BackCardiovascular System: Structure, Function, and Pathophysiology
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Cardiovascular System
Learning Outcomes
Describe the structural and functional properties of cardiac muscle and explain how it differs from skeletal muscle.
Describe and compare action potentials in cardiac pacemaker and contractile cells.
Name the components of the conduction system of the heart and trace the conduction pathway.
Draw and interpret a normal electrocardiogram (ECG) tracing, naming individual waves and intervals and indicating what they represent.
Describe normal heart sounds and how they relate to the cardiac cycle.
Explain the effects of various factors regulating stroke volume, heart rate, and blood pressure.
Discuss the pathophysiology and risk factors of primary hypertension, including the roles of the sympathetic nervous system and the renin-angiotensin-aldosterone system.
Describe the clinical symptoms and underlying pathophysiology of orthostatic hypotension.
Describe the pathophysiology of atherosclerosis, including risk factors.
Structural and Functional Properties of Cardiac Muscle
Special Features of Myocytes
Cardiac myocytes are specialized muscle cells that form the heart's contractile tissue. They possess unique structural and functional characteristics that distinguish them from skeletal muscle cells.
Single nucleus, branched cells: Cardiac myocytes typically have one nucleus and are branched, allowing for a complex network of connections.
Intercalated discs: These specialized junctions connect adjacent cardiac cells and contain gap junctions that facilitate rapid electrical communication.
Pacemaker and contractile cell types: Pacemaker cells generate spontaneous action potentials, while contractile cells respond to these signals to produce forceful contractions.
Functional syncytium: The heart muscle acts as a single coordinated unit due to the presence of gap junctions.
Long refractory period: Cardiac cells have a prolonged refractory period, preventing tetanic contractions and ensuring rhythmic heartbeats.
Abundant mitochondria: Cardiac myocytes contain many mitochondria, supporting continuous aerobic ATP production necessary for sustained contraction.
Comparison with Skeletal Muscle:
Skeletal muscle cells are multinucleated and unbranched, while cardiac cells are single-nucleated and branched.
Skeletal muscle contraction is voluntary and requires nervous stimulation; cardiac muscle can contract autonomously due to pacemaker cells.
Intercalated discs are unique to cardiac muscle, enabling rapid electrical conduction.
Example: The presence of intercalated discs allows the heart to contract in a coordinated manner, essential for effective blood pumping.
Microscopic Anatomy of the Heart
Key Structures
Muscle cell: The basic contractile unit of the heart.
Intercalated disc: Specialized connection between cells.
Mitochondrion: Organelle responsible for ATP production.
T tubule: Invagination of the cell membrane aiding in electrical signal transmission.
Sarcoplasmic reticulum: Organelle storing calcium ions, crucial for muscle contraction.
Sarcolemma: The cell membrane of a muscle cell.
Example: The abundance of mitochondria in cardiac muscle cells supports their high energy demands.
Action Potentials in Cardiac Cells
Pacemaker Cells vs. Contractile Cells
Cardiac action potentials differ between pacemaker cells and contractile cells, reflecting their distinct roles in heart function.
Pacemaker cells: Generate spontaneous action potentials without nervous input. The action potential consists of three phases: pacemaker potential, depolarization, and repolarization.
Contractile cells: Respond to pacemaker cell signals. Their action potential features a rapid depolarization (due to Na+ influx), a plateau phase (due to Ca2+ influx), and repolarization (due to K+ efflux).
Key Ions:
Calcium (Ca2+): Enters pacemaker cells via fast channels, causing depolarization; enters contractile cells via slow channels, prolonging the action potential.
Sodium (Na+): Enters pacemaker cells via slow channels, causing depolarization toward threshold; enters contractile cells via fast channels, triggering action potentials.
Example: The plateau phase in contractile cells prevents premature contractions, ensuring effective heartbeats.
Equation:
Conduction System of the Heart
Components and Pathway
The heart's conduction system ensures the orderly spread of electrical impulses, coordinating contraction.
Sinoatrial (SA) node: Primary pacemaker, initiates impulses.
Atrioventricular (AV) node: Delays impulse, allowing atrial contraction before ventricular contraction.
Bundle of His: Conducts impulses from AV node to ventricles.
Bundle branches: Carry impulses through the interventricular septum.
Purkinje fibers: Distribute impulses throughout ventricular myocardium.
Example: Damage to the SA node can result in arrhythmias due to loss of pacemaker activity.
Electrocardiogram (ECG)
Normal ECG Complex
An ECG records the electrical activity of the heart, displaying characteristic waves and intervals.
P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
T wave: Ventricular repolarization.
PR interval: Time from atrial to ventricular depolarization.
ST segment: Period between ventricular depolarization and repolarization.
Example: Prolonged QRS complex may indicate ventricular conduction abnormalities.
Cardiac Cycle and Heart Sounds
Phases and Sounds
The cardiac cycle encompasses all electrical and mechanical events in one heartbeat, including heart sounds produced by valve closures.
First sound (lub): Closure of tricuspid and mitral valves at the end of ventricular filling.
Second sound (dup): Closure of semilunar valves (aortic and pulmonary) at the end of ventricular ejection.
Example: Abnormal heart sounds (murmurs) may indicate valvular disease.
Regulation of Cardiac Output and Blood Pressure
Factors Affecting Cardiac Output
Cardiac output is determined by stroke volume and heart rate, both regulated by intrinsic and extrinsic factors.
Preload: Volume of blood in ventricles at end of diastole; increased preload increases stroke volume.
Afterload: Resistance to ventricular ejection; increased afterload decreases stroke volume.
Contractility: Strength of cardiac muscle contraction; increased contractility increases stroke volume.
Equation:
Blood Pressure Regulation:
Mean arterial pressure (MAP): Determined by cardiac output and total peripheral resistance (TPR).
Neural regulation: Baroreceptor reflexes adjust heart rate and vessel diameter.
Hormonal regulation: Adrenaline, noradrenaline, ADH, aldosterone, and ANP influence blood pressure and volume.
Example: Sympathetic stimulation increases heart rate and contractility, raising cardiac output and blood pressure.
Pathophysiology of Cardiovascular Diseases
Hypertension
Hypertension is a chronic elevation of blood pressure, increasing the risk of heart disease, stroke, and kidney failure.
Primary hypertension: Accounts for 90-95% of cases; risk factors include family history, age, obesity, alcohol intake, high salt intake, and sedentary lifestyle.
Secondary hypertension: Caused by underlying conditions such as kidney disease or endocrine disorders.
Clinical manifestations: Often asymptomatic early; later symptoms include organ damage, impaired vision, and mobility issues.
Management: Lifestyle modification and pharmacological treatment (diuretics, ACE inhibitors, beta-blockers).
Example: Uncontrolled hypertension can lead to myocardial infarction or stroke.
Orthostatic Hypotension
Orthostatic hypotension is a sustained drop in blood pressure upon standing, leading to dizziness and risk of falls.
Causes: Drugs, immobility, starvation, diabetes, nervous system disorders, older age.
Symptoms: Drop in BP when moving from sitting to standing, dizziness, fainting.
Example: Elderly patients are at increased risk due to impaired autonomic regulation.
Atherosclerosis
Atherosclerosis is the buildup of fatty deposits in arterial walls, leading to reduced blood flow and increased risk of heart attack and stroke.
Pathogenesis: Endothelial injury, inflammation, formation of fatty streaks, development of fibrous plaques, and possible plaque rupture causing thrombosis.
Risk factors: Hypertension, smoking, diabetes, high LDL, low HDL, infection, elevated C-reactive protein.
Clinical manifestations: Transient ischaemic events, infarction, pain and disability in peripheral arteries.
Management: Lifestyle modification, control of diabetes and hypertension, improvement of serum lipids, aspirin therapy.
Example: Coronary artery atherosclerosis is the leading cause of myocardial infarction.
References
Marieb, E.N. & Hoehn, K. (2023). Human Anatomy & Physiology, Global Edition (12th ed.). Pearson Education Inc.
Huether, S.E., McCance, K.L., Brashers, V.L., & List, S.L. (2022). Understanding Pathophysiology (4th ANZ ed.). Elsevier Australia.
Perry, J., Douglas, C., Rebeiro, G., & Waters, D. (2020). Potter and Perry's Fundamentals of Nursing (6th ANZ ed.). Elsevier Australia.