Term
| cardiac output definition |
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Definition
| the volume of blood flowing through either the systemic or pulmonary part of the cardiac cycle, HR x SV, L/min, normal ~5L/min at rest |
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Term
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Definition
| the amount of blood ejected from the ventricle, at 5L/min and 60bpm would be 0.083 L per heartbeat |
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Term
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Definition
| the amount of blood left over after ventricular contraction, bc there is an ejection fraction (amnt of blood pumped out) and only 50-70% of the blood in the ventricle is pumped out. can measure these volumes by echocardiogram, reduction indicates some type of heart failure where the heart isn't functioning |
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Term
| things that can affect cardiac output |
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Definition
| HR, SV- contractility, preload and afterload |
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Term
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Definition
| how fast your heart is beating and with what strength (inotropic property of the heart) |
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Term
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Definition
| how much pressure is on the heart muscle from the filling of the ventricle, amount of blood influences contractility (Frank-Starling relationship). pressure generated at the end of diastole or at the end of ventricular filling (ventricular end diastolic pressure) primarily left but also right. determined by 2 factors: the amount of venous return to the ventricle and the amount of blood that was left in the ventricle after the last beat or the end systolic volume. it this gets too high can cause muscle stretching and decline in cadiac function, so buildup of blood can lead to worse pumping of the heart |
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Term
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Definition
| the resistance, once the heart beats and pumps out blood, how much resistance is it meeting traveling through the vasculature. the resistance to ejection that occurs during systole. high BP can cause inc peripheral resistance and high afterload which pushes back on the heart and can reduce ejection fraction. w dec afterload the heart contracts more rapidly and pumps more bc this is a sign that not enough blood is getting to the periphery. inc afterload can slow the contractions and make the workload higher and lead to damage of the heart muscle and loss of function |
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Term
| Frank-Starling relationship says |
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Definition
| the volume of blood at the end of diastole determines the amount of stretch of the cardiac muscle and the amnt of stretch influences the strength of myocardial contraction, inc blood inc contraction- inotropic effect. pos effect w more fluid, neg effect w less fluid |
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Term
| factors that can change stroke volume |
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Definition
| the force of contraction/intropy/amnt of preload, alterations of activity of the ANS- parasympathetic releases acetylcholine which has a neg inotropic effect and the adrenergic system can release epinephrine to activate beta-1-adrenergic receptors and cause inc HR and contractility and pos inotropic effect. and amnt of oxygen going to the myocardial muscle can influence |
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Term
| agents that can increase myocardial contractility |
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Definition
| positive inotropic agents, inc HR, exercise, cardiac glycosides for heart failure, increasing intracellular calcium, epinephrine and norepinephrine from sympathetic nervous system and adrenal gland (cardioexcitatory), thyroid hormone and dopamine |
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Term
| negative inotropic agents |
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Definition
| dec contractility, AChl from PNS and vagas nerve (cardioinhibitory) , slows down HR and contractility, hypoxia, cardiovacular control centers in the medulla that regulate HR |
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Term
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Definition
| when BP is reduced, sensory neurons in the large vessels that come off the heart (aorta and carotid artery) sense the change in pressure and send signals to cardioexcitatory centers in the brain causing the heart rate to increase and causing arterioles to constrict which increases peripheral resistance and raises BP |
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Term
| cardiomyocyte contraction |
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Definition
| sarcomeres with overlapping actin w head group for ATP->ADP and myosin filaments that move the actin filaments closer together and shortens the sarcomere. creakine kinase and lactase dehydrogenase are also enzymes involved in making energy, myoglobin (oxygen storage), troponins interact w actin and interfere with or allow myosin to interact with the actin, determines whether or not the movement of the myosin heads will occur, these are all part of the cytoskeleton of the muscle so if any are found in the bloodstream is suggests that cardiomyocytes have died |
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Term
| cardiaxc muscle vs skeletal muscle |
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Definition
| cardiac muscle doesn't require any neural input to contract, has automaticity, spread their depolarization through gap junctions and calcium can be spread from cell to cell this way and spread contractions |
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Term
| 2 types of cardiac myocytes found in the heart |
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Definition
| conducting cells (modified, conduct ions from cell to cell and initiate contraction in contractile cells) and contractile cells (depolarize and contract, have gap junctions) |
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Term
| pathway of conducting cells and action potentials in the heart |
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Definition
| begins at the right atrium and sinoatrial node (pacemaker cells- begin the process of conducting depolarization to other myocytes), -> left atrium, atria contract, -> AV node at junction of RT atrium and RT ventricle -> intraventricular septum -> up along the lateral walls of the 2 ventricles (right and left bundle branches joined together by the common bundle/bundle of His) -> up through Purkinje fibers |
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Term
| action potential types in the heart |
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Definition
| depolarize then slowly repolarize. similar in artria and ventricles but atrial are a little bit shorter/not as wide an repolarize mroe quicly. SA node cell action potentials have a very slow onset and then quickly depolarizes at theshhold and then repolarizes slowly- how it creates a rate for the heart |
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Term
| other cells in the heart that can also be pacemakers |
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Definition
| usually just the SA node cells but other cells can as well. they are normally suppressed by SA node cells but if SA node isn't working properly can get latent pacemakers that begin to spontaneously create rhythms that overlay the normal rhythm- called ectopies (can be premature atrial contractions or premature ventricular contractions) |
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