Cardiac Resumes PDF

8 Paola Tuerlinckx Class 59-Introduction:Heart anatomy  Heart: A muscular pump that forces blood around the body  Blood vessels:  Arteries: Carry blood away from the heart  Veins: Bring blood back to the heart  Capillaries: Tiny ve...

8 Paola Tuerlinckx Class 59-Introduction:Heart anatomy  Heart: A muscular pump that forces blood around the body  Blood vessels:  Arteries: Carry blood away from the heart  Veins: Bring blood back to the heart  Capillaries: Tiny vessels branching off from arteries to deliver blood to tissues  Two circulatory systems: Systemic (7 and 8) and pulmonary(3)  AV Valves (Atrioventricular Valves): These valves (Tricuspid and Mitral-bicuspid) are open during the ventricular filling phase, allowing blood to flow from the atria into the ventricles. They are closed during ventricular contraction to prevent backflow of blood into the atria.  Semilunar Valves (Aortic and Pulmonary): These valves are open during the ventricular ejection phase, allowing blood to flow from the ventricles into the aorta and pulmonary artery. They are closed during ventricular relaxation to prevent backflow of blood into the ventricles. he cardiac cycle consists of two main phases:  Cardiac Cycle 1. Diastole (relaxation and filling)-0.62s 2. Systole (contraction and ejection)-0.3s Detailed stages of the cardiac cycle: 1. Ventricular filling (rapid filling, AV valves open) 2. Diastasis (20% of ventricular filling) 3. Atrial systole (contraction) 4. Isovolumetric ventricular contraction 5. Ejection phase (rapid and slow ejection) 6. Isovolumetric ventricular relaxation  Common Cardiovascular Diseases 1. Heart Attack  Symptoms: Chest pain, lightheadedness, pain in jaw/neck/back/arms/shoulders, shortness of breath  Main risk factors: High blood cholesterol, high blood pressure, smoking 2. Stroke  Risk factors: High blood pressure, diabetes, heart disease, smoking, family history, older age, African American heritage  Symptoms: One-sided weakness/numbness, vision problems, speech difficulties, confusion, dizziness, severe headache Effects of Aging  Decreased heart efficiency, especially during physical activity  Increased arterial stiffness leading to higher blood pressure risk Questions 1. Cardiac cycle. Select the correct sequence:  a. Atrial contraction – ventricular ejection – isovolumetric contraction – ventricular filling – isovolumetric relaxation   b. Atrial contraction – isovolumetric contraction - ventricular ejection – isovolumetric relaxation - ventricular filling  c. Atrial contraction – isovolumetric relaxation - ventricular filling - isovolumetric contraction - ventricular ejection  d. Atrial contraction – isovolumetric relaxation - isovolumetric contraction - ventricular ejection - ventricular filling  e. Atrial contraction – ventricular ejection – isovolumetric relaxation -isovolumetric contraction – ventricular filling Answer: b 2. During isovolumetric contraction phase:  a. Atrio-ventricular valves are open  b. Ventricular pressure falls  c. Atrium pressure increase (wave c)  d. Ventricular volume decreases  e. S2 cardiac sound occurs Answer: c 3. During rapid ejection phase:  a. Atrio-ventricular valves are closed  b. Ventricular volume increases  c. EKG shows QRS  d. Ventricular pressure < aortic pressure  e. Correlate with a wave of atrium pressure Answer: a 4. During slow ejection phase:  a. Atrio-ventricular valves remain open  b. Ventricular pressure < aortic pressure  c. Semilunar valves are closed  d. Ventricular volume start increasing  e. Atrium pressure rapidly decreases Answer: b 5. During isovolumetric relaxation phase:  a. All cardiac valves are closed  b. S1 cardiac sound occurs   c. Ventricular pressure increases  d. EKG shows QRS  e. Correlate with a wave of atrium pressure Answer: a 6. During rapid filling phase:  a. Mitral valve is closed  b. Ventricular volume decreases  c. Ventricular pressure initially decreases  d. Occurs before ventricular repolarization  e. Occurs before venous v wave Answer: c 7. During diastase:  a. Ventricular filling is rapid  b. Occurs after atrial contraction  c. Aortic valve is closed  d. Mitral valve is close  e. Atrial contraction occurs before Answer: c 8. During atrial contraction:  a. Atrial pressure decrease  b. Occurs after P wave of EKG  c. Occurs during systole  d. Occurs after S1 cardiac sound  e. Ventricular volume decreases Answer: b Class 60- Heart anatomy-cardiac chambers and valves Section Key Points Clinical Relevance - Pericarditis: - Muscular pump that circulates blood. - Divided into right inflammation of the The Heart (deoxygenated blood) and left (oxygenated blood) sides. - pericardium, causing chest Enclosed in the pericardium. pain. - Heart failure: LV failure - 4 chambers: 2 atria (receiving chambers), 2 ventricles leads to pulmonary Heart Chambers (pumping chambers). - Right side: low-pressure, pulmonary congestion; RV failure circulation. - Left side: high-pressure, systemic circulation. causes systemic edema. - Receives deoxygenated blood from: - Superior vena cava (SVC) (upper body). - Inferior vena cava (IVC) - Atrial septal defect (lower body). - Coronary sinus (heart's own blood (ASD): Patent foramen Right Atrium (RA) supply). - Structures: - Crista terminalis: ridge ovale allows shunting separating smooth and rough areas. - Sulcus terminalis: between RA & LA, leading external groove corresponding to crista terminalis. - to oxygen mixing. Fossa ovalis: remnant of fetal foramen ovale. - Patent foramen ovale Interatrial - Separates right and left atria. - Contains fossa ovalis, a (PFO): Allows abnormal Septum remnant of fetal foramen ovale (which closes after birth). right-to-left shunting, increasing stroke risk. Left Atrium (LA) - Receives oxygenated blood from 4 pulmonary veins. - - Mitral stenosis: narrowing Structures: - Mostly smooth-walled, except for left of mitral valve, causing LA Section Key Points Clinical Relevance auricle. - Mitral valve (bicuspid valve) separates LA from dilation & pulmonary LV. hypertension. - Pumps deoxygenated blood to the lungs via the pulmonary artery. - Structures: - Tricuspid valve regulates inflow from RA. - Trabeculae carneae: - Pulmonary stenosis: muscular ridges that strengthen contraction. - Papillary Right Ventricle Obstruction of pulmonary muscles & chordae tendineae: prevent tricuspid valve (RV) outflow, causing RV prolapse. - Infundibulum (conus arteriosus): smooth- hypertrophy. walled area leading to pulmonary valve. - Pulmonary valve: 3 semilunar cusps, directs blood into pulmonary trunk. - Pumps oxygenated blood into systemic circulation via the aorta. - Structures: - Mitral valve (bicuspid valve) - Aortic stenosis: regulates inflow from LA. - Thickest myocardium for Narrowing of the aortic Left Ventricle high-pressure pumping. - Trabeculae carneae, papillary valve, leading to LV (LV) muscles, and chordae tendineae. - Vestibule: smooth- hypertrophy and heart walled part near the aortic valve. - Aortic valve: 3 failure. semilunar cusps, prevents backflow. - Valve regurgitation: - Ensure unidirectional blood flow. - Two main types: - Backflow of blood due to Heart Valves Atrioventricular (AV) valves: separate atria from ventricles. faulty valves, leading to - Semilunar valves: regulate outflow to arteries. heart murmurs. - Mitral valve prolapse - Tricuspid valve (RA → RV): 3 cusps. - Mitral valve (LA → Atrioventricular (MVP): Leaflets bulge into LV): 2 cusps (bicuspid). - Function: Prevent backflow during Valves (AV) LA, causing regurgitation ventricular contraction (systole). and murmurs. - Pulmonary valve (RV → Pulmonary trunk). - Aortic valve - Aortic regurgitation: Semilunar Valves (LV → Aorta). - Function: Prevent backflow during Backflow from aorta to LV, ventricular relaxation (diastole). leading to heart failure. 1. Atrial Septal Defect (ASD) & Patent Foramen Ovale (PFO) o Failure of foramen ovale to close → Persistent shunting of blood between atria. o Can cause paradoxical embolism, increasing stroke risk. 2. Mitral Valve Disorders o Mitral stenosis: Thickened valve causes left atrial enlargement & pulmonary congestion.  o o Mitral regurgitation: Incompetent valve leads to volume overload in LA & LV. 3. Right Ventricular Hypertrophy (RVH) o Causes: Pulmonary hypertension, pulmonary valve stenosis. o Signs: Right heart failure – edema, ascites, jugular venous distension. 4. Left Ventricular Hypertrophy (LVH) o Causes: Aortic stenosis, hypertension. o Signs: Chest pain, heart failure symptoms. 5. Aortic Valve Disorders o Aortic stenosis: Leads to LV hypertrophy & reduced cardiac output. o Aortic regurgitation: Causes LV volume overload & heart failure. 6. Pulmonary Valve Stenosis o Obstruction leads to RV hypertrophy & cyanosis. Questions Classes 61/62-Overview of the cardiovascular system Key Components Covered 1. The Aorta and its branches 2. Pulmonary and Systemic Circulation 3. Heart Anatomy 4. Coronary Arteries and Cardiac Veins 5. Cardiac Auscultation  Component Details A large, cane-shaped vessel delivering oxygen-rich blood to the Aorta body. Circulatory Loops Pulmonary loop (heart-lungs) and systemic loop (heart-body). Narrowing of the aorta, common in Turner Syndrome, causing Coarctation blood flow issues. Page 2: Anatomy of the Aorta  Structure of the Aorta:  Divided into ascending aorta, aortic arch, thoracic aorta, and abdominal aorta. Section Description Ascending Starts from the heart's left ventricle Aorta Section Description Curves downward, giving rise to major arteries Aortic Arch Passes through the chest cavity. Can be divided into ascending, transverse and descending. Becomes abdominal aorta at the diaphragm. The thoracic aorta can be subdivided in four different portions: Aortic root(origin of the coronary arteries), the ascending aorta (origin of the brachiocephalic trunk), the aortic arch(origin of supra-aortic trunks) and the descending thoracic aorta. Thoracic Aorta Abdominal Aorta Extends through the abdominal cavity  Layers:   Tunica intima (inner layer for smooth blood flow). Contains endothelial cells that enable blood to transport oxygen and nutrient without getting absorved.  Tunica media (middle layer for elasticity).Made of elastin and collagen meeting body’s changing flow needs.  Tunica adventitia (outer layer for structural support).Connects to nearby nerver and tissues.  The vena cava consists of two large veins—superior vena cava (SVC) and inferior vena cava (IVC)—responsible for returning deoxygenated blood from the body to the heart. Type Function Superior Vena Collects deoxygenated blood from the upper body (head, neck, arms, Cava chest). Collects deoxygenated blood from the lower body (abdomen, pelvis, Inferior Vena Cava legs). Pulmonary Circulation  Function:  Transports deoxygenated blood from the heart to the lungs.  Pulmonary arteries carry oxygen-poor blood; pulmonary veins return oxygen-rich blood. The pulmonary trunk splits into the left and right pulmonary arteries (caries deoxygenate blood to the heart) Pulmonary Circulation Details Components Pulmonary Arteries Carry venous blood from the heart to lungs. Pulmonary Circulation Details Components Pulmonary Veins Return oxygenated blood to the left atrium. Coarctation can cause symptoms like chest pain, cold Clinical Note legs, and poor growth. Page 4: Anatomy of the Heart  Key Features:  Central organ of circulation located between the lungs.  Four chambers: left/right atria and left/right ventricles.  Coronary arteries supply oxygen-rich blood to the heart muscle. Heart Component Details Left Coronary Supplies left ventricle/atrium; branches into anterior Artery descending artery. Right Coronary Supplies right ventricle/atrium and conduction system (SA/AV Artery nodes). Blood drains into coronary sinus and directly into the heart Venous Drainage chambers.  There are four main pulmonary veins:  Two from each lung: superior and inferior pulmonary veins.  These veins originate from the lungs' hilum and course medially toward the heart.  They pass anterior to the descending thoracic aorta and through the pericardial sac to enter the left atrium at its smooth posterior wall. Pulmonary Vein Details Superior Pulmonary Veins Drain blood from the upper lobes of each lung. Inferior Pulmonary Veins Drain blood from the lower lobes of each lung. Formation  Pulmonary veins are formed by lobar veins, which receive tributaries from:  Intra-segmental veins within lung parenchyma.  Intersegmental veins, which drain adjacent lung segments. Pulmonary Arteries Pulmonary arteries transport oxygen-poor blood from the heart to the lungs for oxygenation. Key details include: Structure and Pathway  The pulmonary trunk emerges from the right ventricle and splits into:  Right Pulmonary Artery: Arises at a near-right angle to supply the right lung.  Left Pulmonary Artery: A direct continuation of the pulmonary trunk's course, supplying the left lung.  The division occurs at the level between vertebrae T5 and T6. Pulmonary Artery Details Right Pulmonary Artery Supplies oxygen-poor blood to the right lung. Left Pulmonary Supplies oxygen-poor blood to the left lung; follows a Artery straighter path. Coarctation of the Aorta Definition: Coarctation of the aorta is a congenital malformation where part of the aorta is narrowed, making it difficult for blood to pass through. Key Points:  Association: More frequent in individuals with Turner Syndrome and may occur with other congenital heart defects like bicuspid aortic valve, aortic stenosis, ventricular septal defect, and patent ductus arteriosus. Symptoms:  Symptoms vary based on the degree of narrowing and blood flow restriction.  Milder Cases: Symptoms may not appear until adolescence.  Chest pain  Cold feet or legs  Dizziness or fainting  Decreased ability to exercise  Failure to thrive  Leg cramps with exercise  Nosebleed  Poor growth  Pounding headache  Shortness of breath The heart  The heart circulates blood and oxygen throughout the body, directing waste to the lungs for elimination.  Positioned between the lungs, it functions as the central organ of circulation, connecting to major blood vessels. Chambers  The heart is composed of four chambers: the left atrium, the left ventricle, the right atrium, and the right ventricle. Coronary Arteries  Coronary arteries deliver blood to the heart muscle itself.  The two primary coronary arteries are the left main and right coronary arteries. Coronary Arterial Irrigation Artery Origin Supplies Left side of the heart (left ventricle and left atrium). Divides into the anterior Left aortic sinus, interventricular artery Left Coronary passing behind the and the circumflex Artery pulmonary trunk artery. Most of the left ventricle (anterior wall and part of the Arises from the lateral wall), the left coronary anterior two-thirds of artery, runs in the the septum, and part Anterior interventricular of the right Interventricular sulcus.Behind the ventricular outflow Artery pulmonary trunk. tract. Lateral and posterolateral wall of Circumflex Arises from the the left ventricle, the Artery left coronary lateral and posterior artery. wall of the left  Artery Origin Supplies Atrioventricular atrium, and in cases of groove. left dominance, the inferior wall of the left ventricle. Right ventricle, right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes. Typically gives off the posterior descending or Right Coronary Right coronary interventricular artery Artery sinus (in 85% of patients). Coronary Circulation Dominance  Coronary circulation is classified as right-dominant when the posterior descending artery arises from the right coronary artery (85% of patients) and left-dominant when it arises from the circumflex artery (15-25%).  The left coronary artery supplies the most cardiac territory, even in cases of right dominance. Cardiac Veins Vein Location Drains into Anterior interventricular sulcus, alongside the anterior interventricular artery Great Coronary sinus at the point Cardiac where it receives the oblique Vein vein of the left atrium. Middle Cardiac Vein Posterior interventricular groove Coronary sinus  Vein Location Drains into Small Cardiac Atrioventricular groove, next to the posterior Vein interventricular artery Coronary sinus Venous Drainage  Most of the coronary venous blood is drained by veins accompanying the arteries.  Cardiac veins end in the coronary sinus, a large vein that empties into the right atrium.  A portion of coronary circulation blood is collected from the myocardium by small veins that open directly into the four heart chambers. Definition  CAD implies deficient coronary artery irrigation, affecting the heart's ability to receive oxygen- rich blood. Diagnosis  Diagnosis involves examining the heart, with changes in its shape or size indicating disease. 63-Pericardium clas? Topic Details Double-walled sac enclosing the heart, consisting of the fibrous pericardium (tough, dense irregular connective tissue) and serous pericardium (parietal & visceral layers). The pericardial cavity holds 10-50 mL of fluid to reduce friction. Pericardium Fibrous Continuous with the tunica adventitia of great vessels, attached to the sternum via Pericardium sternopericardial ligaments and to the diaphragm via pericardiacophrenic ligaments. Serous The parietal layer lines the fibrous pericardium, while the visceral layer (epicardium) Pericardium covers the heart. The pericardial fluid (15-50 mL) reduces friction. Pericardial Transverse Sinus: Behind the ascending aorta & pulmonary trunk, useful in surgery (e.g., Sinuses CABG), as it separates the arterial vessels from the venous vesses. Oblique Pericardial Sinus: Behind the left atrium, bordered by pulmonary veins & IVC.Allows free movement Topic Details of the heart within the pericardial cavity during contraction. Can serve as a site for fluid accumulation. Cardiac Rapid fluid accumulation in the pericardial cavity compresses the heart, leading to Tamponade biventricular failure. Requires pericardiocentesis. Mainly pericardiophrenic artery(fibrous pericardium and parietal layer of the serous pericardium), musculophrenic (diaphragm and anterior part of the pericardium), Arterial Supply bronchial, esophageal, and superior phrenic arteries (posterior part of the pericardium). Coronary arteries supply only the visceral layer. Venous Drainage Pericardiophrenic, musculophrenic, azygos system, and inferior phrenic veins. Phrenic nerve (C3-C5) carries pain sensation, referred to the shoulder (supraclavicular Nerve Supply region). Functions of Stabilization, protection, lubrication, and prevention of excessive dilation. Pericardium 1. Epicardium (outer, contains adipose tissue, coronary vessels, nerves). 2. Myocardium (middle, thickest, composed of cardiac muscle-cardiomyocytes). 3. Endocardium (inner, smooth endothelial lining, contains Purkinje fibers). Heart Wall Layers Cardiomyocytes have intercalated discs, rich mitochondria, and contract rhythmically. Myocardium The left ventricle has the thickest myocardium. Striated, branched, single or bi-nucleated, high mitochondria content.Calcium dependent Cardiomyocyte contration mechanism. Simpathetic stimulation (via morepinephine) and parasympathetic Features stimulation (vagus nerve) Topic Details Cardiac SA Node (pacemaker, 60-100 bpm) → AV Node (delay station, 40-60 bpm) → Bundle of Conducting His → Right & Left Bundle Branches → Purkinje Fibers. System SA node lacks stable RMP, has automatic depolarization. Sodium influx triggers Membrane prepotential, calcium influx causes depolarization, potassium outflux repolarizes the Potentials cell. Cardiac Conduction System The cardiac conduction system ensures rhythmic and coordinated contractions. The sequence of electrical conduction: 1. Sinoatrial (SA) Node: The pacemaker of the heart, generating impulses at 60-100 bpm. 2. Atrioventricular (AV) Node: Delays impulse by 0.1 sec to allow the atria to empty into the ventricles. 3. Bundle of His: Transmits impulses through the interventricular septum. 4. Right and Left Bundle Branches: Conduct impulses toward the apex of the heart. 5. Purkinje Fibers: Spread throughout the myocardium, initiating ventricular contraction. 6. Ventricular contraction begins Membrane Potentials and Ion Movement  SA Node Cells have no stable resting potential. Instead, they undergo slow depolarization via sodium ion influx.  When the threshold (-40 mV) is reached, calcium channels open, leading to rapid depolarization.  Potassium channels open to repolarize the cell.  This automatic depolarization makes the SA node the natural pacemaker. Class 65-Electrical activity of the heart The heart’s conducting system ensures coordinated contraction of the atria and ventricles, which is critical for efficient blood flow. The SA node, as the natural pacemaker, initiates impulses, which travel through the atria to the AV node. The AV node delays conduction, allowing time for the atria to empty into the ventricles before contraction. The impulse then rapidly propagates through the AV bundle, bundle branches, and Purkinje fibres, triggering coordinated ventricular contraction.Its a one way conducting system, always from the atria to the ventricles. Atria is separated from the ventricle by an insulate and fibrous barrier. Regulation:  Parasympathetic Activity: Decreases heart rate and conduction speed via acetylcholine release, increasing K+ permeability and hyperpolarizing nodal generates electrical impulses.  Sympathetic Activity: Increases heart rate and conduction velocity through norepinephrine release, enhancing Na+ and Ca2+ permeability. The main function of the electrical activity of the heart is:  Generates electrical impulses to initiate rhythmical contraction of the heart muscle~  Conducts electrical impulses rapidly through the heart Component Location Function Key Features Resting membrane potential: -55 to -60 mV, leaky to Na+ and Ca2+, initiates action potentials automatically Superior Primary Main ion channels: slow posterolateral pacemaker of sodium channels, fast wall of the right the heart, sodium channels, calcium Sinoatrial (SA) atrium, near the generates channels and potassium Node opening of the normal channels superior vena rhythmic cava impulses Conduct Includes anterior, middle, Between the SA impulses and posterior pathways; Internodal Bachmann’s bundle node and the AV from the SA Pathways transmits impulses to the node node to the AV node left atrium Delays the impulse before The impulse reaches the AV transmitting node 0.03 after originating Posterior wall of to ventricles, in the SA node. Atrioventricular right atrium, ensuring Delay: 0.09s within the node (AV) Node near the atrial + 0.04s in the AV bundle, tricuspid valve contraction has fewer gap junctions before ventricular contraction AV Bundle Penetrates Conducts Prevents backward impulse (Bundle of His) fibrous tissue impulses conduction, only normal  Component Location Function Key Features between atria from atria to electrical bridge between and ventricles ventricles atria and ventricles Rapid Located beneath Extend from AV endocardium, branches Right and Left conduction of bundle down the spread downward and back Bundle impulses to interventricular toward the base of the Branches Purkinje septum heart fibers Conduct Large fibers with very few Throughout impulses myofibrils, high-speed Purkinje Fibers ventricular rapidly to all transmission (1.5 - 4.0 m/s) myocardium parts of the ensures simultaneous ventricles ventricular contraction Self excitatory mechanism (Sinoatrial node): 1) Open Na+ channels (funny currents) allows Na influx between heart beats (depolarization) 2) When the voltage is -40 , L-type CA2+ channels activate (action potential) 3) After depolarization, K+ repolarizes the cell 4) K+ channels close Fast Na+ channels are always inactivate in these cells The ventricular Purkinje system(highway) -Transmit action potentials at 1.5-4.0 m/s -Almost instantaneous transmission of impulses through the ventricular muscle The cardiac impulse in the ventricular muscles -Slower than in Purkinje fibbers -0.5m/s -From the endocardial surface to the epicardial it requires 0.03s, which is equivalent to the transmission of the entire ventricular Purkinje system Ventricular muscle action potential 1. Rapid upstroke spike(phase 0)- fast Na+ channels opening 2. Initial repolarization (phase 1)- K+ channels opening 3. Plateau phase (phase 2)-Slow Ca2+ channels opening, triggers further calcium release-cardiac contraction 4. Repolarization (phase 3 )- potassium channels open Abnormal pacemakers Topic Key Points - Abnormal pacemakers (ectopic pacemakers) are pacemaker sites outside the SA node that take over heart rhythm. Definition - Can occur in the AV node, Purkinje fibers, atrial, or ventricular muscle. - Blockage of impulse transmission from the SA node. - Abnormal rhythmical discharge from ectopic sites. Causes - Accessory pathways or retrograde conduction may contribute to arrhythmias1. - Ectopic foci display automaticity but are suppressed under normal conditions by the faster SA node rate (overdrive suppression). Mechanism - When activated, they disrupt the normal conduction sequence. - Leads to abnormal contraction sequences, reducing pumping efficiency. - May cause tachycardia (fast heart rate) or bradycardia (slow heart rate), depending on the Effects on Heart ectopic. - Vagus nerve decreases heart rate and slows AV conduction via acetylcholine release. - Hyperpolarization of SA/AV nodes delays excitation; strong stimulation can stop rhythm entirely. SA node -The resting membrane potential becomes more negative Parasympathetic Activity -Delays in threshold excitation  AV node -Hyperpolarization( difficult for small atrial fibres to excite) - Norepinephrine increases heart rate, conduction speed, and contractile force via beta-1 adrenergic receptor activation. - Enhances sodium-calcium permeability and calcium-induced contractility in myocytes(increase strength) SA node: -Sodium-calcium permeability (raises resting potential) -speed up self-excitation and increases heart rate AV node: -Facilitates excitation Sympathetic Activity -Reduce conduction time from atria to ventricles Class 66-Histology of the heart 1. Classification of Muscle Muscle Type Striations Nuclei Location Control Skeletal Yes Multinucleated Attached to bones Voluntary Cardiac Yes Mononucleated Heart Involuntary Smooth (visceral or vascular system) No Mononucleated Viscera, vascular system Involuntary 2. Muscle Tissue Structure 2.1. General Structure  Muscle Tissue: Organized into fascicles containing muscle fibers.  Muscle Fasciculus: A bundle of muscle fibers (cells).  Muscle Fibers: Individual muscle cells, multinucleated in skeletal muscle, mononucleated in cardiac and smooth muscle.  Myofibrils: Long, cylindrical structures within muscle fibers, composed of sarcomeres.  Myofilaments: Contractile proteins (actin and myosin) within myofibrils. 2.2. Myofilaments Filament Type Protein Function Thick Myosin Forms cross-bridges, interacts with actin Thin Actin Binding site for myosin, regulated by troponin and tropomyosin 2.3. Sarcomere The sarcomere is the functional unit of muscle contraction. Structure Composition Function Z line/disc α-actinin (anchors actin filaments) Boundary of the sarcomere; attachment site for actin filaments A band Myosin (thick filaments) Contains both thick and thin filaments (overlap region) I band Actin (thin filaments) Contains only thin filaments Myomesin (connects myosin Middle of the A band; helps maintain the organization of myosin M line filaments) filaments Titin Connects myosin to Z disc Stabilizes myosin and provides elasticity 2.4 Other Proteins Proteins Functions Tropomyosin Covers the myosin-binding site on actin Troponin Complex Binds calcium and regulates the position of tropomyosin on actin Troponin C Binds Calcium Troponin T Binds tropomyosin Troponin I Inhibits actin-myosin interaction 3. Muscle Contraction 3.1. Neuromuscular Junction 1. Nerve action potential reaches the neuromuscular junction. 2. Voltage-gated Ca2+ channels open, allowing Ca2+ influx. 3. Exocytosis of neurotransmitter (acetylcholine). 4. Neurotransmitter binds to receptors on the muscle cell membrane. 5. Endplate potential (EPP) generated, leading to an excitatory postsynaptic potential (EPSP). 6. Spatial/Temporal summation leads to muscular action potential. 3.2. Steps in Muscle Contraction 1. Muscular Action Potential: Spreads through the sarcolemma, T tubules, and sarcoplasmic reticulum.  2. Calcium Release: Ca2+ is released from the sarcoplasmic reticulum. 3. Troponin Binding: Ca2+ binds to troponin C. 4. Tropomyosin Shift: Tropomyosin moves, exposing the myosin-binding site on actin. 5. Cross-Bridge Formation: Myosin heads bind to actin. 6. Power Stroke: Myosin head pivots, pulling the actin filament. 7. Detachment: ATP binds to myosin, causing it to detach from actin. 8. Re-Energizing: ATP is hydrolyzed to ADP and Pi, re-energizing the myosin head. 3.3. Chemomechanical Process Step Details Myosin-Actin Binding Myosin head (with ADP and Pi) has high affinity for actin and binds. Conformational Change (Power Stroke) Myosin head pivots to a 45º angle, pulling actin; ADP and Pi are released. Dissociation ATP binds to myosin, reducing its affinity for actin, causing detachment. ATP is hydrolyzed to ADP and Pi, returning the myosin head to its high-energy, Re-Energizing cocked position (90º angle). 3.4. Relaxation 1. Calcium Removal: Ca2+ is pumped back into the sarcoplasmic reticulum by Ca2+ ATPase. 2. Tropomyosin Blockage: Tropomyosin covers the myosin-binding site on actin. 3. Cessation of Interaction: Actin-myosin interaction ceases. 4. Cardiac Muscle Feature Description Structure Striated, mononucleated cells; branching and anastomosing fibers (Y-shaped) Feature Description Specialized junctions connecting cardiac muscle cells; contain gap junctions for electrical Intercalated Discs coupling Spontaneous Contraction Intrinsic ability to contract rhythmically Modified cardiac muscle cells (Purkinje cells) that form nodes and bundles; facilitate rapid Conducting Cells impulse conduction Neural Control Regulated by the autonomic nervous system Mature cardiac muscle cells do not divide; damage is replaced by fibrous connective tissue Regeneration (scar tissue) 5. Heart Structure Layer Composition Epicardium Mesothelial cells, connective tissue, adipose tissue, blood vessels, and nerves Myocardium Cardiac muscle Endocardium Endothelium, connective tissue, smooth muscle cells, and conducting system 5.1. Heart Components  Papillary Muscles: Projections of cardiac muscle into the ventricles, connected to chordae tendineae.  Fibrous Skeleton: Dense connective tissue encircling the base of the aorta, pulmonary trunk, and atrioventricular orifices; provides structural support.  Interventricular Septum: Separates the ventricles; includes a membranous portion. 5.2. Internal Conducting System Component Function SA Node Pacemaker of the heart; initiates the heartbeat Delays impulse transmission, allowing atrial contraction to complete before ventricular AV Node contraction AV Bundle of His Conducts impulses from the AV node to the ventricles Right/Left Branches Carry impulses down the interventricular septum Purkinje Fibers Rapidly distribute impulses throughout the ventricular myocardium 6. Smooth Muscle Feature Description Structure Non-striated, mononucleated cells T System Absent Contraction Slow and prolonged Present; facilitate coordinated contraction (more difficult to the electrical passage in the Gap Junctions heart ) Spontaneous Activity Can exhibit spontaneous contractile activity Neural Control Nerve terminals in adjacent connective tissue Secretion Secretes connective tissue matrix (collagen, laminin, elastin, proteoglycans) Juxtaglomerular Cells Secrete renin Cell Division Capable of dividing (mitosis) Class 67- Normal electrocardiogram 1. History of ECG Year Event Contributor 1867 First measurement of electricity in the heart Marey 1887 First human ECG published Waller 1895 Naming of the ECG waves Einthoven 1912 Invention of the Einthoven triangle Einthoven 1924 Nobel Prize for ECG; precordial leads added Einthoven 2. ECG Basics  Electrocardiography (ECG): A non-invasive diagnostic tool to assess the electrical activity of the heart by detecting electrical impulses generated by the heart's muscle activity from the skin's surface. 3. Performing a 12-Lead ECG 3.1. Step 1: Preparation Action Details Verify Patient Information Confirm identity and reason for the ECG. THE REASON FOR THE ECG MUST BE CLAR. Inform the patient about the process, reassure them it's painless, and instruct them to Explain Procedure remain still. Ensure the ECG machine is functioning properly and calibrated; gather electrodes, pads, gel, Check Equipment and alcohol wipes. The patient should lie flat on their back with arms at their sides and legs uncrossed. Ensure Positioning the Patient a quiet room. 3.2. Step 2: Electrode Placement Electrode Location RA (Right Arm) Right wrist LA (Left Arm) Left wrist Electrode Location RL (Right Leg) Right ankle (ground electrode) LL (Left Leg) Left ankle V1 Fourth intercostal space, right sternal border V2 Fourth intercostal space, left sternal border V3 Between V2 and V4 V4 Fifth intercostal space, midclavicular line V5 Fifth intercostal space, anterior axillary line V6 Fifth intercostal space, midaxillary line Note: Ensure good skin contact and avoid placing electrodes over bones or muscles. 3.3. Step 3: Performing the ECG 1. Instruct the patient to remain still, breathe normally, and avoid talking. 2. Turn on the ECG machine and ensure all lead connections are secure. 3. Monitor the recording for noise or interference. 4. The procedure should take around 5 minutes. 3.4. Step 4: After the Procedure  1. Gently remove the electrodes. 2. Clean any residual adhesive with alcohol wipes. 4. Interpretation of a Normal ECG 4.1. ECG Leads  12 Leads: Divided into 6 limb leads and 6 precordial/thoracic leads.  Limb Leads: Detect potentials in the frontal plane (I, II, III, aVR, aVL, aVF).  Precordial Leads: Detect potentials in the horizontal plane (V1-V6).  Bipolar Leads: Record voltage between two electrodes.  Unipolar Leads: Record activity directed toward or away from the electrode. 4.2. ECG Components and Intervals Component Represents Normal Interpretation Duration/Amplitude Positive in D II, negative in aVR, may be biphasic in V1. Abnormalities may indicate atrial enlargement Atrial depolarization or conduction issues. P wave < 0.12 seconds; < 2.5 mm Atrial to ventricular 0.12 to 0.20 seconds (3-5 Prolonged: first-degree heart block. Short: pre- PR Interval conduction time small squares) excitation syndromes (e.g., Wolff-Parkinson-White). Should be narrow and sharp. Wide complex may QRS Ventricular < 0.12 seconds (3 small suggest bundle branch block or ventricular Complex depolarization squares) conduction abnormalities. Ventricles fully Elevation or depression may indicate ischemia or ST Segment depolarized Level with baseline injury. Component Represents Normal Interpretation Duration/Amplitude Polarity concordant with QRS complex. Inverted or Ventricular flattened T waves can indicate ischemia, T wave repolarization < 0.20 seconds electrolyte imbalances, or other abnormalities. Total time for ventricular contraction 0.36 to 0.44 seconds Prolonged QT can indicate risk of ventricular QT Interval and relaxation (depending on heart rate) arrhythmias. 4.3. Rate and Rhythm  Normal Rate (Adults): 60-100 bpm  Tachycardia: > 100 bpm  Bradycardia: < 60 bpm  Rhythm Assessment: For irregular rhythms, count R waves in a 6-second strip and multiply by 10. 4.4. Sinus Rhythm Criteria 1. P Waves: Always positive in II (I and aVF), small and rounded, duration < 0.12 sec, amplitude < 2.5 mm, constant morphology.  2. Rhythm Regularity: Constant R-R interval. 3. P Wave Relationship to QRS: Single P wave before each QRS complex, normal PR interval (0.12-0.2 sec) and constant. 4.5. Mnemonic for ECG Interpretation  RATE: Assess heart rate.  RHYTHM: Determine rhythm (sinus, atrial fibrillation, etc.).  INTERVALS: Measure PR, QRS, and QT intervals.  AXIS: Determine the heart's electrical axis.  HYPERTROPHY: Look for signs of atrial or ventricular hypertrophy.  INFARCT: Identify any signs of myocardial infarction (Q waves, ST changes). Class 68-The cardiac cycle diastole and systole Before contraction-depolarization Before relaxation-repolarization Phase Events Pressure Volume Changes ECG Heart Sounds Changes Correlation (if applicable) Ventricular Atrial Atria contract, pushing remaining Atrial pressure volume increases Contraction blood into ventricles. increases. slightly. P wave N/A Ventricular Ventricular Isovolumetric Ventricles contract; all valves are pressure volume remains QRS Contraction closed. increases rapidly. constant. complex N/A Phase Events Pressure Volume Changes ECG Heart Sounds Changes Correlation (if applicable) Ventricular pressure exceeds aortic/pulmonary pressure; Ventricular Ventricular semilunar valves open, blood pressure > aortic volume decreases QRS Rapid Ejection ejected. pressure. rapidly. complex N/A Ventricular pressure Ventricular Continued ventricular ejection, gradually volume continues Slow Ejection but at a slower rate. decreases. to decrease. N/A N/A Ventricular pressure Ventricular Isovolumetric Ventricles relax; all valves are decreases volume remains Relaxation closed. rapidly. constant. T wave S2 Ventricular Ventricular AV valves open; blood rushes into pressure initially volume increases Rapid Filling ventricles from atria. decreases. rapidly. N/A N/A Ventricular pressure Ventricular Diastasis (Slow Ventricular filling slows as gradually volume increases Filling) pressure gradient decreases. increases. slowly. N/A N/A Quiz Questions 1. Cardiac cycle. Select the correct sequence: a. Atrial contraction – ventricular ejection – isovolumetric contraction – ventricular filling – isovolumetric relaxation b. Atrial contraction – isovolumetric contraction - ventricular ejection – isovolumetric relaxation - ventricular filling c. Atrial contraction – isovolumetric relaxation - ventricular filling - isovolumetric contraction - ventricular ejection d. Atrial contraction – isovolumetric relaxation - isovolumetric contraction - ventricular ejection - ventricular filling e. Atrial contraction – ventricular ejection – isovolumetric relaxation -isovolumetric contraction – ventricular filling 2. During isovolumetric contraction phase: a. Atrio-ventricular valves are open b. Ventricular pressure falls c. Atrium pressure increase (wave c) d. Ventricular volume decreases e. S2 cardiac sound occurs 3. During rapid ejection phase: a. Atrio-ventricular valves are closed b. Ventricular volume increases c. EKG shows QRS d. Ventricular pressure < aortic pressure e. Correlate with a wave of atrium pressure 4. During slow ejection phase: a. Atrio-ventricular valves remain open b. Ventricular pressure < aortic pressure c. Semilunar valves are closed d. Ventricular volume start increasing e. Atrium pressure rapidly decreases 5. During isovolumetric relaxation phase: a. All cardiac valves are closed b. S1 cardiac sound occurs c. Ventricular pressure increases d. EKG shows QRS e. Correlate with a wave of atrium pressure 6. During rapid filling phase: a. Mitral valve is closed b. Ventricular volume decreases c. Ventricular pressure initially decreases d. Occurs before ventricular repolarization e. Occurs before venous v wave 7. During diastasis: a. Ventricular filling is rapid b. Occurs after atrial contraction c. Aortic valve is closed d. Mitral valve is close e. Atrial contraction occurs before 8. During atrial contraction: 1. Atrial pressure decrease b. Occurs after P wave of EKG c. Occurs during systole d. Occurs after S1 cardiac sound e. Ventricular volume decreases Class 69-Relationship of the ECG to the cardiac cycle Topic Description A diagnostic tool used to assess the electrical activity of the heart. Electrocardiogram (ECG) The sequence of events that occur during one complete heartbeat, including diastole (relaxation Cardiac Cycle and filling) and systole (contraction and ejection). Topic Description The ECG waveforms (P wave, QRS complex, T wave) correspond to specific events in the cardiac cycle. The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization. These ECG features provide insights into the timing and coordination of the heart's electrical activity during each phase of the Relationship cardiac cycle, allowing clinicians to identify abnormalities in heart function. Class 70-Physiological phases Phases of Systole Phase Key Events Valves Status Isovolumetric Contraction Ventricles contract, pressure rises, but no blood is ejected. All valves closed Blood is ejected into the aorta and pulmonary artery when Semilunar valves open; AV Ejection ventricular pressure exceeds arterial pressure. valves closed  Isovolumetric Contraction: Ventricular pressure increases without volume change as all valves remain closed.  Ejection Phase: Divided into: (semilunar valves open, AV valves are closed)  Rapid Ejection: Blood flows quickly out of the ventricles.  Reduced Ejection: Blood flow slows as ventricles begin to empty. Phases of Diastole Phase Key Events Valves Status Isovolumetric Ventricular pressure decreases without blood flow as all Relaxation valves are closed. All valves closed Rapid blood flow from atria to ventricles due to pressure AV valves open; Semilunar valves Early Diastolic Filling gradient. closed Phase Key Events Valves Status Slower ventricular filling as pressures in atria and ventricles Diastasis equalize. AV valves open Atria contract to "top off" ventricular filling before the next Atrial Contraction systole. AV valves open  Isovolumetric Relaxation: Ventricular pressure drops after semilunar valve closure.  Early Filling (Rapid): Passive blood flow from atria to ventricles.  Diastasis: Slow filling phase.  Atrial Contraction (Atrial Systole): Completes ventricular filling. Key Principles 1. Blood flows from high to low pressure. 2. Valve function depends on pressure gradients:  AV valves open with higher atrial pressure than ventricular pressure.  Semilunar valves open with higher ventricular pressure than arterial pressure.  contraction increase the pressure Factors Influencing Left Ventricular (LV) Function 1. Preload  Definition: The end-diastolic volume (EDV) or the stretch of myocardial fibers before contraction.  Effect: Increased preload enhances stroke volume via Starling's Law.  Clinical Relevance:  High preload: Seen in fluid retention or heart failure.  Low preload: Seen in hypovolemia or severe blood loss. 2. Afterload  Definition: The resistance the LV must overcome to eject blood (systemic vascular resistance).  Effect: Higher afterload reduces stroke volume and increases cardiac workload.  Clinical Relevance:  Chronic high afterload leads to LV hypertrophy and reduced efficiency (e.g., in hypertension or aortic stenosis). 3. Contractility  Definition: The intrinsic ability of myocardial fibers to contract, influenced by calcium levels and sympathetic stimulation.  Effect: Increased contractility improves stroke volume and cardiac output.  Clinical Relevance:  Decreased contractility occurs in conditions like myocardial infarction or heart failure. Transformation of LV Myocardial Function into Pump Function The LV converts myocardial contraction into effective pump function by: 1. Generating sufficient pressure during systole for ejection. 2. Adapting to changes in preload, afterload, and contractility to maintain cardiac output. Key Questions & Answers Question Answer b) Atrial systole → Isovolumetric contraction → Ventricular ejection → Correct order of cardiac cycle phases? Isovolumetric relaxation → Ventricular filling Phase where ventricular pressure rises but no blood is ejected? c) Isovolumetric contraction Event marking the beginning of isovolumetric relaxation? b) Closure of the aortic and pulmonary valves Question Answer What happens to LV pressure during rapid ventricular filling? b) It decreases Best definition of preload? c) Volume of blood returning to the heart, determining EDV Main determinant of afterload? b) Aortic pressure and systemic vascular resistance Best description of contractility? Intrinsic ability of myocardium to contract Class 71-volume pressure loop The pressure-volume (PV) loop is a graphical representation of the changes in pressure and volume within the left ventricle during one cardiac cycle. The loop illustrates four key phases:  Diastolic Filling (A to B): The mitral valve opens, and the ventricle fills with blood, causing both volume and pressure to increase.Ventricular suction  Slow ventricular filling and atrial contraction (B to C)  Isovolumetric Contraction (IVC) (C to D): The mitral valve closes, and the ventricle begins to contract. The volume remains constant as pressure increases.  Rapid Ejection (D to E): The aortic valve opens, and blood is ejected from the ventricle into the aorta. The volume decreases, while pressure initially increases and then decreases.  Slow ejection (E to F)  Isovolumetric Relaxation (IVR) (F to A): The aortic valve closes, and the ventricle begins to relax. The volume remains constant as pressure decreases. F-end of systole , beginning of diastole C-end of diastole, beginning of systole Key points on the PV loop:  ESV: End-systolic volume, the volume of blood remaining in the ventricle at the end of systole. (A and B)  EDV: End-diastolic volume, the volume of blood in the ventricle at the end of diastole.(B or C) Class 72-Cardiac cycle 1. Pressure-Volume Relationships: Used to evaluate systolic and diastolic performance. 2. Preload and Afterload Evaluation:  Preload: End-diastolic pressure or volume.  Afterload: Wall stress during ejection. 3. Contractility Assessment: Measured via end-systolic pressure-volume relationships (ESPVR). 4. Tools include echocardiography, ventriculography, and MRI. 4. Results Phase of Cardiac Cycle Description Systole Begins with mitral valve closure; includes isovolumetric contraction and ejection. Diastole Includes isovolumetric relaxation, early diastolic filling, diastasis, and atrial filling. Stroke Volume (SV) Blood ejected per beat; calculated as SV=EDV−ESVSV=EDV−ESV. Pressure-Volume Relations ESPVR slope reflects contractility; shifts indicate changes in myocardial function. 5. Discussion The discussion elaborates on factors influencing LV function: 1. Preload:+preload=+cardiac output  Defined as the stretch of myocardial fibres before contraction. Its dependent of ventricular filling.  Clinically assessed via pulmonary capillary wedge pressure or end-diastolic volume.  The most important determining factor for preload is venous return  Increased by IV fluids , blood and vasoconstriction  Decrease by diuretics, dehydration , haemorrhage and vasodilatation 2. Afterload:+afterload=-CO  Wall tension during ejection; determined by arterial pressure and ventricular size.  Increased afterload reduces stroke volume without affecting contractility.  Afterload for the right ventricle is determined by pulmonary artery pressure (pressure increases, resistance increases and afterload increases)  Factors which increase afterload( systolic hypertension, Pulmonary hypertension, aortic insufficiency, mitral regurgitation)  Affected by : vascular tone, aortic stiffness, myocardial tension, preload and valvular regurgitation Afterload is increased = aortic stenosis and arterial hypertension  3. Contractility:+contractility +co2  Intrinsic ability of myocardium to contract; measured by ESPVR slope or ejection fraction (EF) that is usually around 50-55%.  Higher contractility increases stroke volume. 4. Diastolic Function:  Assessed by end-diastolic pressure-volume relationships.  Impaired relaxation or reduced distensibility indicates diastolic dysfunction. 5. cardiac output  Cardiac output is the volume of blood pumped each minute  CO=SV*HR 6. Stoke volume  Determined by three: preload, afterload and contractility  Volume of blood that the ventricle has available to pump  SV=EDV-ESV Frank-Starling Principle- The relationship between cardiac output and left ventricular end diastolic volume   Based on length-tension relationship within the ventricle  Cardiac output is directly relate to venous return, the most important factor is preload Key Findings:  Increased preload enhances stroke volume via the Frank-Starling mechanism.  Elevated afterload impairs systolic emptying despite normal contractility.  Diastolic dysfunction reduces LV filling efficiency. Classe 73-heart auscultation Cardiac Auscultation Summary Definition  Heart auscultation involves listening to the heart sounds and murmurs to assess cardiac function. Techniques Cardiac examination comprises inspection and palpation. Auscultation is used for further examination. Inspection and Palpation  Chest Inspection: Evaluates the chest contour for visible cardiac impulses or deformities.  Examples: Pectus carinatum (associated with Marfan or Noonan syndrome) and pectus excavatum (associated with hereditary disorders like Turner, Noonan, and Marfan syndromes).~    Precordial Palpation: Palpates for pulsations to determine the apical impulse.  Normal Apical Impulse: Located in the 4th and 5th intercostal space just medial to the midclavicular line, covering an area less than 2 to 3 cm in diameter.  Abnormal Findings:  Central precordial heave: Suggests severe right ventricular hypertrophy.  Sustained thrust at the apex: Suggests left ventricular hypertrophy. Auscultation  Purpose: Characterize heart sounds and murmurs.  Stethoscope Use:  Electronic devices may offer bell or diaphragm modes, similar to acoustic stethoscopes, though the acoustic characteristics differ.  Auscultation device:  Bell: Low-frequency sounds; should be held lightly against the patient's skin.(tricuspid focus, mitral focus)  Diaphragm: For high-frequency sounds, should be pressed firmly against the skin.(Aortic focus, pulmonary focus, tricuspid focus, left edge of sternum, mitral focus )  May ask the patient to be in the left lateral decubitus or sitting position to increase some sounds like murmurs Auscultation Techniques 1. Patient Position:  Standard: Sitting at 45°  Left lateral decubitus: Enhances mitral murmurs (especially stenosis)  Leaning forward: Best for aortic regurgitation/pericardial rub 2. Auscultation Areas:  Aortic: Right 2nd intercostal space  Pulmonic: Left 2nd intercostal space  Tricuspid: Left lower sternal border (4th ICS)  Mitral: 5th ICS, midclavicular line (apex) 3. Stethoscope Use:  Diaphragm: High-frequency sounds (S1, S2, murmurs)  Bell: Low-frequency sounds (S3, S4, mitral stenosis)  Characteristic Normal Heart Sounds Pathological Heart Innocent Pathological Murmurs Sounds Murmurs Benign turbulent blood flow Sounds from valve Abnormal sounds (no Abnormal turbulent closure during indicating structural flow due to structural Definition cardiac cycle dysfunction disease) issues S1 ("lub"): AV valves close S3: Early diastole (mitral/tricuspid) (HF, volume S2 ("dub"): Semilunar overload) Soft, brief valves close S4: Late diastole sounds Loud (grade III-VI), may Main Sounds (aortic/pulmonary) (stiff ventricles) (grade I-II) radiate S1: Systole onset S3/S4: Diastolic Usually Systolic, diastolic, or Timing S2: Diastole onset gallops systolic continuous - S3: CHF, mitral regurgitation. May be normal in young adults, atlets , - Valve childrens… - Exercise stenosis/regurgitation Common - S4: Hypertension, - Pregnancy - Septal defects Causes Normal valve function aortic stenosis - Anemia - Cardiomyopathy Variable (usually Harsh/rough (stenosis) Pitch High (S1/S2) Low (S3/S4) medium) Blowing (regurgitation) Characteristic Normal Heart Sounds Pathological Heart Innocent Pathological Murmurs Sounds Murmurs Indicates pathology Clinical (e.g., HF, No treatment Requires further Significance Healthy heart hypertrophy) needed evaluation (echo, ECG) Levine Grade III-VI/VI (thrill Grading N/A N/A Grade I-II/VI present if ≥IV) Key Distinctions:  Splitting: Normal S2 splits on inspiration; fixed/widened splitting suggests ASD or RBBB.  Pathologic Murmurs: Associated with symptoms (dyspnea, syncope) or structural abnormalities (e.g., aortic stenosis = crescendo-decrescendo systolic murmur).  Innocent Murmurs: Common in children (50%), disappear with position changes, no thrill. Murmur classification (aortic stenosis murmur radiates to the neck) (Mitral insufficiency murmur radiates to the armpit) Type Timing Quality Common Causes Best Heard At Normal flow (children, Left lower sternal Innocent Systolic Soft, short, musical pregnancy) border Aortic Crescendo- Calcific valve, Right 2nd ICS → Stenosis Systolic decrescendo, harsh bicuspid valve carotids Type Timing Quality Common Causes Best Heard At Mitral Blowing, high- MVP, rheumatic Regurg Holosystolic pitched disease Apex → axilla Mitral Rumbling, low- Apex (bell, left Stenosis Diastolic pitched Rheumatic fever lateral decubitus) Aortic Early Decrescendo Aortic dilation, Left 3rd ICS (Erb's Regurg diastolic blowing endocarditis point) Left lower sternal VSD Holosystolic Harsh Congenital defect border Other abnormalities Sound Description Clinical Significance Pericardial Scratching/grating (3 components: systole, early Acute Rub diastole, atrial contraction) pericarditis Class 75-Blood flow, blood pressure and resistance Blood Flow, Blood Pressure & Resistance — Summary Purpose of Circulation  Delivers oxygen and nutrients; removes waste.  Inadequate perfusion leads to cell dysfunction and tissue death. Hemodynamics: Flow, Pressure & Resistance Blood Flow  Defined as volume of blood passing a point per unit time (mL/min).  At rest: ~5.25 L/min total (cardiac output).  Regional blood flow varies based on tissue demand. Perfusion   Flow per tissue mass (mL/min/g).  Ensures organs receive enough oxygen/nutrients. Core Equation Flow  Flow increases with pressure difference (ΔP).  Flow decreases with increased resistance (R). Factors that may influence blood flow are pressure differences across points and resistance within the vascular system. Blood Pressure (BP)-force exerced by blood on a vessel, initiate by heart contraction.  Systolic Pressure: Peak during ventricular contraction.  Diastolic Pressure: Minimum during relaxation. -The pulse pressure is the difference between SP and DP  Pulse Pressure (PP) = Systolic – Diastolic.  Hearthy person= 120/75 mm Hg  Mean Arterial Pressure (MAP): MAP≈ o Represents average pressure driving blood through tissues. o MAP < 60 mmHg = risk of hypoperfusion. o Influence risks of atherosclerosis, kidney failure, edema, aneurysm and syncope Factors Affecting BP  Elasticity of arteries (↓ with age).  Blood volume.  Cardiac output.  Peripheral resistance.  Resistance to Flow Peripheral Resistance  Opposition to flow in systemic circulation.  Necessary to maintain pressure and control distribution. Determinants of Resistance 1. Blood Viscosity: ↑ viscosity = ↑ resistance (e.g., polycythemia). 2. Vessel Length: Longer vessels = more friction. =less pressure and flow 3. Vessel Radius: Most influential (inversely proportional to flow⁴): Arterioles  Main site of variable resistance.  Adjust organ-specific perfusion via vasomotion. Flow Velocity  Aorta: Fastest flow (low resistance, large diameter).  Capillaries: Slowest (high surface area for exchange).-increase friction over distance, smallest vessel radii  Veins: Flow increases again toward the heart but slower than arteries. Regulation of Blood Flow Local Control (Autoregulation)  Adjusts perfusion based on tissue demand.  Mediated by: o Hypoxia (→ vasodilation)  o Metabolic by-products (CO₂, H⁺, adenosine) o Vasoactive chemicals (histamine, prostaglandins) o Reactive hyperemia: transient increase after occlusion o Angiogenesis: long-term increase in capillary density Neural Control  Sympathetic fibers: o α₁ → vasoconstriction (skin, GI)-activated by norepinephrine o β₂ → vasodilation (skeletal muscle, heart)  Parasympathetic: Minor role; limited to some regions (salivary glands, genitalia) Hormonal Control  Angiotensin II: Potent vasoconstrictor  Aldosterone: Retains Na⁺ → ↑ blood volume/BP  ADH (Vasopressin): Retains water + vasoconstriction  Atrial Natriuretic Peptide (ANP): Vasodilation, promotes salt/water loss  Epinephrine/Norepinephrine: α = vasoconstriction; β = vasodilation (dose and receptor dependent) Vasomotion & Redistribution  Vasomotion = rhythmic contraction/relaxation of vessels.  Allows redistribution of blood based on: o Metabolic need (e.g., exercise → muscle) o Functional state (e.g., digestion → GI tract)  Critical during shock, exercise, and thermoregulation. Key Clinical Concepts  Elastic arteries buffer pressure changes. Loss of elasticity → ↑ systolic BP (common in aging).  Constriction upstream ↑ pressure, but downstream ↓ pressure.  Blood follows the path of least resistance—used therapeutically to reroute flow. Class 76-Introduction to the cardiovascular system-blood vessels and circulation Functions of the Circulatory System Category Description Transport Oxygen, nutrients, metabolic waste, hormones, stem cells Protection White blood cells eliminate microorganisms; platelets prevent blood loss Regulation Fluid distribution stabilization, thermoregulation General Anatomy of Blood Vessels Principal Categories Type Definition Arteries Efferent vessels carrying blood away from the heart (not defined by oxygen content) Veins Afferent vessels returning blood to the heart (not defined by oxygen content) Capillaries Thin-walled microscopic vessels connecting arteries to veins; primary sites for exchange Structural Layers Layer Description Tunica Interna Innermost layer; selectively permeable barrier; secretes chemicals for dilation/constriction Tunica Media Middle layer; smooth muscle regulates vessel diameter Tunica Externa Outermost layer; anchors vessels and provides passage for nerves and smaller vessels. We (adventicia) have vaso vasorum. Arteries-resistants to pressure Classes of Arteries Type Examples Function/Structure Conducting (Large) Aorta, pulmonary trunk Elastic tissue allows expansion/recoil during heartbeats Distributing (Medium) Brachial, renal arteries Distribute blood to specific organs Resistance (Small) Arterioles Control blood flow to organs; thick tunica media relative to lumen size Capillaries Types of Capillaries Type Structure Location/Function Tight junctions; intercellular clefts allow small solutes Skeletal muscles, lungs, most Continuous Capillaries through organs Fenestrated Capillaries Pores for rapid exchange of small molecules Kidneys, endocrine glands Sinusoids Wide gaps between endothelial cells; large fenestrations Liver, bone marrow, spleen Capillary Beds  Organized networks of 10–100 capillaries supplied by one arteriole.  Blood flow regulation via upstream arterioles ensures perfusion based on tissue demand. Veins Classification by Size Type Structure/Function Postcapillary Receive blood from capillaries; highly porous for fluid exchange(primary site for leukocytes Venules emigration ) Muscular Venules Thin tunica externa; smooth muscle layers Type Structure/Function Medium Veins Venous valves prevent backflow; skeletal muscle pump facilitates upward flow Large Veins Thick tunica externa with longitudinal bundles of smooth muscle Venous Sinus  Thin walls with large lumens; incapable of vasoconstriction (e.g., coronary sinus). Circulatory Routes Types Route Type Description/Examples Simplest Route Heart → arteries → capillaries → veins → heart Portal Systems Two consecutive capillary networks (e.g., kidneys, intestines to liver) Anastomoses Convergence points between vessels (arteriovenous shunts, venous or arterial anastomoses) Type of Definition Examples/Locations Function Anastomosis Direct connection Reduces heat loss in cold weather; Arteriovenous between an artery and a increases susceptibility to frostbite Anastomosis vein, bypassing capillaries Fingers, palms, toes, ears in poorly perfused areas Connection between Provides alternative drainage veins, allowing blood to routes; makes vein blockages less Venous flow from one vein to life-threatening than artery Anastomosis another Veins in the forearm blockages Connection between two Coronary circulation (heart), Ensures continuous blood supply to Arterial arteries to provide Circle of Willis (brain), tissues even if one artery is blocked Anastomosis collateral blood supply joints or compressed Lymphatic Connection between Throughout the lymphatic Maintains fluid balance and supports Anastomosis lymph vessels system immunity by redirecting lymph flow Class 77-effects of pressure on vascular resistance and tissue blood flow-capillary exchange The primary purpose of cardiovascular system is to circulate gases, nutrients, wastes and other substances from the cells. Capillary exchange refers to the exchange of material between the blood and the tissue in capillaries. We have three types of capillary exchange: -diffusion -transcytosis -bulk flow Capillary Exchange Mechanisms Energy Mechanism Description What It Moves Direction Key Role Use Passive movement due Gases (O₂, High → Low Primary exchange for Diffusion to concentration CO₂), small No concentration gases/nutrients gradient solutes Important for Vesicular transport Large proteins, Yes Selective, both Transcytosis protein/hormone across endothelial cells antibodies (ATP) directions transport Movement of fluids and Water, ions, Depends on Regulates volume & Bulk Flow No solutes together glucose, etc. pressure gradients pressure in capillaries Starling Forces: What Drives Bulk Flow Bulk flow depends on two main pressures across capillary walls: Pressure Type Description Tends to... Capillary Hydrostatic Pressure Pressure exerted by blood on capillary walls Push fluid out (filtration) (CHP) Blood Colloid Osmotic Pressure Osmotic pull from plasma proteins (e.g., Pull fluid in (BCOP) albumin) (reabsorption)  Net Filtration Pressure (NFP) NFP=CHP-BCOP Capillary Region CHP (mmHg) BCOP (mmHg) NFP (mmHg) Net Movement Effect Arterial end 35 25 +10 Out of capillary Filtration of nutrients, O₂ Mid-capillary ≈25 25 0 No net movement Balance Venous end 18 25 -7 Into capillary Reabsorption of CO₂, waste  About 85% of filtered fluid is reabsorbed.  Remaining 15% (~3.6 L/day) → returned by lymphatic system. Lymphatic System’s Role  Captures excess interstitial fluid.  Returns it to blood via thoracic duct → subclavian vein.  Prevents edema (tissue swelling).  Important in immune surveillance and fat absorption (lacteals). Clinical Cases (Pathophysiology of Capillary Exchange Imbalance) Case Condition Mechanism Disrupted Resulting Change Clinical Outcome Congestive Heart Failure Peripheral edema, 1 ↑ Venous pressure → ↑ CHP ↑ Filtration (CHF) especially in legs Loss of plasma proteins in 2 Nephrotic Syndrome ↓ Reabsorption Generalized edema urine → ↓ BCOP Deep Vein Thrombosis Obstructed venous return → 3 ↑ Filtration Unilateral leg swelling (DVT) ↑ local CHP Hypoproteinemia (e.g., ↓ Albumin production → ↓ Edema, especially in 4 ↓ Reabsorption Kwashiorkor) BCOP abdomen Blocked or removed Accumulated Chronic swelling, often 5 Lymphedema lymphatic vessels interstitial fluid in arms/legs Uterine pressure + venous 6 Pregnancy ↑ CHP in lower limbs Bilateral leg edema obstruction + gravity ↓ Albumin synthesis + ↑ Ascites (fluid in 7 Liver Cirrhosis ↓ BCOP + ↑ CHP portal venous pressure abdomen) Class 78-Circulatory pathways Interaction of the Circulatory System with Other Body Systems The circulatory system interacts with almost every part of the body, impacting cells, tissues, organs, and systems. Key Functions  Transports materials and allows capillary exchange.  Carries white blood cells and antibodies for immunity.  Helps stop bleeding.  Regulates body temperature.  Maintains acid-base balance. Interactions with Specific Systems System Interaction Absorbs nutrients and water, delivers nutrients (except most lipids) to the liver via the hepatic portal vein. The liver provides essential nutrients for hematopoiesis (iron(hemoglobin Digestive production), Vitamin B12(red blood cell maturation ), folic acid (DNA synthesis), proteins like System transferrin and albumin(transport iron), and Vitamin K(clotting factor synthetesis)). System Interaction Several hormones regulate blood pressure: epinephrine (increases heart rate and blood pressure), ANH (lowers blood pressure), Angiotensin II (raises blood pressure), ADH (helps retain water, increasing blood pressure), thyroxine (affects heart rate and metabolism), and estrogen (supports vascular health). Endocrine System Blood carries clotting factors, platelets, and white blood cells for clotting and healing. Blood flow to the skin regulates body temperature. Blood gives skin some of its color. The skin stores Integumentary System extra blood. Lymphatic Transports white blood cells and antibodies, collects extra fluid from tissues, and returns it to System the bloodstream. Blood brings oxygen and nutrients to muscles, removes waste like lactic acid, distributes heat, Muscular and muscle contractions help push blood through veins. Exercise strengthens the heart and System reduces atherosclerosis risk. Skeletal System Blood delivers minerals needed for strong bones and transports hormones controlling bone growth and density (growth hormone, thyroid hormone, calcitonin, parathyroid hormone).  System Interaction Erythropoietin (EPO) stimulates red blood cell production in bone marrow. Bones protect blood vessels. Somatotropin stimulates bone growth, thyroid hormone its for bone metabolism and calcitonin controls calcium levels in bones and blood. Regulates blood flow and heart function, produces cerebrospinal fluid (CSF), helps form the blood-brain barrier, and the cardiac and vasomotor centers in the brainstem control heart rate Nervous System and blood vessel diameter via the autonomic nervous system. Reproductive Blood flow is important for sexual function and erection. The bloodstream transports System gonadotropic hormones (FSH & LH) to regulate reproductive processes. Pulmonary Circulation  Right Ventricle → Pulmonary semilunar valve → Pulmonary trunk (bifurcates into left and right pulmonary arteries) → Smaller arteries and arterioles → Pulmonary capillaries  Gas exchange occurs in the pulmonary capillaries.  Pulmonary capillaries → Pulmonary venules → 4 pulmonary veins (two on the left and two on the right) → Left Atrium Overview of Systemic Arteries  Left Atrium → Left Ventricle → Aorta  The aorta and its branches send blood to every organ. The Aorta  Largest artery in the body.  Arises from the left ventricle and descends to the abdominal region.  Bifurcates at the level of the 4th lumbar vertebra into the two common iliac arteries. Components of the Aorta 1. Ascending Aorta 2. Aortic Arch 3. Descending Aorta (Thoracic and Abdominal) Branches from the Ascending Aorta   Paired coronary arteries (arise from sinuses in the ascending aorta). Aortic Arch Branches 1. Brachiocephalic Artery  Right Subclavian Artery  Right Common Carotid Artery 2. Left Common Carotid Artery 3. Left Subclavian Artery Subclavian Artery Branches 1. Internal Thoracic Artery (mammary artery) 2. Vertebral Artery (supplies blood to the brain and spinal cord) 3. Thyrocervical Artery (supplies the thyroid, cervical region, upper back, and shoulder) Thoracic Aorta Branches  Visceral Branches:  Bronchial Arteries (lungs and visceral pleura)  Pericardial Arteries  Esophageal Arteries  Mediastinal Arteries  Parietal Branches:  Intercostal Arteries (muscles of the thoracic cavity and vertebral column)  Superior Phrenic Arteries (superior surface of the diaphragm) Abdominal Aorta Branches  Single Celiac Trunk:  Left Gastric Artery (stomach and esophagus)  Splenic Artery (spleen)  Common Hepatic Artery  Proper Hepatic Artery (liver)  Right Gastric Artery (stomach)   Cystic Artery (gall bladder)  Branches to the duodenum and pancreas  Superior Mesenteric Artery (SMA) (small intestine, pancreas, large intestine)  Inferior Mesenteric Artery (IMA) (distal large intestine, rectum) Paired Arteries from the Abdominal Aorta  Inferior Phrenic Arteries (inferior surface of the diaphragm)  Adrenal Arteries (adrenal glands)  Renal Arteries (kidneys)  Gonadal Arteries (ovarian or testicular arteries)  Lumbar Arteries (lumbar region, abdominal wall, spinal cord) Common Iliac Arteries  The aorta divides into the left and right common iliac arteries (at L4) and continues as the median sacral artery.  The common iliac arteries provide blood to the pelvic region and lower limbs.  They split into:  External Iliac Artery  Internal Iliac Artery Internal and External Iliac Arteries  Internal Iliac Artery: Supplies the urinary bladder, walls of the pelvis, external genitalia, and the medial portion of the femoral region; in females, supplies the uterus and vagina.  External Iliac Artery: Supplies blood to each of the lower limbs. Arteries Serving the Upper Limbs  Subclavian Artery becomes the axillary artery as it exits the thorax.  Axillary Artery becomes the brachial artery.   Brachial Artery bifurcates into the radial and ulnar arteries.  Radial and Ulnar Arteries: Run parallel to their namesake bones, giving off smaller branches until they reach the wrist.  At the wrist, they form the superficial and deep palmar arches that supply blood to the hand, as well as the digital arteries that supply blood to the digits. Arteries Serving the Lower Limbs  External Iliac Artery becomes the femoral artery as it enters the femoral region.  Femoral Artery branches into the lateral deep femoral artery and the lateral femoral circumflex artery.  Genicular Artery: Supplies blood to the knee region.  Femoral Artery becomes the popliteal artery posterior to the knee.  Popliteal Artery branches into the anterior tibial artery and the posterior tibial artery. Anterior and Posterior Tibial Arteries  Anterior Tibial Artery: Supplies the muscles and integument of the anterior tibial region and becomes the dorsalis pedis artery (supplies the tarsal and dorsal regions of the foot).  Posterior Tibial Artery: Supplies the muscles and integument on the posterior surface of the tibial region, branches into the fibular or peroneal artery, and the medial and lateral plantar arteries (supplying blood to the plantar surfaces). Overview of Systemic Veins  Superior Vena Cava: Drains most areas superior to the diaphragm into the right atrium. Veins Draining into the Superior Vena Cava  Axillary Vein → Subclavian Vein (drains the axillary and smaller local veins near the scapular region).  Subclavian Vein fuses with the external and internal jugular veins.  Vertebral Vein  Internal Thoracic Veins  Brachiocephalic Vein (drains the upper thoracic region)  Azygos Vein  Intercostal Vein (drains the muscles of the thoracic wall)  Esophageal Veins (drains the inferior portions of the esophagus)  Bronchial Veins (drains from the lungs)  Hemiazygos Vein (drains the esophageal veins and the left intercostal veins) Veins of the Head and Neck  Blood from the brain flows into the internal