Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/50

Click to flip

50 Cards in this Set

  • Front
  • Back
Heart muscel and resistance
Has low resistance intercalated disks (1/400 the resistance of cell membrane
Cardiac tissue electrically can be described as
Cardiac tissue is an electrical syncytium
Electrical threshold of cardiac tissue
Resting membrane potential of cardiac muscle is -85 to -95 millivolts
Action potential is 105 millivolts
Plateau lasts ~0.2 -0.3 sec in ventricular muscle (much longer than skeletal muscle)
Phases 0 - 4
0-Fast Na+ channels open then slow Ca++ channels
1-K+ channels open
2-Ca++ channels open more
3-Resting membreane potential
Why don't atria trigger ventricles
Fibrous insulator exists between atrium and ventricle
Results of Action Potential
Ca++ release from sarcoplasmic reticulum.
Ca++ release from T- tubules, which are large, are a very important source of Ca++.
T-tubule Ca++ depends strongly on extracellular Ca++ concentration.
Mucopolysaccharides bind Ca++.
EKG
EKG - P - atrial depol QRS - Ventricular depol, atrial repol T - ventricular repolarization
Systole
Systole - muscle is stimulated by action potential and is contracting
diastole
muscle is reestablishing Na+/K+/Ca++ gradient and is relaxing
Cardiac Cycle graph
Isovolumic contraction
Ejection
Isovolumic relaxation
rapid inflow
diastasis
Atrial systole
Refractory period
During During this time cardiac muscle tissue cannot be re-excited
Lasts 0.25-0.30 sec in ventricles
Lasts 0.15 sec in atria
Excess K+
lowers potential across the membrane and lessens likelihood of depolarization
causes dilation
decreases contractility
causes arrhythmias and fibrillation
slows rate
increases of 2-3x normal can block A-V bundle and cause death
Excess Ca++
spastic contraction
opposite causes effects of K +
Atrial pressure waves
a-wave - atrial contraction c-wave - ventricular contraction (A-V valves bulge) v-wave - flow of blood into atria
Ventricular systole
A-V valves close (ventricular press> atrial press)
Aortic valve opens
Ejection phase
Aortic valve closes
End diastolic volume (each ventricle
120 ml
End systolic volume
50 ml
Ejection volume (stroke volume)
70 ml
120-50 (End diastolic volume - end systolic volume)
Ejection fraction
70ml/120ml = 58% (Stroke volume/end diastolic volume)
normally 60%)
If heart rate (HR) is 70 beats/minute, what is cardiac output?
HR X stroke volume = 70/min. X 70 ml = 4900ml/min.
Total blood volume (ave
5.5 liters
If HR =100, end diastolic volume = 180 ml, end systolic vol. = 20 ml, what is cardiac output?
C.O. = 100/min. * 160 ml = 16,000 ml/min
Cardiac output
HR X stroke volume
Ejection volume (stroke volume)
End diastolic volume - end systolic volume
Valvular Function
-To prevent back-flow.
-Chordae tendineae are attached to A-V valves.
-Papillary muscle, attached to chordae tendineae, contract during systole and help prevent back-flow.
-Because of smaller opening, velocity through aortic and pulmonary valves exceed that through the A-V valves.
Valvular Function and forces
Work output is affected by preload (end-diastolic pressure) and afterload (aortic pressure)
Frank - Starling
states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
Pre-load and After-load
preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. reload is theoretically most accurately described as the initial stretching of cardiac myocytes prior to contraction. This cannot be measured in vivo. Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood
afterload is the tension produced by a chamber of the heart in order to contract
Sympathetic stimulation
causes increased HR + increased contractility with HR = 180-200 and C.O. = 15-20 L/min.
Parasympathetic stimulation
decreases HR markedly and decreases cardiac contractility slightly. Vagal fibers go mainly to atria.
Fast heart rate (tachycardia
can decrease C.O. because there is not enough time for heart to fill during diastole.
(allows atria to contract before ventricles)
Impulse delayed in A-V node
takes impulse into ventricles
A-V bundle
take impulses to all parts of ventricles
Left and right bundles of Purkinje fibers
S.A. Nodal cells
Specialized cardiac/nerve cells within atrial muscle wall.
Acts as pacemaker because membrane leaks Na+ and membrane potential is -55 to -60mV
When membrane potential reaches -40 mV, slow Ca++ channels open causing action potential.
After 100-150 msec Ca++ channels close and K+channels open more, returning membrane potential to -55mV.
Leaky
potentials
sinoatrial (SA) node and travel across the wall of the atrium (arrows) from the SA node to the atrioventricular (AV) node.
Discharge of a single atrial fiber compared to a ventricular fiber
Resting potnetial, Threshold -40 mV, Na+ leak, slow Ca++channels open, K+ channels open more (~1 sec) Ventricular musecle fiber -72 mV (~0.5 sec)
Internodal Pathways
Transmit cardiac impulse throughout atria
Anterior, middle, and posterior internodal pathways
Anterior interatrial band carries impulses to left atrium.
A-V Node
Delays cardiac impulse
Most delay is in A-V node
Delay AV node---0.09 sec.
Delay AV bundle--0.04 sec
Purkinje System
Fibers lead from A-V node through A-V bundle into Ventricles
Fast conduction; many gap junctions at intercalated disks
A-V Bundles
Normally one-way conduction through the bundles
The only conducting path between atria and ventricles is A-V node and A-V bundle
Divides into left and right bundles
Transmission time between A-V bundles and last of ventricular fibers is 0.06 second (QRS time)
Discharge rates
Normal rate of discharge in sinus node is 70-80/min.; A-V node - 40-60/min.; Purkinje fibers - 15-40/min.
Sinus node is pacemaker because of its faster discharge rate
S1
S2
AV valves close
Semilunar valves close
ST segment
Depression: Ischemia
1st, 2nd , 3rd degree AV blocks
1.P-R exceeds 0.20 sec
2. only one out of several atrial waves get through the AV node
3. no atrial waves get through and venticles revert to baseline depolarization.
Main Arrival times
S-A Node 0.00 sec
A-V Node 0.03 sec
A-V Bundle 0.12 sec
VentricularSeptum 0.16 sec
“Ectopic Foci
This is a portion of the heart with a more rapid discharge than the sinus node.
Also occurs when transmission from sinus node to A-V node is blocked (A-V block).
Ectopic…
During sudden onset of A-V block, sinus node discharge does not get through – and sinus is suppressed from previous over run, and next fastest area of discharge becomes pacemaker of heart beat (Purkinje system).
Delay in pickup of the heart beat is the “Stokes-Adams” syndrome. New pacemaker is in A-V node or penetrating part of A-V bundle.
Person faints and/or dies
Parasympathetic effects
Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate S-A node and A-V junctional fibers proximal to A-V node.
Causes hyperpolarization because of increased K+ permeability in response to acetylcholine.
This causes decreased transmission of impulses maybe temporarily stopping heart rate.
Ventricular escape occurs.( Ventricles initiate their own depol
Sympathetic effects
Releases norepinephrine at sympathetic ending
Causes increased sinus node discharge
Increases rate of conduction of impulse
Increases force of contraction in atria and ventricles