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Frog heart
electrical and mechanical properties of the heart
Undergraduate 4

Additional Physiology Flashcards




what is the difference between skeletal muscle and cardiac muscle
- they are both straited but muscle cells are shorter than skeletal and the cardiac muscles are connected by intercalated disks
what are intercalated disks?

desmosomes that contain protiens called adherins that mechanically bind the cells together

gap junctins that electricallhy couple the cells together

explain the electical activity of the heart


Cardiac action potentials originate from the sinoatrial (SA) node
AP from SA node will travel through RA to LA  then to the atrioventricular (AV) node then to the His-Purkinje fiber system and then it travels to the ventricles
 Neural innervation can modulate pacemaker activity but is not necessary for contraction as it is in skeletal

SA node fires APs spontaneously and at regular intervals of 60-100 times/min (Pacemaker Activity

what are the cardiac electrical potentials

different cells in the heart will have different types of action potentials

these aps differ in duartion shape and are caused by differet ion currents

once the venticular muscle is electrically activated it enters an effective refractory period.

what is the difference between refractry period and absolute refractory period

ERP is equivlent to the absoulte refractory period in nerves where the ventricles are not able to be activated

RRP is where and action potential can occur

SA node action potentials: what are the phases

Phase 0: depolarization is caused mostly by calcium influs

Phase 3: repolarization from K efflux

Phase 4: unstable resting potential due to opening of a non- specific cation channel

what is the ventricular action potential phases

Phase 0 rapuid depolarization due to influx of sodium and to a lesser extent calcium

Phase 1: Rapuid repolarization from inactivation of sodium channels

PHase2: plateau caused by continued calcium influx

Phase 3: repolarization due to K efflux and calcium channel inactivation sets the duration of AP

phase 4 resting membrane potential


what is the difference between the cardiac muscle conraction and the skeletal muscle contraction

desribe the mechanism



Increase in Ca2+ in Phase 2 of AP is important for the increase in Ca2+ needed for contraction


A further increase in Ca2+ occurs through Ca2+ induced Ca2+ release (CICR)


Unlike skeletal muscle, L-type Ca2+ channels on the T-tubule are not connected to Ryanodine Receptors (RyR) on the SR


The influx of extracellular Ca2+ is absolutely necessary for Ca2+ efflux from the SR


The increase in intracellular Ca2+ will induce contraction in the same manner as in skeletal muscle  


desrbice the cardiac cycle


Cardiac Cycle – sequence of mechanical and electrical events that repeat with every heartbeat


(1) Ventricular Filling : AV valves open, semilunar valves closed


(2) Isovolumetric Contraction: All valves closed, ventricular contraction causes an increase in Pressure but no change in volume


(3) Ventricular Ejection: Semilunar valves open, ejection of blood causes an increase in pressure and a decrease in volume


(4) Isovolumetric Relaxation: All valves closed, ventricles relax causing a decrease in pressure but no change in volume


Systole: Phases 2 and 3 – contraction and emptying


Diastole : Phases 4 and 1 – relaxation and filling


what is an extrasystole


Extrasystole: premature ventricular contraction


Often caused by depolarization in the ventricle rather than the SA node


An extrasystole will usually cause a skipped beat followed by a stronger beat


But this is dependent on timing, when extrasystole occurs in the cardiac cycle


what is compensatory pause
time period between the extrasystoluic contraction and the normally elicited contraction

how does the parasympathetic sctivity work on the heart




Parasympathetic fibers travel along the vagus nerve to innervate the heart and primarily release ACh, which will bind to muscarinic ACh receptors


ACh will slow pacemaker activity in the SA node to make HR decrease


In the AV node, ACh decreases conduction velocity making it more difficult to depolarize neighboring cells to threshold  


how does sympathetic activity work on the heart


Sympathetic nerves release Norepinephrine or epinephrine which bind to β1-adrenergic receptors to increase HR


Norepi/epi also cause an increase the Calcium current allowing for greater contractions of the heart


Ca increases--- Binding sites increases ----- increase contraction of heart


describe the pacemakers of the heart


The SA nodal cells as well as the AV node and Bundle of His are capable of pacemaker activity


Pacemaker activity will be controlled by the fastest pacemaker cell


The SA node are normally the fastest of the pacemakers so their signal dominates contractility


When faster pacemakers suppress the activity of slower pacemakers it is called overdrive supression


what is vagsal escape

prolonged vagal stimulation will cause bradycardia and eventually lead to cardiac arrest

vagal innercation is not uniform so other pacemaker cells that aren't as stimulated will take over control of the hr


what does the pressure volume loop show
the realtionship between left ventricular pressure and the volum during the cardiac cycle
frankstarling law

the heart will contract with more force during systole if it is filled to a greater extent during dystole

more filling will end diastolic volume

this will lead to an increase in SV

what happens with incread contractility

increasing force of contractility without increasing muscle length

sympathetic activity can increase cbntractility and increase SV

The difference between the frogs heart and human

frog has three chambers and the pacemaker structure is the sinus venosus

the frogs heart aha a collwection of cells that form a funnel between the atria and the centricle that has similar properties to the AV node

does not have a specialised ventricular conduction system

frogs heart do not have a developed SR so the primary source of calcium is extracellular


Pacemakers What are autorhythmic cells? Describe their function and how they affect cardiac muscle contraction
All of the cells of the conduction system are autorythmic, but differ in the rate at which they discharge action potentials. The SA node has the fastest rate of discharge, therefore it sets the pace of the heart. Sometimes a region of the heart other than the SA node develops a even faster rate of discharge and thus takes over the role of pacemaker. A pacemaker other than the SA node is called an ectopic pacemaker
Events of the cardiac cycle Describe the mechanical events during the cardiac cycle. Present a diagram showing the changes in aortic pressure, ventricular pressure, atrial pressure and ECG during systole and diastole . 

The heart undergoes a constant cycle of contractions and relaxations. The period of ventricular contraction is called systole. The period of ventricular relaxation is called diastole.


  1. Ventricles relax
  2. pulmonary and aortic valves close
  3. AV valves open
  4. ventricles fill (about 80% of capacity)
  5. atria contract (ventricles fill another 20%)

systole summary
  1. ventricles contract
  2. AV valves close
  3. aortic and pulmonary valves open
  4. blood is ejected

What is cardiac output?      What are the two determinants of cardiac output? Diagram and present the relationship between end-diastolic volume and stroke volume (Frank-Starling curve). What changes are seen during heart failure?


sv(amount of blood leaving the heart) x Heart rate(how fast the heart beats

-End diastolic volume 

the parasympathetic nervous system and cardiac function . what are the effects? how does it affect cardiac output? bradycardia affects and cardiac arrests? what allowed the heart to return after vagal escape

- parasympathetic id controlled by the neurotransmitter aceylcholine, slows the heart and cardiac output. ACh will slow pacemaker activity in SA node and trhough the APS of the AV node. bradycardia is the slowing of the heart. 


- Pns IS HIGHLY INNERVATED ON THE sa NODE BUT NOT THE av NODE or ectopic cells, other pacemaker takeover as the driver of HR but will not have as fast of rate as SA node. 

Describe sympathetic innervation on the heart. what are the sources what mechanisms are involved in the response

- we used epinephrine injection. This binds to the adrenic resptors that will increase rate of depolarization in pacemaker cells and causes an increase in calcium concentration

also causes increase in myocardial contractility 

describe extasystilic contractions? what was stimulated, when? what will ESc do to contractions? post ESC? what will happen between contractions?

- stimulated the ventricle in early or late diastole to get ESC and this will causes the tensiton to be smaller than the regular contraction and post -esc will have a larger contraction. 

compensatory pause- longer time to contract. 

this is because of frank starling law, if the is more blood filling the ventricle it will take longer to eject and then the heart will return the same amount as returned. 

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