11.1 Cardiovascular Physiology

11.1 Cardiovascular Physiology

Quick Answer: The heart fills and empties in a cardiac cycle of systole (contraction) and diastole (relaxation). S1 marks AV valve closure; S2 marks semilunar valve closure. Cardiac output (CO) = heart rate (HR) × stroke volume (SV). Blood pressure depends on how much blood the heart pumps and how much resistance vessels offer. Pulmonary and systemic circuits keep oxygen-poor and oxygen-rich blood in sequence. Capillaries exchange by diffusion and filtration. On ECG: P = atrial depolarization, QRS = ventricular depolarization, T = ventricular repolarization. This is Human Body function after Chapter 7 anatomy—high-yield for NEX Science.

Anatomy told you what the chambers, valves, and vessels are. Physiology asks how they move blood, generate pressure, exchange materials, and produce the electrical pattern you see on a monitor. Build the cycle first, then output and pressure, then circuit flow and capillaries, then the ECG as a surface readout of the conduction events you already named.

The Cardiac Cycle: Systole and Diastole

One cardiac cycle is one complete heartbeat: atria and ventricles fill and empty in a coordinated sequence so blood moves forward through the valves.

Systole means contraction (and usually ejection for ventricles). Diastole means relaxation and filling. Most ventricular filling is passive early in diastole; atrial contraction adds a late contribution (the atrial “kick”). At rest, diastole lasts longer than systole—important because coronary arteries fill mainly during ventricular diastole when the myocardium is less compressed.

Pressure logic (no physics deep-dive): Blood flows from higher pressure to lower pressure. Ventricular pressure must rise above atrial pressure to close AV valves and above arterial pressure to open semilunar valves. When ventricles relax, arterial pressure exceeds ventricular pressure and semilunar valves shut; atrial pressure then exceeds ventricular pressure and AV valves open for filling.

Heart Sounds: S1 and S2

Normal heart sounds come mainly from valve closure and the vibrations that follow—not from the valves “slamming like doors” in isolation, but from abrupt cessation of reverse flow as cusps meet.

S1 occurs when rising ventricular pressure forces AV valves shut so blood cannot regurgitate into the atria. S2 occurs when falling ventricular pressure allows arterial backpressure to close the aortic and pulmonary valves so blood cannot fall back into the ventricles.

Extra sounds (S3/S4) and murmurs from turbulent flow across stenotic or regurgitant valves appear in clinical courses; for NEX Science, lock S1 = AV closure and S2 = semilunar closure.

Cardiac Output: CO = HR × SV

Cardiac output (CO) is the volume of blood each ventricle ejects per minute (usually stated for the left ventricle into the systemic circuit).

If HR is 70 beats/min and SV is 70 mL/beat, CO ≈ 4,900 mL/min ≈ 5 L/min. Both sides of the heart must match output over time: right ventricular CO into the lungs equals left ventricular CO into the body under steady conditions, or blood would pool in one circuit.

What changes stroke volume? At intro level, think of three influences:

1. Preload — stretch of ventricular muscle before contraction (related to venous return and end-diastolic volume); within limits, more stretch → stronger contraction (Frank–Starling idea).
2. Contractility — strength of contraction at a given preload (sympathetic stimulation and circulating catecholamines increase contractility).
3. Afterload — the pressure the ventricle must overcome to eject (higher arterial pressure makes ejection harder and can reduce SV if the heart cannot compensate).

Sympathetic stimulation raises HR and contractility; parasympathetic (vagus) mainly slows HR. Exercise raises CO by increasing both HR and SV.

Blood Pressure Determinants (Intro)

Blood pressure (BP) is the force blood exerts on vessel walls. Arterial BP is often written as systolic/diastolic (e.g., 120/80 mm Hg): peak pressure during ventricular ejection and lowest pressure during diastole.

Mean arterial pressure conceptually reflects a balance of CO × systemic vascular resistance (plus central venous pressure, often treated as small). For NEX: if CO falls (e.g., pump failure) or resistance falls sharply (e.g., widespread vasodilation in some shocks), arterial pressure falls. Baroreceptors and autonomic reflexes adjust HR, contractility, and vessel tone to stabilize BP—detailed reflex arcs can wait; know that pressure is not “set by the cuff” but by pump and pipes.

Pulse pressure = systolic − diastolic. A very wide or narrow pulse pressure can be clinically meaningful later; intro exams mainly want systolic vs diastolic identity and the CO/resistance idea.

Pulmonary vs Systemic Flow and Oxygen Content

Function follows the dual-circuit anatomy from Chapter 7.

Path of a drop of blood (function focus):

1. Deoxygenated systemic venous blood → right atrium → right ventricle → pulmonary arteries → pulmonary capillaries (pick up O₂, unload CO₂)
2. Oxygenated blood → pulmonary veins → left atrium → left ventricle → aorta → systemic arteries → tissue capillaries (unload O₂, pick up CO₂)
3. Deoxygenated blood → systemic veins → venae cavae → right atrium again

Remember: artery/vein names track direction relative to the heart, not oxygen content. Pulmonary arteries are the large exception students forget—they carry deoxygenated blood.

Capillary Exchange: Diffusion and Filtration Overview

Capillaries are the exchange vessels. Two major processes matter at intro level:

Diffusion

Diffusion moves individual molecules down their concentration gradients across the thin capillary wall and interstitial fluid into (or out of) cells.

Lipid-soluble gases cross easily; water-soluble substances use clefts, fenestrations, or transporters depending on capillary type. The huge total capillary surface area and short diffusion distance make exchange efficient.

Filtration and Reabsorption (Fluid)

Filtration pushes fluid out of the capillary; reabsorption pulls fluid in. Two opposing “pressures” dominate textbook summaries:

Typically, net filtration occurs at the arterial end of a capillary bed and net reabsorption at the venous end; lymphatics return the small net fluid leftover to the blood. If hydrostatic pressure stays high (e.g., venous congestion) or plasma proteins fall, more fluid remains in tissues → edema. This is the physiologic bridge from vessel anatomy to fluid-balance nursing assessments.

ECG Waves: P, QRS, and T (Intro Meaning)

An electrocardiogram (ECG/EKG) records electrical activity of the heart from the body surface—not mechanical contraction itself, though electrical events trigger mechanical ones.

PR interval (start of P to start of QRS) includes AV nodal delay—time for atrial emptying before ventricles fire. ST segment sits between ventricular depolarization and repolarization; clinically watched for ischemia, but intro NEX needs wave meanings more than interval numbers.

Link to conduction anatomy: SA node starts atrial depolarization (P); AV node delay then ventricular depolarization via His–Purkinje (QRS); ventricular recovery produces T. No P wave with organized QRS can suggest atrial electrical failure or junctional rhythms in later coursework—here, know the normal triad.

Clinical and Nursing Anchors

• Vital signs: HR and BP are direct readouts of cardiac cycle rate and pressure determinants; weak pulse may reflect low SV.
• Auscultation: S1/S2 timing frames systole vs diastole when you listen for murmurs.
• Shock and heart failure: Low CO threatens tissue perfusion; edema implicates capillary filtration balance.
• ECG monitoring: Recognize that P–QRS–T map to atrial then ventricular electrical events before interpreting rhythms.
• Oxygen delivery: Systemic flow must match tissue demand; pulmonary flow must match ventilation for gas exchange (Section 11.2).

Exam Traps

• S1 vs S2: S1 = AV valves; S2 = semilunar valves—not the reverse.
• Systole ≠ always “blood pressure number”: Systole is the contraction phase; systolic BP is the peak arterial pressure during that phase.
• CO formula: CO = HR × SV—not BP × SV.
• Pulmonary artery blood: deoxygenated until it reaches pulmonary capillaries.
• ECG vs pulse: Electrical activity can exist briefly without effective pulse (pulseless rhythms)—electrical ≠ guaranteed mechanical output.
• P wave ≠ ventricular: P is atrial; QRS is ventricular depolarization.

Study Map for NEX

1. Sketch one cardiac cycle: label systole/diastole and mark when AV vs semilunar valves are closed.
2. Write CO = HR × SV and compute one sample (e.g., 75 × 70 mL).
3. List BP determinants: CO, resistance, volume, arterial elasticity.
4. Trace oxygenated vs deoxygenated path through both circuits aloud.
5. Assign P / QRS / T to atrial depolarization, ventricular depolarization, ventricular repolarization.

With cycle, output, pressure, circuits, capillaries, and ECG meanings in place, respiratory physiology can explain how pulmonary capillary blood actually gains O₂ and loses CO₂—the next section’s job.