Cardiovascular System

Cardiovascular System

Part 1 of 4 — The Heart, the Cardiac Cycle & the ECG

Two Circuits, One Pump

The two circuits are in series: every liter the right heart pumps must be pumped by the left heart. The organs within the systemic circuit, by contrast, are arranged in parallel off the aorta.

• The left ventricle has the thickest wall — it generates systemic pressure (~120 mmHg peak) versus the right ventricle's ~25 mmHg pulmonary peak.
• "Arteries carry blood away from the heart" is defined by direction, not oxygenation — the pulmonary artery is the classic exception trap.

Valves and Heart Sounds

• S1 ("lub") = AV valves (tricuspid + mitral) close at the start of ventricular systole.
• S2 ("dub") = semilunar valves (aortic + pulmonary) close at the start of diastole.
• Valves open and close passively from pressure differences — the chordae tendineae and papillary muscles only prevent AV-valve prolapse; they do not open the valves.

Phases of the Cardiac Cycle

1. Atrial systole — atria contract, topping off ventricular filling (the "atrial kick," ~10–30% of filling at rest; most filling is passive).
2. Isovolumetric contraction — ventricles contract with all four valves closed; pressure rises, volume constant.
3. Ejection — ventricular pressure exceeds arterial pressure → semilunar valves open → blood ejected.
4. Isovolumetric relaxation — all valves closed again; ventricular pressure falls.
5. Passive filling — AV valves open when atrial pressure exceeds ventricular pressure.

Key volumes: end-diastolic volume (EDV) ≈ 120 mL, end-systolic volume (ESV) ≈ 50 mL, so

$SV = EDV - ESV \approx 70 \text{ mL}, \qquad EF = \frac{SV}{EDV} \approx 55\text{-}60\%$

The Conduction System

$\text{SA node} \to \text{atrial muscle} \to \text{AV node (delay)} \to \text{Bundle of His} \to \text{bundle branches} \to \text{Purkinje fibers}$

• SA node is the pacemaker: its cells depolarize spontaneously (a slow inward Na$^+$ leak, then Ca$^{2+}$ influx), intrinsic rate ~100 bpm. Cardiac muscle is myogenic — the beat originates in the heart itself; nerves only modulate it.

• The pacemaker currents have names: the "funny" Na$^+$ current ($I_f$) and T-type Ca$^{2+}$ channels.

• AV node delay (~0.1 s) lets the atria finish emptying before ventricular contraction; it is the only electrical path between atria and ventricles (the fibrous skeleton insulates them).
• Gap junctions in intercalated discs let depolarization spread cell-to-cell, so the myocardium contracts as a functional syncytium.
• Autonomic control: sympathetic (norepinephrine, beta-1) raises rate and contractility; parasympathetic (vagus, acetylcholine, muscarinic) slows the SA node. Resting "vagal tone" is why resting HR (~70) is below the SA node's intrinsic rate.

The ECG

The ECG records electrical events; contraction (mechanical) follows each depolarization. QRS therefore comes just before ventricular pressure rises and S1.

Heart & Cardiac Cycle 🎯

Worked Examples — Cardiac Cycle & Conduction

Question: A patient has EDV = 140 mL, ESV = 70 mL, and HR = 80 bpm. Find SV, EF, and CO. Is the EF normal?

Solution:

1. $SV = EDV - ESV = 140 - 70 = 70$ mL ✓
2. $EF = SV/EDV = 70/140 = 50\%$ — borderline low (normal ≈ 55–70%); the elevated ESV suggests the ventricle is not emptying well.
3. $CO = HR \times SV = 80 \times 70 = 5600$ mL/min = 5.6 L/min ✓

MCAT note: A "normal-looking" SV can hide a failing heart if EDV is inflated — always check EF, not just SV.

Question: Place in temporal order: (a) S1, (b) QRS complex, (c) aortic valve opens, (d) mitral valve closes.

Solution:

1. QRS — electrical depolarization must precede mechanical contraction.
2. Ventricular pressure rises above atrial pressure → mitral valve closes, producing S1 (d and a are essentially simultaneous; closure causes the sound).
3. Pressure keeps rising through isovolumetric contraction until it exceeds aortic pressure → aortic valve opens (c). ✓

Order: b → d/a → c.

Why it matters: Passage figures often overlay ECG, pressure, and volume traces — anchor every mechanical event to the electrical one just before it.

Question: In an animal experiment, both vagus nerves to the heart are severed. Resting heart rate rises from 70 to about 100 bpm. Explain.

Solution:

1. The SA node's intrinsic firing rate is ~100 bpm.
2. At rest, parasympathetic (vagal) tone dominates, holding the rate near 70.
3. Removing vagal input unmasks the intrinsic SA rate → HR climbs to ~100 bpm. ✓

Contrast: Blocking sympathetic input at rest changes HR only slightly (small resting sympathetic tone); blocking muscarinic receptors with atropine mimics vagotomy.

Key Takeaways — Part 1

• Pulmonary and systemic circuits are in series; systemic organs are in parallel. Pulmonary artery = deoxygenated, pulmonary veins = oxygenated.
• $SV = EDV - ESV$; $EF = SV/EDV$ (normal ≈ 55–70%); $CO = HR \times SV$.
• S1 = AV valves close (start of systole); S2 = semilunar valves close (start of diastole); valves are passive.
• Conduction: SA node (myogenic pacemaker) → AV node (delay, only atria-ventricle path) → His–Purkinje. P = atrial depolarization, QRS = ventricular depolarization, T = ventricular repolarization.
• Sympathetic NE (beta-1) speeds and strengthens; vagal ACh slows — resting HR sits below the SA node's intrinsic ~100 bpm because vagal tone dominates.

• Low-yield extras: the pacemaker currents are named the "funny" Na$^+$ current ($I_f$) and T-type Ca$^{2+}$ channels

Cardiovascular System

Part 2 of 4 — Pressure, Flow & Resistance (Hemodynamics)

The Ohm's-Law Analogy

Bulk blood flow is driven by a pressure gradient against a resistance:

$Q = \frac{\Delta P}{R}$

Applied to the whole systemic circulation:

$CO = \frac{MAP - P_{RA}}{TPR} \approx \frac{MAP}{TPR} \quad\Rightarrow\quad MAP \approx CO \times TPR$

since right atrial pressure is near zero. Every blood-pressure question reduces to this: pressure changes only if cardiac output or total peripheral resistance changes.

Mean Arterial Pressure and Pulse Pressure

$MAP \approx P_{dias} + \frac{1}{3}(P_{sys} - P_{dias}), \qquad \text{Pulse pressure} = P_{sys} - P_{dias}$

• MAP is weighted toward diastolic because the heart spends about two-thirds of each cycle in diastole at rest.
• Pulse pressure rises with larger stroke volume or stiffer arteries (less elastic damping — why isolated systolic hypertension appears with age).
• Elastic arteries act as a pressure reservoir: they stretch during systole and recoil during diastole, keeping flow continuous.

• This elastic-reservoir behavior of the large arteries is called the Windkessel effect.

Poiseuille's Law — Radius Rules

$R = \frac{8 \eta L}{\pi r^4}$

• Resistance scales with viscosity ($\eta$) and length, but with the fourth power of the inverse radius: halving $r$ multiplies $R$ by 16.
• Arterioles are the "resistance vessels": their smooth muscle tone is the main site of TPR control and the largest pressure drop in the circuit.
• Viscosity rises with hematocrit — polycythemia raises resistance; severe anemia lowers it.

Series vs. Parallel Vessels

Because systemic organs sit in parallel, losing a parallel bed (e.g., amputation, vasoconstriction of one organ) raises TPR, while opening more beds (exercise, pregnancy) lowers it.

Continuity: Velocity vs. Total Cross-Sectional Area

$v = \frac{Q}{A_{total}}$

• Flow rate $Q$ (volume/time) is the same through each series segment of the circulation — what leaves the aorta per minute passes through the capillaries per minute.
• Capillaries individually are tiny, but their total cross-sectional area is by far the largest, so velocity there is slowest (~0.03 cm/s vs ~30 cm/s in the aorta) — maximizing time for exchange.
• Veins are capacitance vessels: thin-walled and distensible, they hold ~60–70% of blood volume at rest; venoconstriction mobilizes this reservoir to boost venous return.

Where Pressure Falls

Aorta (MAP ~93) → arterioles (largest drop, to ~35) → capillaries (~35 → 15) → veins (~15 → ~0 at the RA). Skeletal-muscle pumping and respiratory pressure swings help venous return against this tiny remaining gradient; venous valves prevent backflow.

Hemodynamics 🎯

Worked Examples — Pressure, Flow & Resistance

Question: During vigorous exercise, cardiac output rises from 5 to 20 L/min, yet MAP only rises from ~93 to ~110 mmHg. Reconcile this with $MAP = CO \times TPR$.

Solution:

1. If TPR were constant, quadrupling CO would nearly quadruple MAP — it doesn't.
2. Exercising skeletal-muscle arterioles dilate massively (local metabolites: CO2, H$^+$, adenosine, K$^+$), opening huge parallel beds → TPR falls to roughly a third to a quarter of resting value (MAP rises only modestly because CO quadruples).
3. $MAP = 20 \times TPR_{new} \approx$ only modestly above resting MAP. ✓

Takeaway: Local metabolic vasodilation in active muscle overrides sympathetic vasoconstriction there; the net effect is high flow at nearly constant pressure.

• The override of sympathetic vasoconstriction by local metabolites in exercising muscle is called functional sympatholysis.

Question: Two vascular beds each have resistance $R = 12$ units. Compare total resistance when they are in parallel versus in series, and state which arrangement the body uses for its organs.

Solution:

1. Parallel: $\frac{1}{R_{tot}} = \frac{1}{12} + \frac{1}{12} = \frac{2}{12} \Rightarrow R_{tot} = 6$ units.
2. Series: $R_{tot} = 12 + 12 = 24$ units — four times the parallel value.
3. Systemic organs branch in parallel off the aorta ✓ — so each organ receives fully oxygenated blood at full arterial pressure, flow to one organ can be adjusted without starving the others, and total resistance stays low.

Question: A trauma patient loses 1 L of blood. Predict the immediate changes in MAP, and the reflex changes in HR and TPR that follow.

Solution:

1. Blood loss → decreased venous return → decreased preload → decreased SV (Frank–Starling) → CO and MAP fall.
2. Baroreceptors (carotid sinus, aortic arch) fire less → brainstem raises sympathetic and withdraws parasympathetic output.
3. Reflex: HR up, contractility up, arteriolar constriction (TPR up), venoconstriction (mobilizes venous reservoir) → MAP is defended. ✓

Clinical signature: tachycardia + cool, pale skin (skin/gut beds sacrificed) + narrowed pulse pressure — before MAP itself collapses.

Key Takeaways — Part 2

• $Q = \Delta P / R$; for the whole circuit, $MAP \approx CO \times TPR$.
• $MAP \approx P_{dias} + \frac{1}{3}(\text{pulse pressure})$ — weighted toward diastole.
• Poiseuille: $R \propto \eta L / r^4$ — radius dominates; arterioles are the resistance (and largest pressure-drop) site.
• Parallel organ beds keep total resistance low; opening beds lowers TPR, closing them raises it.
• $v = Q / A_{total}$: capillaries have the largest total area → slowest velocity → best exchange. Veins are the volume reservoir (~2/3 of blood).

• Low-yield extras: the arterial pressure-reservoir effect is named the Windkessel effect; metabolic override of sympathetic constriction in exercising muscle is named functional sympatholysis

Cardiovascular System

Part 3 of 4 — Starling Forces, Frank–Starling & Blood Pressure Regulation

The Three Determinants of Stroke Volume

Frank–Starling Mechanism

The heart pumps what it receives. Greater end-diastolic volume stretches cardiac sarcomeres toward optimal actin–myosin overlap → stronger contraction → larger stroke volume.

• This automatically matches the outputs of the two ventricles: if the right heart briefly pumps more, the extra volume reaches the left heart, stretches it, and the left output rises to match.
• Sympathetic stimulation shifts the whole Starling curve up and left (more SV at the same preload) — that is a contractility change, not a preload change. Distinguishing the two is a favorite MCAT discrimination.

Capillary Exchange — Starling Forces

Net fluid flux across the capillary wall:

$J_v \propto (P_c - P_i) - (\pi_c - \pi_i)$

• Arteriolar end: $P_c$ high (~35 mmHg) → net filtration out. Venular end: $P_c$ low (~15) while $\pi_c$ ≈ 25 → net reabsorption in.
• The slight net excess filtered each day (~2–4 L) returns via lymphatics.
• Edema logic: ↑$P_c$ (heart failure, venous obstruction), ↓$\pi_c$ (low albumin — liver failure, nephrotic syndrome, malnutrition), ↑ capillary permeability (inflammation → protein leaks, raising $\pi_i$), or lymphatic blockage — each tips the balance toward the interstitium.

Small solutes and gases cross by diffusion down their gradients (O$_2$ and CO$_2$ straight through membranes; ions/glucose via pores or clefts); Starling forces govern bulk fluid, not gas exchange.

The Baroreceptor Reflex — Short-Term Pressure Control

1. Stretch receptors in the carotid sinus and aortic arch fire in proportion to arterial pressure.
2. Signals reach the medulla (cardiovascular centers).
3. Pressure falls → less baroreceptor firing → ↑ sympathetic, ↓ parasympathetic output → ↑ HR, ↑ contractility, arteriolar constriction, venoconstriction → pressure restored.
4. Pressure rises → the mirror image.

• Afferent nerves: the carotid sinus signals via the glossopharyngeal nerve (CN IX), the aortic arch via the vagus (CN X).

This is a classic negative feedback loop acting within seconds. Long-term pressure control belongs to the kidneys (blood volume via RAAS/ADH — covered in the renal lesson).

Hormonal Modulators (Preview)

• Epinephrine (adrenal medulla): beta-1 → ↑HR/contractility; alpha-1 → vasoconstriction in skin/gut; beta-2 → vasodilation in skeletal muscle.
• Angiotensin II and ADH (vasopressin): vasoconstrictors that also expand volume via the kidney.
• ANP (stretched atria): promotes Na$^+$ and water excretion — the heart's own volume-lowering hormone.

Starling Forces & Regulation 🎯

Worked Examples — Regulation & Exchange

Question: Arteriolar end: $P_c = 37$, $P_i = 1$, $\pi_c = 25$, $\pi_i = 3$ mmHg. Venular end: $P_c = 16$, others unchanged. Find the net pressure at each end and the direction of fluid movement.

Solution:

1. Arteriolar: $(37 - 1) - (25 - 3) = 36 - 22 = +14$ mmHg → filtration OUT. ✓
2. Venular: $(16 - 1) - (25 - 3) = 15 - 22 = -7$ mmHg → reabsorption IN. ✓
3. Filtration (+14) exceeds reabsorption (−7): the small daily surplus is drained by lymphatics — block them and lymphedema follows.

Question: On a graph of SV (y) versus EDV (x), distinguish: (a) an IV saline infusion, and (b) an epinephrine infusion.

Solution:

1. (a) Saline expands volume → venous return and EDV rise → the heart moves up along the SAME curve (a preload change). ✓
2. (b) Epinephrine (beta-1) raises contractility → the entire curve shifts up/left: at ANY given EDV, SV is larger. ✓

Test skill: "Along the curve" = preload; "new curve" = contractility. Afterload increases shift the curve down.

Question: A patient with failing left-ventricular function develops fluid in the lungs (pulmonary edema). Trace the mechanism using Starling logic.

Solution:

1. Weak LV → blood is not moved forward effectively → volume and pressure back up into the left atrium and pulmonary veins.
2. Pulmonary capillary hydrostatic pressure ($P_c$) rises.
3. Filtration now exceeds reabsorption in pulmonary capillaries → fluid enters the interstitium and alveoli → impaired gas exchange, dyspnea. ✓

Symmetry: RIGHT-heart failure backs pressure into the systemic veins instead → peripheral (ankle) edema and jugular venous distension.

Key Takeaways — Part 3

• SV depends on preload (↑SV), afterload (↓SV), contractility (↑SV). Frank–Starling: more filling → stronger contraction; it balances the two ventricles automatically.
• Starling forces: filtration = $(P_c - P_i) - (\pi_c - \pi_i)$; hydrostatic pushes out, oncotic (albumin) pulls in; lymphatics clear the surplus.
• Edema causes: ↑$P_c$, ↓$\pi_c$, ↑ permeability, lymph blockage.
• Baroreceptor reflex (carotid sinus + aortic arch → medulla) is the seconds-scale negative-feedback controller of MAP; kidneys control pressure long-term via volume.
• Preload changes move you along a Starling curve; contractility changes create a new curve.

• Low-yield extras: baroreceptor afferents run in the glossopharyngeal nerve (carotid sinus) and the vagus (aortic arch)

Cardiovascular System

Part 4 of 4 — MCAT-Style Integration: Loops, Pathology & Passage Skills

Reading a Pressure–Volume (PV) Loop

A left-ventricular PV loop (pressure on y, volume on x) is traversed counterclockwise:

1. Bottom edge (left → right): diastolic filling — mitral open, volume rises to EDV.
2. Right edge (up): isovolumetric contraction — all valves closed, pressure rises at EDV.
3. Top edge (right → left): ejection — aortic valve open, volume falls to ESV.
4. Left edge (down): isovolumetric relaxation — all valves closed at ESV.

• Loop width = stroke volume (EDV − ESV); loop area ≈ stroke work of the ventricle.
• ↑ Preload → right edge moves right (wider loop). ↑ Afterload → taller loop, ejection ends early (narrower SV). ↑ Contractility → lower ESV (left edge shifts left, wider loop).

Classic Valve Pathologies as Physics Problems

You don't memorize murmurs for the MCAT — you derive consequences from flow physics: where does blood back up, and what pressure must rise?

Categories of Shock (Inadequate Perfusion)

Distributive shock is the outlier: warm skin, LOW resistance, pressure falls despite normal-to-high output.

Oxygen Delivery & the Fick Principle

$\text{O}_2 \text{ consumption} = CO \times (C_a - C_v)$

where $C_a$ and $C_v$ are arterial and venous O$_2$ contents. Rearranged, this measures cardiac output from measured O$_2$ uptake and the arteriovenous O$_2$ difference — a standard experimental-passage setup. During exercise, both CO and extraction ($C_a - C_v$) rise.

Passage-Skill Checklist

• Anchor every trace: ECG events precede mechanical events; valve sounds mark phase boundaries.
• Perturbation questions: identify whether the change hits preload, afterload, contractility, HR, or TPR — then propagate through $CO = HR \times SV$ and $MAP = CO \times TPR$.
• Units discipline: CO in L/min; convert mL ↔ L before multiplying.
• Reflex second-guess: after any primary change, ask what the baroreflex does next — many wrong answers describe the un-compensated state when the question asks about the compensated one (or vice versa).

Integration & Pathology 🎯

Worked Examples — MCAT-Style Passages

Question: A passage reports that a stenotic aortic valve's effective orifice radius is 60% of normal. By roughly what factor does the valve's resistance to ejection rise, and what chronic ventricular change follows?

Solution:

1. $R \propto 1/r^4 \Rightarrow R_{new}/R_{old} = 1/(0.6)^4 = 1/0.1296 \approx 7.7$ — nearly 8× the resistance.
2. The LV must generate much higher systolic pressure to maintain flow → chronic pressure overload → concentric hypertrophy (wall thickens, chamber not dilated).
3. Long-term: thick stiff wall impairs filling (diastolic dysfunction) and raises O2 demand. ✓

Contrast: volume overload (regurgitation) → eccentric hypertrophy (chamber dilates).

Question: In a trial, propranolol (beta-adrenergic antagonist) is given before treadmill exercise. Compared with placebo, predict exercise HR, contractility, and CO.

Solution:

1. Exercise normally raises HR and contractility via sympathetic NE/epinephrine on beta-1 receptors.
2. Blocking beta-1 blunts both: exercise HR and contractility rise far less.
3. $CO = HR \times SV$: the ceiling on both factors caps CO; exercise capacity falls. Frank–Starling (preload from muscle-pump venous return) still contributes some SV increase — CO rises, just much less. ✓

Distractor alert: propranolol does not block the vagus — resting bradycardia deepens because sympathetic support is gone while vagal tone remains.

Question: A passage table shows, 10 minutes after moderate hemorrhage: HR 115 (was 72), MAP 88 (was 92), TPR elevated. A student concludes "the hemorrhage was mild because pressure is nearly normal." Critique.

Solution:

1. Near-normal MAP does NOT mean minimal blood loss — it means the baroreflex is working: tachycardia and high TPR are the fingerprints of active compensation.
2. The proper severity clues are the compensation markers themselves (HR ↑ 60%, vasoconstriction) — pressure is the DEFENDED variable, so it is the last number to move.
3. If losses continue, compensation fails: MAP then drops precipitously (decompensated shock). ✓

Passage skill: in regulated systems, judge the disturbance by the effort of the regulator, not by the regulated variable.

Key Takeaways — Part 4

• PV loop: width = SV, counterclockwise; preload moves the right edge, afterload the top, contractility the left (ESV).
• Valve lesions are flow-physics problems: find where blood backs up and which chamber faces pressure vs. volume overload.
• Shock taxonomy: hypovolemic and cardiogenic = low CO with reflex high TPR; distributive (septic) = low TPR with warm skin and often high CO.
• Fick: $CO = \text{O}_2 \text{ consumption}/(C_a - C_v)$ — a recurring experimental design.
• In any perturbation question: classify the change (preload/afterload/contractility/HR/TPR), propagate through the two master equations, then apply the baroreflex.