Anatomy & Physiology of the Heart PDF

Section One: Anatomy & Physiology of the Heart, Heart Wall Disorders, Cardiac Muscle Contraction and Electrocardiography 1. Locate and define major structures of the heart Apex : Definition: Pointed tip of the heart directed downward, forward, and to the left. Locati...

Section One: Anatomy & Physiology of the Heart, Heart Wall Disorders, Cardiac Muscle Contraction and Electrocardiography 1. Locate and define major structures of the heart Apex : Definition: Pointed tip of the heart directed downward, forward, and to the left. Location: Formed by the left ventricle, at the 5th intercostal space near midclavicular line. Function: Landmark for auscultating heart sounds. Base ️: Definition: Broad, flat upper portion of the heart. Location: Near the 2nd rib, opposite the apex. Function: Entry/exit point for great vessels (aorta, pulmonary trunk). Atria : Definition: Upper chambers receiving blood. Right Atrium: From SVC, IVC, coronary sinus (deoxygenated). Left Atrium: From pulmonary veins (oxygenated). Interatrial Septum: Separates left/right atria. Fossa ovalis : Remnant of fetal foramen ovale. Ventricles : Definition: Lower chambers pumping blood out. Right Ventricle: To pulmonary arteries (deoxygenated to lungs). Left Ventricle: To aorta (oxygenated to body). Interventricular Septum : Thick wall dividing ventricles. Atrioventricular (AV) Valves : Tricuspid: Between RA & RV. Mitral (Bicuspid): Between LA & LV. Semilunar Valves ️: Pulmonary Valve: RV to pulmonary trunk. Aortic Valve: LV to aorta. Chordae Tendineae & Papillary Muscles : Chordae Tendineae: Tendon-like cords anchoring AV valves. Papillary Muscles: Contract during systole to prevent valve prolapse. 2. Major vessels delivering blood to/from the heart Aorta : Largest artery, carries oxygenated blood from LV to systemic circulation. Pulmonary Trunk & Arteries : From RV to lungs for oxygenation. Pulmonary Veins : Return oxygenated blood from lungs to LA. Superior Vena Cava (SVC) ️: Drains upper body deoxygenated blood into RA. Inferior Vena Cava (IVC) : Drains lower body deoxygenated blood into RA. Coronary Sinus : Collects venous blood from myocardium, empties into RA. 3. Atrial vs. Ventricular Septal Defects ⚠️ Atrial Septal Defect (ASD) : Hole in interatrial septum. Left-to-right shunt, ↑ pulmonary flow, right heart strain. Mild symptoms or asymptomatic. Ventricular Septal Defect (VSD) : Hole in interventricular septum.  Left-to-right shunt at ventricular level. More severe: Pulmonary hypertension, heart failure, murmur. Comparison: ASD: Atria-level defect, less symptomatic. VSD: Ventricle-level defect, more severe hemodynamic changes. 4. Major layers of the heart wall 1. Endocardium : Inner lining (endothelial). Smooth surface, prevents clots. 2. Myocardium : Middle muscular layer. Contraction for pumping action. 3. Epicardium (Visceral Pericardium) : Outer layer with fat, vessels. Protects & reduces friction. 4. Parietal Pericardium (Fibrous Sac): Not part of the wall, but surrounds heart. Anchors heart, prevents overdistension. 5. Cardiac vs. Skeletal & Smooth Muscle Cardiac Muscle: Striated, branched, intercalated disks ⚡. Involuntary, rhythmic contractions. Gap junctions for synchronized beating. Skeletal Muscle: Striated, long cylindrical fibers. Voluntary control, multiple nuclei. Requires nerve stimulation. Smooth Muscle: Non-striated, spindle-shaped. Involuntary, found in organ walls. Sustained, slower contractions. 6. Heart sounds & associations S1 ("lub") : AV valves closing at start of systole. Best at apex. S2 ("dub") : Semilunar valves close at end of systole. Best at base. S3: Rapid filling, can indicate HF in adults. S4: Atrial contraction into stiff ventricle. Suggests LV hypertrophy. 7. Blood flow through the heart Deoxygenated: 1. RA ← SVC/IVC/Coronary Sinus. 2. Through tricuspid → RV. 3. Pulmonary valve → Pulmonary arteries → Lungs. Oxygenated: 1. LA ← Pulmonary veins. 2. Mitral valve → LV. 3. Aortic valve → Aorta ️ → Body. 8. Pericardial space, tamponade, pericardiocentesis Pericardial Space: Between parietal & visceral layers. Fluid reduces friction. Cardiac Tamponade : Fluid accumulation under pressure. Beck’s Triad: Hypotension , JVD, muffled sounds. Pericardiocentesis : Needle drainage of pericardial fluid. Relieves pressure on heart. 9. Pericarditis, Myocarditis, Cardiomyopathies, Endocarditis Pericarditis : Inflammation of pericardium. Sharp chest pain, friction rub. Myocarditis : Inflammation of myocardium. Viral, can lead to dilated cardiomyopathy. Cardiomyopathies : Dilated (weak, stretched), Hypertrophic (thickened), Restrictive (stiff). Affect filling and pumping. Endocarditis : Infection of valves/endocardium. Vegetations, risk in IV drug use, prosthetic valves. 10. Antibiotic prophylaxis in dental procedures Prevents infective endocarditis in high-risk patients. Dental manipulations cause transient bacteremia. Antibiotics reduce bacteria, protecting damaged/prosthetic valves. 11. Cardiac muscle contraction events ⚡ Sarcomeres (actin/myosin) : Basic contractile units. T-tubules & SR : Ca²⁺ influx triggers CICR. Cross-bridge cycling → contraction. Calcium reuptake → relaxation. 12. Intercalated disks in cardiac muscle ⚡ Gap Junctions: Electrical coupling, synchronous contraction. Desmosomes: Mechanical support. Ensures unified heartbeat. 13. Excitation-contraction coupling & comparison to skeletal muscle ⚙️ Cardiac: Relies on extracellular Ca²⁺ + SR Ca²⁺. Pacemaker-driven, involuntary. Gap junctions for syncytium. Skeletal: Only SR Ca²⁺. Needs nerve input. Fibers contract independently. 14. Troponin in angina vs. MI  Angina: No muscle death, troponin normal. MI: Necrosis, troponin release ️. Elevated troponin = myocardial injury. 15. Cardiac conduction system ⚡ SA Node (Pacemaker) → AV Node (delay) → Bundle of His → Bundle Branches → Purkinje Fibers. Ensures orderly, timed depolarization and contraction sequence. 16. Cardiac vs. Neuronal AP ⚡ Cardiac: Longer AP (200–400 ms). Plateau phase (Ca²⁺ influx). Neuronal: Short AP (1–2 ms). No plateau, faster signaling. 17. Non-pacemaker vs. pacemaker potentials ⚡ Non-Pacemaker: Stable resting potential, fast Na⁺ upstroke. Plateau from Ca²⁺ balance. Pacemaker: No true rest, slow depolarization (funny current), Ca²⁺-driven upstroke. Automaticity (self-firing). 18. Absolute vs. Relative Refractory Periods Absolute: No new AP possible. Ensures relaxation before next beat. Relative: Strong stimulus can trigger AP. Gradual return of excitability. 19. Autonomic effects on conduction ⚡ SNS (Norepi) : ↑HR, ↑AV conduction, ↑Contractility. PNS (ACh) ​♀️: ↓HR, ↓AV conduction. Minimal contractility change. Balance ensures appropriate heart rate & output. 20. 3-lead vs. 12-lead ECG 3-lead: Basic rhythm monitoring. Limited view. 12-lead: Diagnostic view of heart’s electrical activity from multiple angles. Identifies ischemia, infarction, arrhythmias. 21. Label and define the various parts of an electrocardiogram (ECG) ⚡ P Wave: Represents atrial depolarization.  Normal: Smooth, upright in most leads. Clinical Note: Abnormal P waves may suggest atrial enlargement or arrhythmias. PR Interval : Time from start of P wave to start of QRS complex. Reflects AV nodal delay. Normal: 0.12–0.20 s. Prolongation: Could indicate AV block. QRS Complex : Ventricular depolarization. Normal Duration: ≤0.12 s. Widened QRS: Suggests bundle branch block or ventricular origin of beats. ST Segment : Early ventricular repolarization. Normally isoelectric (flat). Elevation: Myocardial injury/infarction. Depression: Ischemia. T Wave: Ventricular repolarization. Inversion may suggest ischemia. Peaked T waves often indicate hyperkalemia. QT Interval : Start of QRS to end of T wave. Reflects total ventricular depolarization & repolarization. Prolonged QT: Risk of torsades de pointes (dangerous arrhythmia). 22. Define and explain the concept of overdrive suppression Overdrive Suppression: Faster pacemaker (SA node) suppresses slower latent pacemakers (AV node, Purkinje fibers). High firing rate keeps potential pacemakers depolarized, preventing their spontaneous activity. Ensures a single, dominant pacemaker (SA node) controls heart rhythm. If SA node fails, a latent pacemaker can emerge as a backup, but at a slower rate. 23. Identify basic dysrhythmias on the electrocardiogram (ECG) ⚡ Atrial Fibrillation (AFib) : Irregularly irregular rhythm, no distinct P waves. Risk of stroke due to clot formation. Atrial Flutter : "Sawtooth" flutter waves. Atrial rate ~250–350 bpm. Ventricular Tachycardia (VT) : Rapid, wide QRS complexes. Can progress to VFib if untreated. Ventricular Fibrillation (VFib) : Chaotic rhythm, no QRS complexes. Requires immediate defibrillation. Heart Blocks (AV Blocks) : First-degree: Prolonged PR interval. Second-degree: Dropped beats. Third-degree: Complete dissociation between atria and ventricles. 24. Predict and explain the underlying pathophysiology of basic ECG abnormalities ST Elevation : Transmural infarction (STEMI). Indicates acute myocardial injury. ST Depression ️: Subendocardial ischemia. Seen in stable angina or reciprocal changes in STEMI. Inverted T Waves : Ischemia or previous MI. Altered repolarization patterns.  Prolonged QT Interval : Delayed repolarization. Risk of torsades de pointes. Peaked T Waves ☄️: Hyperkalemia. Excess extracellular K⁺ speeds repolarization phase. 25. Explain how devices such as an automated external defibrillator (AED) and cardiac pacemakers work to correct some of these dysrhythmias ⚙️⚡ Automated External Defibrillator (AED): Delivers an electrical shock to depolarize all cardiac cells simultaneously. Allows SA node to resume normal pacing. Life-saving in VFib or pulseless VT. Cardiac Pacemakers : Electronic devices that provide electrical impulses when the heart’s intrinsic rate is too slow or unreliable. Temporary or permanent. Modern pacemakers adjust rate based on patient’s activity, improving quality of life. Clinical Impact: AEDs are crucial in out-of-hospital cardiac arrests. Pacemakers ensure a stable rhythm in patients with bradyarrhythmias or AV blocks.