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Lecture 10
cardiac muscle physiology
Question | Answer |
---|---|
Cardiac Muscle: cardiac muscle is ___ and has an intracellular sarcomere structure that is similar to that of skeletal muscle | striated |
Cardiac Muscle: unlike skeletal muscle, cardiac muscle cells (myocytes) form a ____ | highly branched network |
Cardiac Muscle: myocyte to myocyte connections occur at structures called __ | intercalated disks |
Cardiac Muscle: gap junctions in intercalated disks provide ____ | low electrical resistance |
Cardiac Muscle Structure: a single adequate stimulus for ___ in one myocyte results in the rapid spread of ___ to all myocytes via ___. This is known as the ___electrical response of the heart | action potential, excitation, gap junctions; all or none |
Cardiac Muscle Structure: in the patient with coronary ischemia, areas of heart muscle can begin to randomly ___ | depolarize |
Cardiac Muscle Structure: these myocytes are referred to as "___" | irritable |
Cardiac Muscle Structure: depolarization of one irritable myocyte rapidly ___via the all or none principle, which can lead to a fatal ___ | propagates, arrhythmia |
Na/K Pump: like other cells in the body, the axon maintains the resting electrical membrane potential such that the outside is ____ than the inside | more positive |
Na/K Pump: the pump moves 3 sodium ____ the cell for every __ potassium brought in. however potassium leaks back outside the cell more easily than sodium leak backs in. this maintains the ____ | outside; 2; resting membrane potential |
Na/K Pump: there are separate voltage dependent sodium and potassium channels that are vital to generation of ___. these open or close depending on the state of the membrane electrical potential to allow selective movement of Na and K = generate a ___ | action potentials, traveling potential |
Nerve impulses: sodium rushes into the cell = __. occurs so fast the inside of the cell can become even neural or positive to the outside causing a ____opening neighboring voltage dependent ___ | depolarization; lateral shift, sodium gates |
Nerve impulses: as it spreads the axon recovers due to ___the sodium gates and the opening of the voltage dependent potassium gates allowing K to rush out ____membrane potential = __ | shutting off, restoring, repolarization |
Nerve impulses: once this happens it cannot ___until membrane potential is restored = ____ | fire again, refractory period |
Enter Calcium Channels: there is another important gate ___ | Ca++ |
Enter Calcium Channels: Ca++ is normally much higher ___than intracellularly due to a ___pump that pumps it outside the cell | extracellularly, calcium |
Enter Calcium Channels: voltage dependent opening of the Na+ channels may be accompanied by the voltage dependent opening of the ___channels which causes further ___ | calcium, depolarization |
Enter Calcium Channels: Ca++ channels are ___than Na+ channels so in cells like the heart where Ca++ channels are plentiful there is a ___in the action potential and recovery of membrane potential are ___. | slower, plateau, delayed. this is good because we like prolonged and complete contractions of the heart |
Ventricular Muscle Action Potentials: action potentials arriving at the ventricular muscle from the ventricular conducting system trigger the rapid spread of action potential in all ____ | ventricular myocytes |
Ventricular Muscle Action Potentials: the ventricular muscle action potential has a very long ____ | duration |
SA node action potentials: SA nodal cells are ___because their membrane potential depolarizes spontaneously during ___, which is called the ____or ____ | pacemakers, Phase 4, pacemaker potential or diastolic depolarization |
SA node action potentials: in other words, the SA node action potentials (AP) are self generating and require ____ | no stimulus |
SA node action potentials: action potential generation in the AV node is similar to the SA node but has a ____phase 4 depolarization | slower |
Atrial and Ventricular Contraction: in atrial and ventricular muscle cells we see a large plateau due to the _____ | slow calcium channels |
Atrial and Ventricular Contraction: protects us from ___and allows for complete ____and ___of the atria and ventricles | tachycardia, contraction, emptying |
Purkenje Fibers | note the plateau and the refractory period. protects again from rapid heart rates and full ventricular contraction. Slow calcium channels are important to regulating both rate and strength of muscular contraction |
Why do we care? There are four classes of ____ based on their site of ___ | antiarrhythmics, action |
Why do we care? Class I = __, Class II = ___, Class III = ____, Class IV = ___ | sodium channel blockers, beta blockers, potassium channel blockers, calcium channel blockers |
Why do we care? The SA node and AV node action potential upstroke is ____ dependent, whereas the ventricular upstroke is ____dependent | Ca++, Na+ |
Why do we care? As such, class I are effective in the treatment of ____, and class IV are effective in slowing conduction in the ____ | ventricular ectopy, SA and Av nodes |
Electrolyte abnormalities can make the heart very ___ or ___. Too much K+ = ____. Too little K+ = ____ | excitable, calm. bad and excitable. bad and lazy |
Sympathetic: sympathetic stimulation ____ both both heart rate and myocardial contractility which increased ____ | increases, cardiac output |
Parasympathetic: parasympathetic stimulation ____ both heart rate and myocardial contractility | decreases |
Sympathetic: norepinephrine released by sympathetic fibers interacts with ____receptors on cardiac muscle leading to increased cardiac contractility through increased ____ | beta 1, calcium influx |
Sympathetic: increased heart rate by increasing the firing rate of the SA node and the ____channels and increases conduction velocity | Na, K, Ca |
Parasympathetics: work through the release of ____. More selective in their innervation. Decrease cardiac pumping by innervating the ____and ____ | acetylcholine, SA and AV nodes |
Parasympathetics: this ___ the HR through its SA node influence and conduction velocity through the AV node. note it has no influence on the ___. | decreases. ventricles |
Chronotropic = ___; changes in ___ | time, heart rate. ANS effects of HR |
Dromotropic = ___; affects the ____ | running, conduction speed |
Inotropic = strength of ___ | muscular contractions |
Parasympathetic = rest/digest = slow = ____chronotropic effects | negative. acetylcholine released from parasympathetic fibers activate muscarinic (M2) receptors in SA node |
Sympathetic = fight/flight = fast = ____chronotropic effects | positive. norepinephrine released from sympathetic fibers activate B1 receptors in SA node |
Dromotropic effects = change in conduction ____ | velocity |
Dromotropic effects on AV node: parasympathetic = rest/digest = slow = ___dromotropic effects | negative |
Dromotropic effects on AV node: sympathetic = fight/flight = fast = ___dromotropic effects | positive |
Excitation-contraction coupling | cardiac muscle cells contract without nervous stimulation |
Excitation-contraction coupling | pacemaker cells spontaneously generate action potentials, which spread through gap junctions |
Excitation-contraction coupling | action potentials conducted along T tubules open voltage-gated Ca2+ channels causing entry of extracellular Ca2+ into the cells |
Excitation-contraction coupling | Ca2+ induced Ca2+ release is triggered from internal sarcoplasmic reticulum stores |
Excitation-contraction coupling | almost all Ca2+ that interacts with troponin C to initiate contraction is derived from internal stores |
Excitation-contraction coupling | contraction occurs via the sliding filament mechanism |
Determinants of Contractility (inotropy): increasing contractility/positive inotropy | sympathetic activation, medications, increase in preload |
Determinants of Contractility (inotropy): decreasing contractility/negative inotropy | parasympathetic activation, anoxia and hypercapnia, loss of parts of the myocardium |
Stroke volume definition | volume of blood ejected with each beat |
ejection fraction definition | % of SV as compared to end-diastolic volume. measure of efficiency |
cardiac output definition | total amount of SV's per unit of time |
Frank Starling** | as volume increases and the myocardial fibers begin to stretch the corresponding pressure created by the ensuing muscle contraction becomes greater |
Frank Starling** | stroke volume increases in response to increased venous return. increased end diastolic volume increases stroke volume |