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Describe three mechanisms of how adrenergic stimulation of nodal cells and/or cardiocytes increases heart rate and contraction strength.
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- Parasympathetic stimulation decreases the heart rate by Decreasing permeability of SA node cells to Ca2+ increasing ion influx, thus increasing the rate of depolarization. Increasing the permeability of SA node cells to Ca2+. Increasing the permeability of SA (sinoatrial) node cells to K+.Slow conduction in the atrioventricular node is associated with which of the following? Group of answer choices Prolonged PR interval Prolonged QRS interval Shortened QT interval Elevated ST segmentIdentify physiological processes involved in STROKE
- When a heart is transplanted into a patient, it is not possible to connect autonomic neurons from the medullary cardiovascular centers to the new heart. Will such a patient be able to increase cardiac output during exercise? Hint: Recall the effects of circulating catecholamines and changes in venous return on cardiac output.Describe the interactions of actin, myosin, and the troponin-tropomyosin complex in controlling heart function.A drug that blocks the cardiac muscarinic receptor might be expected to: Increased heart rate Decreased heart rate Open mechanically-gated K channels Decreased contractility Decrease pacemaker potential
- Why is it possible for acetylcholine to actually cause an increase in stroke volume, even though increased parasympathetic activity causes an overall decrease in cardiac output?The following medications are used to treat an exacerbation of congestive heart failure. Each one of them is actually used to counteract mechanisms the body has naturally set in place in response to a drop in blood pressure and presumed drop in tissue perfusion. For each medication, explain its affect(s) on A, B, and C. If you feel it has no effect on a particular parameter, then say "no effect". Specifically for each: A) affect on TPR (total peripheral resistance) and how/why it changes it B) affect on cardiac output (contractility, heart rate, stroke volume) and how/why it changes it C) blood volume/pressure and how/why it changes it ACEIs (ACE inhibitors) Beta blockers Digoxin Nitrates (nitroglycerin, isosorbide) Diuretics like LasixYou are testing a compound as cardioactive drug. You know the compound is an agonist of acetylcholine (ACh) at the relevant ACh receptor (AChR) on sinoatrial (SA) node cells. Briefly describe how the action of the drug likely would affect the electrical signal produced by the SA node cells. In respect of cardiac output, what would you expect to be the effect of this drug?
- Describe nervous and chemical factors that alter heart rate, stroke volume, and cardiac output.Autorhythmic cells in the SA node intrinsically fire at a rate of - 90 action potentials per minute. At rest, the heart rate is lowered primarily through modulation by: O Decreased delivery of acetylcholine and increased delivery of norepinephrine Increased delivery of acetylcholine and decreased delivery of norepinephrine Cardiac contractile cells Decreased delivery of acetylcholine and decreased delivery of norepinephrine Increased delivery of acetylcholine and increased delivery of norepinephrine O O ODefine the term 'distributive shock' and briefly explain why two of the three types of distributive shock result in increased heart rate, whilst the third type results in decreased heart rate.
