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53 Cards in this Set
- Front
- Back
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Mechanical Events of the Cardiac Cycle |
The heart alternately contracts to empty and reacts to fill - systole and diastole -mid-. late and end ventricular diastole |
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Cardiac Output |
- measure of Cardiac performance - CO= HR x SV - HR controlled by ANS - changing HR is fastest way to change CO - SV remains constant |
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parasympathetic stimulation on HR |
slows HR |
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sympathetic stimulation on HR |
speeds it up |
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CO depends on... |
- heart rate - stroke volume |
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Regulators of the heart: sympathetic neurons |
-NE - integrating center: cardiovascular control center in medulla oblongata - efferent path: sympathetic neurons (NE) - Effector: B1 receptors of auto rhythmic cells - Tissue response: increased Na+ and CA2+ influx - Tissue response: increased rate of depolarization - Tissue response: increased HR |
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Regulators of the heart: parasympathetic neurons |
- Ach - integrating center: cardiovascular control center in medulla oblongata - efferent path: parasympathetic neurons (Ach) - Effector: muscarinic receptors of auto rhythmic cells - Tissue response:increased K+ efflux and decreased CA2+ influx - Tissue response: hyper polarizes cell and decreases rate of depolarization - Tissue response: decreased HR |
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Extrinsic regulation via autonomic innervation of the heart: Sympathetic |
- assymetric innervation leads to different response of LV (contraction) and RV (rate) - beta receptors (cAMP/G-protein) - slow (over many beats) time course - slow release of NE - second messenger system (adenylyl cyclase) - slow re-uptake of NE |
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Extrinsic regulation via autonomic innervation of the heart: Parasympathetic |
- muscarinic receptor, blocked by atropine - fast (beat by beat) time course - direct action on K channels - suppress second messenger systems - cholinesterase |
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SA node effect of parasympathetic stimulation |
decreases the rate of depolarization to threshold - decreased the HR |
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SA node effect of sympathetic stimulation |
- increases the rate of depolarization to threshold - increases the HR |
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AV node effect of PNS |
- decreases excitability - increases the AV nodal delay |
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AV node effect of SNS |
- increased excitability - decreases the AV node delay |
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ventricular conduction pathway- PNS |
- no effect |
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Ventricular conduction pathway- SNS |
- increases excitability
- hastens conduction through th bundle of His and Purkinje cells |
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Atrial muscle- PNS |
- decreases contractility - weakens contraction |
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Atrial muscle- SNS |
- increases constractility - strengthens contraction |
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Ventricular muscle- PNS |
- no effect |
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Ventricular muscle- SNS |
- increases contractility - strengthens contraction |
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adrenal medulla- PNS |
no effect |
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adrenal medulla- SNS |
- promotes secretion of epinephrine |
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epinephrine |
a hormone that augments sympathetic nervous system actions |
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veins- PNS |
no effect |
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veins- SNS |
increases venous return, which increases the strength of cardiac contraction via intrinsic control |
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Effects of Epiniephrine on HR |
- positive chronotype - secreted by the adrena medulla in response to sympathetic activation - increases HR - stimulation of SA nodal beta receptors - increase rate of spontaneous depolarization- increase HR - increase conduction velocity through AV node and other parts of the conduction system- decrease duration of systole |
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adrenocortical steroids- effect on HR |
positive inotropic but mechanism unclear |
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thyroid hormones- T3 and T4 effect on HR |
- increases rate and contractility - effects both direct and indirect via sympathetic |
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insulin effect on HR |
positive inotropic - mechanism unclear |
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pituitary hormones effect on HR |
- generally positive inotropic - combined effect with other hormones |
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positive chronotrope |
- sympathetic stimulation - stimulation of SA nodal beta receptors increase rate of spontaneous depolarization ---> increase HR - increase conduction velocity through AV node and other parts of conduction system --> decrease duration of systole |
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negative chronotrope |
- parasympathetic stimulation - stimulation of SA nodal muscarinic receptors ---> decrease rate of spontaneous depolarization --> decreases HR - decrease conduction velocity through AV node and other parts of the conduction system ---> increase duration of systole |
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Stroke Volume |
- determined by extent of venous return and by sympathetic activity - influenced by two types of controls - intrinsic control- preload and afterload - extrinsic control - both factors increase stroke volume by increases strength of heart contraction |
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3 variables SV is regulated by |
- EDV (preload) - contractility (strength of contraction) - total peripheral resistance (after load) |
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variables affecting contractility |
- starling's law of the heart (intrinsic control) - sympathetic nervous system (extrinsic control) - normall, strength of contraction is sufficient to about 70-80 ml/beat out of total EDV of 110-120 ml - ejection fraction about 60% |
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extrinsic chronotropic factors or Chronotropes |
- have an effect on HR - pacemaker potential - conduction velocity |
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extrinsic and intrinsic inotropic factors or Inotropes |
- have an effect on SV - contractility - force of ventricular contraction |
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Controlling SV |
- increased end-diatomic volume results in increased SV - intrinsic control of stroke volume: heart's inherent ability to vary SV - Frank-Starling law of the heart: intrinsic relationship between EDV and SV - advantages and mechanism of the cardiac length-tension relationship |
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contractility |
- strength of contraction at any given EDV |
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sympathetic stimulation and contractility |
increases contractility of the heart |
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factors affecting SV and cardiac output |
-SV can be graded by varying the initial length of the muscle fibers and varying the extent of sympathetic stimulation |
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Frank-Starling law of the hear |
- heart normally pumps out during systole the volume of blood returned to it during diastole - describes the relationship between the EDV and stroke volume |
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intrinsic factors that affect SV |
- ventricular contractility - EDV - afterload |
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ventricular contractility affecting SV |
- increases contractility --> increases ejection fraction - increases sympathetic activity --> increased contractility - increased Epinephrine --> increased contractility - sympathetic activity and epinephrine are positive inotropes |
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EDV affecting SV |
- Starling's Law of Heart - increased EDV--> increased ventricular contraction force |
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after load affect SV |
increased afterload --> increased end systolic volume |
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What can cause EDV to increase? |
- decrease HR--> increased filling time --> increased venous return --> increased atrial pressure - increase central venous pressure --> increased venous return --> increased atrial pressure - atrial contraction --> increased atrial pressure |
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High blood pressure |
- increases the workload of the heart - after load: workload imposed on the heart after contraction has begun - sustained extra workload placed on the heart can eventually cause pathological changes in the heart that lead to heart failure |
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Heart failure |
- failing heart cannot pump out enough blood - inability of CO to keep pace with the body's demands for supplies and removal of wastes - systolic and diastolic - defect in systolic heart failure - prime defect is decreased cardiac contractility |
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Parameters of the healthy heart |
- EDV= (110-130mL) - ESV= 40-50mL - SV= EDV- ESV (70 mL) - ejection fraction= 50-65% - CO= 5-35l/min |
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EDV |
- end diastolic volume - volume of blood in ventricle at end of diastole |
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ESV |
- end systolic volume - volume of blood in ventricle at end of systole |
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Ejection fraction |
- fraction of end-diastolic volume ejected in a single heart beat - Ef= SV/EDV |
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Cardiac index (CI) |
- vasodynamic parameter that relates the CO to body surface area (BSA) thus relating heart performance to the size of the individual. - l/min/m2 -normal range= 2.6-4.2 L/min per square meter - CI= CO/BSA= SV*HR/BSA |
