Video 3 - Cardiac Cycle, Cardiac Output & Heart Pathologies

Cardiac Cycle Overview

• The cardiac cycle = one complete “beat-to-beat” sequence.
  • Begins with atrial contraction → ventricular contraction → relaxation/pause → repeats.
  • Provides a “day-in-the-life” snapshot of heart function (athlete vs. couch potato).
• Cardiodynamics = study of speed & efficiency of the cycle (how well / how fast the heart moves blood).

Basic Terminology (Squeeze vs. Relax)

• Systole – contraction phase ("S for Squeeze").
  • Atrial systole: atria push blood ↓ through AV valves.
  • Ventricular systole: ventricles eject blood ↑; semilunar valves open, AV valves slam shut.
• Diastole – relaxation phase ("not-squeezed").
  • Ventricular diastole triggers closure of pulmonary & aortic semilunar valves and the general “reset.”

Key Volume Definitions

• End Diastolic Volume (EDV)
  • Max blood volume in ventricle after filling, before contraction.
• End Systolic Volume (ESV)
  • Min blood volume remaining after ejection.
• Stroke Volume (SV) – amount ejected per beat.
  • Formula: SV = EDV - ESV
  • Analogy: A pitcher starts with 1000\,\text{mL} (EDV). If 800\,\text{mL} remains (ESV), poured out 200\,\text{mL} (SV).

Sample Calculations

• Given EDV = 130\,\text{mL} and ESV = 50\,\text{mL}:
  • SV = 130 - 50 = 80\,\text{mL/beat}.
• Cardiac Output (CO) – blood volume pumped per minute.
  • Formula: CO = SV \times HR
  • Dimensional proof: (\text{mL/beat})(\text{beats/min}) \Rightarrow \text{mL/min}.
  • Example: SV = 80\,\text{mL/beat},\; HR = 60\,\text{beats/min} → CO = 4800\,\text{mL/min}.
  • Standardizing SV over time lets clinicians compare athletes vs sedentary patients with identical HR or SV.

Factors Affecting Heart Rate (HR)

• Autonomic nervous system (ANS)
  • Medulla oblongata houses cardio-regulatory centers.
  • Cardio-accelerator (sympathetic): releases (\text{NE}/\text{E} → ↑HR.
  • Cardio-inhibitory (parasympathetic): vagus nerve releases acetylcholine (ACh) → ↓HR.
  • Dual (sympathetic & parasympathetic) innervation sets autonomic tone for rapid adjustment.
• Reflexes
  • Baro- & chemoreceptors detect pressure and gas changes, feed back to medulla.
• Hormones
  • Circulating (\text{E},\text{NE}, T3, T4) elevate HR (fight-or-flight or metabolic ramp-up).

SA Node Electrical Modulation

• Intrinsic SA node resting potential ≈ -60\,\text{mV} (vs. ventricular muscle -90\,\text{mV}) → easier to reach threshold (≈ -45\,\text{mV} → depolarize to +15\,\text{mV}).
• Sympathetic effect: (\text{NE}) opens Ca²⁺ channels → partial depolarization (e.g., shift to -50\,\text{mV}) = quicker threshold, more beats/​min.
• Parasympathetic effect: ACh opens K⁺ channels → hyperpolarization (e.g., ↓ to -70\,\text{mV}$$) = longer climb, fewer beats/​min.
  • Diagrammatically: 5 spikes vs 3 vs 2 spikes in equal time windows (fast ↔ normal ↔ slow).

Factors Affecting Stroke Volume

Determinants of EDV ("Filling")

• Filling time – duration of ventricular diastole (↓ at high HR).
• Venous return – quantity of blood delivered to atria (↓ with vascular disease or hypovolemia).

Determinants of ESV ("Emptying")

• Preload – stretch on ventricular walls at end-diastole (Frank-Starling law: ↑stretch → ↑force).
• Contractility – intrinsic force of cardiac muscle (affected by Ca²⁺, sympathetic tone, inotropes).
• Afterload – pressure in aorta & pulmonary trunk opposing ejection.
  • High systemic or pulmonary hypertension → ventricles leave more residual blood (↑ESV).

Exercise & Cardiac Output

• Heavy exercise can ↑CO by 300 – 500 %.
  • Practical implication: regular training maintains myocardial "fitness" & vascular elasticity.

Clinical Conditions & Pathologies

• Mitral Valve Prolapse (MVP)
  • One cusp inverts upward, allowing regurgitation into left atrium.
  • Risk: blood swirl → clot → potential atrial fibrillation → stroke.
• Myocardial Infarction (MI)
  • Blocked coronary artery → downstream hypoxia → tissue death.
  • Severity: small distal branch (often survivable) vs. large proximal artery (often fatal).
• Cardiomegaly – enlarged heart; often secondary to chronic hypertension or infections.
• Congestive Heart Failure (CHF) & Edema
  • Left-sided failure → pulmonary edema (fluid in lungs).
  • Right-sided failure → systemic edema (legs, ankles, extremities).
  • Cause: mismatch between right/left ventricular outputs.

EKG / ECG Abnormalities

• Premature Ventricular Contractions (PVCs)
  • Occasional extra ventricular beat; usually benign.
  • Provoked by stress, dehydration; resolve with hydration/electrolytes.
• Atrial Fibrillation (AFib)
  • Erratic atrial electrical activity; absent/irregular P waves.
  • Leads to inefficient atrial emptying → clot risk (esp. with MVP).
• Atrial Flutter
  • Rapid, repetitive atrial depolarizations → "sawtooth" EKG pattern.
  • More aggressive variant; still exhibits irregular ventricular response.

Practical / Ethical / Real-World Connections

• Encouraging exercise has direct cardiac benefits (↑CO reserves, ↓afterload). Ethical duty for clinicians to promote lifestyle change.
• Accurate SV & CO calculations underpin drug dosing (inotropes, beta-blockers) and critical-care decisions.
• Understanding arrhythmia patterns guides timely anti-coagulation to prevent stroke in AFib.
• Early detection of valve prolapse or CHF via auscultation & imaging prevents progression to life-threatening edema or hypoxia.

Looking Ahead (Vascular Integration)

• Chapter 20 extends these principles to blood vessels:
  • How cardiac output distributes through arteries, capillaries, veins.
  • Interaction between vascular resistance and the heart’s workload.

Reminder from instructor: Complete the heart quiz before starting the vasculature module.