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Immuno/Pathology and Physiology > Physiology Week 2 > Flashcards

Physiology Week 2 Flashcards

1
Q

How do APs travel?

A

Through gap junctions

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2
Q

What does an ECG detect?

A

Extracellular voltages

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3
Q

What are connexons? Connexins?

A

Part of intercalated disks. Connexon is the complete channel, connexin is the subunit protein. Can become disrupted in HF

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4
Q

what are the two main determinants of how fast an AP travels?

A

number of gap junctions between cells and the inward current responsible for the AP upstroke.

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5
Q

What is the waveform mathematically?

A

V2-V1=AP1-AP2

OR dV/dt

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6
Q

What’s the difference between AP shapes in the endocardium and epicardium?

A

Epicardial ventricular cells have more pronounced Phase 1 (doesn’t show up on ECG) and shorter APs (v. imp for ECG). This comes from different expression of K channels

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7
Q

What causes an upward deflection?

A

A depolarization wave moving toward an electrode

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8
Q

What is Einthoven’s Triangle?

A

Where you set up the bipolar ECG limb leads. LA, RA, LL. RA is neg neg, LA neg pos, LL pos pos. Start at RA.

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9
Q

What are precordial leads?

A

placed in transverse plane to provide info in anterior to posterior direction. Can be helpful in finding where an MI is.

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10
Q

What is the P wave?

A

Atrial depolarization

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11
Q

What is the QRS complex?

A

Ventricular depolarization

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12
Q

What the T wave?

A

Ventricular repolarization

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13
Q

Why is there no signal from conducting tissues (SA node)?

A

Not enough tissue mass. The amplitude of a deflection on the ECG depends both on tissue mass and the magnitude of the derivative.

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14
Q

What is the QT interval?

A

Ventricular depolarization to repolarization, so AP duration

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15
Q

What is the PR interval?

A

atrial to ventricular depolarization, so propagation through the AV node. Should be .12 to .20 seconds

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16
Q

Why is conduction through AV node slow?

A

AV nodal upstroke are carried by LTCCs, which are slow

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17
Q

How does parasympathetic negative dromotropy work?

A

Activation of muscarinic Ach receptors go to Gi prot and inhibit AC, which leads to decreased phosphorylation of LTCCs. This decreases upstroke velocity in AV nodal cells

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18
Q

How does sympathetic positive dromotropy work?

A

Activation of beta adrenergic receptor, coupled with Gs protein, activates AC and increases phosphorylation of LTCCs. This increases upstroke velocity in AV nodal cells

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19
Q

How long should the QRS be?

A

less than .12 seconds

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20
Q

What is the scale of ECG boxes?

A

1 small box is 0.04s, 1 large box is 0.2s, 5 large boxes is 1s.

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21
Q

How do you find the electrical axis of the heart?

A

From the leads that produces the largest QRS complex.

  1. look for maximum positive R with no negative, this is closest.
  2. look for closest QRS with integral of zero (up and down balance). Axis is perpendicular to this.
  3. If 2 R waves are equally tall, axis is between these.
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22
Q

What can cause a shift to negative values for electrical axis?

A

LV hypertrophy. Some consider -30 to 0 to be WNL

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23
Q

What can cause a wide QRS?

A

Ventricular propagation - not going through conduction system, slow. Ventricles exciting themselves. Can be premature ventricular contractions (PVCs)

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24
Q

What does a first degree AV block look like?

A

First degree means delayed - delay between P and R. PR interval should be 120-200ms.

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25
Q

What does a second degree AV block look like?

A

Some impulses fail to propagate to ventricles, so some P waves will not be followed by QRS.

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26
Q

What does atrial flutter/ fibrillation look like?

A

P waves are random and irregular, R-R intervals are irregular.

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27
Q

What if two PVCs have different shapes?

A

Premature ventricular contractions can have diff shapes if there are multiple ectopic foci so QRS look diff every time.

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28
Q

What does monomorphic ventricular tachycardia look like?

A

Wide QRS complexes with not enough time R-R. All complexes look similar. Very dangerous. Can be from ventricular focus (one site) or reentry.

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29
Q

Initiation of Reentry?

A

A stimulus delivered late will propagate on both sides and collide.

A premature stimulus will encounter refractory tissue and be blocked only on the right side. It will propagate slowly on the left. By the time it propagates around the bottom, the right side will have recovered

This is why cardiologists consider “dispersion of repolarization“ to increase arrhythmia risk

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30
Q

What does ventricular fibrillation look like

A

Irregular, no identifiable patten. Will cause death in mins.

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31
Q

Why is the T wave usually upright?

A

because although endocardium is activated first, it repolarizes after the epicardium

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32
Q

WHY is the ST segment flat?

A

There’s no difference between the endocardium and epicardium – both declining at same time in the plateau. Must have difference between endo and epi to show up on ECG.

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33
Q

When would you see ST segment elevation?

A

ECG BRUGADA SIGN. Rare. Key thing is a much more dramatic effect on AP in either endo or epi. Example is very shortened AP in epicardium.

Acute ischemia also.

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34
Q

When would you see a negative T wave?

A

Negative T wave would come from the endocardium repolarizing first

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35
Q

What leads should be positive?

A

Lead 1 and aVF. aVR usually negative.

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36
Q

What does left ventricular hypertrophy look like?

A

Left ventricular hypertrophy give you a negative electrical axis and positive aVL.

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37
Q

How is arterial BP determined?

A

primarily by resistance in the arterioles

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38
Q

What is Ohm’s law?

A

Q=(P1-P2)/R Where Q is flow and R is resistance

For BP:

MAP=COxTPR

Which has a causal relationship, don’t rearrange: changes in CO or TPR lead physiologically to changes in MAP, but an increase in MAP does not lead to an increase in CO.

MAP - mean arterial pressure
CO - cardiac output
TPR - total peripheral resistance

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39
Q

What is MAP?

A

At rest:

MAP = 2/3DP + 1/3SP

Because diastole usually lasts longer than systole

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40
Q

How does body sense BP?

A
  1. Baroreceptors
  2. atrial volume receptors (release atrial natriuretic peptide)
  3. chemoreceptors (carotid bodies and aortic arch)
  4. mechanoreceptors in kidney afferent arterioles
41
Q

What is the baroreceptor reflex?

A

Increased pressure leads to more impulses from the baroreceptors to medulla, decreased pressure leads to fewer impulses.

42
Q

What’s the equation for cardiac output?

A

CO=HRxSV

43
Q

What does ANP do?

A

vasodilates blood vessels, which decreases TPR, decreases MAP, blocks renal Na reabsorption (more excreted), which decreases blood volume.

How heart serves as endocrine organ - ANP released from atria

44
Q

What do the central chemoreceptors do?

A

Located in carotid bodies and aorta, they respond primarily to decreases in blood O2. Decrease O2 leads to increased sympathetic output to arterioles which leads to increased resistance. Restricts blood flow to renal, skel muscle, etc. in favor of vital organs.

45
Q

What does angiotensin II cause? What is RAAS?

A

increased aldosterone, which increases sodium reabsorbtion in the kidney, increasing blood volume.

Also causes vasoconstriction, which increases TPR.

Renin-angiotensin-aldosterone-system

46
Q

Why don’t baroreceptors respond to angiotensin-based changes?

A

Angiotensin II can reset baroreceptor response.

47
Q

What does the Frank-Starling relationship describe?

A

increased filling of the ventricle will increase cardiac output (SV vs. LVEDP)

48
Q

What does increased afterload do?

A

increased afterload aka increased pressure in the arteries leads to decreased cardiac output/decreased muscle shortening

49
Q

What does increased preload do?

A

increases CO/ degree of muscle shortening. Ventricular filling is the preload. Increases stroke volume and arterial BP.

50
Q

When does the mitral valve close?

A

When LVP is greater than LAP. Then isovolumic contraction.

51
Q

When does the aortic valve open?

A

When LVP is greater than aortic pressure

52
Q

What is the atrial kick?

A

contraction of atria that pushes more blood into ventricles

53
Q

What are the first and second heart sounds in the Wiggers diagram?

A

1st: Closing of AV valves
2nd: closing of aortic and pulmonary valves

54
Q

Where is pressure high and low in the heart?

A

Atrial pressure is low, ventricular and aortic pressures are high.

55
Q

What does the Wiggers diagram measure?

A

pressure, volume, ECG, heart sounds vs time

56
Q

What are the 4 stages of the cardiac cycle PV loop?

A
  1. isovolumic contraction
  2. ejection
  3. isovolumic relaxation
  4. diastolic filling
57
Q

What is SV on PV Loop?

A

stroke volume is the horizontal distance inside the loop. EDV-ESV. Stroke volume is proportional to CO (CO=SVxHR)

58
Q

What is EDV on PV loop?

A

Distance from far outer loop to Y axis.

59
Q

What is the EF?

A

ejection fraction = SV/EDV

60
Q

Where is EDP on loop?

A

Far bottom right (end diastolic pressure)

61
Q

Where is LAP on loop?

A

left bottom (left atrial pressure)

62
Q

Where is Pes on loop?

A

Top left. End systolic pressure.

63
Q

Where is SBP on loop?

A

systolic blood pressure is the topmost point of loop.

64
Q

Where is DBP on loop?

A

diastolic blood pressure is at the beginning of ejection, the top part of the loop.

65
Q

What is the ESPVR? The EDPVR?

A

end systolic pressure volume relations. ESPVR is top left corner of loop, EDVPR is bottom right. Both are BOUNDARIES and are independent of preload and afterload

66
Q

Why isn’t an EDPVR curve linear?

A

At low volume the ventricle is compliant and easy to fill, whereas as higher volumes, the slope is larger because the ventricle is stiff and more difficult to fill.

67
Q

Is the ESPVR curve linear?

A

YES.

68
Q

What is preload?

A

The load imposed on the ventricle at the end of diastole. The most common measures of preload include end-diastolic volume (EDV) and end-diastolic pressure (EDP). These are found along the EDPVR in the bottom right corner.

69
Q

What does increased preload do to the PV loop?

A

Shifts up and to the R

70
Q

What causes increased preload?

A

fluid retention as found in advanced HF, constriction of veins

71
Q

What causes decreased preload?

A

blood loss, dilation of veins.

72
Q

What is afterload?

A

The mechanical load on the ventricle during ejection. Under normal physiological conditions, this is determined by the arterioles. The most common index of afterload is total peripheral resistance (TPR):

TPR = MAP/CO

Increased TPR leads to decreased SV and increased pressure

73
Q

What causes increased afterload?

A

Temporary constriction of arterioles, chronic hypertension, aortic stenosis

74
Q

What causes decreased afterload?

A

dilation of arterioles

75
Q

What is the slope of the ESPVR curve? Why is it important?

A

The slope (Ees) changes when inotropic drugs are given, but it is independent of preload and afterload. Ees is considered an index of ventricular contractility.

76
Q

What causes increased contractility?

A

beta adrenergic stimulation of ventricles, increased plasma Ca, increase in muscle mass (physiological hypertrophy).

77
Q

What causes decreased contractility?

A

beta adrenergic receptor blocker, Ca channel blockers, decreased energy supply (ischemia or hypoxia can cause), decreased muscle mass

78
Q

Does an increase in stroke volume mean an increase in contractility?

A

not necessarily. SV can also change based on increased preload or decreased afterload.

79
Q

What do we use clinically to measure contractility?

A

Ejection fraction (EF) because the slope Ees of the ESPVR curve is too hard to measure.

80
Q

What is ejection fraction? What affects it?

A

SV/EDF. EF varies with contractility. There are minor effects based on preload but afterload affects EF significantly.

81
Q

What variables alter the venous return curve? How do they change the return curve?

A
  1. arterial resistance (rotates venous return curve, no change to X intercept)
  2. venous compliance (rotation of venous return curve with no change in Y intercept)
  3. blood volume (parallel shift)
82
Q

What’s the relationship of atrial pressure to flow into atrium on the venous return curve? When does maximal flow occur? What controls maximal flow?

A

Lower atrial pressure makes it easier for blood to flow into atrium.

Maximal flow occurs with no atrial pressure (intercept of venous return curve). Maximal flow determined most by arterioles.

83
Q

What does a steady state venous return look like?

A

cardiac output=venous return

84
Q

What happens to the venous return curve with increase in blood volume?

A

Parallel shift as it increases pressure with zero flow, but also maximal flow.

85
Q

What happens to the venous return curve when you decrease TPR (arteriolar dilation)?

A

No change in the no-flow atrial pressure (most of the blood is in the veins) but maximal flow increases because resistance decreases. X intercept same

86
Q

What happens to the venous return curve with venoconstriction?

A

Increases no-flow atrial pressure, no change in maximal flow bc this is determined by arterioles

87
Q

What changes occur due to HF?

A
  1. decrease in contractility (due to damaged myocardium) - decrease in cardiac output and increase in venous pressure
  2. retaining fluids to increase preload - increases cardiac output but w increased venous pressure
  3. chronic sympathetic stimulation to improve myocardial performance (damages myocardium). CO almost back to normal but venous pressure increased
88
Q

What does increased atrial pressure mean for the lungs?

A

Also increased pressure there - why heart failure is CONGESTIVE

89
Q

How do we determine steady-state cardiac output?

A

the intersection of the Starling Curve with the Venous Return Curve

90
Q

What’s a metarteriole?

A

a shunt pathway - doesn’t get closed by sphincter when blood is diverted.

91
Q

What kind of fluid movements occur in the arteries vs veins?

A

filtration at arterial end, absorption at venous

92
Q

What is the Starling equation?

A

Describes fluid movement.

Q=K((Pc-Pi)-(Pic-Pii))

93
Q

What determines pressure in the capillaries?

A

Increased venous pressure - less about increased MAP. Pressure back-up

94
Q

What is active hyperemia?

A

Metabolic activity, particularly in skeletal muscle, produces many vasodilating agents which increases blood flow.

Possible examples: Lactic acid intravascular O2adenosineCO2 H+ ions Extracellular K+

95
Q

What is endothelial-vascular communication?

A

Increased shear stress causes endothelial cells to produce NO. NO diffuses from endothelial to smooth muscle cells  vasodilation. NO turns off cGMP which downregs MLCK

NO in this context is sometimes still called Endothelium-Derived Relaxing Factor

96
Q

What is autoregulation?

A

Autoregulation: ↑ local pressure ↑ local flow which leads to vasoconstriction (opposite end effect of EDRF (aka NO))

97
Q

What encourages turbulent flow?

A

high velocities, low fluid viscosity (decreased hematocrit), narrow blood vessels (increases velocities)

98
Q

What is EDRF?

A

aka NO. Maybe regulates turbulent flow as apposed to laminar flow (smooth flow)

99
Q

How are arterial pressure and volume related?

A

through arterial compliance (veins same but less pressure, more volume)

Immuno/Pathology and Physiology (8 decks)

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