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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

what causes the rising phase of AP in pacemaker cells?

A

Long lasting (L-type) Ca++ channels resulting in Ca++ influx

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2
Q

what causes the falling phase of AP in pacemaker cells?

A

Inactivation of L type Ca++ channels and activation of K++ channels resulting in k++ efflux

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3
Q

what is cell to cell current flow via?

A

gap junctions

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4
Q

why is there an AV nodal delay?

A

to allow atrial systole to precede ventricular systole

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5
Q

phase 0-4 of AP in cardiac myocytes

A

0- fast Na+ inflex
1- closure of Na+ channels and transient K+ efflux
2- mainly Ca++ influx
3- closure of Ca++ channels and K+ efflux
4- resting membrane potential

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6
Q

what is the plateau phase due to?

A

Influx of Ca++ through L-type channels

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7
Q

resting potential of cardiac myocytes?

A

-90mV

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8
Q

what part of the heart does the vagus nerve supply?

A

SA node and AV node

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9
Q

consequence of vagal stimulation in the heart

A

increased AV nodal delay to slow HR

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10
Q

parasympathetic receptor and neurotransmitter

A

Muscarinic M2 receptors and acetylcholine

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11
Q

effect of vagal stimulation on pacemaker cells?

A
  • Takes longer to reach threshold
  • Slope of pacemaker potential decreases
  • Frequency of AP decrease
  • Negative chronotropic effect
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12
Q

what part of the heart do cardiac nerves supply?

A

AV node, SA node and myocardium

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13
Q

effect of sympathetic stimulation on the heart

A

increased HR, increased force of contraction and decreased AV nodal delay

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14
Q

neurotransmitter and receptors for cardiac nerve supply

A

noradrenaline and Bi adenoreceptors

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15
Q

effect of noradrenaline on pacemaker cells

A

• Slope of pacemaker potential increases
• Pacemaker potential reaches threshold quicker
• Frequency of AP increases
Positive chronotropic effect

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16
Q

arrangement of cardiac muscle

A

striated, regular arrangement of contractile protein

17
Q

what is required to turn on cross bridge formation between myosin and actin

A

Ca++ from the sarcoplasmic reticulum released in the presence of extra-cellular Ca++

18
Q

what is the refractory period?

A

A period following an AP in which it is not possible to produce another AP. The long refractory period prevents generation of tetanic contraction

19
Q

what is stroke volume?

A

The volume of blood ejected by each ventricle per heart beat

SV = (End diastolic volume) – (End systolic volume)

20
Q

what determines the end diastolic volume?

A

the diastolic stretch of myocardial fibres

21
Q

France-Starling Hypothesis

A

the more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be during the resulting contraction (SV)

22
Q

what does stretch increase the affinity of?

A

Troponin for Ca++

23
Q

what is skeletal muscles optimal fibre length?

A

resting muscle length

24
Q

what is cardiac muscle optimal fibre length?

A

Stretched muscle length

25
Q

what is after load?

A

the pressure into which the heart is pumping

26
Q

consequence of prolonged increased after load?

A

ventricular hypertrophy

27
Q

postive inotropic effect

A

increased force of contraction

28
Q

positive chronotropic effect

A

increased rate of contraction

29
Q

what is the Cardiac output?

A

The volume of blood pumped by each ventricle per minute

30
Q

what are the four events of the cardiac cycle?

A
  1. Passive filling
    Pressure in atria and ventricles are close to zero. AV valves are open so blood fills ventricles. Ventricles become 80% full.
  2. Atrial Contraction
    P wave shows atria depolarisation. Atria contracts between P-wave and QRS. Atrial contraction complete EDV (130ml)
  3. Isovolumetric ventricular contraction
    Ventricular contraction starts at QRS. Ventricular pressure rises. When V pressure > A pressure, AV valves shut. First heart sound (LUB). Aortic valve is still shut too so the blood is TRAPPED IN THE VENTRICLES
  4. Ventricular Ejection
    When V pressure > aorta/PA pressure, valves open, and aortic pressure rises. T waves in ECG signal ventricular repolarisation. Ventricles relax and V pressure falls. When V pressure < Aortic/pulmonary pressure, aortic/pulmonary valves shut (DUB) 2nd heart sound
  5. Isovolumetric ventricular relaxation
    Signalled by closure of aortic/pulmonary valves. Ventricle is a closed box again as the AV valve is shut. When ventricular pressure < atrial presure, AV valves open (silent) and a new cycle starts here
31
Q

two calculations for MAP

A 
MAP = [(2xDBP) + (SBP)]/3
MAP = DBP + 1/3 PP
32
Q

normal ranges for MAP

A

Normal range is 70-105 mm HG

33
Q

MAP equation

A 
MAP = SVR x CO
MAP = SVR x HR x SV
34
Q

what are the major resistance vessels?

A

arterioles

35
Q

resistance to flow equation

A

R directly proportional to n (blood viscosity) and length of blood vessel
R is directly proportional to radius of blood vessel to the power 4

36
Q

what are some humeral agents that can cause vasodilation? intrinsic control

A
  • Serotonin
  • Thromboxane A2
  • Leukotrienes
  • Endothelin
37
Q

causes of vasodilation by relaxation of arteriolar smooth muscles?

A
  • Decreased local PO2
  • Increased local PCO2
  • Increased local H+
  • Increased extracellular K+
  • Increased osmolarity of ECF
  • Adenosine release from phosphate
  • Histamine
  • Bradykinin
  • Nitric Oxide

Cardiovascular (4 decks)

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