Overview
This lecture explains the cardiac cycle, the mechanical and electrical events controlling heart function, key determinants of cardiac output, and how various factors and dysfunctions impact heart performance.
Cardiac Cycle Phases
- Cardiac cycle refers to the mechanical events during one heartbeat.
- Five stages: passive filling, atrial systole, isovolumetric contraction, ventricular ejection, isovolumetric relaxation.
- Passive filling: both atria and ventricles are relaxed (diastole); 80% of ventricular filling happens spontaneously.
- Atrial systole: atria contract to push the remaining 20% of blood into ventricles; ventricles remain in diastole.
- Isovolumetric contraction: ventricles contract with all valves closed, causing pressure to rise but no blood ejection.
- Ventricular ejection: ventricular pressure exceeds afterload, semilunar (aortic/pulmonary) valves open, blood leaves the heart.
- Isovolumetric relaxation: ventricles relax with all valves closed, pressure drops, no blood enters or exits.
Heart Sounds and ECG
- S1 ("lub"): AV valves close at start of isovolumetric contraction (after QRS complex).
- S2 ("dub"): Semilunar valves close at start of isovolumetric relaxation (after T wave).
- ECG: P wave = atrial contraction; QRS = ventricular contraction; T wave = ventricular relaxation.
Cardiac Volumes and Pressures
- End-diastolic volume (EDV): blood in ventricle at end of filling (preload).
- End-systolic volume (ESV): blood remaining after ejection.
- Stroke volume (SV) = EDV - ESV; blood ejected per beat.
- Afterload: pressure that must be overcome to eject blood, set by diastolic arterial pressure.
Cardiac Output and Regulation
- Cardiac output (CO) = SV × heart rate; quantity of blood pumped per minute.
- CO determined by preload (venous return), afterload, contractility, and heart rate.
- Sympathetic stimulation increases heart rate and contractility (via more calcium).
- Parasympathetic stimulation (vagus nerve) decreases heart rate (vagal tone).
Frank-Starling Law & Preload
- Increasing preload (EDV) stretches ventricular muscle, leading to stronger contractions and higher stroke volume, up to an optimal point.
- Sarcomere length determines muscle tension; optimal overlap increases contraction efficiency.
Factors Affecting Heart Rate
- Sympathetic increases heart rate and contractility; parasympathetic decreases heart rate.
- Chemicals (epinephrine, thyroxine), ion balance (K+, Ca2+), age, gender, and fitness affect heart rate.
- Athletes have increased vagal tone and lower resting heart rate, but higher stroke volume.
Clinical Relevance & Dysfunction
- Blocked coronary arteries limit blood to the heart, causing ischemia or infarction.
- Arrhythmias disrupt coordinated electrical activity, impairing cardiac output.
- Changes in cardiac output, chemical imbalances, and congenital defects affect heart performance.
Key Terms & Definitions
- Preload — Volume of blood in the ventricle at end diastole, or the initial stretch of the heart muscle.
- Afterload — Pressure against which the ventricle must work to eject blood.
- Stroke Volume (SV) — Amount of blood ejected from the ventricle per heartbeat.
- Cardiac Output (CO) — Total blood volume pumped by the ventricle per minute (SV × heart rate).
- Frank-Starling Law — Ventricular contraction increases as preload increases (within limits).
- Isovolumetric Contraction/Relaxation — Phases when all heart valves are closed and volume remains constant.
Action Items / Next Steps
- Review diagrams of the cardiac cycle stages and relate them to ECG and heart sounds.
- Practice identifying each phase, valve status, and pressure changes in the cycle.
- Study the effects of preload, afterload, and autonomic regulation on cardiac output.