The Cardiac Cycle
The cardiac cycle includes systole (contraction) and diastole (relaxation) coordinated by electrical signals.
| Phase | Valves | Key Events |
|---|---|---|
| Isovolumetric contraction | All closed | Pressure rises, no volume change; follows QRS on ECG |
| Rapid ejection | Aortic/pulmonic open | 70% of SV ejected; peak systolic pressure |
| Isovolumetric relaxation | All closed | Pressure falls, no volume change; follows T wave |
| Rapid filling | Mitral/tricuspid open | 80% of ventricular filling (passive); S3 sound here if pathologic |
| Atrial kick | Mitral/tricuspid open | Final 20% filling; S4 sound here if pathologic; lost in A-fib |
⭐ Heart SoundsS1 = mitral/tricuspid closure (systole onset). S2 = aortic/pulmonic closure (systole end). S3 = rapid filling (volume overload, HFrEF, normal in young). S4 = atrial kick against stiff ventricle (hypertension, LVH, AS).
Cardiac Action Potentials
| Phase | Ion Flow | Significance |
|---|---|---|
| Phase 0 — Rapid depolarization | Na+ in (fast channels) | Absent in SA/AV nodes; blocked by Class I antiarrhythmics |
| Phase 1 — Early repolarization | K+ out (Ito) | Notch on AP; prominent in Brugada syndrome |
| Phase 2 — Plateau | Ca2+ in, K+ out (balance) | Unique to cardiac muscle; sustains contraction; blocked by Class IV (CCBs) |
| Phase 3 — Rapid repolarization | K+ out (IKr, IKs) | Blocked by Class III antiarrhythmics (amiodarone, sotalol); prolongs QT |
| Phase 4 — Resting potential | K+ leak; pacemaker If (funny current) | SA node spontaneous depolarization; blocked by ivabradine |
🩹 SA vs Ventricular APSA/AV node AP: no Phase 0 fast Na+; relies on slow Ca2+ channels (Phase 0). Slow conduction. Blocked by Class IV (CCBs) and Class II (beta-blockers). Ventricular AP: fast Na+ dependent; Class I antiarrhythmics work here.
Cardiac Output and Determinants
CO = HR x SV (normal ~5 L/min at rest)
| Determinant | Definition | Increases With | Decreases With |
|---|---|---|---|
| Heart rate | Beats per minute | Sympathetic, catecholamines, hyperthyroidism | Parasympathetic (vagal), beta-blockers, hypothyroidism |
| Preload | Ventricular EDV (stretch) | Increased venous return, fluid bolus | Diuretics, venodilatation (nitrates) |
| Afterload | Resistance ventricle pumps against | Hypertension, aortic stenosis, vasoconstriction | Vasodilators (ACEi, ARB, hydralazine) |
| Contractility (inotropy) | Intrinsic force at same preload | Catecholamines, digoxin, Ca2+, dobutamine | Beta-blockers, heart failure, acidosis, hypoxia |
Frank-Starling Law
The Frank-Starling law states that stroke volume increases with increased preload (end-diastolic volume), up to a point. Greater stretch of cardiac muscle fibers → greater force of contraction due to optimal actin-myosin overlap.
⭐ Boards ApplicationIn heart failure, the Frank-Starling curve is shifted DOWN and to the RIGHT — same preload produces less stroke volume. Inotropes shift the curve UP (more SV at same preload). This explains why HF patients decompensate with fluid challenges.
🧐 Quick Formula ReviewCO = HR x SV. MAP = DBP + 1/3 (SBP-DBP). SVR = (MAP - RAP) / CO x 80. Ejection fraction = SV/EDV (normal >55%).
Blood Pressure and Hemodynamics
BP = CO x SVR (systemic vascular resistance). Arterioles are the primary site of resistance. The baroreceptor reflex (carotid sinus, aortic arch) provides moment-to-moment BP regulation.
| Pressure Type | Normal Value | Clinical Note |
|---|---|---|
| Systolic BP | 90-120 mmHg | Reflects CO and arterial compliance |
| Diastolic BP | 60-80 mmHg | Reflects SVR and arterial tone |
| MAP | 70-100 mmHg | Perfusion pressure; organs autoregulate within this range |
| Pulse pressure | SBP - DBP (~40 mmHg) | Widened in aortic regurgitation, aortic dissection; narrowed in cardiac tamponade, severe AS |
| CVP (RAP) | 2-8 mmHg | Reflects preload; elevated in RHF, tamponade, tension pneumo |
Autonomic Regulation of the Heart
| Effect | Sympathetic (NE, Epi) | Parasympathetic (ACh) |
|---|---|---|
| Heart rate | Increase (beta-1) | Decrease (M2) |
| Contractility | Increase (beta-1) | Slight decrease (atria mainly) |
| AV conduction | Faster (shorter PR) | Slower (longer PR; AV block with excess) |
| Coronary vessels | Dilate (beta-2); constrict (alpha-1) | Dilate (indirect via metabolic demand) |
🩹 Valsalva Maneuver PhasesStrain phase: increased intrathoracic pressure → decreased venous return → decreased CO → reflex tachycardia. Release phase: venous return surges → CO spike → reflex bradycardia. Used to terminate SVT (increases vagal tone).
Clinical Pearls
⭐ Ejection Fraction ClassificationHFrEF: EF less than 40% (systolic dysfunction). HFmrEF: EF 40-49%. HFpEF: EF 50% or greater (diastolic dysfunction). HFpEF is now more common than HFrEF; associated with hypertension, obesity, DM, elderly women.
🩹 Starling Forces (Capillary Exchange)Filtration favored by: high capillary hydrostatic pressure (Pc), low interstitial oncotic pressure. Absorption favored by: high plasma oncotic pressure (albumin), low Pc. Edema: when filtration exceeds lymphatic drainage.
🧐 Orthostatic Hypotension ReflexStanding: gravity pools blood in legs → decreased venous return → decreased CO → baroreceptors detect BP drop → sympathetic activation → tachycardia + vasoconstriction → BP restored. Failure = orthostatic hypotension (20 mmHg systolic or 10 mmHg diastolic drop).