Clinical Cardiology

114 flashcards by MentisLibrary

Cardiac physiology, coronary syndromes, heart failure, arrhythmias, valve disease, hypertension and lipids, vascular and pericardial disease, for medical students and clinicians reviewing the specialty.

What two variables determine cardiac output?
Heart rate and stroke volume, so $CO = HR \times SV$.
Define preload, and name the law that links it to stroke volume.
Preload is ventricular wall stress at end diastole, approximated by end diastolic volume. The Frank-Starling law states that greater stretch increases stroke volume up to a limit.
Define afterload, and give the clinical variables that reflect it.
Afterload is the wall stress the ventricle must overcome to eject blood. Systolic blood pressure and systemic vascular resistance are its usual surrogates.
What is ejection fraction, and what range is normal?
The fraction of end diastolic volume ejected with each beat. Normal is roughly 55 to 70 percent.
Why is coronary perfusion mainly a diastolic event?
Left ventricular systole compresses the intramural coronary arteries, so most left coronary flow occurs during diastole.
Name the main determinants of myocardial oxygen demand.
Heart rate, contractility and ventricular wall stress.
What is the baroreceptor reflex response to a fall in blood pressure?
Carotid sinus and aortic arch stretch receptors fire less, sympathetic outflow rises and vagal tone falls, producing tachycardia and vasoconstriction.
How does the renin angiotensin aldosterone system worsen chronic heart failure?
Low renal perfusion drives renin release; angiotensin II causes vasoconstriction and aldosterone causes sodium and water retention, raising both afterload and preload.
What stimulates release of B-type natriuretic peptide?
Ventricular wall stretch from pressure or volume overload. BNP promotes natriuresis and vasodilation and opposes the renin angiotensin system.
What does a widened pulse pressure suggest?
A large gap between systolic and diastolic pressure, seen with aortic regurgitation, a stiff aorta in older adults, and high output states such as thyrotoxicosis, anemia or arteriovenous fistula.
What happens to stroke volume when afterload rises in a failing ventricle?
It falls sharply, because a failing ventricle is far more afterload sensitive than a normal one.
Describe the pathogenesis of an atherosclerotic plaque.
Endothelial injury lets LDL enter the intima where it is oxidized, monocytes become lipid laden foam cells, and smooth muscle migrates and builds a fibrous cap over a lipid core.
What defines stable angina?
Predictable chest discomfort brought on by a fixed level of exertion or emotional stress and relieved within minutes by rest or nitroglycerin.
How does unstable angina differ from stable angina?
It occurs at rest, is new in onset, or is increasing in frequency, duration or severity, and reflects plaque rupture with partial thrombosis rather than a fixed stenosis.
Unstable angina vs NSTEMI: what separates them?
Troponin. Both share partial coronary occlusion by thrombus, but NSTEMI has detectable myocardial necrosis and unstable angina does not.
What distinguishes STEMI from NSTEMI?
STEMI reflects complete occlusion causing transmural ischemia with ST segment elevation; NSTEMI reflects partial occlusion causing subendocardial injury without persistent ST elevation.
Describe the time course of cardiac troponin after myocardial infarction.
It rises within about 3 to 4 hours of injury, peaks around 24 hours, and stays elevated for 7 to 10 days.
Which patients most often present with atypical infarction symptoms?
Older adults, women and people with diabetes.
What is the reperfusion goal in STEMI?
Primary percutaneous coronary intervention within 90 minutes of first medical contact at a PCI capable hospital.
Why is aspirin given immediately in acute coronary syndrome?
It irreversibly inhibits platelet cyclooxygenase-1, blocking thromboxane A2 mediated aggregation, and it lowers mortality.
Which four drug classes make up standard secondary prevention after myocardial infarction?
Antiplatelet therapy, a high intensity statin, a beta blocker, and an ACE inhibitor or ARB.
Which mechanical complication of infarction causes a new holosystolic murmur with sudden pulmonary edema?
Papillary muscle rupture producing acute mitral regurgitation, usually 3 to 5 days after the infarct.
What is ventricular free wall rupture, and when does it occur?
Rupture of necrotic myocardium, most often 3 to 14 days after infarction, causing hemopericardium and tamponade.
What is Dressler syndrome?
An immune mediated pericarditis that appears weeks to a few months after myocardial infarction.
What causes Prinzmetal, or vasospastic, angina?
Focal coronary artery smooth muscle spasm, not a fixed stenosis.
Match each coronary artery to the myocardial wall it supplies.
The left anterior descending supplies the anterior wall and septum, the left circumflex supplies the lateral wall, and the right coronary artery supplies the inferior wall.
Why are nitrates dangerous in right ventricular infarction?
The infarcted right ventricle is preload dependent, so venodilation drops filling and causes profound hypotension.
What is myocardial stunning?
Reversible contractile dysfunction that persists after blood flow has been restored, recovering over hours to days.
How do heart failure with reduced and with preserved ejection fraction differ?
HFrEF is a failure of contraction with an ejection fraction of 40 percent or less; HFpEF is a failure of relaxation and filling with a preserved ejection fraction.
Which symptoms point to left sided heart failure?
Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea and pulmonary crackles.