Phisiology
isovolumetric contraction
This event causes STEMI/NSTEMI and unstable angina
plaque rupture
A congenital heart disease (CHD) that causes a continuous “machinery-like” murmur
Patent Ductus Arteriosus (PDA)
Sharp chest pain which is relived by leaning forward
Acute pericarditis
Mechanism of action of nitrates in angina
venodilation -> decreased venous return -> decreased preload -> decreased O2 demand
Mechanism of S1 and S2 heart sounds
Closure of mitral and tricuspid valves
Closure of aortic and pulmonic valves
This type of hypertrophy results from pressure overload (e.g., hypertension, aortic stenosis) and involves sarcomeres added in parallel
Concentric
This low-frequency heart sound, always pathologic in adults, occurs just before S1 due to atrial contraction against a stiff ventricle
S4
Classic clinical triad for cardiac tamponade
Hypotension – due to ↓ stroke volume.
Jugular venous distension (JVD) – due to impaired venous return.
Muffled or distant heart sounds – due to fluid around the heart.
Drug which causes prolonged QT but has low probability of causing torsades
Amiodarone
Main factor which determines diastolic blood pressure
PVR
Mechanism of S3 sound
Rapid passive filling of a very compliant or volume-overloaded ventricle during early diastole (right after S2)
Classic finding in ASD
wide, fixed splitting of S2
This valve is most commonly affected in infective endocarditis due to IV drug use
Tricuspid
antiarrhythmic drug which can cause LSE-like syndrome
Procainamide
Increasing afterload (such as with hypertension or aortic stenosis) has this effect on stroke volume, assuming contractility and preload remain constant
decrease
Which signs are caused by wide pulse pressure in aortic regurgitation?
Musset head bobbing
Quincke capillary pulsations in nail beds
Traube "pistol-shot” sounds over femoral artery
Classic auscultation finding in hypertrophic cardiomyopathy
Harsh crescendo–decrescendo systolic murmur, best heard at the left sternal border, that increases with Valsalva or standing and decreases with squatting or handgrip.
Septic shock changes of CVP PCWP CO SVR
CVP ↓, PCWP ↓, CO ↑, SVR ↓
5 classes of drugs which have proven mortality benefit in CHF
ACE inhibitors (or ARBs) – ↓ afterload, ↓ preload, inhibit maladaptive remodeling.
ARNI (angiotensin receptor–neprilysin inhibitor, e.g., sacubitril/valsartan) – improves outcomes beyond ACEi/ARB alone.
Beta blockers (specific ones: carvedilol, metoprolol succinate, bisoprolol) – improve EF and survival.
Mineralocorticoid receptor antagonists (MRAs) – spironolactone, eplerenone; ↓ mortality in HFrEF.
SGLT2 inhibitors (dapagliflozin, empagliflozin) – now proven to reduce mortality and hospitalization in HFrEF (even without diabetes).
This region of the myocardium is the most susceptible to ischemia because it experiences the highest wall stress, is compressed during systole, and is farthest from coronary blood supply
subendocardial layer
Pulsus paradoxus mechanism
Inspiration → ↑ venous return to RV
RV cannot expand outward (fluid-filled pericardium restricts)
RV pushes interventricular septum leftward → ↓ LV filling
↓ LV stroke volume → marked fall in systolic BP (>10 mmHg) = pulsus paradoxus
The murmur decreases with handgrip but increases with squatting. Name the condition
Aortic stenosis
A post-menopausal woman develops acute chest pain after severe emotional stress. Her ECG shows ST-segment elevation and troponins are mildly elevated, but coronary angiography is normal. Echocardiography reveals apical ballooning of the left ventricle. Name the condition
Takotsubo
Sacubitril-Valsartan mechanism of action
Neprilisin inhibitor -> increased ANP BNP -> increased natriuresis, decreased aldosterone, vasodilation