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Cardiovascular Physiology: Heart Function and Blood Pressure Regulation

Cardiovascular Physiology: Heart Function and Blood Pressure Regulation

Cardiovascular Physiology: Heart Function and Blood Pressure Regulation

Published: 2024-12-08T00:00:00.000Z

The cardiovascular system is the body's transport network, delivering oxygen and nutrients while removing waste products. Understanding cardiovascular physiology is crucial for interpreting clinical findings, ECGs, and managing cardiac patients. This comprehensive guide explores the cardiac cycle, electrical conduction, hemodynamics, and regulatory mechanisms that maintain cardiovascular homeostasis.

Human heart model

Cardiac Cycle

Phases of the Cardiac Cycle

Systole (Ventricular Contraction):

  1. Isovolumetric contraction: All valves closed, pressure rises
  2. Ejection phase: Aortic/pulmonary valves open, blood ejected

Diastole (Ventricular Relaxation):

  1. Isovolumetric relaxation: All valves closed, pressure falls
  2. Rapid filling: AV valves open, passive filling
  3. Atrial contraction: Active filling (contributes ~20% of ventricular volume)

Normal ejection fraction is 55-70%. Learn more about cardiac function at NCBI Cardiac Physiology.

Heart Sounds

  • S1 (lub): Closure of mitral and tricuspid valves (start of systole)
  • S2 (dub): Closure of aortic and pulmonary valves (start of diastole)
  • S3: Rapid ventricular filling (normal in young, pathologic in heart failure)
  • S4: Atrial contraction against stiff ventricle (always pathologic)

For clinical examination of heart sounds, see our Clinical Examination Guide.

Electrical Conduction System

ECG monitor display

Conduction Pathway

  1. SA node: Pacemaker (60-100 bpm)
  2. Atrial conduction: Bachmann's bundle, internodal pathways
  3. AV node: Delays impulse (0.1 sec) - allows atrial emptying
  4. Bundle of His: Rapid conduction to ventricles
  5. Right and Left Bundle Branches
  6. Purkinje fibers: Rapid ventricular depolarization

Cardiac Action Potential

Pacemaker cells (SA node):

  • Phase 4: Spontaneous depolarization (funny current, If)
  • Phase 0: Calcium influx
  • Phase 3: Potassium efflux (repolarization)

Ventricular myocytes:

  • Phase 0: Rapid sodium influx (depolarization)
  • Phase 1: Brief repolarization (K+ efflux)
  • Phase 2: Plateau (Ca²⁺ influx = K⁺ efflux)
  • Phase 3: Repolarization (K⁺ efflux)
  • Phase 4: Resting potential

Electrocardiogram (ECG)

ECG Waves and Intervals

  • P wave: Atrial depolarization
  • PR interval: AV nodal delay (0.12-0.20 sec)
  • QRS complex: Ventricular depolarization (<0.12 sec)
  • ST segment: Ventricular plateau phase
  • T wave: Ventricular repolarization
  • QT interval: Total ventricular depolarization and repolarization

Common ECG Abnormalities

  • ST elevation: Myocardial infarction
  • ST depression: Ischemia, digitalis effect
  • Wide QRS: Bundle branch block, ventricular origin
  • Prolonged PR: First-degree heart block
  • Prolonged QT: Risk of torsades de pointes
Medical monitoring equipment

Hemodynamics

Key Equations

Cardiac Output (CO):

CO = Heart Rate × Stroke Volume

Normal: 5 L/min at rest

Blood Pressure:

BP = Cardiac Output × Systemic Vascular Resistance

MAP = Diastolic BP + 1/3(Systolic BP - Diastolic BP)

Ohm's Law (Hemodynamic):

Flow = Pressure gradient / Resistance

Factors Affecting Cardiac Output

Preload:

  • End-diastolic volume (venous return)
  • Frank-Starling mechanism: ↑ stretch → ↑ contractility

Afterload:

  • Resistance against which ventricle pumps
  • ↑ Afterload (hypertension) → ↓ Stroke volume

Contractility:

  • Intrinsic force of myocardial contraction
  • Increased by: Sympathetic stimulation, catecholamines, calcium
  • Decreased by: Heart failure, beta-blockers, calcium channel blockers

Heart Rate:

  • Sympathetic: ↑ HR (beta-1 receptors)
  • Parasympathetic: ↓ HR (muscarinic receptors)

Blood Pressure Regulation

Short-term Regulation

Baroreceptor Reflex:

  • Located in carotid sinus and aortic arch
  • ↑ BP → ↑ firing → ↓ sympathetic, ↑ parasympathetic → ↓ BP
  • Responds within seconds

Chemoreceptors:

  • Respond to ↓ O₂, ↑ CO₂, ↑ H⁺
  • Increase sympathetic activity

Long-term Regulation

Renin-Angiotensin-Aldosterone System (RAAS):

  1. Kidney releases renin (in response to ↓ BP, ↓ Na⁺, sympathetic stimulation)
  2. Renin converts angiotensinogen → angiotensin I
  3. ACE converts angiotensin I → angiotensin II
  4. Angiotensin II: Vasoconstriction, aldosterone release, ADH release
  5. Aldosterone: ↑ Na⁺ and water reabsorption

Antidiuretic Hormone (ADH/Vasopressin):

  • Released by posterior pituitary
  • ↑ Water reabsorption in collecting ducts
  • Vasoconstriction at high doses

Atrial Natriuretic Peptide (ANP):

  • Released by atrial stretch
  • ↑ Na⁺ and water excretion
  • Vasodilation
  • Opposes RAAS

For pharmacological interventions, see our Pharmacology Guide.

Clinical Correlations

  • Heart Failure: Reduced ejection fraction, compensatory mechanisms
  • Hypertension: Dysregulation of BP control, target organ damage
  • Arrhythmias: Abnormal conduction patterns
  • Valvular Disease: Altered hemodynamics, murmurs
  • Shock: Inadequate tissue perfusion

External Resources

Conclusion

Mastering cardiovascular physiology is essential for clinical medicine. Understanding the cardiac cycle, ECG interpretation, and hemodynamic principles enables effective patient assessment and management. Practice with our Question Bank and explore related topics in our blog section.

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