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Cardiovascular > Anatomy, physiology, hemodynamics > Flashcards

Anatomy, physiology, hemodynamics Flashcards

1
Q

What does the right coronary artery supply?

A

-RV
-SA and AV nodes
-posterior and inferior surfaces of the LV

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2
Q

What makes up the left coronary system?

A

Circumflex and LAD

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3
Q

What does the left coronary artery supply?

A

-IV septum
-conduction system below the AV node
-anterior and lateral LV walls

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4
Q

What determines end diastolic volume?

A

Ventricular compliance and transmural pressure

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5
Q

By what mechanisms can diastolic compliance be reduced?

A

-myocardial thickening/dysfunction (MI, HTN, valve dysfunction)
-pericardial disease (tamponade)
-extrinsic compression (PEEP, TPTX, RV dilation, impaired chest wall compliance)

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6
Q

What is one commone consequence of sudden diastolic dysfunction?

A

Flash pulmonary edema

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7
Q

In diastolic dysfunction what does ventricular filling become dependent on?

A

Terminal-phase atrial contraction (“atrial kick”)

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8
Q

Definition of afterload?

A

Muscular tension that must be developed during systolic per unit of blood flow

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9
Q

How does a normal heart accommodate for changes in afterload?

A

Increases in:
-contractility
-preload
-heart rate

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10
Q

What happens if preload reserves have been exhausted but there is still a rising/elevated afterload?

A

Cardiac output depression

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11
Q

Which ventricle is more sensitive to increasing afterload?

A

RV

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12
Q

What can influence contractility independent of preload or afterload?

A

-sympathetic impulses
-circulating catecholamines
-acid/base and electrolyte disturbances
-ischemia
-anoxia
-chemodepressants
-hormones (high dose insulin)

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13
Q

No PE signs reliably reflect alterations in contractility but what can suggest impaired contractility?

A

-S3 gallop
-narrow pulse pressure
-poorly audible heart tones

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14
Q

What is the equation to grossly predict the maximum atrial rate before cardiac output and myocardial perfusion are reduced?

A

(220 - age)/min1

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15
Q

On a capillary level what leads to an increase in interstitial fluids?

A

-incresed venous and capillary pressures
-fall in serum oncotic pressures
-increased number and leakiness of capillary pores

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16
Q

What is the basic definition of CHF?

A

Condition in which the filing pressures of the left heart are increased enough to cause dyspnea or weakness at rest or mild exertion

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17
Q

Is a normal functioning LV sensitive or not sensitive to afterload? How about a failing LV?

A

-normal LV is insensitive to changes in ageless but sensitive to preload
-failing LV is sensitive to afterload and fairly insensitive to preload

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18
Q

What are some radiologic findings that suggest acute heart failure?

A

-perivascular cuffing
-widened perivascular pedicle
-blurring of the hilar vasculature
-diffuse infiltrates

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19
Q

How do infiltrates in acute heart failure differ from those found in ARDS and PNA?

A

AHF infiltrates lack air bronchograms and are usually unaccompanied by an acute change in heart size

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20
Q

What are some radiologic findings that suggest chronic heart failure?

A

-Kerley B lines
-dilated cardiac chambers
-increased cardiac dimensions

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21
Q

What are the 2 endogenous natriuretic peptides are released in response to myocardial stretch (ie. ventricular overload)?

A

-ANP atrial natriuretic peptide
-BNP B-type natriuretic peptide

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22
Q

What effects on other endogenous peptides do cardiac natriuretic peptides have?

A

-lower excessive levels of angiotension 2
-lowers aldosterone
-lowers endothelial 1

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23
Q

What systemic effects do cardiac natriuretic peptide have?

A

-arterial and venous dilation
-enhanced diuresis
-inhibition of sodium reabsorption

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24
Q

Which cardiac natriuretic peptide is only stored in small amounts in ventricular granules so an increase is more indicative of ventricular dysfunction and myocardial stretch?

A

BNP

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25
Q

Other than myocardial stretch what else cam cause BNP elevation?

A

-lung diseases
-renal insufficiency
-sepsis
-inflammatory states

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26
Q

What are potential causes of LV insufficiency CHF with normal LV cavity size?

A

-mitral stenosis
-tamponade
-constrictive pericarditis
-acute myocardial infarction
-hypertrophic cardiomyopathy
-diastolic dysfunction

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27
Q

What had the signature echo findings of apical ballooning with preserved ballast basilar contraction?

A

Takotsubo cardiomyopathy (stress cardiomyopathy)
-these findings are temporary

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28
Q

What does generalized hypokinesis with normal chamber size on echo reflect and what causes it?

A

Stunned myocardium
-trauma
-diffuse ischemia
-drug overdose
-toxin ingestion
-post-tachycardia dysfunction

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29
Q

What 6 questions should be asked to determine pulmonary venous congestion etiology?

A

-is forward output adequate to perfuse tissue?
-evidence of systolic dysfunction
-LV size?
-global or regional LV hypokinesis?
-valvular dysfunction?
-evidence of increased pulm vascular permeability or hypoalbuminemia?

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30
Q

What should be used in CHF with LV insufficiency when there is elevated SVR and/or valvular insufficiency with adequate preload and BP?

A

ACE inhibitors (captopril, enalapril) and/or systemic vasodilators

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31
Q

What medication can help aid in CHF with LV insufficiency with cardiac ischemia?

A

Nitrates
-but can precipitate hypotension in patients with borderline or inadequate filling pressures

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32
Q

What are the pros and cons of using beta-blockers for CHF w/ LV dysfunction?

A

Pro
-reduce myocardial oxygen consumption by decreasing HR and contractility

Con
-can precipitate CHF
-can cause conduction system disturbances
-can cause bronchospasm

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33
Q

What are the pros and cons of using Ca channel blockers for CHF w/ LV dysfunction?

A

Pro
-controls HTN
-slows tachycardia
-reverses coronary spasm

Con (only use in well selected patients)
-depress cardiac contractility
-can impair conduction

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34
Q

What is nesiritide?

A

Recombinant human BNP
-for acutely decompensated CHF w/ dyspnea at rest/minimal exertion
-affects: vasodilation, diuresis, natriuresis, decreases plasma NE and aldosterone, decreases preload
-does not change heart rate
-SE: profound hypotension, bradycardia, renal dysfunction

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35
Q

Most CHF with RV dysfunction arise from which disease conditions?

A

-ischemia
-infarction
-cor pulmonale
-ARDS

36
Q

Where does the RV get its blood supply from?

A

RCA

37
Q

What type of MI typically leads to RV dysfunction?

A

Seen in 30% of inferior MIs

38
Q

When should RV dysfunction from a MI be suspected?

A

Systemic venous HTN and ST segment elevation or Q waves over right precordium (V4R)

39
Q

For MI with subsequent RV dysfunction what does prognosis depend on?

A

-size of infarct
-presence or absence of increased PVR

40
Q

What defines cor pulmonale?

A

In response to excessive PVR not d/t pulmonary venous HTN or LV failure get:
-hypertrophy
-dilatation
-RV failure

41
Q

What are 3 causes of pulmonary hypertension?

A

-restricted capillary bed
-alveolar hypoxia
-acidosis

42
Q

What is the maximum pulmonary arterial pressure that normal RVs can overcome?

A

35mmHg

43
Q

What is the most common cause of acute cor pulmonale in a patient without prior cardiopulmonary abnormality?

A

Massive PE

44
Q

What can cause cor pulmonale in a mechanically ventilated patient?

A

Lung overdidtention with capillary compression

45
Q

How much of the pulmonary capillary bed can be obstructed before the pulmonary arterial pressure rises?

A

One half

46
Q

What values help differentiate RV dysfunction from LV dysfunction?

A

-CVP
-PVR
-wedge pressure

47
Q

What are the physical findings of acute cor pulmonale?

A

Same findings as pulmonary hypertension
-hypoperfusion
-RV gallop
-loud P2

48
Q

What are the physical findings of RV failure and severe pulmonary HTN?

A

-pulsatile hepatomegaly
-systemic venous congestion
-parasternal lift
-peripheral edema

49
Q

What are the radiographic signs of cor pulmonale?

A

dilated, sharply tapering central pulmonary arteries with peripheral vascular “pruning”

50
Q

What happens to LV systolic function in true cor pulmonale?

A

Nothing out should be unaffected

51
Q

What are the basic principles in cor pulmonale management?

A

-maintain adequate RV filling
-reverse hypoxia and acidosis
-establish a coordinated cardiac rhythm
-reverse atelectasis
-treat underlying disease

52
Q

What is the treatment for polycythemia in chronic hypoxemia in RV dysfunction?

A

Slowly reduce Hct to 55% to reduce blood viscosity and RV afterload
-this helps improve myocardial perfusion

53
Q

What are the pros and cons to diuresis in a patient with RV dysfunction and cor pulmonale?

A

Pro
-reduction of RV distention and myocardial tension
-improves RV afterload and perfusion
-reduction in pulmonary arterial pressure via decreased CO

Con
-some patients require RV distention and ventricular interdependence to maintain stroke volume so be gentle with diuresis
-to ensure no adverse affects closely watch CVP

54
Q

What are the pros to digitalis in a patient with RV dysfunction and cor pulmonale?

A

-may be helpful in chronic cor pulmonale
-rate control of AFib w/ RVR (slow effect) without depressing myocardial function

55
Q

What are the pros and cons to inotropes (dopamine and dobutamine) in a patient with RV dysfunction and cor pulmonale?

A

Pro
-improve LV function
-boosts perfusion pressure of RV
-improved RV function via ventricular interdependence

Con
-associated arrhythmias
-conduction disturbances
-these can disrupt AV coordination that is vital to RV filing

56
Q

What are the pros and cons to Ca channel blockers in a patient with RV dysfunction and cor pulmonale?

A

These effects are only true for minority of patients. Check during cardiac cath first
Pro
-reduces PVR
-decreased RV afterload which increases CO

Con
-depress myocardial function
-reduce coronary perfusion pressure

57
Q

What are the pros and cons to inhaled NO in a patient with RV dysfunction and cor pulmonale?

A

Pro
-helps when there’s a reversible component to pulm HTN
-good bridge to definitive therapy

Con
-tolerance develops quickly

58
Q

What are causes of acute pericarditis?

A

-infections (viral, TB, bacterial, fungal)
-dissecting aneurysm
-rheumatic
-Dressler syndrome
-anticoagulation
-MI
-malignancy
-uremia
-radiation
-drugs
-trauma

59
Q

What is the characteristic complaint in acute pericarditis?

A

CP relieved by sitting up and forward; exacerbated by laying down, coughing, deep inspiration, swallowing

60
Q

What is the PE of pericarditis?

A

Friction rub best heard with patient leaning forward

61
Q

What is an on EKG in patient with pericarditis?

A

-concave upward ST segment elevation in all leads but AVR and V1
-PR segment depression

62
Q

What is the management of pericarditis?

A

-monitoring
-treat underlying cause
-NSAIDS

63
Q

How much pericardial fluid is needed before it is detected on CXR?

A

250mL

64
Q

What is normal intrapericardial pressure similar to?

A

Intrpleural pressure and less than LV and RV diastolic pressures
-rapid accumulation of pericardial fluid can lead to equalization of RA and LA pressures

65
Q

How does the body compensate for early tamponade?

A

Increased heart rate and adrenergic tone to maintain CO
-means things that reduce venous return or cause bradycardia (hypoxemia, beta-blocker) can quickly lead to shock

66
Q

What are the most common physical findings of tamponade?

A

-JVD
-pulsus paradoxus

67
Q

Why is intubating a patient with cardiac tamponade risky?

A

-positive pressure can further reduce cardiac filling
-vasodilation can drop needed central pressures for compensation

68
Q

What are the general trends seen on SG catheter for pt in distributive shock?

A

-normal PCWP
-increased CO
-decreased SVR
-increased MVO2

69
Q

What are the general trends seen on SG catheter for pt in cardiogenic shock?

A

-increased PCWP
-decreased CO
-increased SVR
-decreased MVO2

70
Q

What are the general trends seen on SG catheter for a pt in hypovolemic shock?

A

-increased SVR
-decreased PCWP
-decreased CO
-decreased MVO2

71
Q

What is the normal value of MVO2 on SG catheter?

A

65%

72
Q

What is the normal value for SVR on SG catheter?

A

900-1300dyne-sec/cm^5

73
Q

What is the normal value for CO on SG catheter?

A

5-7L/min

74
Q

What is the normal value for PCWP on SG catheter?

A

8-12mmHg

75
Q

What is the initial treatment of choice for a pt w/ acute RHF following a MI?

A

fluid resuscitation until PCWP > 15 (if using SG catheter)

76
Q

What are the 3 common pathophysiologic pathways to diastolic heart failure?

A

-impaired ventricular wall relaxation
-LA pressure > LV pressure leading to pulmonary edema
-increased stiffness of ventricle d/t increased wall thickness and decreased internal diameter
-seen in poorly controlled HTN
-excess collagen deposition d/t ischemia
-impairs contractility

77
Q

On a CVP waveform what mechanical event and cardiac cycle event is represented by the a wave?

A

atrial contraction
end diastole

78
Q

On a CVP waveform what mechanical event and cardiac cycle event is represented by the c wave?

A

isovolumic contraction
early systole

79
Q

On a CVP waveform what mechanical event and cardiac cycle event is represented by the v wave?

A

systolic filling of the atrium
late systole

80
Q

On a CVP waveform what mechanical event and cardiac cycle event is represented by the x descent?

A

atrial relaxation, systolic collapse
mid-systole

81
Q

On a CVP waveform what mechanical event and cardiac cycle event is represented by the y descent?

A

early diastolic filling, diastolic collapse
early diastole

82
Q

How much does an IABP tend to decrease afterload?

A

by 10-30%
-it decreases aortic systolic pressure and end-diastolic aortic pressure
-also reduces myocardial oxygen consumption by decreasing isometric phase of LV contraction
-decreases LV wall tension by 20%
-increases LV EF by up to 30%

83
Q

How do vasodilators increase cardiac function in acute decompensated HF?

A

increase CO
-ex. nitroprusside and nitroglycerin
-decrease preload, decrease afterload, decrease myocardial O2 demand, increase CO and SV

84
Q

What murmur is associated w/ AR?

A

-blowing, decrescendo, diastolic murmur at 3rd intercostal space along L sternal border
-low pitched rumbling mid-diastolic murmur at the apex

85
Q

What is the equation to calculate LVEF w/ radionuclide angiography?

A

LVEF = (net counts in end-diastolic frame - net counts in end systolic frame)/(net counts in end-diastolic)

86
Q

What is the normal EF in females? In males?

A

-54-74%
-52-72%

87
Q

What is pulsus paradoxus and in what disease process is it seen?

A

-lack of decline in jugular pressure w/ inspiration
-constrictive pericraditis

Cardiovascular (7 decks)

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