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743 Exam 3 - Heart

Lecture Terms for Heart

TermDefinition
Myocardial Infarction Dead cardiac tissue --> pinkish. Area infiltrated by neutros, lymphs, macros. Tissue eventually becomes granulated.
Cardiac Cycle Passive filling --> AV valves open. Atrial contraction --> top off tanks. Isovolumetric ventricular contraction --> all valves closed. Ventricular ejection --> semilunar valved open. Isovolumetric ventricular relaxation --> all valves closed.
Stroke Volume (SV) Amount of blood pumped per beat. End diastolic vol (EDV) - end systolic vol (ESV).
Increased Preload ↑ EDV. ↑ SV. Slightly increases ESV.
Decreased Preload ↓ EDV. ↓ SV. Slightly decreases ESV.
Preload Degree of myocyte stretch prior to ventricular contraction. Changed by venous pressure, HR, aortic pressure, atrial contractility, ventricular compliance.
Afterload Force or load that ventricular contraction must work against (to eject blood). Changed by changes in aortic diastolic pressure, resistance.
Increased Afterload ↑ EDV. ↓ SV. Slightly increases ESV.
Decreased Afterload ↓ EDV. ↑ SV. Slightly decreases ESV.
Causes of Changed Afterload HTN, aortic stenosis, drugs that alter systemic resistance.
Causes of Changed Preload Ventricular failure, valve stenosis, arrhythmias.
Inotropy Degree of myocyte contractility, or force generation. Changed by Ca2+ balance, HR, sympathetic activity, adrenergic agents.
Increased Intropy ↓ EDV & ESV. ↑ SV and EF.
Ejection Fraction (EF) EF = SV / EDV.
Decreased Intropy ↑ EDV & ESV. ↓ SV and EF.
Causes of Changed Intropy Exercise training, ischemia/infarct, arrhythmias, heart failure, inotropic drugs (digitalis).
Laminar Flow Parallel movement of blood layers. All RBCs moving in same direction. Centerline velocity is highest.
Turbulent Flow Neither parallel nor layered. Whirls/eddie currents created by incomplete valve closure. Not necessarily random. Can be used to identify murmors.
Cardiac Output (CO) Volume of blood pumped by each ventricle/min. Normally the same for pulmonary and systemic circulations. CO = HR x SV
Resting CO 5 L/min
Exercise CO ~20-25 L/min. SV is maximal at ~50% of capacity.
At Rest Parasympathetic NS dominates.
Exercise Sympathetic recruitment. Parasympathetic withdrawn.
Epinephrine Also influences HR and SV. Secreted from adrenal medulla.
Intrinsic Control Venous blood return. Length-tension relationship. Frank-Starling Law of the Heart.
Extrinsic Control Via sympathetic nerve activity. Increases HR and SV.
Frank-Starling Curve Increased venous return = increased SV.
Frank-Starling Curve Functions Matches left and right heart SV. Immediately accommodates increased CO.
Frank-Starling Curve Mechanism Stretching reduces space b/n myofilaments. Increases cross-bridge binding sites.
Frank-Starling Curve: Sympathetic Influence Increased Ca2+ influx into the myocyte. Stimulates venous constriction. Stimulates adrenal medulla to secrete E.
Heart Failure Inability of heart to match CO w/ collective organ demands.
Heart Failure Causes Ischemia, infarction, stenotic valve, HTN.
Heart Failure Compensation Sympathetic stimulation. Renal sodium retention.
Cardiac Myocytes ~40% of volume = mitochondria. Elevated myoglobin = can store limited amounts of O2.
Coronary Blood Flow Majority occurs during diastole. Remaining ~30% occurs during systole.
Heart Attack Severity depends on location of clot. Collateral circulation can offset severity.
Infarction Outcomes Immediate death, delayed death, functional recovery, impaired recovery (cardiac invalid).
Plaque Bulging Interrupts paracrine signaling (NO). Disrupts nutrient exchange. Impairs/compromises vasodilation.
Angina Pectoris Myocardial ischemia. Nitroglycerin offsets by dilating coronary arteries.
Created by: liviticus
 

 



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