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CH.18 Heart (Diseases (Pericardial effusion: abnormal increases in…
CH.18 Heart
Diseases
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mitral valve prolapse: disorder with excessively “floppy” bicuspid valve; incr flexibility prevents the valve from closing properly, leading to backflow of blood
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Occlusion/blockage of the coronary circulation is a charac of coronary artery disease; in the left anterior descending artery is commonly referred to as the “widow maker” because of its extremely low survival rate
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Atrial cells will continue to be paced by the SA node, and ventricular cells by the purkinje fibers, but without the AV node to conduct the signals through the septum the two processes uncoupled.
Cardiac arrhythmias characterized by abnormal electrical activity within the heart that often lead to changes in pumping activity
fibrillation = fast, spastic depolarization of the myocardium, localized to the atria (atrial fibrillation) or ventricles (ventricular fibrillation)
heart murmurs = abnormalities in heart sounds & most commonly occur due to incomplete closure of valves
Basics
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Multi-layer organ
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Myocardium: thickest layer w/ myocytes in concentric pattern + cardiac skeleton (= electrical insulator)
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Left versus right
Right side: pulmonary circulation that pumps deoxygenated blood to the heart & returns oxygenated blood to heart
Left side: systematic circulation that pumps oxygenated blood to body & returns deoxygenated blood to heart
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Cardiac Muscle
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Intercalated discs (fusions in sarcolemmas) so no recruitment -> syncytium = single coordinated function through desmosomes & gap junctions
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Types of cells
Pacemaker
Ectopic Pacemakers: in response to changes in ion concentrations that alter HCN channels, histological changes, or failure SA node
Source of autorhythmicity: non-contractile cells that form intrinsic conduction system of heart & spontaneously generates AP & propagates through heart
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cycles
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Cardiac Cycle
Early ventricular systole & atrial diastole follow atrial systole: ventricles (myocytes here) contract + vol decr + isometric/isovolumetric + pressure > atrial but less than major vessels
Late ventricular systole (ventricular systole II) : pressure now more than major vessels + SL valves open + isotonic + also called ejection phase
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Regulation IDKKK
Extrinsic
Parasympthetic through vagus nerve from brainstem in cardioinhibitory center -> preganglionic fibers innervate postganglionic parasympathetic cells in heart wall ->
postganglionic fibers send axons to the SA and AV nodes, coronary blood vessels, and atrial myocardium -> stimulation has a general inhibitory effect : blocking parasympathetic connections to the heart (physically or pharmacologically) induces tachycardia (increased heart rate).
Sympathetic through sympathetic nerves & mass discharge of epinephrine and norepinephrine from adrenal medulla (flight or fight) in cardioacceletory
preganglionic fibers (originally in spinal cord thoracic region) -> stim postganglionic cells in inferior cervical and superior thoracic ganglia
B1-adrenergic receptors = G-coupled receptors lead to generation cAMP -> effects Protein Kinase A (PKA) -> PKA alters intracellular proteins with phosphorylation -> incr strength of cardiac contraction bc: phosphorylates L-type Ca channel (incr conductance) + phosphorylation ryanodine receptor (incr open) + phosphorylation of troponin C (incr Ca sensitivity) + phosphorylation regulatory protein phospholamban (PLB) (incr activity SERCA)
in pacemakers: cAMP incr speed cardiac contraction thro: incr conduction thro HCN channels (which are gated by cyclic nucleotides like cAMP) & accelerate pacemaker potential + phosphorylate L and T type Ca channels so incr conductance
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heart rate incr -> less time for the heart to fill during atrial diastole, decreasing the EDV, preload, and stroke volume. overall incr in cardiac output, heart rate incr at the expense of stroke volume
effects mediated by acetylcholine, the parasympathetic postganglionic neurotransmitter -> works thro muscarinic receptors on the myocardium. Bc no innervation of ventricular contractile myocytes, the parasympathetic nervous system little impact on contractility.
exerts its effects primarily on pacemaker cells in the atria-> decr speed of cardiac contraction through: Incr conductance through ligand gated potassium channels, efflux of K acts to hyperpolarize SA node cells, moving them closer to the equilibrium potential for potassium, which makes pacemaker potential more difficult to form + Decr cAMP decreases conductance through HCN channels
Strong parasympathetic inhibition of the heart decr heart rate but has little effect on stroke volume. If venous return remains constant during parasympathetic inhibition, the stroke volume will incr, occurs because of increased preload (recall the Frank-Starling Law of the heart)
Intrinsic
venous return = amt blood passively enters heart during diastole
preload = incr in venous return -> incr in EDV -> ventricles stretch
afterload = additional force generated by ventricle to overcome diastolic pressure in aorta AKA how much effort by heart to eject blood; how resistance opposes flow
Frank Starling Law = force of cardiac muscle contraction proportional to resting length of its fibers -> max cross-bridge formation -> incr Ca release
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