBPM ≥ 150/95 4. Hypertensive Urgency: Systolic ≥ 180 and/or Diastolic ≥ 120 5. Hypertensive Emergency: Systolic ≥ 180 and/or Diastolic ≥ 120 with end organ damage.

Answer 426

ASCVD risk calculator or QRISK 2-2015

Answer 427

1. Urinalysis: for protein, albumin:creatinine ratio & hematuria 2. Blood tests: glucose, electrolytes, creatinine, eGFR & total & HDL cholesterol 3. ECG: to detect Left Ventricular Hypertrophy (LVH) 4. Clinical history & examination for secondary causes.

Answer 428

1. Blood vessels: atherosclerosis, aneurysms, aortic dissection 2. Chronic kidney disease: hematuria, uremia, proteinemia 3. Cardiac failure: pulmonary edema, myocardial infarction, LVH 4. Stroke/TIA: hemorrhage or infarction, seizures, vascular dementia

Answer 429

1. Grade 1: tortuosity of retinal arteries with increased reflectiveness (silver wiring) 2. Grade 2: Grade 1 + arteriovenous nipping 3. Grade 3: Grade 2 + flame-shaped hemorrhages & soft exudates 4. Grade 4: Grade 3 + papilledema (blurring of the optic disc)

Answer 430

1. Diet: high in vegetables & fruits, low-fat diet. 2. Reduction of sodium intake: 5-6g/day & use of low sodium salt. 3. Regular exercise: 30 min of moderate-intensity aerobic exercise 5-7 days/week. 4. Reduction of alcohol. 5. Smoking cessation. 6. Weight reduction: BMI < 25, waist circumference < 102 cm for men & < 88 cm for women.

Answer 431

In patients with mean home or daytime ambulatory BP ≥135 mmHg systolic or ≥85 mmHg diastolic (or average office BP ≥140 mmHg systolic or ≥90 mmHg diastolic), or with BP ≥130 mmHg systolic or ≥80 mmHg diastolic and one or more risk factors.

Answer 432

1. Established clinical cardiovascular disease. 2. Type 2 diabetes mellitus. 3. Chronic kidney disease. 4. Age 65 years or older. 5. An estimated 10-year risk of atherosclerotic CVD of at least 10%.

Answer 433

An ACE inhibitor (or ARB if ACE cannot be tolerated).

Answer 434

Start with a calcium channel blocker (CCB) or a thiazide-like diuretic if there is heart failure or ankle edema.

Answer 435

Combine ACE-inhibitor (or ARB) with CCB (or thiazide-like diuretic).

Answer 436

Add a thiazide-like diuretic.

Answer 437

Refer the patient to a specialist.

Answer 438

Less than 140/90.

Answer 439

Less than 150/90.

Answer 440

Inadequate blood pressure control on three or more antihypertensive drugs.

Answer 441

Spironolactone 25 mg daily if K+ ≤ 4.5 mmol/L.

Answer 442

An increased dose of thiazide-like diuretic can be used with monitoring of electrolytes.

Answer 443

Endovascular renal denervation of sympathetic nerves with radio-frequency catheter may be effective.

Answer 444

Post MI, diabetes or CKD with microalbuminuria, renal impairment, benign prostatic hypertrophy, depression, asthma, hyperthyroidism, osteoporosis, pregnancy.

Answer 445

ACEI first then BB, BB first then ACEI, ACEI, ARB, CCB, alpha blockers.

Answer 446

Beta blockers.

Answer 447

Gout, asthma, grade 2 or 3 AV block, tachyarrhythmia, heart failure.

Answer 448

Hyperglycemia, ankle edema, flushing, dizziness, hypotension, headache, bradycardia, cardiac conduction defects, dry cough, first dose hypotension, hyperkalemia, rash, renal impairment.

Answer 449

Angioneurotic edema, hyperkalemia.

Answer 450

Bilateral renal artery stenosis, stage 4 & 5 renal failure, pregnancy.

Answer 451

BP ≥ 180 systolic and/or ≥ 120 diastolic (asymptomatic severely high BP)

Answer 452

May be due to undiagnosed hypertension or nonadherence to previously described antihypertensive therapy. ## Footnote Usually treated on an outpatient basis; mainstay of treatment is oral antihypertensives.

Answer 453

Clonidine (α agonist), nifedipine (CCB), captopril (ACEI), and labetalol (BB).

Answer 454

Target is < 160/100 in the first few hours, then reduce over few hours/days.

Answer 455

The patient must be seen within 1-2 weeks to ensure that the blood pressure is improving and that there are no further complications of uncontrolled hypertension.

Answer 456

CNS: encephalopathy, stroke, SAH; Renal: AKI; Retinopathy: papilledema, loss of vision; Cardiogenic shock.

Answer 457

Must be admitted for immediate initiation of treatment.

Answer 458

Aim is to lower the mean arterial pressure by 10-20% in the first hour, then gradually lower in the next 2-3 hours to reach 25% lower of baseline.

Answer 459

IV nitroprusside, IV nitroglycerin, IV nicardipine, IV labetalol.

Answer 460

Must rapidly lower BP ASAP. Target is 100 to 120 systolic.

Answer 461

Slower lowering of BP.

Answer 462

Warm extremities, low BP, high HR, low CVP, low PCWP ## Footnote Causes include sepsis and neurogenic shock.

Answer 463

Low BP, high HR, high CVP, increased SVR, cold extremities ## Footnote Causes include ACS, valve failure, dysrhythmias, high PCWP.

Answer 464

Low BP, high HR, low CVP, increased SVR, cold extremities ## Footnote Caused by decreased circulatory volume or GI bleed.

Answer 465

Low BP, high HR, high CVP or normal, increased SVR ## Footnote Causes include cardiac tamponade, tension pneumothorax, pulmonary embolism.

Answer 466

ABC, consider intubation, oxygen, IV fluids ## Footnote If hypovolemic, consider blood transfusion.

Answer 467

Epinephrine, dopamine, vasopressin.

Answer 468

Antibiotics (broad spectrum).

Answer 469

Thrombolysis, anticoagulation.

Answer 470

Cardiocentesis.

Answer 471

CVP: Central Venous Pressure, RVP: Right Venous Pressure, PA: Pulmonary Artery Pressure, PAWP: Pulmonary Artery Wedge Pressure, CI: Cardiac Index, SVRI: Systemic Vascular Resistance Index.

Answer 472

Stable angina secondary to coronary artery disease.

Answer 473

ECG: 70% normal; some ST depression/TWI. ## Footnote Stress test: exercise (If patient can't walk → pharmacological). If ECG shows LBBB → myocardial perfusion test.

Answer 474

Angiography and stenting.

Answer 475

Aspirin, Statin (given after dinner), beta blocker, and Nitrate.

Answer 476

Muscle pain, with severe cases leading to rhabdomyolysis and renal failure.

Answer 477

Acute left ventricular failure or Acute pulmonary edema.

Answer 478

Large infarctions, recurrent infarction, arrhythmia (atrial fibrillation, ventricular tachycardia), and mechanical complications (acute MR, septal rupture).

Answer 479

Admit to CCU, propped up position, oxygen, IV furosemide, morphine, and IV nitrate. Inotropic if low systolic function (Dobutamine), aortic balloon.

Answer 480

Acute pericarditis complicated by cardiac tamponade.

Answer 481

Pericardiocentesis, colchicine, and NSAIDs.

Answer 482

Chronic stable RHD, now decompensated by LHF and RHF.

Answer 483

A. Fib. and rhythm disturbance, recurrence of rheumatic fever (if younger), pregnancy complicating heart disease, anemia, pulmonary thromboembolism, progressive valve destruction, infection (IE).

Answer 484

Anti-failure treatment plus finding and treating the cause.

Answer 485

Peripartum cardiomyopathy and pulmonary thromboembolism.

Answer 486

SOB, orthopnea, PND, pedal edema, ascites, elevated JVP, S3 (HF-REF), bibasal crackles, pansystolic murmur (MR from annular dilation).

Answer 487

Investigate and treat like DCM.

Answer 488

Diagnosis by pulmonary CT Angio.

Answer 489

Supraventricular tachycardia, accessory pathway atrioventricular SVT, AV nodal, paroxysmal A. Fib., paroxysmal V. Tach.

Answer 490

Manage accordingly.

Answer 491

Fever, bilateral knee and ankle pain, and a pansystolic murmur at the apex.

Answer 492

Endocarditis: MR and AR (murmur or echo), myocarditis: enlarged heart or HF (gallop/JVP), pericarditis: rub or effusion.

Answer 493

Bed rest, eradicate strept. by penicillin/erythromycin, anti-inflammatory agent (aspirin if no carditis, steroid if carditis).

Answer 494

Long acting penicillin once a month till 40 years or for 10 years, whichever is longer (if carditis) OR till 21 years (if no carditis).

Answer 495

Infective Endocarditis (IE) ## Footnote Fever with cardiac background suggests IE.

Answer 496

Blood cultures (3 to 6 with different puncture sites), Echo, and if not informative, serology for Q fever, Brucella, and unusual organisms.

Answer 497

IV antibiotics: combination of bactericidal and synergistic activity like penicillin/gentamicin for 4-6 weeks.

Answer 498

Severe heart failure, severe valve damage, perivalvular abscess, large vegetation, fungal vegetation, and prosthetic valve endocarditis.

Answer 499

No prophylaxis.

Answer 500

Previous prosthetic valve, previous cyanotic congenital heart disease, past history of treatment for IE, and previous cardiac transplantation related valvular disease.

Answer 501

Palpitations, weakness of the right upper limb, and difficulty to speak.

Answer 502

Warfarin takes 5 days to work.

Cardiology Flashcards

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