In a normal left ventricular cycle with competent valves, what bounds isovolumetric relaxation?

It begins with aortic valve closure, associated with A2 and the aortic pressure trace’s dicrotic notch. It ends when left ventricular pressure falls below left atrial pressure and the mitral valve opens. Both valves are closed while ventricular pressure falls at constant volume.

How do HFrEF and HFpEF differ, and why is ejection fraction alone insufficient to diagnose heart failure?

HFrEF has left ventricular ejection fraction (LVEF) ≤40%; HFpEF has LVEF ≥50% with evidence of increased left ventricular filling pressures at rest or with provocation. Heart failure is a clinical syndrome, not an EF value alone. Reduced contractility and dilation are common in HFrEF; impaired relaxation or increased stiffness are common in HFpEF, but remodeling patterns are not obligatory or exclusive.

How can mean arterial pressure be estimated from systolic and diastolic pressures at a normal resting heart rate?

MAP ≈ DBP + (SBP − DBP)/3. This is an approximation: arterial pressure spends more of a resting cycle nearer the diastolic level. True MAP is the time-average arterial pressure over a cardiac cycle; heart rate and waveform shape affect the accuracy of the estimate.

What ECG findings define the WPW pre-excitation pattern, and how does it differ from WPW syndrome?

The classic pattern is a short PR interval ( 120 ms, due to antegrade ventricular activation through an accessory pathway. The degree of pre-excitation varies. An ECG pattern alone is not WPW syndrome, which also entails related tachyarrhythmia or symptoms.

What is the typical murmur of chronic mitral regurgitation?

A high-pitched, blowing holosystolic murmur, usually loudest at the apex and often radiating toward the left axilla. Timing and radiation can vary with the regurgitant jet and valve lesion.

What defines complete AV block, and what jugular pulse finding may accompany it?

No atrial impulses conduct to the ventricles, so atrial activity and the ventricular escape rhythm proceed independently; the escape rate is usually slower. Intermittent cannon a waves may occur when the atrium contracts against a closed tricuspid valve. AV dissociation alone is not synonymous with complete AV block.

What produces the a and v waves of the jugular venous pulse?

The a wave reflects right atrial contraction in late diastole. The v wave reflects venous filling of the right atrium while the tricuspid valve is closed during ventricular systole.

What identifies Mobitz II AV block, and when does the 2018 ACC/AHA/HRS guideline recommend permanent pacing?

With a stable atrial rhythm, conducted beats have unchanged PR intervals before and after an intermittently non-conducted P wave. The block is usually in the His–Purkinje system. Acquired Mobitz II not due to a reversible or physiological cause warrants permanent pacing regardless of symptoms. A 2:1 pattern alone cannot be classified as Mobitz I or II.

What circuit underlies typical atrial flutter, and what ECG pattern is common?

It is a right atrial macro-reentrant circuit around the tricuspid annulus that depends on the cavotricuspid isthmus. Flutter waves often form a sawtooth pattern in inferior leads at about 300/min. With 2:1 AV conduction the ventricular rate is about 150/min, but atrial rates and conduction ratios vary.

How do standing and squatting usually change the click and murmur of mitral valve prolapse?

Standing reduces left ventricular volume, so prolapse and the click tend to occur earlier, with a longer systolic murmur. Squatting increases ventricular filling and afterload, tending to delay the click and shorten the murmur.

How does the Frank–Starling mechanism relate ventricular filling to stroke volume?

Within the physiological range, greater end-diastolic filling increases myocardial stretch and usually stroke volume at a given afterload and contractile state. Length-dependent activation, including increased myofilament calcium sensitivity, contributes. The relationship is not an unlimited increase in output with added filling.

What is the classic Mobitz I (Wenckebach) second-degree AV-block pattern?

The PR interval progressively lengthens until a P wave fails to conduct, producing no QRS for that beat; the cycle then resets with a shorter PR interval. The block is usually in the AV node.

What ECG features suggest atrial fibrillation, and where do common triggers arise?

AF has no consistent discrete P waves and usually an irregularly irregular ventricular response; fibrillatory baseline activity may be visible. The ventricular rhythm need not be irregular with complete AV block or pacing. Pulmonary vein myocardial sleeves are important trigger sites, especially in paroxysmal AF, but not the only source.

How is cardiac output calculated from stroke volume or by the oxygen Fick principle?

CO = stroke volume × heart rate. At steady state, CO = whole-body oxygen consumption / (arterial oxygen content − mixed venous oxygen content). Use oxygen content, not saturation alone, and consistent units: mL O₂/min divided by mL O₂/L blood gives L blood/min.

How do Valsalva strain and handgrip usually affect the murmur of obstructive hypertrophic cardiomyopathy?

Valsalva strain reduces venous return and left ventricular volume, tending to increase dynamic outflow obstruction and intensify the murmur. Handgrip increases afterload and usually softens it. This describes dynamic obstruction, not every form of hypertrophic cardiomyopathy.

What event produces the first heart sound (S1), and where is it usually best heard?

S1 arises from vibrations associated with mitral and tricuspid valve closure at the start of ventricular systole. It is usually best heard near the apex, normally around the left fifth intercostal space at the midclavicular line.

How do cardiac β₁ and M₂ receptors influence rate, conduction and contractility?

β₁ receptors couple to Gs, increasing cAMP and PKA activity, which increases heart rate, AV conduction and contractility. Vagal M₂ receptors couple to Gi, reduce cAMP and activate potassium channels, slowing the SA and AV nodes. Direct vagal reduction of contractility is mainly atrial; ventricular effects are smaller.

What produces S4, and why is it absent in atrial fibrillation?

S4 occurs in late diastole when atrial contraction fills a poorly compliant ventricle, for example with hypertensive hypertrophy, aortic stenosis or myocardial ischemia. It requires organized atrial contraction, so it is absent in atrial fibrillation. Stiffness does not necessarily imply hypertrophy.

What defines first-degree AV block, and how should its significance be interpreted?

The PR interval is >200 ms with 1:1 AV conduction: every P wave conducts to a QRS. At 25 mm/s this is more than five small boxes. The delay is often AV-nodal but can be elsewhere; clinical significance depends on the degree of delay, symptoms and cause.

What produces S2, and why does its normal split widen during inspiration?

S2 accompanies aortic (A2) and pulmonary (P2) valve closure. A2 normally precedes P2. Inspiration increases right-heart filling and prolongs right ventricular ejection, delaying P2 and widening the physiological split.

What do loop diuretics do in heart failure, and what is established about their mortality effect?

They relieve fluid congestion by inhibiting the Na⁺/K⁺/2Cl⁻ cotransporter in the thick ascending limb, increasing salt and water excretion. A long-term mortality benefit has not been established; that is not proof of no benefit. They do not replace disease-modifying HFrEF therapy.

What is torsades de pointes, and what treatment priority does the 2025 AHA guidance give to sustained polymorphic VT?

Torsades is polymorphic ventricular tachycardia associated with QT prolongation; early afterdepolarizations can trigger it. Sustained polymorphic VT requires immediate unsynchronized shock (defibrillation). IV magnesium may be considered for recurrent torsades with long QT, alongside correction of electrolyte abnormalities and withdrawal of QT-prolonging drugs; it does not replace an indicated shock.

What murmur and carotid pulse findings classically suggest severe aortic stenosis?

A harsh systolic crescendo–decrescendo murmur near the right upper sternal border often radiates to the carotids. A weak, delayed carotid upstroke is pulsus parvus et tardus. These findings are not universal, and murmur loudness alone does not grade severity; echocardiography is used to assess the valve.

What auscultatory and pulse findings are typical of significant chronic aortic regurgitation?

An early-diastolic, high-pitched decrescendo murmur is often heard along the left sternal border, aided by leaning forward at end-expiration. A wide pulse pressure and bounding, rapidly collapsing pulse may accompany significant chronic regurgitation; they are not always present.

In a normal left ventricular cycle with competent valves, what bounds isovolumetric contraction?

It begins with mitral valve closure and ends when left ventricular pressure exceeds aortic pressure and the aortic valve opens. Both valves are closed during the interval, so ventricular pressure rises without a change in volume.

What are the classic auscultatory findings of rheumatic mitral stenosis?

A low-pitched diastolic rumble is best heard at the apex in the left lateral position. An opening snap may occur after A2. The A2-to-snap interval alone is not a reliable severity measure; echocardiography assesses stenosis severity.

What does CHA₂DS₂-VASc score in atrial fibrillation, and how do the 2023 US and 2024 ESC guidelines differ?

It counts heart failure/LV dysfunction (1), hypertension (1), age ≥75 (2), diabetes (1), prior stroke/TIA/thromboembolism (2), vascular disease (1), age 65–74 (1) and female sex (1). Count only one age category; female sex alone is not an anticoagulation indication. The 2023 US guideline recommends anticoagulation at estimated stroke risk ≥2%/year, exemplified by ≥2 in men or ≥3 in women. The 2024 ESC guideline uses CHA₂DS₂-VA without sex: consider anticoagulation at 1 and recommend it at ≥2. Individual risks and valve-specific indications still matter.

What are preload, afterload and contractility, the main determinants of stroke volume?

Preload is myocardial stretch at end-diastole, often indexed by end-diastolic volume. Afterload is the load opposing ventricular ejection; arterial pressure, outflow obstruction and ventricular geometry contribute. Contractility is the myocardium’s force-generating state at a given preload and afterload. Afterload is not identical to systemic vascular resistance.

What is Kussmaul sign, and what does it suggest?

Jugular venous pressure rises or fails to fall during inspiration because the right heart cannot accommodate increased venous return normally. It can occur in constrictive pericarditis, restrictive cardiomyopathy and right ventricular infarction; it is not specific to one diagnosis.

Which ECG findings strongly favor VT over SVT with aberrancy in a wide-complex tachycardia?

AV dissociation, capture beats and fusion beats strongly favor ventricular tachycardia. Extreme axis deviation and certain very broad QRS patterns also support it. No single QRS-width cutoff is definitive, and absence of these signs does not exclude VT; interpret the full ECG and clinical context.

What are the four foundational drug classes for eligible adults with symptomatic chronic HFrEF in the 2022 AHA/ACC/HFSA guideline?

An angiotensin receptor–neprilysin inhibitor (ARNI; sacubitril/valsartan), or an ACE inhibitor/angiotensin receptor blocker when appropriate; an evidence-based beta blocker (carvedilol, metoprolol succinate or bisoprolol); a mineralocorticoid receptor antagonist (spironolactone or eplerenone); and an SGLT2 inhibitor (dapagliflozin or empagliflozin). These form outcome-improving therapy; selection and monitoring depend on factors such as blood pressure, kidney function and potassium.

When is S3 heard, and what does a pathological S3 suggest?

S3 is a low-frequency sound during rapid early-diastolic ventricular filling. When pathological, it suggests increased filling volume or ventricular dysfunction, as in heart failure, dilated cardiomyopathy or significant regurgitation. It can be physiological in younger people and does not diagnose a disease by itself.

Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias

32 review cards on cardiac physiology, bedside cardiovascular signs, heart failure and common ECG rhythms. Assumes basic anatomy and ECG knowledge; treatment summaries identify their guideline context.

Level: basic
Languages: en → en
Cards: 32
Markdown: Cardiology & Cardiovascular Physiology — Hemodynamics, Cardiac Cycle, Murmurs, Heart Failure & Arrhythmias (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	In a normal left ventricular cycle with competent valves, what bounds isovolumetric relaxation?	It begins with aortic valve closure, associated with A2 and the aortic pressure trace’s dicrotic notch. It ends when left ventricular pressure falls below left atrial pressure and the mitral valve opens. Both valves are closed while ventricular pressure falls at constant volume.
2	How do HFrEF and HFpEF differ, and why is ejection fraction alone insufficient to diagnose heart failure?	HFrEF has left ventricular ejection fraction (LVEF) ≤40%; HFpEF has LVEF ≥50% with evidence of increased left ventricular filling pressures at rest or with provocation. Heart failure is a clinical syndrome, not an EF value alone. Reduced contractility and dilation are common in HFrEF; impaired relaxation or increased stiffness are common in HFpEF, but remodeling patterns are not obligatory or exclusive.
3	How can mean arterial pressure be estimated from systolic and diastolic pressures at a normal resting heart rate?	MAP ≈ DBP + (SBP − DBP)/3. This is an approximation: arterial pressure spends more of a resting cycle nearer the diastolic level. True MAP is the time-average arterial pressure over a cardiac cycle; heart rate and waveform shape affect the accuracy of the estimate.
4	What ECG findings define the WPW pre-excitation pattern, and how does it differ from WPW syndrome?	The classic pattern is a short PR interval (<120 ms), a delta wave and a widened QRS, often >120 ms, due to antegrade ventricular activation through an accessory pathway. The degree of pre-excitation varies. An ECG pattern alone is not WPW syndrome, which also entails related tachyarrhythmia or symptoms.
5	What is the typical murmur of chronic mitral regurgitation?	A high-pitched, blowing holosystolic murmur, usually loudest at the apex and often radiating toward the left axilla. Timing and radiation can vary with the regurgitant jet and valve lesion.
6	What defines complete AV block, and what jugular pulse finding may accompany it?	No atrial impulses conduct to the ventricles, so atrial activity and the ventricular escape rhythm proceed independently; the escape rate is usually slower. Intermittent cannon a waves may occur when the atrium contracts against a closed tricuspid valve. AV dissociation alone is not synonymous with complete AV block.
7	What produces the a and v waves of the jugular venous pulse?	The a wave reflects right atrial contraction in late diastole. The v wave reflects venous filling of the right atrium while the tricuspid valve is closed during ventricular systole.
8	What identifies Mobitz II AV block, and when does the 2018 ACC/AHA/HRS guideline recommend permanent pacing?	With a stable atrial rhythm, conducted beats have unchanged PR intervals before and after an intermittently non-conducted P wave. The block is usually in the His–Purkinje system. Acquired Mobitz II not due to a reversible or physiological cause warrants permanent pacing regardless of symptoms. A 2:1 pattern alone cannot be classified as Mobitz I or II.
9	What circuit underlies typical atrial flutter, and what ECG pattern is common?	It is a right atrial macro-reentrant circuit around the tricuspid annulus that depends on the cavotricuspid isthmus. Flutter waves often form a sawtooth pattern in inferior leads at about 300/min. With 2:1 AV conduction the ventricular rate is about 150/min, but atrial rates and conduction ratios vary.
10	How do standing and squatting usually change the click and murmur of mitral valve prolapse?	Standing reduces left ventricular volume, so prolapse and the click tend to occur earlier, with a longer systolic murmur. Squatting increases ventricular filling and afterload, tending to delay the click and shorten the murmur.
11	How does the Frank–Starling mechanism relate ventricular filling to stroke volume?	Within the physiological range, greater end-diastolic filling increases myocardial stretch and usually stroke volume at a given afterload and contractile state. Length-dependent activation, including increased myofilament calcium sensitivity, contributes. The relationship is not an unlimited increase in output with added filling.
12	What is the classic Mobitz I (Wenckebach) second-degree AV-block pattern?	The PR interval progressively lengthens until a P wave fails to conduct, producing no QRS for that beat; the cycle then resets with a shorter PR interval. The block is usually in the AV node.
13	What ECG features suggest atrial fibrillation, and where do common triggers arise?	AF has no consistent discrete P waves and usually an irregularly irregular ventricular response; fibrillatory baseline activity may be visible. The ventricular rhythm need not be irregular with complete AV block or pacing. Pulmonary vein myocardial sleeves are important trigger sites, especially in paroxysmal AF, but not the only source.
14	How is cardiac output calculated from stroke volume or by the oxygen Fick principle?	CO = stroke volume × heart rate. At steady state, CO = whole-body oxygen consumption / (arterial oxygen content − mixed venous oxygen content). Use oxygen content, not saturation alone, and consistent units: mL O₂/min divided by mL O₂/L blood gives L blood/min.
15	How do Valsalva strain and handgrip usually affect the murmur of obstructive hypertrophic cardiomyopathy?	Valsalva strain reduces venous return and left ventricular volume, tending to increase dynamic outflow obstruction and intensify the murmur. Handgrip increases afterload and usually softens it. This describes dynamic obstruction, not every form of hypertrophic cardiomyopathy.
16	What event produces the first heart sound (S1), and where is it usually best heard?	S1 arises from vibrations associated with mitral and tricuspid valve closure at the start of ventricular systole. It is usually best heard near the apex, normally around the left fifth intercostal space at the midclavicular line.
17	How do cardiac β₁ and M₂ receptors influence rate, conduction and contractility?	β₁ receptors couple to Gs, increasing cAMP and PKA activity, which increases heart rate, AV conduction and contractility. Vagal M₂ receptors couple to Gi, reduce cAMP and activate potassium channels, slowing the SA and AV nodes. Direct vagal reduction of contractility is mainly atrial; ventricular effects are smaller.
18	What produces S4, and why is it absent in atrial fibrillation?	S4 occurs in late diastole when atrial contraction fills a poorly compliant ventricle, for example with hypertensive hypertrophy, aortic stenosis or myocardial ischemia. It requires organized atrial contraction, so it is absent in atrial fibrillation. Stiffness does not necessarily imply hypertrophy.
19	What defines first-degree AV block, and how should its significance be interpreted?	The PR interval is >200 ms with 1:1 AV conduction: every P wave conducts to a QRS. At 25 mm/s this is more than five small boxes. The delay is often AV-nodal but can be elsewhere; clinical significance depends on the degree of delay, symptoms and cause.
20	What produces S2, and why does its normal split widen during inspiration?	S2 accompanies aortic (A2) and pulmonary (P2) valve closure. A2 normally precedes P2. Inspiration increases right-heart filling and prolongs right ventricular ejection, delaying P2 and widening the physiological split.
21	What do loop diuretics do in heart failure, and what is established about their mortality effect?	They relieve fluid congestion by inhibiting the Na⁺/K⁺/2Cl⁻ cotransporter in the thick ascending limb, increasing salt and water excretion. A long-term mortality benefit has not been established; that is not proof of no benefit. They do not replace disease-modifying HFrEF therapy.
22	What is torsades de pointes, and what treatment priority does the 2025 AHA guidance give to sustained polymorphic VT?	Torsades is polymorphic ventricular tachycardia associated with QT prolongation; early afterdepolarizations can trigger it. Sustained polymorphic VT requires immediate unsynchronized shock (defibrillation). IV magnesium may be considered for recurrent torsades with long QT, alongside correction of electrolyte abnormalities and withdrawal of QT-prolonging drugs; it does not replace an indicated shock.
23	What murmur and carotid pulse findings classically suggest severe aortic stenosis?	A harsh systolic crescendo–decrescendo murmur near the right upper sternal border often radiates to the carotids. A weak, delayed carotid upstroke is pulsus parvus et tardus. These findings are not universal, and murmur loudness alone does not grade severity; echocardiography is used to assess the valve.
24	What auscultatory and pulse findings are typical of significant chronic aortic regurgitation?	An early-diastolic, high-pitched decrescendo murmur is often heard along the left sternal border, aided by leaning forward at end-expiration. A wide pulse pressure and bounding, rapidly collapsing pulse may accompany significant chronic regurgitation; they are not always present.
25	In a normal left ventricular cycle with competent valves, what bounds isovolumetric contraction?	It begins with mitral valve closure and ends when left ventricular pressure exceeds aortic pressure and the aortic valve opens. Both valves are closed during the interval, so ventricular pressure rises without a change in volume.
26	What are the classic auscultatory findings of rheumatic mitral stenosis?	A low-pitched diastolic rumble is best heard at the apex in the left lateral position. An opening snap may occur after A2. The A2-to-snap interval alone is not a reliable severity measure; echocardiography assesses stenosis severity.
27	What does CHA₂DS₂-VASc score in atrial fibrillation, and how do the 2023 US and 2024 ESC guidelines differ?	It counts heart failure/LV dysfunction (1), hypertension (1), age ≥75 (2), diabetes (1), prior stroke/TIA/thromboembolism (2), vascular disease (1), age 65–74 (1) and female sex (1). Count only one age category; female sex alone is not an anticoagulation indication. The 2023 US guideline recommends anticoagulation at estimated stroke risk ≥2%/year, exemplified by ≥2 in men or ≥3 in women. The 2024 ESC guideline uses CHA₂DS₂-VA without sex: consider anticoagulation at 1 and recommend it at ≥2. Individual risks and valve-specific indications still matter.
28	What are preload, afterload and contractility, the main determinants of stroke volume?	Preload is myocardial stretch at end-diastole, often indexed by end-diastolic volume. Afterload is the load opposing ventricular ejection; arterial pressure, outflow obstruction and ventricular geometry contribute. Contractility is the myocardium’s force-generating state at a given preload and afterload. Afterload is not identical to systemic vascular resistance.
29	What is Kussmaul sign, and what does it suggest?	Jugular venous pressure rises or fails to fall during inspiration because the right heart cannot accommodate increased venous return normally. It can occur in constrictive pericarditis, restrictive cardiomyopathy and right ventricular infarction; it is not specific to one diagnosis.
30	Which ECG findings strongly favor VT over SVT with aberrancy in a wide-complex tachycardia?	AV dissociation, capture beats and fusion beats strongly favor ventricular tachycardia. Extreme axis deviation and certain very broad QRS patterns also support it. No single QRS-width cutoff is definitive, and absence of these signs does not exclude VT; interpret the full ECG and clinical context.
31	What are the four foundational drug classes for eligible adults with symptomatic chronic HFrEF in the 2022 AHA/ACC/HFSA guideline?	An angiotensin receptor–neprilysin inhibitor (ARNI; sacubitril/valsartan), or an ACE inhibitor/angiotensin receptor blocker when appropriate; an evidence-based beta blocker (carvedilol, metoprolol succinate or bisoprolol); a mineralocorticoid receptor antagonist (spironolactone or eplerenone); and an SGLT2 inhibitor (dapagliflozin or empagliflozin). These form outcome-improving therapy; selection and monitoring depend on factors such as blood pressure, kidney function and potassium.
32	When is S3 heard, and what does a pathological S3 suggest?	S3 is a low-frequency sound during rapid early-diastolic ventricular filling. When pathological, it suggests increased filling volume or ventricular dysfunction, as in heart failure, dilated cardiomyopathy or significant regurgitation. It can be physiological in younger people and does not diagnose a disease by itself.