3 Cardio

Heart and Circulation-C

  • Lecturer: Dr. R. Ahangari

  • Institution: University of Central Florida, Orlando

  • Text References: Human Physiology by Linda S. Constanzo, Medline Plus

  • Course Code: 20000

Myocardial Cells—Nodal/Conducting Cells

  • Definition: Nodal or conducting cells in the heart contract weakly due to low contractile elements (myofibrils).

  • Key Traits:

    • Spontaneously generate action potentials without nervous input, unlike regular neurons.

    • Conduct action potentials rapidly to atrial and ventricular muscle.

  • Function:

    • Provide a self-excitatory and transmission system for the heart.

    • Main site of impulse generation is the sinoatrial (SA) node.

  • Location of SA Node: Upper posterior wall of the right atrium.

  • Role of SA Node:

    • First area to depolarize and produce an action potential, known as the pacemaker of the heart.

    • The action potential spreads through the atria to the atrioventricular (AV) node, then to the Bundle of His, and subsequently through the Purkinje Fibers to the ventricular muscle.

Myocardial Cells—Conducting System of the Heart

  • Action Potential Transmission:

    • Generated at the SA node and travels throughout the heart.

    • Causes contraction of the atrial muscle, followed by transmission to the ventricles.

  • Electrical Isolation of Atria and Ventricles:

    • Atria are electrically isolated from the ventricles due to fibrous tissue.

    • Action potential passes through the AV node before reaching the ventricles.

  • Propagation Pathway:

    • SA node → Atrial contraction → AV node → Bundle of His → Purkinje Fibers → Ventricular contraction.

Autonomic Effects on Heart Rate and Conduction Velocity

  • Chronotropic Effects:

    • Definition: Changes in heart rate.

    • Negative chronotropic effect: Decreases heart rate by lowering firing rate of SA node.

    • Positive chronotropic effect: Increases heart rate by raising firing rate of SA node.

  • Dromotropic Effects:

    • Definition: Changes in conduction velocity, primarily through the AV node.

    • Negative dromotropic effect: Slows conduction through AV node, increases PR interval.

    • Positive dromotropic effect: Increases conduction through AV node, decreases PR interval.

  • Inotropic Effects:

    • Definition: Changes in the force of contraction.

    • Negative inotropic effect: Decreases force of contraction.

    • Positive inotropic effect: Increases force of contraction.

Autonomic Nervous System and Heart Function

  • Sympathetic and Parasympathetic Interactions:

    • Sympathetic Effects:

    • β1-Adrenergic receptors:

      • Positive effects on chronotropic, dromotropic, and inotropic function (increased heart rate and contractility).

      • Coronary arteries respond with vasodilation.

    • Parasympathetic Effects:

    • Negative effects on chronotropic (decreased heart rate) and inotropic function (decreased contraction).

Heart Rate and Arrhythmias

  • Normal Heart Rate:

    • Resting heart rate: 50 to 99 beats per minute.

  • Arrhythmia Definition:

    • Result from abnormalities in impulse formation or conduction.

    • Sinus Tachycardia: Heart rate > 100 bpm (exercise, anxiety, fever).

    • Sinus Bradycardia: Heart rate < 50-60 bpm (regular rhythm in both cases).

Supraventricular and Ventricular Arrhythmias

  • Supraventricular Arrhythmia:

    • Caused by atrial or nodal extrasystole (ES).

    • Abnormal or ectopic impulses arise from the atria or AV node.

    • Atrial ES deforms the P wave, but the QRS complex is normal.

    • Nodal ES presents with negative P wave, often masked by QRS complex.

  • Ventricular Extrasystole:

    • Ventricular premature complexes (VPCs) arise from areas distal to His-Purkinje system.

    • Mechanisms for VPCs:

    1. Automaticity: New depolarization site in non-nodal ventricular tissue.

    2. Reentry Circuits: Slow-conducting tissue adjacent to normal tissue.

Causes and Symptoms of Ventricular Extrasystole

  • Possible Causes of PVCs:

    • Ischemia, medications (e.g., digoxin), myocarditis, cardiomyopathy, hypoxia, hypercapnia, mitral valve prolapse, smoking, alcohol, drugs (cocaine, caffeine, magnesium and potassium deficiencies, calcium excess), thyroid disorders, heart attack.

  • Symptoms:

    • Chest pain, faint feelings, fatigue, hyperventilation post-exercise.

  • Ventricular Tachycardia Relation:

    • Frequent PVCs can lead to VT due to extra electrical impulses.

Treatment of Ventricular Extrasystole (PVC)

  • Approach:

    • Restore balance of potassium, magnesium, calcium within the body.

  • Pharmacological Agents:

    • Class I: Sodium channel blockers (e.g., Lidocaine, Phenytoin).

    • Class II: Beta blockers (e.g., Atenolol, Propranolol, Metoprolol); block catecholamines at β1 receptors, decreasing sympathetic activity.

    • Class III: Potassium channel blockers (e.g., Sotalol) prolonging repolarization without affecting conduction velocity.

    • Class IV: Calcium channel blockers (e.g., Verapamil, Diltiazem); decrease conduction through AV node and shorten plateau of cardiac action potential.

Cardiac Muscle and Output

  • Types of Myocardial Cells:

    • Contractile Cells:

    • Similar to skeletal muscle, contain actin and myosin in myofibrils, surrounded by sarcoplasmic reticulum.

    • One nucleus and abundant mitochondria (1/3 of volume).

    • Efficient in oxygen extraction (80% from blood).

    • Joined by intercalated discs (tight junctions) and gap junctions facilitate ionic movement for action potential conduction.

  • Excitation-Contraction Coupling Process:

    1. Action potential spreads to T tubules.

    2. Ca2+ conductance increases during plateau; Ca2+ enters cell.

    3. Triggers Ca2+ release from sarcoplasmic reticulum (Ca2+ induced Ca2+ release).

    4. Ca2+ binds to troponin C; muscle contraction occurs.

    5. Relaxation happens with reaccumulation of Ca2+.

Contractility and Cardiac Performance

  • Contractility Definition:

    • Intrinsic ability of cardiac muscle to develop force; also known as inotropism.

    • Related to intracellular Ca2+ concentration.

    • Ejection Fraction (EF): Ratio of stroke volume to end-diastolic volume; normal EF is 0.55 (55%).

  • Positive Inotropic Factors:

    • Increased heart rate (more action potentials for Ca2+ influx).

    • Sympathetic stimulation increases inward Ca2+ current.

    • Cardiac glycosides (like digitalis).

  • Negative Inotropic Factors:

    • Parasympathetic stimulation (Ach) reduces inward Ca2+ current, decreasing contraction force.

Length-Tension Relationship and Ventricular Mechanics

  • Preload:

    • Equivalent to end-diastolic volume; increases with venous return.

    • Stretches ventricular muscle fibers.

  • Afterload:

    • Left Ventricle: Aortic pressure impacts afterload; increased aortic pressure increases afterload.

    • Right Ventricle: Pulmonary artery pressure impacts afterload similarly.

  • Sarcromere Length and Force:

    • Determines max cross-bridge formations; affects tension and contraction force.

  • Velocity of Contraction:

    • Maximal when afterload is zero; increases in afterload decrease contraction velocity.

  • Frank-Starling Relationship:

    • Increased end-diastolic volume results in increased stroke volume and cardiac output; matches cardiac output with venous return.

Cardiac Cycle

  • Cycle Steps Overview:

    1. Isovolumetric Contraction (1-2): Begins with depolarization; pressure increases with contraction, valves closed.

    2. Ventricular Ejection (2-3): Aortic valve opens; blood is ejected, reducing volume.

    3. Isovolumetric Relaxation (3-4): Pressure drops; all valves closed, volume constant.

    4. Ventricular Filling (4-1): Mitral valve opens; blood fills ventricle, volume increases.

Pressure-Volume Loop Changes

  • Increased Preload: Increases stroke volume due to enhanced venous return, reflected in wider pressure-volume loop.

  • Increased Afterload: Results in decreased stroke volume (narrowing loop) as the ventricle faces higher ejection pressure.

  • Increased Contractility: Results in higher stroke volume and lower end-systolic volume.

Cardiac Output Measurements

  • Equations and Relationships:

    • Stroke Volume (SV):

    • Defined as SV = End-diastolic volume - End-systolic volume.

    • Cardiac Output (CO):

    • CO = SV x Heart Rate (HR).

    • Ejection Fraction (EF):

    • EF = Stroke Volume / End-Diastolic Volume; normally 0.55.

Cardiac Oxygen Consumption

  • Relation to Cardiac Performance:

    • O2 consumption corresponds to ventricular tension.

    • Increased by factors:

    • Afterload increase, heart size enlargement, contractility increase, heart rate elevation.

Fick Principle for Cardiac Output

  • Measurement Formula:

    • Cardiac output (CO) = O2 consumption / (O2 in pulmonary vein - O2 in pulmonary artery).

Cardiac Cycle—Ejection Period

  • Essential Criteria: Ventricular pressure must exceed aortic pressure (~80 mmHg) to open aortic valve for blood ejection.

Heart Sounds

  • Valve Function Sounds:

    • AV valves closure produces first heart sound (low pitch, long duration).

    • Aortic and pulmonary semilunar valves closure produces second sound (high pitch, short duration).

    • Third heart sound may occur during diastole, harder to detect.

Cardiac Output and Exercise

  • Resting Cardiac Output: Roughly 5 liters/min at rest; can increase to 20 l/min in exercise and 35-40 l/min in athletes.

  • CO Calculation: At rest, HR = 70 bpm and SV = ~70 ml; CO = ~5 l/min.

Autonomic Control of Heart Rate

  • Overview:

    • The ANS largely regulates heart rate and contractility.

    • Parasympathetic Nervous System (PSYN):

    • Decreases heart rate and force of contraction.

    • Sympathetic Nervous System (SYN):

    • Increases heart rate and force of contraction.

  • Natural Heart Rate: Heart beats at ~100 bpm without ANS influence; resting heart rate is ~70 bpm due to PSYN activity.

Atherosclerosis

  • Definition: A patchy intimal plaque formation in medium and large arteries, consisting of lipids, inflammatory cells, smooth muscle cells, and connective tissue.

  • Pathophysiology: Arteries may become blocked by fats and cholesterol, affecting many artery types (e.g., coronary, carotid).

Risk Factors and Complications of Atherosclerosis

  • Risk Factors Include:

    • Dyslipidemia, diabetes, smoking, family history, sedentary lifestyle, obesity, hypertension.

  • Complications:

    • Symptoms such as shortness of breath and chest pain; potential consequences include strokes and damage to organs.

Inflammatory Response in Atherosclerosis

  • Role of Endothelial Dysfunction:

    • Damages nitric oxide production, causing inflammation and recruitment of inflammatory cells, which thickens the plaque.

  • Cellular Mechanism:

    • Monocytes transform into macrophages within plaques and produce enzymes leading to plaque rupture.

    • Lipid oxidation occurs in the sub-endothelium.

Atrial Fibrillation and Flutter

  • Definitions:

    • Atrial fibrillation: irregular atrial rhythm; atrial muscles contract erratically.

    • Atrial flutter: regular but fast atrial rhythm.

  • Outcome: In atrial fibrillation, pooled blood may lead to clot formation.

Causes and Symptoms of Atrial Fibrillation/Flutter

  • Common Causes:

    • Various heart diseases, stress, anxiety, caffeine, alcohol, tobacco, diet pills, and prior surgeries.

Heart Murmurs

  • Definition: Turbulent blood flow inside or outside the heart, can be benign or pathological.

  • Causes of Abnormal Murmurs:

    • Stenosis: restricts valve opening, causing blood turbulence.

    • Valve insufficiency: allows backflow of blood when valves are supposed to close, causing turbulence.