Physiology Flashcards
Tissues layers in Heart
endocardium - inner lining of chamber
epicardium - outer lining of chambers
pericardiu, - surrounds entire heart (composed of visceral and parietal layer)
Papillary muscules
attach to AV valves via chordae tendinae
- do not help close the valves
- help in prevevnting regurgitation into atria
mitral valve closes at the beginning of ______
isovolumetric contraction
(ventricular systole)
Intracellular [K+]
140
Extracellular [K+]
4
Nersnt equilibrium potential of K and Na
K+ = -90
Na+ = +70
Intracellular [Na+]
10
Extracellular [Na+]
140
Na+-K+-ATPase pump
maintains negative potential
3 Na out for 2 K in
Na+-H+ exchanger
regulates intracellular pH
H+ out and Na+ in
Cardiac Action Potential
[phase 0]
activation of fast Na+ channels (iNa)
- increases membrane conductance 100x
- generates inward current
Cardiac Action Potential
[phase 1]
inactivation of iNa and activation of transient outward K current (iTO)
- decreases membrane potential which favors Ca2+ entry
- influences plateau length
- more K efflux = shorter plateau phase
Cardiac Action Potential
[phase 2]
opening of L-type Ca2+ channels (iCa-L) and Na-Ca exchanger
Cardiac Action Potential
[phase 3]
opening of delayed rectifier K (iKV)
- increased K+ conductance
- size of current determines plateau duration
Cardiac Action Potential
[phase 4]
“pacemaker potential”
- small Na+ current (ib) and inward rectifier (Kir)
inward rectifier K+ channel (iK1)
maintains high K+ permeability during phase 4
fast Na+ voltage channel
accounts for phase 0
L-type Ca2+ channel
responsible for phase 2
- enhanced by sympathetic stimulation and Beta agonists
Ca-ATPase
sequesters calcium back into SR
- regulated by phospholamban (inhibitor)
- catecholamines decrease inhibitor effect
absolute refractory period
[during which phases]
0, 1, 2, and 3
chronic heart failure
[ion channels]
decreased K+ (iTO) expression
- delays repolarization, prolongs plateau, and arryhthmogenic
Long QT syndrome
[ion channel]
abnormality of delayed rectifier channel (iK)
- prolongs plateau and results in Ca2+ overload after depolarization
Early After Depolarizations
secondary depolarizations that occur before the end of phase 3
- increased frequency with slow heart rate
- may lead to Torsades de pointes
Purkinje cells
[beats per minute]
15
AV node
[beats per minute]
50 - 60
SA node
[beats per minute]
70 - 80
Pacemaker Action Potential
[which phases are not involved?]
pacemaker action potentials do not include phase 1 and 2
chronotropy
increase heart rate
dromotropy
increase AV node conduction
inotropy
increased contractility
lusitropy
increased rate of myocyte relaxation
Phosphodiesterase Inhibitors
[effects]
inotropy and chronotropy
Phosphodiesterase Inhibitor
[examples]
caffeine, theophylline, milrinone, and amrinone
Muscarinc M1 Receptor
[location]
cortex and hippocampus
Muscarinic M2 Receptors
[location]
heart
Muscarinic M3 Receptors
exocrine glands and GI tract
Muscarinic M4 Receptor
[location]
neostriatum
Muscarinic M5 Receptor
[location]
substantia nigra
Hypocalcemia
[effects]
prolonged QT interval
- possible result is EAD and torsades
Hypocalcemia
[possible causes]
loop diuretics
osteomalacia
hypoparathyroid
respiratory alkalosis
Hypercalcemia
[effects]
shortens QT interval
Hypercalcemia
[causes]
adrenal insufficiency
hyperparathyroid
kidney failure
malignancy
Hyperkalemia
[effects]
wide QRS and peaked T waves
- hyperkalemia decreases equilibrium potential and closes Na+-voltage channels
- wide QRS
- enhanced K+ channel activity
- peaked T-waves
Hyperkalemia
[causes]
potassium-sparing diuretics
ACE inhibitors
metabolic acidosis
MH
blood transfusions
Hypokalemia
[effects]
wide QRS with U-wave
- reduces K+ channel activity
- prolongs plateau and repolarization
Temperature’s effect on HR
Hyperthermia: increase 10 bpm per 1oC
Hypothermia: conduction slows and ST segment elevates; J or Osnorne wave
Ivabradine
funny channel blocker (if)
- decreases rate of pacemaker decay
- decreases HR
Adenosine
activates A-1 Receptors
- slows AV conduction and slows HR
Bainbridge Reflex
increased CVP → stretch and increased HR
- detected by baroreceptors
Spontaneous Ventilation effect on HR
Inhalation: decreases intrathoracic pressure and increases venous return (increases HR) via bainbridge reflex
Exhalation: increased pressure activates baroreceptor reflex to decrease HR
Beta-Blocker
[overdose treatment]
glucagon
cardiac myocytes resting membrane potential
about -90 mV
p-wave
[electrical event]
altrial repolarization
PR interval
[electrical event]
delay of conduction by the AV node
T-wave
[electrical event]
ventricular repolarization
phase 3
QT interval
[electrical event]
ventricle depolarization and repolarization
Bazett’s Formula
QTc = QT/sqrt(RR)
p-wave
[normal time]
0.08 - 0.12
PR interval
[normal time]
0.12 - 0.20
QRS complex
[normal time]
0.06 - 0.11
Horizontal plane leads
V1 - V6
- view across horizontal plane
- each lead is positive
Bipolar leads
Lead I - III
Unipolar leads
aVr, aVL, aVf
- amplify the voltage of waves in Leads I - III
V1
[location]
right side of sternum
4th intercostal
V2
[location]
left side of sternum
4th intercostal
V4
[location]
left midclavicular line
5th intercostal
V5
[location]
left anterior axillary
5th intercostal
V6
[location]
left mid-axillary line
5th intercostal
which leads correspond to the high lateral wall?
Leads I and aVL
which leads correspond to the inferior wall?
Leads II, III and aVF
which leads correspond to the septal wall?
Leads V1 and V2
which leads correspond to the anterior wall?
Leads V3 and V4
which leads correspond to the lateral wall?
Leads V5 and V6
Junctional Rhythm
[heart rate]
40 - 60 bpm
Ventricular Escape Rhythm
20 - 40 bpm
- esentially regular
(3) mechanisms associated with tachy-arrhythmias
enhanced automaticity
triggered automaticity
re-entry
QT interval
[normal time]
0.45 in men and 0.46 in women
normal heart axis
-30o to +90o
[axis of heart]
If QRS is positive in Lead I and aVF
normal
[axis of heart]
If QRS is negative in Lead I, but positive in aVF
right axis deviation
[axis of heart]
If QRS is positive in Lead I, but negative in aVF
LAD
sinus node
[location]
lateral edge of right atrium
First degree heart block
prolonged PR interval
(greater than 0.2 seconds)
Second Degree - Type I
progressive prolongation of the PR interval followed by a droped QRS
Second Degree - Type II
dropped QRS not preceded by PR prolongation
Third Degree Heart block
atria and ventricular rhythms are independent
- no impulses are transmitted through the AV node
Right Bundle Branch Block
due to myocardial infarction of the Purkinje system
- rabbit ears on V1
Tri-fascicular Block
first degree AV block
RBBB
and LAFB or LPFB
Atrial Fibrillation
loss of synchrony during excitation and resing phases
- ventricular irregularly irregular rhythm
- greater than 300 bpm
Atrial Flutter
re-entry circuit in the right atrium
- 240-340 bpm
Wolf Parkinson White
accessory pathway (bundle of Kent)
- contains delta wave and short PR interval
Bowditch Effect
increased HR causes increased contractility
- due to increase SR calcium store
Extracellular
[composition]
3L of plasma
and
12L interstitial fluid
“conduit vessels”
arteries
“resistance vessels”
arterioles
“exchange vessels”
capillaries
“capacitance vessels”
veins
which electrolytes are higher interstitially?
Na+ and Ca2+
which electrolyte is higher intracellularly?
K+
Heart sounds
[S1]
begining of systole due to AV valve closure
- best heart at apex
- during isovolumetric contraction