Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
102 Cards in this Set
- Front
- Back
What determines conduction velocity?
|
- amplitude of action potentials
- rate of rise od phase 0(dP/dt) |
|
What is the effect of the following on conduction of fast response AP?
- elevated resting potential |
slow conduction velocity (due to decreased amplitude of AP)
|
|
What is the effect of the following on conduction of fast response AP?
- Na channel blockers |
slow conduction velocity (due to decreased amplitude of AP and slow rate of rise of phase 0)
|
|
What is the effect of the following on conduction of slow response AP?
- raised resting potential |
slow conduction velocity (due to decreased amplitude of AP)
|
|
What is the effect of the following on conduction of slow response AP?
- Ca channel blockers |
slow conduction velocity (due to decreased amplitude of AP and slow rate of rise of phase 0)
|
|
What is the effect of the following on conduction of slow response AP?
- intensive hyperpolarization |
block conduction
|
|
Fast vs. slow response action potential: phases
|
Fast:
- phase 0: rapid depolarization (Na influx) - phase 1: transient K+ efflux - phase 2: plateau, balance of Ca and K fluxes - phase 3: K efflux - phase 4: stable membrane potential Slow: - phase 4: stable membrane potential(nonpacemaker), slow depolarizing pacemaker potential(slow Na influx, reduced K efflux) - phase 0: depolarization (Ca influx) - phase 3: K efflux |
|
Fast vs. slow response action potential: location
|
Fast:
- myocardial fibers(atria, ventricles) - ventricular conducting fibers (purkinje fibers, L,R bundles) Slow: - SA node - AV node |
|
Fast vs. slow response action potential: resting potential
|
Fast: -95mV
Slow: -65mV |
|
Fast vs. slow response action potential: conduction
|
Fast:
- Na channel activated at -70mV, rapidly inactivates. - must return to -95mV to allow full recovery Slow: - Ca channles activated at -40mV, slowly inactivates - must return to -65mV and allow time to allow full recovery |
|
Fast vs. slow response action potential: Effective refractory period
|
Fast:
- phase 0 to a point in phase 3 Slow: - phase 0 to a point in phase 3 |
|
Fast vs. slow response action potential: relative refractory period
|
Fast:
- end of ERP to beginning of full repolarization - Na, Ca begin to recover - Ca recover first - AP generated early resemble slow response Slow: - end of ERP to phase 4 - early AP susceptible to block |
|
What is the HR generated by the following?
- SA node - AV node - Purkinje fibers |
- SA node: 70-80/min
- AV node: 40-60/min - Purkinje fibers: 30-40/min |
|
What happens when AV node becomes the primary pacemaker?
|
Ventricles depolarize first because conduction pathway to ventricles are faster.
|
|
What happens when Purkinje fibers become the primary pacemaker?
|
Atria will not depolarize
|
|
What is this?
conduct signal from SA to AV node. |
internodal fibers (anterior, middle, posterior)
|
|
What is this?
conduct signal from SA to atrial muslces. |
Bachmann's bundle
|
|
Describe the conduction in the ventricles.
|
- depolarization in interventricular septum
- spreads to right and left endocardial surfaces - spreads from endocardium to epicardium |
|
If right bundle in the heart is blocked, will right ventricle still contract?
|
Yes, but happens after left ventricle contracts due to time lag in gap juction conduction from left to right ventricle.
|
|
What are some possible causes of bidirectional block?
|
- intense vagal stimulation
- cellular damage (infarction) |
|
What may be the cause of unidirectional block?
|
- ischemia ( damaged but not dead cells)
- build up of lactic acid -> gap closed -> refractory period out of sync - high extracellular K+ -> depolarized membrane potential -> slow action potential -> reentry arrythmia |
|
What causes reentry arrhythmua?
|
unidirectinal conduction block and slow conduction or shortened refractory period.
|
|
How to treat a unidirectional block?
|
block Na channel using lidocaine to convert it into a bidirectional block.
|
|
How is cardiac E-C coupling different from skeletal E-C coupling?
|
- always need trigger Ca2+ from outside: because ryanidine receptor reset its sensitivity to Ca2+.
- glycocalyx holds Ca2+ in T tubules - calcium induced Ca2+ release in pH sensitive: maximal release at 7.4, strong inhibition at 6.5. |
|
Why is cardiac muscle unlikely to undergo rigor?
|
Lots of mitochondria!
|
|
How are Ca2+ removed from cardiac cell?
|
- sarcoplasmic reticulum Ca2+ pump
- sarcolemmal Ca2+ pump - Na-Ca exchanger: remove 1 Ca2+ for every 3 Na+. |
|
What is the effect of phospholamban?
|
speeds up sarcoplasmic reticulum Ca2+ pump when phosphorylated by cAMP-protein kinase
|
|
How does digitlais treat congestive heart failure?
|
block Na-K pump -> Na+ build up inside -> Na-Ca exchanger reverse direction -> more Ca2+ inside
|
|
What is the relationship between velocity and force of contraction?
|
inversely related
|
|
Describe the isotonic contraction in which the cardiac muscle is both preloaded and afterloaded.
|
- ventricle preloaded: stretching of the muscle due to filling of blood
- isovolumic contraction: elastic fiber stretching, no external shortening - rapid ejection of blood: maximum velocity of muscle shortening. |
|
What is always associated with increase in contractility?
|
Ca2+ influx
|
|
T/F: Increase preload can increase contractility.
|
F. It increases force of contraction.
|
|
What are some good estimates of contractility?
|
- dP/dt
- ejection fraction: stroke volume/end-diastolic volume |
|
How to treat a dilated heart?
|
- diuretics to reduce venous return
- sit up (gravity) to reduce venous return. |
|
Describe the change in pressure-volume loop when there is an increase in afterload.
|
- initially: smaller stroke volume, similar work
- Frank-starling compensation: increase stroke volume to the same level as before, maintaining the same CO as before but with more work. |
|
Describe the change in pressure-volume loop when there is an increase in preload.
|
- larger stroke volume
- does more work |
|
Describe the change in pressure-volume loop when there is an increase in contractility.
|
- same preload
- same afterload - increased stroke volume and aterial pressure - more cardiac work |
|
What can cause a left shift in ventricular function curve?
|
NE-> increase contractility
|
|
What can cause a right shift in ventricular function curve?
|
cardiac failure -> decrease contractility
|
|
What is the equation for Fick's principle?
|
Q = q2/[O2(pv)-O2(pa)]
q2: O2 consumption computed from volume and O2 content of expired air. O2(pv): needle puncture at peripheral arterial pressure O2(pa): catheter in pulmonary artery |
|
How to calculate CO using Dye method?
|
Q = q/c(t2-t1)
q: injected dye c: mean dye concentration t1: time first able to measure dye t2: time dye concentration goes to 0 (need to extrapolate). |
|
Describe the thermodilution method used to get cardiac output.
|
- inject ice cold saline into or near right atrium.
- measure temperature in pulmonary artery. |
|
How to calculate CO using Echo-Doppler method?
|
Q = cross-section area of aorta x velocity
|
|
What is the single most important determinant for adequate ATP production in the heart?
|
O2 delivery by coronary artery flow.
|
|
How to calculate stroke work?
|
SW = SV x MAP
|
|
Name the two external cardiac work.
|
- stroke work: SV x MAP
- kinetic work: pushing blood from ventricles |
|
What does internal cardiac work do?
|
activities in E-C coupling
- ion transport - internal eventsin contraction - overcome internal viscosity to contract cell |
|
Which require more energy, external or internal cardiac work?
|
Internal cardiac work
|
|
How to estimate cardiac efficiency?
What should be the primary determinant for cardiac efficiency? |
- external work/O2 consumption
- internal work |
|
What is the best way to estimate energy requirements of cardiac work?
|
Double product = HR x MAP
- index for O2 consumption - can be used in dilated heart |
|
What is the intrinsic heart rate?
|
100/min
|
|
What are the innervation of the following? be specific.
- SA node - AV node |
- SA node: both left and right vagal
- AV node: right vagal parasympathetic origniate in medulla oblongata, DMN of vagus or nucleus ambiguous. |
|
How does parasympathetics slow HR?
|
- slow steepness of phase 4 depolarization in pacemaker
- increase K+ conductance, hyperpolarizing membrane potential - decrease Ca conductance, slow phase 4 depoloarization and make threshold more less negative |
|
How does sympathetics increase HR?
|
- increase leak current thus increase steepness of phase 4 depolarization
- increase Ca conductance, increase phase 4 depoloarization and make threshold more more negative |
|
How does parasympathetics provide beat-to-beat regulation?
|
- ACh opens special K channel which inactivate fast
- SA and AV node rich in cholinesterase which removes Ach quickly. |
|
What are some sympathetic receptors in nodal region in the heart?
|
- beta receptors: stimulated by isoproterenol, NE, inhibited by propranolol
|
|
Differentiate left and right sympathetic innervation of the heart.
|
left: more on contractility
right: more on heart rate |
|
Does sympathetic system provide beat to beat control of heart rate?
|
No.
- effects decay gradually - regulation through 2nd messenger system |
|
What are the higher center for cardiac control?
|
medulla oblongata
- solitary tract nucleus: baroreceptor reflex - caudal and rostral ventrolateral medulla |
|
Where are baroreceptors located?
|
- aortic arch
- carotid sinuses |
|
How does baroreceptor regulate high blood pressure?
|
high BP -> increase firing of baroreceptor -> vagal stimulation -> slow HR
|
|
T/F: Baroreceptor reflex is reduced in patients with chronic hypertension.
|
T.
|
|
Give 2 two examples where baroreceptor reflex provide beat to beat variation in HR.
|
1. incomplete AV block
- at the beat blocked: low arterial pressure -> remove vagal stimulation -> increase HR - at next beat: 2xblood and Ca -> more forceful contraction -> increase BP -> vagal stimulation -> decrease HR 2. PVC - feeble response: low blood filling, low Ca store -> low force of contraction -> low BP -> remove vagal stimulation -> increase HR - strong response: 2x Ca -> forceful ocntraction -> increase BP -> vagal stimulation -> decrease HR |
|
What happen to HR when blood is transfused to patients with low HR?
|
Bainbridge reflex:
- increased right atrial pressure -> stimulate atrial receptors -> increase HR ANF(diuretic, natriuretic, vasodilator) is released by atria in response to increases in blood volume |
|
What happen to HR when blood is transfused to patients with fast HR?
|
Bainbridge reflex overpowered by baroreceptor reflex:
- increased right atrial pressure -> increased CO -> increased aterial pressure -> decrease HR ANF(diuretic, natriuretic, vasodilator) is released by atria in response to increases in blood volume |
|
What happens to HR during inspiration?
|
increase:
- sympathetic fibers coincides with phrenic nerve - low intrathoracic pressure -> increase venous return -> bainbridge reflex - if increased CO produces an increased aterial pressure, baroreflex will counteract the bainbridge reflex |
|
What happens to HR during expiration?
|
decrease:
- vagal fiber activity |
|
How does coughing affect HR?
|
increased intrathoracic pressure -> decreased venous return -> less vagal stimulation (baroreceptor reflex) -> increase HR
|
|
What happens to heart rate when there is low O2 and high CO2 level according to chemoreceptor reflex?
|
- decrease HR
- respiratory activity will increase HR: hypocapnia and increased lung strength -> decrease vagal stimulation -> increase HR |
|
What should you do before changing the ventilation tube of quadraplegic patients?
|
hyperventilate them
|
|
What happens to HR when endocardial receptors are stimulated?
|
slows HR and decrease peripheral resistance (ventricular receptor reflexes)
|
|
What is this?
An increase in contraction frequency produces a progressive increase in force |
Staircase/Treppe phenomenon:
- effect of more ca build up |
|
Why does the strong response in PVC have a higher amplitude (more force)?
|
feeble response causes inadequate ventricular filling and too little time to sequester ca to SR -> more ca build up -> more force of contraction
|
|
Effect of left sympathetic nerve on heart.
|
- increase peak pressure and rate of pressure rise
- reduce duration of systole - increase the rate of ventricular relaxation during early diastole: enable adequate ventricular filling - increase HR - increase contractility |
|
Effect of parasympathetic influence on heart.
|
- inhibit pace maker, atrial myocardium and AV conduction tissue
- decrease peak left ventricular pressure - decrease max rate of pressure development (dP/dt) - decrease the max rate of relaxation during diastole - decrease HR - decrease contractility |
|
Sympathetic activity shift the ventricular functional curve to the ____.
|
Left
|
|
Parasympathetic activity shift the ventricular functional curve to the ____.
|
right
|
|
Mechanism of sympathetic action on heart.
|
- release NE which interact with beta receptor
- Gs stimulated to activate adenylate cyclase, raise cAMP level - phosphorylation of L-type Ca channel - indrease ca influx during plateau phase - increased contractility, shift ventricular function curve to the left. |
|
Mechanism of parasympathetic action on heart.
|
- release Ach which interact with muscarinic receptors and inhibit release of NE from sympathetic neurons
- stimulate Gi to inhibit adenylate cyclase - reduces cAMP - reduction in ca influx during plateau phase - decrease in contractility and shift ventricular functional curve to the right |
|
Hormonal control on heart.
- hypothyroidism |
- slow HR
- decrease CO |
|
Hormonal control on heart.
- hyperthyroidism |
- increase HR (may have arrhythmias such as atrial fibrillation)
- increase CO - enhance contractility - affect vasculature, sympthetic neural activity, density of beta receptors |
|
Hormonal control on heart.
- insulin |
- positive ionotropic effect on heart (not prevented when adrenergic receptors are blocked or glucose is given)
|
|
How does high CO2 in blood affect heart function?
|
reduce pH -> decrease ca release from SR and sensitivity of myofilaments to ca -> decrease contractility
|
|
How is cardiac muscle different from skeletal muscle?
|
- transversetubules (only in ventricular muscle cells): filled with glycocalyx which attract Ca2+
- diad: single transverse tubule and SR - intercalated disk - functional syncytium: gap juncitons. Artrial syncytium is separated from ventricular syncytium. - large amount of mitochondria - rich capillary supply |
|
What is the resting length of sarcomere?
|
2-2.4 uM: need to stretch it first.
|
|
What is the primary difference between contractile cells and non-contractile cells in the heart?
|
presence/absence of myofibrils
|
|
Which cardiac chamber is this?
- thin walled - low pressure chamber - not important as a pump, but important during tachycardia |
left/right atria
|
|
Which cardiac chamber is this?
- principle pumps of the heart - thickness related to pressure generated |
left/right ventricle
|
|
Where does heart attack usually start? epicardium or endocardium?
|
endocardium
|
|
Movements of cardiac valves are ____. (active/passive)
|
passive
|
|
Function of pericardium.
|
- prevent suddenn overextension of the chambers of the heart
- hypertrophy of the heart may gradually stretch the pericardium |
|
What is the effect of increase in pressure in one ventricle to the other ventricle?
|
- decrease compliance (non-distensible pericardium) -> induce an increase in pressure
|
|
Which type of vessel is this?
- large diameter - large elastic component - high velocity - high pressure - pulsatile |
aorta
|
|
Which type of vessel is this?
- large smooth muscle component with small elastic component - higher systolic pressure than aorta - lower diastolic pressure than aorta - pulsatile |
arteries
|
|
Which type of vessel is this?
- small diameter - large muscle component - little elastic component - "resistance" vessels - can cut off blood flow - respond to metabolic need - steady flow |
arterioles
|
|
Which type of vessel is this?
- large total cross sectional area - small diameter - single cell thick walls - O2 satuartion around 50-80% |
capillaries
|
|
Which type of vessel is this?
- endothelium and fibrous tissue - no smooth muscle |
venules
|
|
Which type of vessel is this?
- pressure low near heart - velocity increase near heart - smooth muscle, elastic component and fibrous tissue |
veins
|
|
Compare the mean pressure in pulmonary vessels to systemic vessels.
|
1/7th of that of systemic vessels
|
|
What is the O2 saturation in pulmonary capiallary after exchange?
|
94-98%
|
|
At which pulmonary O2 saturation is considered asthmatic attack?
|
lower than 90% saturation
|
|
T/F: Venous pressure is roughly the same throughout the body when a person is recumbant.
|
T.
|