Cardiovascular Anatomy & Physiology PDF

NOTES NOTES CARDIOVASCULAR ANATOMY & PHYSIOLOGY CARDIOVASCULAR ANATOMY & PHYSIOLOGY osms.it/cardiovascular-anatomy-physiology CARDIOVASCULAR SYSTEM ▫ Sits on...

NOTES NOTES CARDIOVASCULAR ANATOMY & PHYSIOLOGY CARDIOVASCULAR ANATOMY & PHYSIOLOGY osms.it/cardiovascular-anatomy-physiology CARDIOVASCULAR SYSTEM ▫ Sits on top of diaphragm (main ▪ Cardia-, cardi-, cardio- breathing muscle) ▫ Heart, which pumps blood ▫ Behind sternum (breast bone) ▪ Vascular: blood vessels (carry blood to ▫ In front of vertebral column body, return it to heart) ▫ Between lungs ▪ Delivers oxygen, nutrients to organs, ▫ Enclosed, protected by ribs tissues ▫ Right, left sides separated by muscular ▪ Removes waste (carbon dioxide, other septum cellular respiration by-products) from organs, tissues Heart wall layers ▪ Epicardium: covers surface of heart, great vessels (AKA visceral pericardium) MORPHOLOGY ▪ Myocardium: muscular middle layer ▪ Size: about size of person’s first (correlated with person’s size) ▫ Cardiac muscle cells: striated branching cells with many mitochondria, ▪ Shape: blunt cone-shaped intercalated disks for synchronous ▪ Position: slightly shifted to left side contraction ▪ Location ▫ Cardiac myocytes: striated, branching ▫ Lies in mediastinum in thoracic cavity cells with fibrous cardiac skeleton Figure 14.1 Heart location relative to other thoracic structures. OSMOSIS.ORG 83  (supports muscle tissue, crisscrossing ▫ Serous pericardium: simple squamous connective tissue collagen fibers); epithelium layer coronary vessels (lie on outside of heart, ▫ Parietal pericardium: lines fibrous penetrate into myocardium to bring pericardium blood to that layer) ▫ Visceral pericardium (epicardium): ▪ Endocardium: innermost layer covers outer surface of heart ▫ Made of thin epithelial layer, underlying ▫ Cells of parietal, visceral pericardium connective tissue secrete protein-rich fluid (pericardial ▫ Lines heart chamber, valve fluid) → fills space between layers ▪ Pericardium: double-layered sac (lubricant for heart, prevents friction) surrounding heart ▫ Fibrous pericardium: outer layer; tough fibrous connective tissue anchors heart within mediastinum Figure 14.2 Heart wall layers, from superficial to deep. Figure 14.3 Layers of the pericardium (the double-layered sac surrounding the heart.) 84 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology Atrioventricular valves ventricle → pulmonary valve → pulmonary ▪ Separate atria from ventricles trunk → pulmonary arteries → pulmonary ▪ Tricuspid valve arterioles → pulmonary capillaries → alveoli ▫ Three cusps with chordae tendinae ▪ Blood collects oxygen from alveoli, removes (tether valve to papillary muscle) carbon dioxide ▫ Prevents blood backflow into right ▪ Oxygenated blood travels through atrium (right ventricle contracts → pulmonary venules → pulmonary veins → papillary muscles contract, keep chordae left atrium → bicuspid/mitral valve → left tendineae taut) ventricle → aortic valve → aorta → organs, tissues ▪ Bicuspid / mitral valve ▪ Deoxygenated blood returns to heart ▫ Two cusps: anterior, posterior leaflet ▫ Both have chordae tendineae tethered to papillary muscles in left ventricle SYSTEMIC VS. PULMONARY ▫ Prevents blood backflow back into left CIRCULATION atrium ▪ Pulmonary, systemic circulation both pump same amount of blood Semilunar valves ▪ Located where two major arteries leave Pulmonary circulation ventricles ▪ Low pressure system ▪ Pulmonary valve ▪ Right side of heart pumps deoxygenated ▫ Three half-moon shaped cusps blood through pulmonary circulation to collect oxygen ▫ Prevents blood backflow into right ventricle ▫ Right atrium → right ventricle → pulmonary arteries → lungs ▪ Aortic valve ▫ Three cusps Systemic circulation ▫ Prevents blood backflow into left ▪ High pressure system ventricle ▪ Left side of heart pumps oxygenated blood to systemic circulation Blood flow physiology ▫ Pulmonary veins → left atrium → left ▪ Deoxygenated blood enters right side of ventricle → aorta → body heart via superior, inferior vena cava (veins) ▫ Left ventricle three times thicker than ▪ Coronary sinus (tiny right atrium opening) right ventricle (↑ systemic circulation collects blood from coronary vessels → resistance) right atrium → tricuspid valve → right Figure 14.4 The four heart valves. The chordae tendineae and papillary muscles attached to the atrioventricular valves prevent blood backflow into the atria. OSMOSIS.ORG 85  Figure 14.5 Blood flow physiology starting with the superior and inferior vena cavae bringing deoxygenated blood from the body to the right atrium of the heart. VENTRICULAR SYSTOLE VS. of four heart chambers DIASTOLE ▪ 15% (750ml/0.2gal) in systemic arteries Systole ▫ 15% to brain ▪ Ventricular contraction/atrial relaxation ▫ 5% nourishes heart ▪ Occurs during S1 sound ▫ 25% to kidneys ▫ Aortic, pulmonic valves open → blood ▫ 25% to GI organs pushed into aorta, pulmonary arteries ▫ 25% to skeletal muscles ▪ Systolic blood pressure ▫ 5% to skin ▫ Arterial pressure when ventricles ▪ 5% (250ml/0.07gal) in systemic capillaries squeeze out blood under high pressure ▪ 65% (3.25L/0.86gal) in systemic veins ▫ Peripheral pulse felt ▪ Numbers can change (e.g. exercise) Diastole ▪ Ventricular relaxation/atrial contraction BLOOD FLOW TERMINOLOGY ▪ Occurs during S2 sound Preload ▫ Tricuspid, mitral valves open → blood ▪ Amount of blood in left ventricle before fills ventricles contraction ▪ Diastolic blood pressure ▪ Determined by filling pressure (end diastolic ▫ Ventricles fill with more blood (lower pressure) pressure) ▪ “Volume work” of heart Afterload BLOOD DISTRIBUTION ▪ Resistance (load) left ventricle needs ▪ Average adult: 5L/1.32gal total blood to push against to eject blood during volume (not cardiac output) contraction ▪ 10% of total volume (approx. ▪ “Tension work” of heart 500ml/0.13gal) in pulmonary arteries, ▪ Components include capillaries, pulmonic circulatory veins ▫ Amount of blood in systemic circulation ▪ 5% of total volume (250ml/0.07gal) in one 86 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ▫ Degree of arterial vessel wall Venous return constriction (for left side of heart, main ▪ Blood-flow from veins back to atria afterload source is systemic arterial resistance; for right side of heart, main Ejection fraction (EF) afterload source is pulmonary arterial ▪ Percentage of blood leaving heart during pressure) each contraction ▪ EF = (stroke volumeend diastolic volume) * Stroke volume (SV) 100 ▪ Blood volume (in liters) pumped by heart per contraction Frank–Starling Mechanism ▪ Determined by amount of blood filling ▪ Ventricular contraction strength related to ventricle, compliance of ventricular amount of ventricular myocardial stretch myocardium ▪ Maximum contraction force achieved when myocardial actin, myosin fibers are Cardiac output (CO) stretched about 2–2.5 times normal resting ▪ Blood volume pumped by heart per minute length (L/min) ▪ CO = SV * heart rate ▪ Example BLOOD VESSEL LAYERS (“TUNICS”) ▫ SV = 70mL ejected per contraction Tunica intima (interna) ▫ HR = 70bpm ▪ Innermost layer ▫ CO = 70 * 70 = 4900mL/min = 4.9L/min Figure 14.6 A: Total blood volume distribution in an average adult. B: Systemic arterial blood distribution. OSMOSIS.ORG 87  ▪ Endothelial cells create slick surface for Types smooth blood flow ▪ “Elastic” arteries (conducting arteries) ▪ Receives nutrients from blood in lumen ▫ Lots of elastin in tunica externa, media ▪ Only one cell thick ▫ Stretchy; allows arteries to expand, ▫ Larger vessels may have subendothelial recoil during systole, diastole basement membrane layer (supports ▫ Absorbs pressure endothelial cells) ▫ Largest arteries closest to heart (aorta, main branches of aorta, pulmonary Tunica media arteries) have most elastic in walls ▪ Middle layer ▪ Muscular arteries (distributing arteries) ▪ Mostly made of smooth muscle cells, elastin ▫ Carry blood to organs, distant body protein sheets parts ▪ Receives nutrients from blood in lumen ▫ Thick muscular layer Tunica externa ▪ Arterioles (smallest arteries) ▪ Outermost layer ▫ Artery branches when they reach ▪ Made of loosely woven fibers of collagen, organs, tissues elastic ▫ Major systemic vascular resistance ▫ Protects, reinforces blood vessel; regulators anchors it in place ▫ Bulky tunica media (thick smooth ▪ Vaso vasorum (“vessels of the vessels”) muscle layer) ▫ Tunica externa blood vessels are very ▫ Regulate blood flow to organs, tissues large, need own blood supply ▫ Contract (vasoconstriction) in response to hormones/autonomic nervous system, ↓ blood/↑ systemic resistance ARTERIES ▫ Vasodilate (relax) ↑ blood flow to Key features organs/tissues, ↓ systemic resistance ▪ High pressure, thicker than veins, no valves ▫ Ability to contract/dilate provides thermoregulation VEINS Key features ▪ Low pressure ▪ Cannot tolerate high pressure but are distensible → adapts to different volumes, pressures ▪ Have valves (folds in tunica interna) to resist gravity, keep blood flowing unidirectionally heart Types ▪ Venules: small veins that connect to capillaries CAPILLARIES ▪ Only one cell thick (flat endothelial cells) ▪ Oxygen, carbon dioxide, nutrients, Figure 14.7 The three layers, or “tunics,” of a metabolic waste easily exchanged between blood vessel. tissues; circulation through capillary wall by diffusion 88 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ▪ Fluid moves out of vessel, into interstitial Key features space (space between blood vessels, cells) ▪ Moves large amounts of water, substances ▫ Water-soluble substances (ions) cross in same direction through fenestrated capillary wall through clefts, between capillaries endothelial cells, through large pores in ▪ Material movement fenestrated capillary walls ▪ Faster transport method ▫ Lipid-soluble molecules (oxygen, ▪ Regulates blood, interstitial volume carbon dioxide) dissolve, diffuse across ▪ Filtration, reabsorption endothelial cell membranes ▪ Continuous fluid mixing between plasma, interstitial fluid BULK FLOW ▪ Passive water, nutrient movement across Types capillary wall down concentration gradient ▪ Filtration: bulk flow when moving from blood to interstitium ▪ Reabsorption: bulk flow when moving from interstitium to blood Other characteristics ▪ Kidney: major site of bulk flow where waste products are filtered out, nutrients reabsorbed ▪ Fluid filters out of capillaries into interstitial space (net filtration) at arteriolar end, reabsorbed (net reabsorption) at venous end ▫ Hydrostatic interstitial fluid pressure draws fluid into capillary ▫ Hydrostatic capillary pressure pushes fluid out of capillary ▫ Colloid interstitial fluid pressure pushes fluid out of capillary ▫ Colloid capillary pressure draws fluid into capillary MICROCIRCULATION ▪ Microcirculation: arterioles + capillaries + venules ▪ Arteriole blood flow through capillary bed, to venule (nutrient, waste, fluid exchange) ▫ Capillary beds composed of vascular shunt (vessel connects arteriole, venule to capillaries), actual capillaries ▫ Terminal arteriole → metarteriole → thoroughfare channel → postcapillary venule ▫ Precapillary sphincter: valve regulates blood flow into capillary ▫ Various chemicals, hormones, Figure 14.8 Key features of different blood vasomotor nerve fibers regulate amount vessel types. of blood entering capillary bed OSMOSIS.ORG 89  LYMPHATIC ANATOMY & PHYSIOLOGY osms.it/lymphatic-anatomy-physiology LYMPHATIC SYSTEM ▪ Carries particles away from inflammation sites/injury towards bloodstream, stopping Function first through lymph nodes that filter out ▪ Fluid balance harmful substances ▫ Returns leaked interstitial fluid, plasma ▪ Overlapping endothelial cells create valves; proteins to blood, heart via lymphatic prevent backflow, infectious spread vessels ▪ Lacteals: specialized lymphatic capillaries ▫ Lymph: name of interstitial fluid when in found in small intestine villi lymph vessels ▫ Carry absorbed fats into blood ▫ Lymphedema: lymph dysfunctional/ ▫ Chyle: fat-containing lymph absent (lymph node removal in cancer) → edema forms Larger lymphatics ▪ Immunity ▪ Capillaries → collecting vessels → trunks → ▪ Fat absorption ducts → angle of jugular, subclavian veins; right lymphatic duct empties into right Lymphatic capillaries angle, thoracic into left ▪ Collect interstitial fluid leaked by capillaries ▪ Collecting vessels have more valves, more ▪ Found in all tissues (except bone, teeth, anastomoses than veins marrow) ▫ Superficial collecting vessels follow ▫ Microscopic dead-ended vessels unlike veins blood capillaries, helps fluid remain ▫ Deep collecting vessels follow arteries inside ▪ Lymphatic trunks ▫ Usually found next to blood capillaries ▫ Paired: lumbar, bronchomediastinal, ▪ Lymph moves via breathing, muscle subclavian, jugular contractions, arterial pulsation in tight ▫ Singular: intestinal tissues Figure 14.9 Lymphatic vessels collect interstitial fluid (which is then called lymph) and return it to the veins. Lymphatic capillaries have minivalves that open when pressure in the interstitial space is higher than in the capillary and shut when pressure in the interstitial space is lower. 90 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology Figure 14.10 Lymphatic system structures and their locations in the body. ▪ Ducts ▫ Found in larger organs (lymph nodes)/ ▫ Upper right lymphatic drains right arm; individually (mucosa) right thorax; right side of head, neck ▫ Thoracic duct drains into cisterna chyli LYMPHOID ORGANS (a dilation created to gather all lymph drained from body area that’s not Spleen covered by upper right lymphatic duct) ▪ Largest lymphoid tissue in body ▪ Located below left side of diaphragm LYMPHOID CELLS ▪ Blood supplied by splenic artery; blood ▪ Lymphocytes: T subtype activate immune leaves spleen via splenic vein response; B subtype → plasma cells, ▫ Capsules with projections into organ, produce antibodies form splenic trabeculae ▪ Macrophages: important in T cell activation, ▪ Function phagocytosis ▫ Macrophages remove foreign particles, ▪ Dendrocytes: return to nodes from pathogens from blood inflammation sites to present antigens ▫ Red blood cell turnover ▪ Reticular cells: similar to fibroblasts; create ▫ Compound storage (e.g. iron) mesh to contain other immune cells ▫ Platelet/monocyte storage ▫ Blood reservoir: stores about LYMPHOID TISSUES 300mL/0.08gal ▪ Reticular connective tissue ▫ Fetal erythrocyte production ▪ Composition: macrophage-embedded ▪ Histology reticular fibers ▫ White pulp: lymphocyte, macrophage ▪ Loose islands that surround central arteries ▫ Diffuse lymphoid tissue ▫ Red pulp: composed mostly of red ▫ Venules enter, filters blood blood cells, macrophages; macrophages remove old red blood cells, platelets; ▫ Found in all organs splenic cords (reticular tissues running ▪ Dense between venous sinusoids) ▫ Follicles/nodules ▫ Mostly contain germinal centers OSMOSIS.ORG 91  Figure 14.11 In lymph nodes, dendritic cells present pieces of pathogens they come across to B cells. If a dendritic cell presents something foreign to a B cell, the B cell turns into a plasma cell and starts secreting antibodies, which flow into the lymph and exit the lymph node. Figure 14.12 Spleen location, histology. Lymph nodes ▪ Kidney-shaped formations ▪ Hundreds scattered throughout body, often ▫ Built like tiny spleens, 1–25cm/0.4–9.8in grouped along lymphatic vessels long ▫ Superficial, deep ▫ Covered by capsule with trabeculae, ▫ Many found in inguinal, axillary, cervical extend inward; trabeculae divide nodes regions sectionally ▪ Function ▪ Cortex ▫ Lymph filtration, immune system ▫ Subcapsular sinus, lymphoid follicle, activation germinal center 92 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ▪ Medulla Appendix ▫ Medullary cord, medullary sinus ▪ Worm-like large bowel extension ▪ Lymph flows through afferent lymphatic ▪ Contains numerous lymphoid follicles vessels → enters node through hilum → ▪ Fights intestinal infections subcapsular sinus → cortex → medullary sinus → exiting via efferent lymphatic vessels in hilum ▫ Fewer efferent vessels than afferent vessels, slows traffic down → allows node to filter lymphatic fluid ▪ Swollen painful nodes indicate inflammation, painless nodes may indicate cancer Thymus ▪ Located between sternum, aorta in mediastinum ▪ Two lobes, many lobules composed of cortex, medulla ▫ Cortex: T lymphocyte maturation site (immature T lymphocytes move from bone marrow to thymus for maturation) ▫ Medulla: contains some mature T lymphocytes, macrophages, cell-clusters Figure 14.13 Thymus location. called thymic corpuscles (corpuscles contain special T lymphocytes thought to be involved in preventing autoimmune disease) ▪ Lymphocyte production site in fetal life ▫ Active in neonatal, early life; atrophies with age Bone marrow ▪ B cells: made, mature in bone marrow ▪ T cells: made in bone marrow, mature in thymus Mucosa-associated lymphoid tissue (MALT) ▪ Lymphoid tissue that is associated with mucosal membranes ▪ Tonsils: lymphoid-tissue ring around pharynx Figure 14.14 Tubal, pharyngeal (adenoid), ▫ Have crypts (epithelial invaginations) palatine, and lingual tonsils create a which trap bacteria lymphoid-tissue ring around pharynx. ▫ Palatine: paired tonsils on each side of pharynx (largest tonsils, most often inflamed) ▫ Lingual: near base of tongue ▫ Pharyngeal: near nasal cavity (called adenoid when inflamed) ▫ Tubal: near Eustachian tube ▪ Peyer’s patches: small bowel MALT OSMOSIS.ORG 93  NORMAL HEART SOUNDS osms.it/normal-heart-sounds HEART SOUNDS S1 heart sound ▪ “Lub”: low-pitched sound Causes ▪ Marks beginning of systole/end of diastole ▪ Opening / closing cardiac valves ▪ Early ventricular contraction (systole) → ▪ Blood movement: into chambers, through ventricular pressure rises above atrial pathological constrictions, through pressure → atrioventricular valves close → pathological openings S1 ▪ S1: mitral, tricuspid closure WHERE ARE THEY HEARD? ▫ Intensity predominantly determined by ▪ By auscultating specific points individual mitral valve component, loudest at apex sounds can be isolated ▪ S1 (lub) louder, more resonant than S2 ▫ These points are not directly above (dub) their respective valves, but are where ▪ S1 displays negligible variation during valve sounds are best heard; however, breathing they generally map a representation of different heart chambers S2 heart sound ▪ Knowing normal heart size, auscultation ▪ “Dub”: higher-pitched sound locations allows for enlarged (diseased) ▪ Marks end of systole/beginning of diastole heart detection ▪ S2: semilunar valves (aortic, pulmonic) snap Optimal auscultation sites shut at beginning of ventricular relaxation (diastole) → short, sharp sound ▪ Aortic valve sounds: 2nd intercostal, right sternal margin ▪ Best heard at Erb’s point, 3rd intercostal space on left, medial to midclavicular line ▪ Pulmonary valve sounds: 2nd intercostal space, left sternal margin ▪ Splits on expiration ▪ Tricuspid valve sounds: 4/5th intercostal, left ▫ During expiration S2 split into earlier sternal margin aortic component; later, softer pulmonic component (A2 P2). Lower intrathoracic ▪ Mitral valve sounds: 5th intercostal space, pressure during inspiration → ↑ right midclavicular line (apex) ventricular preload → ↑ right ventricular systole duration → delays P2 NORMAL HEART SOUNDS ▫ ↓ left ventricular preload during ▪ Two sounds for each beat inspiration → shorter ventricular systole, ▫ Lub (S1), dub (S2) earlier A2 ▪ Factors affecting intensity ▫ A2, P2 splitting during inspiration ▫ Intervening tissue, fluid presence, usually about 40ms quantity ▫ A2, P2 intensity roughly proportional ▫ Mitral valve closure speed (mitral valve to respective systemic. pulmonary contraction strength) circulation pressures ▫ P2 best heard over pulmonic area 94 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology Figure 14.15 Valves that close to produce S1 and S2 sounds and optimal auscultation sites. ABNORMAL HEART SOUNDS osms.it/abnormal-heart-sounds ABNORMAL S1 drift towards each other before onset of systole Loud S1 ▫ Shorter PR interval → less time to drift ▪ As left ventricle fills, pressure increases closure → wider closure distance → ▪ As left atrium empties, pressure increases louder S1 as it empties against increasingly pressure- ▫ Short PR interval → incomplete loaded ventricle; as atrium approaches ventricular emptying → higher empty, pressure begins to decrease ventricular filling pressure → ventricular ▪ Differential diagnosis: short PR interval, pressure crosses critical atrioventricular mild mitral stenosis, hyperdynamic states valve closing threshold while atrial ▪ Short PR interval (< 120ms) pressures are still high → load snap ▫ Normally atrioventricular valve leaflets OSMOSIS.ORG 95  ▪ Mild mitral stenosis ventricle ▫ Significant force required to close stenotic mitral valve → large ABNORMAL S2 atrioventricular pressure gradient required Split S2 ▫ Slam shut with increased force, ▪ Physiological S2 splitting producing loud sound ▫ Expiration: S1 A2P2 (no split) ▪ Hyperdynamic states ▫ Inspiration: S1 A2....P2 (40ms split) ▫ Shortened diastole → large amount of ▪ Wide split ongoing flow across valve during systole ▫ Detection: splitting during expiration → leaflets wide apart, pressure remains ▫ Expiration: S1 A2..P2 (slight split) high ▫ Inspiration: S1 A2…....P2 (wide split) ▫ Results in forceful atrioventricular valve closure ▫ Differential diagnosis: right bundle branch block, left ventricle preexcitation, Soft S1 pulmonary hypertension, massive ▪ Differential diagnosis: long PR intervals, pulmonary embolism, severe mitral severe mitral stenosis, left bundle branch regurgitation, constrictive pericarditis block, chronic obstructive pulmonary ▪ Fixed split disease (COPD), obesity, pericardial ▫ Splitting during both expiration, effusion inspiration; does not lengthen during ▪ Long PR intervals (> 200ms) inspiration ▫ Atrium empties fully → low pressure ▫ Expiration: S1 A2..P2 (slight split) → low ventricular pressure required ▫ Inspiration: S1 A2..P2 (slight split) to close atrioventricular valves → ▫ Differential diagnosis: atrial septal valves close when ventricle is in early defect, severe right ventricular failure acceleration phase (low pressures) → ▪ Reversed split soft sound ▫ Split during expiration, but not ▪ Severe mitral stenosis inspiration ▫ Leaflets too stiff, fixed to change ▫ Expiration: S1 P2….A2 (moderate split) position ▫ Inspiration: S1 P2A2 Variable S1 ▫ Differential diagnosis: left bundle branch ▪ Auscultatory alternans block, right ventricle preexcitation, aortic ▫ When observed with severe left stenosis/AR ventricular dysfunction, correlate of Abnormal single S2 variants pulsus alternans ▪ Loud P2 ▪ Differential diagnosis: atrioventricular dissociation, atrial fibrillation, large ▫ Expiration: S1 A2P2 pericardial effusion, severe left ventricular ▫ Inspiration: S1 A2….P2! dysfunction ▫ Diagnosis: pulmonary hypertension ▪ Left ventricular outflow obstruction Split S1 ▫ Absent A2 ▪ S1 usually a single sound ▫ Expiration: S1 P2 ▫ Near-simultaneous mitral, tricuspid ▫ Inspiration: S1 P2 valve closures; soft intensity of tricuspid valve closure ▫ Diagnosis: severe aortic valve disease ▪ Splitting usually from tricuspid valve closure ▪ Fused A2/P2 being delayed relative to mitral valve ▫ Expiration: S1 A2P2 closure ▫ Inspiration: S1 A2P2 ▪ Differential diagnosis: right bundle ▫ Differential diagnosis: ventricular septal branch block, left-sided preexcitation, defect with Eisenmenger’s syndrome, idioventricular rhythm arising from left single ventricle 96 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ADDED HEART SOUNDS ▪ Auscultatory summary: S1... S2.S3… S1 S3 heart sound S4 heart sound ▪ S3 (ventricular gallop) ▪ S4 (atrial gallop): low pitched late diastolic ▫ Low-pitched early diastolic sound (pre-systolic) sound, best heard in mitral/ ▫ Best heard in mitral/apex region apex region, left lateral decubitus position ▫ Left lateral decubitus position ▪ Associated with hypertension, left ventricular hypertrophy, ischaemic ▪ Associated with volume overload cardiomyopathy conditions ▪ Pressure overload: thought to be caused by ▪ Early diastolic sound, produced in rapid atrial contraction into stiff / non-compliant filling phase → excessive volume filling ventricle ventricle in short period → rapid filling → chordae tendineae tensing → S3 sound ▪ Chronic heart contraction effort against increased pressure → hypertrophy → stiff ▪ Children/adolescents: may be normal ventricle (concentric hypertrophy) ▪ Middle aged/elderly person: usually ▪ Always pathological pathological ▪ Auscultatory summary: S4.S1...S2...S4.S1 ▫ Over 40 years old: indicative of left ventricular failure Figure 14.16 Linear representation of A: normal (S1, S2), B: S3, and C: S4 heart sounds. OSMOSIS.ORG 97  Summation gallop ▪ Location ▪ Superimposition of atrial, ventricular gallops ▫ Location on chest wall where murmur is during tachycardia best heard ▪ Heart rate ↑ → diastole shortens more than ▪ Radiation systole → S3, S4 brought closer together ▫ Location where murmur is audible until they merge despite not lying directly over heart ▫ Generally radiate in same direction as HEART MURMURS turbulent blood is flowing ▫ Aortic stenosis: carotid arteries Key features ▫ Tricuspid regurgitation: anterior right ▪ Blood flow silent when laminar, thorax uninterrupted ▫ Mitral regurgitation: left axilla ▪ Turbulent flow may generate abnormal ▪ Shape sounds (AKA “heart murmurs”) ▫ How sound intensity changes from ▪ Murmurs can be auscultated with onset to completion stethoscope ▫ Shape determined by pattern of Causes pressure gradient driving turbulent flow, ▪ May be normal in young children, some loudest segment occurring at time of elderly individuals greatest gradient (moment of highest velocity) ▪ ↓ blood viscosity (e.g. anaemia) ▫ Three basic shapes: crescendo- ▪ ↓ diameter of vessel, valve, orifice (e.g. decrescendo, uniform (holosystolic when valvular stenosis, coarctation of aorta, occurring during systole), decrescendo ventricular septal defect) ▫ Crescendo-decrescendo, uniform ▪ ↑ blood velocity through normal structures generally systolic; decrescendo murmurs (e.g. hyperdynamic states—sepsis, generally diastolic hyperthyroid) ▪ Regurgitation across incompetent valve (e.g. valvular regurgitation) Describing heart murmurs ▪ Specific language used to describe murmurs in diagnostic workup ▪ Timing: refers to timing relative to cardiac cycle ▫ Systolic “flow murmurs”: aortic, pulmonic stenosis; mitral, tricuspid regurgitation; ventricular septal defect; aortic outflow tract obstruction ▫ Diastolic: aortic, pulmonic regurgitation; mitral, tricuspid stenosis ▫ Continuous murmurs are least common, generally seen in children with congenital heart disease (e.g. patent ductus arteriosus, cervical venous hum) ▫ Occasionally may have two related murmurs, one systolic, one diastolic; gives impression of continuous murmur (e.g. concurrent aortic stenosis, aortic regurgitation) Figure 14.17 Three basic heart murmur shapes: crescendo-decrescendo, decrescendo, uniform/holosystolic. 98 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ▪ Pitch ▫ ↓ intrathoracic pressure → ↑ pulmonary ▫ High pressure gradients → high pitched venous return to right heart → ↑ right murmurs (e.g. mitral regurgitation, heart stroke volume → right sided ventricular septal defect) murmurs → ↑ intensity ▫ Large volume of blood-flow across ▫ Dilation of pulmonary vascular system low pressure gradients → low pitched → ↓ pulmonary venous return to left murmurs (e.g. mitral stenosis) side of heart → ↓ left heart stroke ▫ If both high pressure, high flow volume → left side murmurs → ↓ (severe aortic stenosis), both high, low intensity pitches are produced simultaneously ▪ Expiration → subjectively unpleasant/“harsh” ▫ ↑ intrathoracic pressure → ↓ venous sounding murmur return to right heart → ↓ right ventricle ▪ Intensity stroke volume → ↓ intensity of right ▫ Murmur loudness graded on scale from sided murmurs I–VI ▫ ↑ pulmonary venous return to left side ▫ Dependent on blood velocity generating → ↑ left ventricle stroke volume → left murmur; acoustic properties of sided murmur → ↑ intensity intervening tissue; hearing; examiner ▪ Valsalva maneuver experience; stethoscope used, ambient ▫ Forceful exhalation against closed glottis noise presence ▫ ↓ venous return to heart → ↓ left ▫ I: barely audible ventricular volume → ↓ cardiac output ▫ II: faint, but certainly present ▫ Murmurs of hypertrophic obstructive ▫ III: easily, immediately heard cardiomyopathy, occasionally mitral ▫ IV: associated with thrill (palpable valve prolapse → ↑ intensity vibration over involved heart valve) ▫ All other systolic murmurs → ↓ intensity ▫ V: heard with only edge of stethoscope ▪ Isometric handgrip touching chest wall ▫ Squeeze two objects (such as rolled ▫ VI: heard without stethoscope (or towels) with both hands without it making direct contact with ▫ Do not simultaneously Valsalva chest wall) ▫ If unconscious, simulate by transient ▪ Quality arterial occlusion (BP cuffs applied ▫ Subjective, attempt to describe timbre, to both upper arms, inflated to 20– depends on how many different base 40mmHg above systolic blood pressure frequencies of sound are generated, for 20 seconds) relative amplitude of various harmonics ▫ ↑ venous return, ↑ sympathetic tone → ▫ Mitral regurgitation: blowing/musical ↑ heart rate, systemic venous return ▫ Mitral stenosis: rumbling → ↑ cardiac output → murmurs from mitral regurgitation, aortic regurgitation, ▫ Aortic stenosis: harsh ventricular septal defect → ↑ intensity ▫ Aortic regurgitation: blowing ▫ Murmur from hypertrophic obstructive ▫ Still’s murmur (benign childhood): cardiomyopathy → ↓ intensity musical ▫ Murmur from aortic stenosis → most ▫ Patent ductus arteriosus: machine-like commonly unchanged Diagnostic maneuvers (dynamic ▪ Leg elevation auscultation) ▫ Lying supine, both legs raised 45° ▪ Some maneuvers may elicit characteristic ▫ ↑ venous return → ↑ left ventricular intensity/timing changes (changes in volume hemodynamics during maneuvers) ▫ Murmur from hypertrophic obstructive ▪ Dynamic auscultation: listening for subtle cardiomyopathy → ↓ intensity changes during physical maneuvers ▫ Murmurs from aortic stenosis, mitral ▪ Inspiration regurgitation may → ↑ intensity OSMOSIS.ORG 99  ▪ Müller’s maneuver ▫ Radiates to neck/carotids (murmur ▫ Nares closed, forcibly suck on incentive occurs in aorta, these are its first spirometer/air-filled syringe for 10 branches) seconds (conceptual opposite of ▫ Auscultatory summary: S1. Ejection Valsalva) click. Crescendo-decrescendo murmur. ▫ ↓ venous return → ↓ left ventricular S2 volume → ↓ systemic venous resistance ▪ Pulmonic stenosis murmur from hypertrophic obstructive ▫ Pulmonary valve auscultation site: 2nd myopathy → ↑ intensity intercostal space, left sternal margin ▫ Murmur from aortic stenosis may → ↓ ▫ S1, closing of tricuspid valve, during intensity systole ▪ Squatting to standing ▫ Heart contracts against closed pulmonic ▫ Abruptly stand up after 30 seconds of valve → pressure builds during systole, squatting forcing open stenotic pulmonic valve → ▫ ↓ venous return → ↓ left ventricular valve pops open → ejection click volume ▫ Flow rate increases as heart contracts ▫ Murmur from hypertrophic obstructive more forcefully to empty right ventricle cardiomyopathy → ↑ intensity → murmur gets louder as flow across ▫ Murmur from aortic stenosis may → ↓ partially open valve increases → intensity chamber empties → pressure, flow diminishing → ↓ murmur intensity ▪ Standing to squatting ▫ Radiates to neck/carotids, back ▫ From standing upright, squat down ▫ Auscultatory summary: S1. Ejection ▫ If unable to squat, examiner can click. Crescendo-decrescendo murmur. passively bend knees up towards S2 abdomen to mimic maneuver ▪ Mitral regurgitation ▫ ↑ venous return → ↑ left ventricular volume ▫ Mitral valve auscultation site: 5th intercostal space, midclavicular line/apex ▫ Murmur from hypertrophic obstructive cardiomyopathy → ↓ intensity ▫ Holo-/pansystolic murmur (occurs for systole duration) ▫ Murmur from aortic stenosis may → ↑ intensity ▫ Normal S1 as mitral valve closes → in mitral regurgitation, valve cannot ▫ Murmur from aortic regurgitation → ↑ completely close → pressure builds in intensity left ventricle (with closed aortic valve) Systolic murmurs → blood forced back through partially ▪ Aortic stenosis closed mitral valve → murmur occurs along with S1 as long as pressures ▫ Aortic valve auscultation site: 2nd remain high enough intercostal, right sternal margin ▫ Aortic valve will open to redirect ▫ S1, closing of mitral valve, during majority of blood → left ventricle systole → heart contracts against closed continues contracting → continuously stenotic aortic valve → pressure must raised pressures → blood continuously rise during systole to force open stenotic flowing through partially closed mitral aortic valve → valve pops open → valve (whole of systole) produces ejection click ▫ As heart continues to contract, pressure ▫ Followed by ↑ flow as heart contracts ↑, but atrium becomes more compliant. more forcefully to empty left ventricle Even though blood-flow across partially → murmur intensity ↑ as flow across closed valve may ↑, pressure in atrium partially open valve ↑ does not significantly increase ▫ Chamber begins to empty → pressure, ▫ Left ventricle pressure notably higher flow diminish → ↓ murmur intensity than left atrium → sound does not 100 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology change throughout murmur mitral regurgitation may follow ▫ Referred to as “flat” murmur because ▫ Auscultatory summary: S1. Mid systolic intensity does not change click with late systolic murmur. S2 ▫ Radiates to axilla due to direction of regurgitant jet Diastolic murmurs ▫ Auscultatory summary: S1. Flat ▪ Aortic regurgitation murmur. S2 ▫ Aortic regurgitation auscultation site: ▪ Tricuspid regurgitation left parasternal border ▫ Tricuspid valve auscultation site: 4/5th ▫ Blood flows back through incompletely intercostal, left sternal margin closed aortic valve ▫ Holo-/pansystolic murmur ▫ Occurs between S2, S1 ▫ Normal S1 occurs due to tricuspid ▫ S2, aortic valve closure → mitral valve valve closure → pulmonic valve closed, opens, heart in diastole → blood enters pressure rises in right ventricle left ventricle through regurgitant valve, through normal filling via mitral valve ▫ In tricuspid regurgitation, valve cannot completely close → pressure builds in ▫ Initially, low pressure in ventricle right ventricle → blood forced back out (compared to systemic blood pressure through partially closed tricuspid valve forcing blood through regurgitant valve) → murmur is continuous as long as → ventricle fills → as pressure mounts, pressures remain high enough less flow through regurgitant valve → decrescendo murmur ▫ Pulmonic valve opens to redirect blood → left ventricle maintains contraction ▫ Early diastolic decrescendo murmur (thus raises pressure) → blood ▫ Auscultatory summary: S1. S2. Early continues flowing through partially diastolic decrescendo murmur. S1 closed tricuspid valve (through whole ▪ Pulmonic regurgitation systole) ▫ Pulmonic regurgitation auscultation ▫ Arium becomes more compliant as it fills site: upper left parasternal border → atrium pressure does not significantly ▫ Blood flows back through incompletely increase closed pulmonic valve ▫ Right ventricle pressure notably higher ▫ Occurs between S2, S1 than that of right atrium → murmur ▫ S2 aortic valve closure → tricuspid valve sound does not change throughout opens, heart in diastole → incomplete murmur pulmonic valve closure → right ventricle ▫ Referred to as “flat” murmur (intensity fills via incompletely closed pulmonic does not change) valve as well as tricuspid valve ▫ Auscultatory summary: S1. flat murmur. ▫ Initially → low ventricle pressure allows S2 for high flow through regurgitant ▪ Mitral valve prolapse valve → pressure rises, ↓ flow through ▫ Mitral valve auscultation site: 5th regurgitant valve → decrescendo intercostal space, midclavicular line/apex murmur ▫ Mitral valve billows into left atrium → ▫ Early diastolic decrescendo murmur clicking sound (unlike aortic stenosis, ▫ Auscultatory summary: S1. S2. Early not associated with ejection of blood, diastolic decrescendo murmur. S1 non-ejection click, mid-late systolic) ▪ Mitral stenosis ▫ Ventricle contracts → mitral valve ▫ Mitral valve auscultation site: 5th closure → S1 → pressure rises → intercostal space, midclavicular line/apex mitral valve accelerates into left atrium ▫ Mitral valve can’t open efficiently → stops abruptly (chordae tendineae ▫ S2 → aortic valve closure → restraint) → rapid tensing → click milliseconds later, mitral valve should ▫ Often associated with mitral open (fill ventricle during diastole), only regurgitation → after click murmur of small opening occurs OSMOSIS.ORG 101  Figure 14.18 Causes of systolic murmurs. 102 OSMOSIS.ORG  Chapter 14 Cardiovascular Physiology: Cardiovascular Anatomy & Physiology ▫ Beginning of diastole, highest flow of blood comes from left atrium to left ventricle (rapid filling), fills more blood at beginning of diastole (beginning due to highest pressure difference) → most intense phase of murmur ▫ Aortic valve closure → mitral valve opens, due to stenotic leaflets, they can only open slightly → chordae tendineae snap as limit is reached Figure 14.19 Diastolic murmurs are heard as (similar to ejection snap) → opening a “whoosh” after S2. snap from stenotic leaflets shooting open (milliseconds after S2) → highest intensity of murmur thereafter Murmur Identification → murmur diminishes as pressure ▪ Detect murmur? equalises ▫ Yes/no ▫ End of diastole atrium contracts to ▪ Identify phase? force remaining blood into left ventricle ▫ Systolic/diastolic: S1 -systole- S2 → atrial kick sound (presystolic -diastole- S1 (in tachycardia, feel pulse accentuation at end of murmur) → tapping → ejection phase, therefore ▫ Auscultatory summary: S1. S2. Opening S1) snap. Decrescendo mid diastolic rumble. ▪ Which valves normally open/which valves Atrial kick. S1 normally closed ▪ Tricuspid stenosis ▫ Systole, aortic and pulmonic, open ▫ Tricuspid valve auscultation site: 4/5th (mitral and tricuspid, closed) intercostal space, left sternal margin ▫ If systolic murmur, either open valves ▫ Tricuspid valve can’t open efficiently stenotic/closed valves regurgitant (1/4 ▫ S2 → pulmonic valve closure → choice) milliseconds later, tricuspid valve should ▫ Diastole, mitral and tricuspid, open open (fill ventricle during diastole), only (aortic and pulmonic, closed) (1/4 small opening occurs choice) ▫ Beginning of diastole, high flow of ▪ To choose between four resultant options blood comes from right atrium to right auscultate over respective areas, employ ventricle (rapid filling), fills more blood maneuvers as required at beginning of diastole (due to highest pressure difference) → most intense murmur phase MISCELLANEOUS HEART SOUNDS ▫ Pulmonic valve closure → tricuspid ▪ Mechanical valve clicks valve opens (due to stenotic leaflets, ▫ Distinctly audible, harsh, metallic sound they can only open slightly) → chordae ▪ Pericardial knock tendineae snap as limit is reached ▫ Sound occasionally heard in constrictive (similar to ejection snap) → opening pericarditis; similar in acoustics, timing snap from stenotic leaflets shooting to S3 open (milliseconds after S2) → highest ▪ Tumor plop murmur intensity thereafter → murmur diminishes as pressures equalise ▫ Rare low-pitched early diastolic sound, occasionally heard in atrial myxoma ▫ End of diastole atrium contracts to presence force remaining blood into left ventricle → atrial kick sound (presystolic ▫ Occurs when relatively mobile tumour accentuation at end of murmur) moves in front of mitral valve during diastole → functional mitral stenosis ▫ Auscultatory summary: S1. S2. Opening along with low pitched diastolic snap. Decrescendo mid diastolic rumble. rumbling murmur Atrial kick. S1 OSMOSIS.ORG 103