Lecture 2 Flashcards
Explain preload or EDV.
end-diastolic volume (EDV) or preload is the amount of stretch on the myocardial wall prior to contraction, in a normal health adult.
Explain Contractility.
Intrinsic control of contraction strength in relation to EDV.
Extrinsic control of contraction depends on the activity of the sympathoadrenal system.(Epinephrine from adrenal an NE from sympathetic nerve endings.)
Explain afterload.
Pressure against which the ventricle must work in order to eject blood = pressure resisting the ejection of blood during systole.
Identify the general differences between cardiac, skeletal and smooth muscle.
Skeletal - voluntary, not self stimulating, have motor units, under nervous system control, striated appreaence, able to stretch and return to original shape, fast contracting, multi-nucleatd.
Smooth - involuntary, unstriated, found in walls of hollow organs (stomach, esophagus, bronchii, blood vessels) slow cycle (prolonged contraction) of myosin/actin cross bridging, low energy requirement, maximum force of contraction is often greater than in skeletal.
Cardiac - wall of heart (3 types = atrial, ventricular, specialized excitatory and conductive), also striated, under nervous/endocrine/chemical control, resistant to fatigue, branching chains w/single nuclei, self stimulating (impulse spread from cell to cell)
Normal values of cardiac output (CO).
CO (L/min) = HR (bpm) x SV (L)
Normal resting CO = 4-8 L/min (with resting HR of 70bpm; resting SV of 71 ml/beat)
Explain the difference between CO and Cardiac index (CI).
CI = CO/BSA
Normal CI range = 2.6 - 4.2 L/min/m^2
CI expresses the CO in relations to body surface area (BSA), provides more complete CO, more exact measurement of blood flow.
Explain how HR is regulated in a person who is healthy.
Normal resting HR = 60-100 bpm Chronotropic effects (alter cardiac rate) - positive chronotropic: epinephrine (adrenal) and norepinephrine (sympathetic) & negative chronotropic: acetylcholine (vagus n./parasympathetic) Sympathetic effects - vasodilate coronary arteries to incr blood flow to heart or increase myocardial contraction. Parasympathetic effets - vasoconstriction coronary arteries or depress myocardial contraction.
Explain how SV is regulated in a health adult (preload, contractility, afterload).
(preload) Frank Starling Mechanism - intrinsic property of heart muscle to include SV based on pre contractile myocardial cell length. The force of contraction increases as blood volume increases (in left ventricle). AKA amount of stress on the myocardial wall, healthy heart reacts to this stress, diseased hearts don’t.
(contractility) Epinephrine from adrenal and NE from sympathetic nerve endings produce positive effects and increase myocardial contractility. Reduction of sympathetic stimulation and reduced HR will reduce contractility.
(afterload)Pressure against which the ventricle must work in order to eject blood = pressure resisting the ejection of blood during systole. Hypertension results in increase in afterload.
Increase in afterload causes decreased SV.
Decrease in afterload causes an increase in SV.
Explain physiologic response in heart contractility in a diseased heart.
In a normal heart, there is a linear relationship between myocardial oxygen consumption (MVO^2) and coronary blood flow, but not in a diseased heart.
Any increase in HR and/or BP will increase MVO^2.
Problems include inability of myocardial cells to extract oxygen from arterial blood, decreased oxygen carrying capacity of arterial blood, and impaired delivery of oxygenated blood through coronary arteries.
Known factors influencing contractility/inotropism
Positive inotropic influences - increase sympathetic tone, and endogenous catecholamines. digitalis, sympathetic amines, increase HR, glucagon, angiotensin, aldactone, corticosteroids, hyperthyroidism, serotonin.
Negative inotropic influences - Beta blockers, calcium antagonists barbiturates, acidosis, hypoxia, general anesthesia, anti-arrhythmic agents, heart failure, decreased function ventricle muscle mass & myocardial oxygen demand, circulating myocardial depressant facts.
Define ejection fraction and values in a healthy adult.
EF = SV/EDV
Normal EF = 60-70%
Definition EF = % of ventricular filling that is ejected with each heart beat.
Explain the factors that affect CO
Heart Rate - intrinsic great of pacemaker function (SA), balance of SNS & PNS stimulation, levels of circulating catecholamines and other substances.
Stroke Volume - increase preload = increase SV: active atrial contraction, HR, venous blood return, total blood volume & state of hydration, ventricular compliance.
Afterload - increase afterlaod = decrease SV: total peripheral resistance, aortic compliance, EDV & SV, blood viscosity, presence of outflow obstruction.
Contractility - increase contractility = increase SV: affected by positive & negative inotropic factors.
Explain ventricular compliance.
Ease to which the ventricle distends when filling with blood. Decreased compliance (stiff ventricles or hypotrophy): a given volume of filling will result in a higher EDV. Increased compliance (dilation): a given volume will effect a lower EDV.
