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M2 Cardiology > 1. Cardiovasc Physiology > Flashcards

1. Cardiovasc Physiology Flashcards

0
Q

What are the 2 parts of systemic circulation that don’t have arterioles?

A

CNS/brain, and Heart

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1
Q

Starting with the Right Atrium, name the order in which blood flows through the heart. (chambers and valves)

A

RA, Tricuspid Valve, RV, Pulmonary valve, Pulm Arteries, Lungs, Pulm Veins, LA, Mitral Valve, LV, Aortic Valve, Aorta, Systemic Circ

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2
Q

What parts of the heart does the R Coronary Artery supply? The Left Coronary Artery?

A

R Coronary Artery: becomes posterior descending artery. Supplies posterior 1/3 of Septum, AV node, mainly right side of heart?
L coronary artery: Splits to Circumflex artery and Left Anterior Descending (LAD) artery. Supplies anterior 2/3 of septum (bundles of conduction system are here), mainly left side of heart?

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3
Q

Which parts of conduction system have slow upstrokes vs fast/sudden upstrokes?

A

Slow/gradual: SA node and AV node. Rest is bundles, Purkinje fibers, muscle tissue: fast/sudden upstroke.

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4
Q

How does the brain know what the BP is?

A

Baroreceptors at aorta. they detect BP via stretch: if stretched, BP is high. Can also have stretch receptors in RA – these tell you what the volume is.

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5
Q

Describe Carotid Sinus Massage.

A

Physician puts pressure on carotid at area of sinus/carotid body. activates the stretch receptors, thereby lowers BP. also decreases sympathetic tone, and increases vagal tone to the AV node.

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6
Q

Vagal efferents to the heart do what? what types of nerves are they?

A

Vagi are parasympathetic. Stimulation would slow the sinus rate, and decrease conduction through the AV node.

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7
Q

P cells stand for what? what is the quality that they have that is unique?

A

P for pale (could also be for pacemaker). AV node cells and SA node cells. they have automaticity – they produce the sinus impulses.

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8
Q

Why does the cardiac myocardium require so much ATP?

A

huge amount of energy required to maintain trans-membrane potential – 10000 fold difference between Ca conc in and Ca conc out.

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9
Q

Which protein wraps around the actin filament and moves in order to allow the myosin to access the ____complex: troponin or tropomyosin?

A

Tropomycin wraps around in a spiral pattern, troponin is the I, T, C complex. Calcium binds to troponin, moving it and tropomyosin, and the myosin heads can then interact with actin.

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10
Q

Define inotropy

A

Like contractility. But more specific: refers to the amount of calcium, and the rate at which it flows into the cell.

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11
Q

Define lusitropy.

A

Opposite of Inotropy. Amount and rate of removal of Ca into SR.

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12
Q

What are the 3 determinants of LV systolic function?

A

Preload, Contractility, Peripheral Vascular Tone.

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13
Q

Define preload

A

Fiber length. related to heart size. may also be considered fiber tension prior to contraction.

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14
Q

Define afterload

A

resistance by systemic vasculature. SVR = systemic vascular resistance. PVT = peripheral vascular tone. essentially what the heart is pushing against.

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15
Q

what is the effect of increased contractility/inotropy on fiber tension?

A

Not sure

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16
Q

what are a few ways to increase inotropy?

A

use digitalis to get more Ca2+ in cell, use catecholamines for same purpose. also can give vasodilators to decrease Systemic Vasc Resistance.

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17
Q

What measures are a proxy for preload?

A

sarcomere length, LV diastolic volume, LV diastolic pressure, pulm wedge pressure.

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18
Q

what measure are a proxy for cardiac output?

A

stroke volume, LV fiber shortening, LV fiber tension (?)

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19
Q

name 2 ways to increase cardiac output?

A

increase contractility, or decrease SVR.

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20
Q

3 ways to improve LV systolic function?

A

increase preload, increase contractility, decr SVR.

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21
Q

What is the main user of myocardial 02 consumption? why is this impt?

A

afterload. impt because if you have coronary artery disease, increased use of 02 is critical/difficult given your compromised delivery of 02 to the heart.

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22
Q

how would we calculate afterload (wall tension after contraction)?

A

calculate from heart size and BP. Tension = (Systolic BP * LV radius (ventricle only))/(2xwall thickness)

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23
Q

What are the good and bad qualities of a big heart?

A

Good: stronger.
Bad: consumes inc 02. because as you enlarge the heart to generate more pressure, you need more tension, so you incr the thickness of the wall.

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24
Q

what are a few things that determine arteriolar resistance to blood flow?

A

vasoconstrictor and vasodilator fibers, blood-borne excitatory and inhibitory chemicals, vasodilator action of tissue metabolites, adenosine.

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25
Q

what’s impt about adenosine?

A

impt vasodilator. major metabolite that determines local tone of arteriole.

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26
Q

what is the initial event in systole?

A

mitral valve closure. aortic valve is initially closed. as LV pressure increases, aortic valve opens, stays open during contraction.

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27
Q

what is the initial event in diastole?

A

aortic valve closes when pressure is higher in aorta than LA. mitral valve then opens as LV fills.

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28
Q

what are 5 determinants of LV diastolic function?

A
  1. Lusitropy
  2. LA pressure (aka LV filling pressure)
  3. LV compliance
  4. HR (affects diastolic filling time)
  5. atrial kick at end of filling
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29
Q

what is compliance?

A

stiffness of body that you’re filling. eg stiffness of balloon being blown up.

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30
Q

what are some causes of decreased LV compliance?

A

ischemia, infarction, LV hypertrophy

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31
Q

2 ways to improve LV diastolic function?

A

treat underlying causes: ischemia or hypertrophy

decr heart rate to allow more time for filling.

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32
Q

Importance of LV function: three realms.
How does LV function impact prognosis?
Diagnosis?
Treatment?

A

Prognosis: the degree of LV dysfunction predicts poor prognosis in patients with heart disease.
Diagnosis: Dyspnea can be due to pulmonary or cardiac disease. If there is LV dysfunction, the cause is cardiac.
Therapy: tailored to the type of dysfunction. Systolic prob: improve contraction. Diastolic prob: improve filling.

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33
Q

What is a normal ejection fraction?

A

around 50%

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34
Q

what is the correlation between ejection fraction and mortality in post-MI patients?

A

lower the EF, higher the mortality

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35
Q

where would we place a swan-ganz catheter? for what purpose?

A

place in pulmonary artery (go through SVC, RA, tricuspid, RV, pulmonary valve, to pulm artery).
purpose: measures LV preload. measures pressure of blood on way to lungs = estimate for BP on way back from lungs to LA.

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36
Q

where is pulm artery wedge pressure taken?

A

in pulm artery, just past RV and prior to entry to lungs.

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37
Q

if the balloon on the swan-ganz catheter is inflated, what pressure are you measuring? if it is deflated?

A

inf: measuring pulm artery pressure.
def: measuring pulm vein presure, proxy for filling pressure of LA.

38
Q

how can you use the wedge pressure to guide your IV use?

A

when wedge pressure is normal, prob have given enough fluids. if you give too much fluids, it will leak out of the pulm capillaries and cause pulm edema.

39
Q

what is the formula for calculating ejection fraction?

A

stroke volume/end-diastolic volume.
stroke volume = EDV-ESV
so: EF = (EDV-ESV)/EDV

40
Q

what is diffuse hypokinesis?

A

heart not pumping out as much blood as normal. smaller amount of movement all around LV.

41
Q

what is dyskinesis?

A

many parts of the heart’s contraction may be normal, but there is a section that is not pumping. may be due to ischemia, may be termed “aneurysm”

42
Q

Where does most of the pressure drop take place within the arterial system?

A

in the arterioles.

43
Q

what is the normal distribution of blood volume?

A

50% in systemic veins and venules
30% in heart and pulm vessels
13% in arteries
7% in arterioles and capillaries

44
Q

what will be the effect of arteriolar constriction to the rest of the system, and to preload/afterload?

A

arteriolar constriction diverts blood flow to brain and heart, also raises BP. increases LV afterload.

45
Q

what will be the effect of systemic venoconstriction to the rest of the system and to preload/afterload?

A

shifts blood volume from systemic compartment to pulmonary compartment. increases LV preload

46
Q

the central venous pressure is the same as pressure in what heart chamber?

A

RA

47
Q

pulm wedge pressure indicates the pressure in what heart chamber?

A

LA.

48
Q

What is the equation for cardiac output?

A

CO = HR x SV.

49
Q

What are 6 factors affecting total blood volume?

A
  1. renal blood flow
  2. Angiotensin II
  3. Aldosterone
  4. vasopressin/ADH
  5. Atrial natriuretic hormone
  6. renal arteriolar sympathetic tone
50
Q

what are 6 factors affecting cardiac output?

A
  1. blood volume (= preload)
  2. Cardiac tone (inotropy)
  3. arteriolar sympathetic tone
  4. venous sympathetic tone
  5. angiotensin II
  6. cardiac hypertrophy
51
Q

systemic venoconstriction inc/dec LV preload?

inc/dec cardiac output?

A

inc preload

inc CO

52
Q

increased arteriolar tone inc/dec BP?

A

inc

53
Q

3 forms of cardiac stress?

A
  1. volume load. creates need for a larger stroke volume.
  2. Pressure load. creates need for higher BP
  3. ventricular underloading. small LV -> low output and pressure
54
Q

3 responses to cardiac stresses?

A
  1. sympathetic stimulation. tachycardia, increased inotropy. arteriolar and venous constriction.
  2. salt and water retention. leads to increased BV and increased preload.
  3. cardiac hypertrophy. if volume load, Eccentric LVH. if pressure load, Concentric LVH.
55
Q

describe eccentric hypertrophy

A

response to a volume load. sarcomeres added in series, increasing wall length. the same shortening/sarcomere with more sarcomeres yields a greater stroke volume. volume solution to a volume problem.

56
Q

describe concentric hypertrophy

A

sarcomeres added in parallel to increase wall thickness. the same tension/sarcomere with more sarcomeres generates a greater systolic pressure. pressure solution to a pressure problem.

57
Q

describe the Valsalva maneuver. what can be the result? why?

A

Valsalva: exhalation against a closed glottis. less blood flow in chest, less blood in right heart, less bloodflow into lungs, less into LV -> LV underloading. result = DROP in BP. can lead to fainting.

58
Q

most common cause of LV underloading?

A

hemorrhage.

59
Q

describe the path leading to orthostatic hypotension/syncope

A

from sitting, rise to standing posture. blood pooled in leg veins -> decr venous return. decreased CO and BP. BP drop can lead to orthostatic syncope.

60
Q

what response do we rely on to prevent orthostatic syncope?

A

sympathetic NS. reflex tachycardia. also, baroreflex plays a role. stand up -> BP falls -> decr stretch in receptors -> HR increases -> BP inc, inotropy incr, venoconstriction.

61
Q

what kind of exercise can create a pressure load?

A

isometric. reason: the muscle constricts the arterioles, so need to raise the BP to get through. the brain knows to raise BP and may do it in anticipation.
Will cause a concentric LVH.

63
Q

what kind of exercise can cause a volume load?

A

endurance. because cardiac output needs to be able to rise quickly. volume load -> eccentric hypertrophy.

64
Q

Vagal efferents are primarily distributed where? What would be the effect of stimulation?

A

distributed to sinus and AV nodes. cardiac vagal stimulation decreases the HR and conduction velocity of sinus and AV nodes.

65
Q

Vagal afferents are located where? what do they control/what are they sensitive to?

A

stretch receptors in the aorta and carotid sinus are sensitive to blood pressure, and contribute to the baroreflex.

66
Q

what is the dominant effect of sympathetic vascular stimulation?

A

arteriolar and venous constriction, mediated by alpha-adrenergic receptors.

67
Q

what is the dominant effect of cardiac sympathetic stimulation?

A

increases automaticity (HR), conduction velocity of sinus and AV nodes, and myocardial contractility

68
Q

what is the first part of systole (on a molecular level?) Phase 0, Phase 2?

A

cardiac impulse travels along myocardial sarcolemma, sodium influx = Phase 0 of action potential. This triggers Phase 2 of action potential (calcium influx). Ca concentration allows interaction of actin and myosin.

69
Q

what happens during diastole?

A

Ca is pumped back into SR and sarcotubules, lowering intracellular Ca concentration back to pre-systolic levels.

70
Q

systolic contraction of the LV is affected by 3 things: what are they?

A

preload, contractility, afterload. (latter is affected by systemic vascular resistance)

71
Q

what types of drugs increase contractility?

A

positive inotropic agents: beta-adrenergics, digitalis, catecholamines

72
Q

in terms of vascular resistance, what can improve cardiac contractility?

A

decr systemic vascular resistance.

73
Q

what is the formula for systemic vascular resistance?

A

SVR = (BP-CVP)/CO

74
Q

what is the major determinant of myocardial 02 requirement?

A

afterload.

75
Q

what are the 5 phases of diastole?

A
  1. resequestration of Ca into SR. measured by lusitropy (rate and amount)
  2. isovolumic relaxation
  3. early diastolic LV filling. just after mitral valve opens. affected by LV compliance, and LV filling pressure.
  4. diastasis. little change in volume
  5. Atrial kick. LA contraction.
76
Q

When a Starling curve shifts up, what might be two reasons for the shift?

A
  1. increased sympathetic tone

2. decr systemic vascular resistance

77
Q

why is cardiomegaly a useful sign of heart failure?

A

Starling’s law: a big heart is a stronger heart.

78
Q

what is the definition of cardiomegaly?

A

on CXR, if the transverse cardiac diameter is more than half the trans-thoracic diameter = cardiomegaly.

79
Q

afterload is clinically estimated by what measure?

A

systolic BP

80
Q

increased renal blood flow will increase what?

A

glomerular filtration rate

81
Q

increased Angiotensin II will increase what?

A

efferent arteriolar tone, inc glomerular filtration rate

82
Q

increased aldosterone will increase what?

A

increased Na retention in the distal tubule/collecting duct, inc blood volume

83
Q

increased vasopressin will increase what?

A

water reabsorption

84
Q

increased Atrial Natriuretic Hormone will increase what?

A

increased Na excretion, decreased renin and aldosterone.

85
Q

increase renal arteriolar sympathetic tone will increase what?

A

renal vascular tone, renin secretion. sim to renal arteriolar stenosis

86
Q

where are the receptors that detect blood volume?

A

cardiac stretch receptors

87
Q

where are the receptors that detect blood pressure?

A

arterial stretch receptors (aorta). aortic baroreceptors. in all arteries.

88
Q

what is the definition of a volume load?

A

LV needs to generate a higher cardiac output

89
Q

what is the definition of a pressure load?

A

LV needs to generate a higher BP

90
Q

what is underloading?

A

decreased LV filling (decr preload)

91
Q

what is the response to the aortic stretch receptors detecting a decr in BP? (sympathetic baroreflex)

A

tachycardia, increased inotropy and lusitropy, arteriolar constriction, venous constriction.

92
Q

what is the heart’s response to a volume load (need for higher CO)?

A

eventually, will add sarcomeres in series –> eccentric hypertrophy

93
Q

what is the heart’s response to a pressure load (need for higher BP)?

A

eventually, will add sarcomeres in parallel –> concentric hypertrophy

M2 Cardiology (32 decks)

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