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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.