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40 Cards in this Set
- Front
- Back
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How are skeletal and cardiac mm similar
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striated
sliding filament mechanism requires Ca++ inc sodium leads to action potential |
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How is cardiac mm unique to skeletal mm?
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short, fat, branched and interconnected. 1-2 nuclei
~1% - conduction cells |
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How is membrane repolarization achieved in cardiac mm
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Return of Ca++ and K+ permeability to normal (not Na+ returning to its normal permeability)
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How does cardiac mm avoid tetany?
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An increased refractory period
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Define mid-late diastole
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AV valves are open, Aortic and pulmonary (A/P) valves are closed, ventricles are filling. P increases in atria and ventricles and decreases in the aorta. At the end of diastole SA node fires and atria depolarize and contract, delivering the residual blood out of the atria into the ventricles. At this point the blood in the ventricles = end-diastolic volume (EDV)
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Define Ventricular systole
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Isovolumetric contraction - as P in ventricles increases AV valves close. A/P valves remain close for a moment and ventricular P rises.
Ventricular contraction/Ejection - A/P valves are forced open as vent P exceeds that of great vessels. Blood moves into aorta and pulmonary trunk. Blood remaining in ventricles is End-systolic volume (ESV) |
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Define Early Diastole
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Druing the brief phase following repolarization, ventricles relax and ventricular P goes down (quickly). A/P valves close, AV valves still closed. P in atria quickly exceeds and AV valves open. Cycle starts again
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What is the S1 heart sound (Lub)
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AV vaves closing in early systole
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What is the S2 heart sound (Dub)
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A/P valves closing in early diastole.
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What is P wave
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Ventricular filling/atrial contraction, AV valves open (1st part of Diastolic)
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What is QRS
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Isovolumetric ventricular contraction
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What increases heart contractility
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Enhanced Ca++ influx into the cytoplasm from extracellular fluid and SR
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What hormones increase heart contractility
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Norepinephrine and Epinephrine
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What makes a more forceful cardiac contraction according to Starling Forces
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Greater EDV, greater stretch
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Cardiac Out Put =
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CO = Stroke volume X Heart Rate
Amount of blood pumped out by each ventricle in 1 min. |
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What can change force of contraction of the heart?
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1. Increase EDV/inc heart stretch - inc volume or speed of venous return
2. Sympathetic stimulation |
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What effect does the PNS have on the SA node?
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decreases intrinsic rate of SA not at rest
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What effect does the SNS have on the SA node?
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increase in rate in times of stress
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What effects do thyroid hormones have on the heart?
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slower, more sustained increase in HR and enhance the effect of Epi and NE on the heart
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What are the two autocrine transmitters that alter coronary artery resistance in response to O2 demand?
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Adenosine and Nitric Oxide
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What is functional sympatholysis?
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The vasodilating effect that SNS stimulation has on the heart:
1. SNS stimulated by stressor 2. alpha 1 receptors activated - vasoconstriciton (short lived) 3. Local production of nitric oxide - activate beta-1 adrenergic recptors - vasodilation |
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What increases heart contractility
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Enhanced Ca++ influx into the cytoplasm from extracellular fluid and SR
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What hormones increase heart contractility
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Norepinephrine and Epinephrine
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What makes a more forceful cardiac contraction according to Starling Forces
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Greater EDV, greater stretch
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Cardiac Out Put =
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CO = Stroke volume X Heart Rate
Amount of blood pumped out by each ventricle in 1 min. |
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What can change force of contraction of the heart?
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1. Increase EDV/inc heart stretch - inc volume or speed of venous return
2. Sympathetic stimulation |
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What effect does the PNS have on the SA node?
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decreases intrinsic rate of SA not at rest
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What effect does the SNS have on the SA node?
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increase in rate in times of stress
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What effects do thyroid hormones have on the heart?
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slower, more sustained increase in HR and enhance the effect of Epi and NE on the heart
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What are the two autocrine transmitters that alter coronary artery resistance in response to O2 demand?
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Adenosine and Nitric Oxide
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What is functional sympatholysis?
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The vasodilating effect that SNS stimulation has on the heart:
1. SNS stimulated by stressor 2. alpha 1 receptors activated - vasoconstriciton (short lived) 3. Local production of nitric oxide - activate beta-1 adrenergic recptors - vasodilation |
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what effect does nitric oxide have on the heart?
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Vasodilatation of the coronary vessels
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What effect does SNS have on the heart coronary vessels
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Transient vasoconstriction by activating alpha-1 adrenergic receptors. (endogenous nitric oxide is the produced to vasodialate area)
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What effect does PNS have on the heart coronary vessels
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Moderate vasodilatation, if blood flow exceeds O2 demand local autoregulation induces vasoconstriction.
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What are the layers of blood vessels?
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Lumen --> Tunica intima -> Tunica media --> Tunica adventitia
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Tunica intima
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inner most layer of blood vessels - comprised of endothelium, larger vessels have a layer of connective tissue as well.
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Tunica media
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middle layer of the blood vessels. Smooth mm and elastin
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Tunica adventitia
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Outer most layer of blood vessels. Loosely woven collagen fibers - protect and anchor vessels, keep from over stretching. Larger vessels - contains vasa vasorum - nn fibers, lymph, tiny blood vessels.
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P of Pulmonary circulation
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Low resistance, low pressure, little control
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P of systemic circulation
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high resistance, high pressure and many control systems
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