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Fall'20 A&P III > CV Diseases > Flashcards

CV Diseases Flashcards

1
Q

s/s of LHF

A

orthopnea
paroxysmal nocturnal dyspnea
pulmonary edema

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2
Q

s/s of RHF

A

hepatomegaly
JV distension
peripheral edema

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3
Q

MCC of CHF?

A

ischemia and MI

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4
Q

Pump dysfunction primary etiology of what?

A

CHF

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5
Q

name 4 elements of CHF etiology:

A
  1. pump dysfunction
  2. decreased contractility
  3. increased afterload
  4. increased preload
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6
Q

pump dysfunction leads to

A

congestion and low perfusion

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7
Q

causes of decreased contractility:

A
  • ischemia/MI
  • cardomyopathy
  • valvular heart disease
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8
Q

Valvular stenosis causes

A

pressure overload

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9
Q

valvular regurgitation causes

A

volume overload

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10
Q

systemic hyptertension causes

A

increased afterload

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11
Q

increased preload leads to symptoms of

A

pulmonary vascular congestion

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12
Q

s/s of increased preload include:

A

dyspnea
orthopnea
paroxysmal nocturnal dyspnea
pulmonary edema

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13
Q

MCC of Right sided HF

A

left sided HF

the RV may fail secondary to pulmonary disease (COPD) which causes increase in pulmonary vascular resistance, resulting in right sided pressure overload

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14
Q

• Backward congestion symptoms

A

o Dyspnea , orthopnea, PND
o JV distension ( venous pressure)
o Peripheral pitting edema

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15
Q

signs and symptoms of CHF

A 
•	Signs
o	Tachycardia
o	S3 (ventricular gallop), S4 (atrial gallop)
o	Rales
o	Cardiomegaly
o	Ascites
o	Hepatic congestion ( increased CVP)
o	Systolic dysfunction 
o	Diastolic dysfunction
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16
Q

o Diastolic dysfunction (to ef, edv, etc)

A

heart unable to dilate/relax; becomes stiff

Preserved EF, normal EDV, ↓ compliance (↑EDP) often secondary to myocardial hypertrophy

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17
Q

o Systolic dysfunction (to EF, EDV, etc.)

A

Reduced EF, ↑ EDV, ↓ contractility often secondary to ischemia/MI or dilated cardiomyopathy

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18
Q

heart sounds associated with HF

A

o S3 (ventricular gallop), S4 (atrial gallop)

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19
Q

Diagnostics for HF

A
  • BNP 100-300 (normal ~ 100)
  • EKG - evidence of ischemia, chamber enlargement
  • CXR - cardiomegaly, pleural effusion/edema
  • Echo - systolic and diastolic dysfunction
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20
Q

Treatment for HF (broad goals):

A
  • treat diminished contractility
  • treat high preload
  • treat high afterload
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21
Q

specific treatment for HF contractility

A

Amrinone (PDE inhibitor)
Beta agonist - Dopamine
Digoxin

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22
Q

Specific treatment of HF for high afterload

A

ACE inhibitors or ATR blockers

-reduce afterload and improve survival

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23
Q

Role of digoxin in HF treatment

A

o Inhibit Na/K ATPase
o BEWARE digoxin toxicity with hypokalemia (with diuretics) , elderly and renal insufficiency
o EKG finding in toxicity
—- PVC’s
—–ST depression ‘ dig effect’
—–Paroxysmal atrial tachycardia with varying block

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24
Q

ABCDE tx of HF

A

ABCDE

	-ACE Inhibitors- reduce afterload
	-Beta-blockers
	-Calcium Channel Blockers
	-Diuretics
-	Endothelin Receptor Blockers -->  decrease pulmonary vascular resistance
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25
Q

Anesthesia concerns for HF

A
  • elevated head posture
  • fluid status sensitive
  • risk of OD due to slow circulation
  • monitor I/O
  • sensitive to gases
  • avoid N2O in severe HF
  • watch for arrhythmia - poorly tolerated
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26
Q

• Mean Arterial Pressure =

A

Cardiac output x SVR

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27
Q

Stroke volume x Heart Rate

A

Cardiac Output =

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28
Q

• Stroke volume is determined by three factors:

A

1.) preload, 2.) afterload 3.) contractility

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29
Q

• Preload is determined by two factors:

A

1.) intravascular volume 2.) venous tone

o Venous constriction –> high preload

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30
Q

what is the major determinant of intravascular volume?

A

NA in the body

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31
Q

** most important hormone for controlling vascular volume?

A

aldosterone

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32
Q

Normal EF =

A

60-80%

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33
Q

Ejection Fraction is …

A

the fraction of the end diastolic volume ejected in EACH stroke volume

Is an index of ventricular contractility- “systolic function”

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34
Q

formula for EF

A

EF = SV / EDV

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35
Q

** formula for SVR =

A

SVR = [ (MAP-CVP) / CO ] x 80

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36
Q

major determinant of SVR ?

A

arterioles

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37
Q

normal SVR?

A

1200-1500 dynes/sec/cm^-5

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38
Q

Afterload is

A

Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure).

The lower the afterload, the more blood the heart will eject with each contraction. Like contractility, changes in afterload will raise or lower the Starling curve relating stroke volume index to LAP.

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39
Q

Preload is:

A

preload is a measure of the degree of the ventricular stretch when the heart is at the end of diastole

LVEDP (supplied by: DBP)

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40
Q

** 5% of cardiac output. 250 ml/min @ rest

A

coronary circulation

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41
Q

**Coronary perfusion pressure =

A

arterial diastolic pressure - LVEDP (preload)

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42
Q

maximum flow of coronary circuclation occurs during

A

diastole

– this is why diastolic dysfunctions interrupt blood supply

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43
Q

hypoxia and adenosine cause:

A

vasodilation

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44
Q

name two factors that reduce coronary blood flow:

A
  1. tachycardia (shorter diastolic time)

2. aortic stenosis

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45
Q

Autoregulation MAP =

A

50-120mmHG

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46
Q

how does the autonomic system influence coronary circulation?

A

minimally

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47
Q

the myocardium utilizes all the O2 from arterial blood. what does this result in?

“extraction ratio”

A

if demand increases, it must be met
so, coronary blood flow increases

*parallel

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48
Q

What are the major determinants of coronary blood flow?

A

LVEDP & HR

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49
Q

resulf of stenosis on Coronary blood flow?

A

stenosis –> angina

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50
Q

at rest, coronary circulation accounts for what % of CO?

A

5%

250ml/min

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51
Q

increased pressure (vol) at the end of diastole causes

A

coronary compression
(coronaries lie under the heart)

-coronaries perfuse with diastolic relaxation

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52
Q

most volatiles are ideal for MI because they

A

are coronary vasodilators

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53
Q

the RV is perfused throughout

A

systole and diastole

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54
Q

the LV is perfused largely during

A

diastole

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55
Q

name three things that can decrease coronary perfusion:

A
  1. decreased aortic pressure
  2. increased HR (d/t decreased diastolic time)
  3. Increased LVEDP (preload)
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56
Q

main coronary artery? what percent?

A

80% Left CA

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57
Q

name two forms of myocardial hypertrophy

A
  1. concentric hypertrophy

2. eccentric hypertorphy

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58
Q

form of hypertrophy d/t chronically elevated afterload (pressure overload) is:

A

concentric hypertrophy

**Increased systolic pressure

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59
Q

form of hypertrophy d/t chronically elevated preload (vol overload) is:

A

eccentric hypertrophy

**increased diastolic pressure

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60
Q

concentric hypertrophy results in:

A

o Increased Thickness of ventricular walls, (due to Increased ejection of blood)

o Chamber size remains normal

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61
Q

o Conditions causing LV concentric hypertrophy

A

 Chronic untreated hypertension
 Chronic aortic stenosis
 Coarctation of aorta (“a kink”)

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62
Q

o Conditions causing RV concentric hypertrophy

A

 Pulmonary artery HTN

 Pulmonary valve stenosis

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63
Q

Eccentric hypertrophy is due to?

what happens to heart?

A

• Due to chronically elevated preload (volume overload)
• Chamber size increases to accommodate larger volume
a

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64
Q

• Causes of eccentric hypertrophy:

A

o Excessive intravascular volume
o Chronic mitral or aortic regurgitation (“leaking of volume”)
o Morbid obesity

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65
Q

x axis on PV loop =

A

preload (LV volume)

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66
Q

y axis on PV loop=

A

afterload (LV pressure)

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67
Q

MV opens at what point on PV loop?

A

A

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68
Q

Point A on PV loop =

A

MV opens
ESV
S3

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69
Q

Point B on PV loop =

A

MV Closes = S1
EDV
S4
** ATRIAL KICK!!

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70
Q

Point C on PV loop =

A

aortic valve opens

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71
Q

Point D on PV loop =

A

aortic valve closes = S2

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72
Q

b/w point A and B on PV loop=

A

filling period

Stroke volume

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73
Q

b/w point B and C on PV loop=

A

isovolumetric contraction

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74
Q

b/w point C and D on PV loop=

A

period of ejection

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75
Q

b/w point D and A on PV loop=

A

isovolumetric relaxation

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76
Q

the beginning of contraction and indication of compliance is at what point on the PV loop?

A

point B

o	Beginning of contraction
o	Heart is biggest as it gets
o	Shows EDP/EDV relationship
o	Shows LVEDV. Pressure is fairly low
o	Indicates compliance; how easily ventricle takes in blood without significant rise in pressure
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77
Q

Ca ++ is releasing from troponin and going back into the SR at what point on the PV loop?

A

Point D

o Ventricle start relaxing
o Ca++ is releasing from troponin and going back to sarcoplasmic reticulum
o Shows ESP/ESV relationship
o ( or ) shows regurgitation

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78
Q

insert image assessment of ventricular function

A =
B=
C=
D=

A
  • ‘A’ is normal single ventricular contraction
  • ‘B’ shows increasing preload with constant contractility and afterload
  • ‘C’ shows increasing afterload with constant preload and contractility
  • ‘D’ shows increasing contractility with constant preload and afterload

ESP= End systolic point; EDP= End diastolic point

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79
Q

In Systolic failure, there is increase in LVEDV and reduction of SV. LVEDP is increased b/c LV vol is increased. Diastolic portion of PV loop has shifts

A

to the RIGHT

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80
Q

In Diastolic failure, diastolic portion of PV loop shifts

A

UP

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81
Q

o Heart is unable to pump to meet the need
o Low CO–> fatigue, oxygen debt and acidosis
o Damming –> pulmonary or systemic congestion
o Causes: CAD, valvular dysfunction or arrhythmia

What form of HF is this?

A

Systolic

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82
Q

Causes: HTN, CAD, hypertrophic cardiomyopathy and pericardial diseases

What form of HF?

A

diastolic

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83
Q

normal atrial pressure =

A

8

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84
Q

according to the Heart Association classification of heart disease, class 1 is:

A

asymptomatic

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85
Q

according to the Heart Association classification of heart disease, class IV (4) is:

A

symptomatic at rest

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86
Q

in mitral stenosis; atrial pressure is=

A

high!!! 25/14 (normal is 8)

LA has to squeeze hard through a tight hole ==> less LV filling

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87
Q

what effects does Mitral stenosis have on the PV loop?

ABCD..

A

all decrease. loop shift DOWN and LEFT

preload
LVEDV
LVEDP
SV
EF
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88
Q

features of Mitral stenosis include:

A

• Delayed complication of RHD (antibodies), may occur 15-20 years after RF
• Normal left ventricle
• Narrowing of the mitral valve (Normal 4-6 cm2)  rise in left atrial pressure which limits the pulmonary venous drainage –> increased PA pressure –> pulmonary hypertension –> RVH
o Ascites, peripheral edema, high risk of a.fib

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89
Q

PE of Mitral Stenosis

A 
o	Loud S1
o	Opening snap
o	Loud P2
o	Low pitched late diastolic murmur (mid diastolic murmur), best heard at apex
o	LA >> LV pressure during diastole
o	Right ventricular lift
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90
Q

symptoms of mitral stenosis

A

o Dyspnea, orthopnea , PND (due to pulm. congestion) “backup”
o Hemoptysis
o A fib –> embolization

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91
Q

dx of mitral stenosis

A

o ECG signs of left atrial enlargement, RVH (normal LV)
o A.fib
o CxR: straightening of the left heart border
o Dilation of pulmonary veins
o Echo : Narrowed, “fish mouth” – shaped orifice

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92
Q

medical tx for mitral stenosis includes:

A

MS = “ADDS”

  • Anticoagulant
  • diuretics (pulm congestion)
  • Digoxin/ Diltiazem (afib)
  • Surgical replacement
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93
Q

Anesthetic goals for patient with Mitral Stenosis would be:

*in regards to Heart Rate and rhythm, preload, afterload, contractility.

A
  • Slow/Low HR (for LV filling)
  • NSR
  • Not too full, tight, or strong (maintain preload, afterload/SVR, and contractility

“remember: slow, regular, not too full/tight/strong”

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94
Q

causes of mitral valve regurgitation:

A

o Chronic: due to rheumatic heart disease, incompetent valve or destruction of mitral valve annulus

o Acute: due to ischemia, MI (papillary muscle dysfunction (D3 post MI), infective endocarditis (Bacterial Staph) or chest trauma

o Mitral valve prolapse

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95
Q

what effects does Mitral regurgitation have on the PV loop?

ABCD..

A 
Afterload decreases
SV decreases
SVR decreases
CO decreases
-Acute: atrial compliance is normal or decreased (pulm congestion)
Left Atrial Pressure increases
contractility increases 
LVEDV Increases 
LVEDP Increases
-Chronic: atrial compliance is increased (low CO)
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96
Q

what form of hypertrophy develops as a result of mitral regurgitation?

A

eccentric

LV hypertrophy due to regurg vol > SV

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97
Q

symptoms of mitral regurgitation may include:

A

o Due to backward regurgitant flow: dyspnea, orthopnea, PND

o Regurgitation symptoms
 <30 % mild symptoms
 30-60 % moderate
 > 60% severe symptoms

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98
Q

PE for mitral regurgitation:

A

o Diffuse and hyperdynamic ventricular impulse
o Holosystolic murmur best heard at apex, radiating to axilla
o Wide splitting S2
o S3 due to volume overload in left atrium

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99
Q

wide splitting S2 and holosytolic murmur are associated with what valvular heart disease?

A

MR

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100
Q

dx of MR includes:

A 
o	EKG: left atrial enlargement and left ventricular hypertrophy
o	Cx: enlarge left atrium
o	Echo: may show ruptured chordae
o	Cath: large v wave
o	TEE and doppler
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101
Q

a large V wave is associated with what valvular heart dx?

A

MR

  • Present in chronic phase
  • Shows decreased atrial and pulmonary compliance and
  • increased pulmonary blood flow and regurgitant volume
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102
Q

Loud S1, opening snap, and a low pitched late diastolic murmur are associated with what valvular heart dx?

A

Mitral stenosis

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103
Q

Medical tx for Mitral regurg are:

A

MR = “VADDS”

  • Vasodilator (ACE inhibitors) - reduce afterload; move fwd
  • Anticoagulant
  • diuretics (pulm congestion)
  • Digoxin/ Diuretics (afib)
  • Surgical replacement
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104
Q

Anesthetic goals for patient with Mitral Regurgitation would be:

*in regards to Heart Rate and rhythm, preload, afterload, contractility.

A
  • Increase HR (avoid brady b/c regurg worsens)
  • NSR
  • Maintain Preload (increase PL = Increased regurg; decreased= decreased CO)
  • Decrease Afterload - move flow fwd.
  • Maintain Contractility (dig)

**remember: Fast, FWD, Regular and not too strong”

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105
Q

the most frequent valvular lesion commonly found in young women is

A

MV prolapse

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106
Q

clinical features of MV prolapse include:

A

-most asymptomatic; atypical chest pain or tachyarrhythmia

  • pregnancy
  • murmurs when supine to rising; infective endocarditis
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107
Q

Management of MV Prolapse:

A

minimal. most don’t require tx. complications are rare.

  • Beta Blocker for palpitation
  • abx prophylaxis with MR
108
Q

major anesthesia concerns for MV prolapse

A

avoid increasing HR

avoid histamine release

109
Q

valvular disease associated with pregnancy?

A

MV prolapse

-ideal to allow for tolerance in the increased blood volume associated with pregnancy.

110
Q

in mitral stenosis; what are the considerations for spinal/epidural use?

A

avoid

don’t want to decrease preload

111
Q

Aortic Stenosis - when you see this dx, what should we automatically associate it with?

A

coronary perfusion!!!

112
Q

what effects does Aortic Stenosis have on the PV loop?

ABCD..

A

-SV Decreases

-Due to the stenosis; almost everything INCREASES:
LVESP = 200mmhg
LVESV
LVEDV/ Preload
Contraction

This moves the loop to the RIGHT and UP - isovolumetric sides.

113
Q

aortic stenosis is what form of hypertrophy?

A

Concentric LV hypertrophy

114
Q

Clinical symptoms of Aortic Stenosis:

A

AS = “SAD”

  • Syncope (fall in SV and BP)
  • Angina (decreased O2 supply)
  • Dyspnea
115
Q

PE for Aortic Stenosis:

A

o Paradoxical splitting of S2
o P2 comes before A2 in expiration
o Very narrow pulse pressure due to low systolic BP
o S4
o Systolic ejection murmur, with LV pressure&raquo_space; aortic pressure during systole

116
Q

splitting of S2
S4 (‘atrial kick’)
and systolic ejection murmur

associated with what valvular disease?

A

aortic stenosis

117
Q

low pulse pressure d/t low SBP is associated with:

A

aortic stenosis

118
Q

does age matter in regards to AV replacement?

A

no

if you need it, you need it.

119
Q

Anesthetic goals for patient with Aortic Stenosis would be:

*in regards to Heart Rate and rhythm, preload, afterload, contractility.

A

MAINTAIN!!

Maintain HR / NSR (avoid brady ) 
Maintain/increase Preload &amp; Afterload
Maintain Contractility (not too strong)

MAINTAIN coronary perfusion

“remember: slow, full, tight, regular, and not too strong”

120
Q

coronaries feed during

A

diastole

121
Q

**Normal aortic valve distance =

A

[ N=2.5-3.5 cm2]

narrowed aortic valve: 0.7-0.9 cm2

122
Q

in aortic stenosis; what are the considerations for spinal/epidural use?

A

contraindicated in severe stenosis

-can lead to decrease in SVR

123
Q

what effects does Aortic Regurgiation have on the PV loop?

ABCD..

A

NO isovolumetric relaxation or contraction as blood is still coming in during systole.

INCREASED:
LVEDV
SV
LVESP

Moves the loop to the RIGHT and UP (major volume increase)

124
Q

causes associated with aortic regurgitation:

A 
o	Rheumatic heart disease or congenital 
o	Infective endocarditis
o	3 Syphilis 
o	Aortic dissection
o	Marfan’s syndrome
o	Collagen vascular disease e.g. SLE
125
Q

in AR the Regurgitant flow from aorta during diastole results in

A

left ventricular dilatation and volume overload

126
Q

a widened pulse pressure is often associated with what valvular disease?

A

AR

Reduction in systemic diastolic blood pressure leading to increased pulse pressure – Widened pulse pressure (160/50)

127
Q

clinical features of AR

A

“AR = SAL”

o Syncope, weakness due to reduction in the diastolic arterial pressure
o Angina- because reduce coronary blood flow (coronary arteries are perfused during diastole)
o Left ventricular failure (PND) due to volume overload

128
Q

o High pitch “blowing” diastolic murmur is associated with

A

AR

129
Q

rapid rise followed by a rapid fall of carotid pulse is known as:

A

Corrigan pulse

130
Q

A Pistol-shot –

A

femoral pulse “bounding”

131
Q

a diastolic bruit over the femoral artery

A

Duroziez sign –

132
Q

 De Musset’s sign

A

– bobbing motion of head

133
Q

systolic blushing and then diastolic blanching of the fingernail bed

A

Quincke’s pulse –

134
Q

Anesthetic goals for patient with Aortic Regurgitation would be:

*in regards to Heart Rate and rhythm, preload, afterload, contractility.

A

“remember: Fast, Full, and forward”

  • Maintain HR/NSR and maybe slightly tachy
  • Increase Preload
  • decrease Afterload (TPR)
135
Q

avoid vasoconstrictors in what valvular disease?

A

AR

136
Q

in AR, what’s the rule for spinal and epidural management?

A

they’re generally well tolerated

137
Q

insert pic PV loops

A 
A=normal, 
B= mitral stenosis, 
C= aortic stenosis, 
D= mitral regurgitation (chronic), 
E= aortic regurgitation (chronic)
138
Q

insert pic abnormal pressure pulse

A

know

139
Q

this decreases compliance of arterial tree, thus leading to increase in pulse pressure.

A

Arteriosclerosis

140
Q

this is associated with low diastolic pressure and high systolic pressure, net result is very high pulse pressure.

A

Patent ductus arteriosus

141
Q

this condition associated with backward flow of blood through the aortic valve. Low diastolic and high systolic pressure leads to high pulse pressure.

A

aortic regurgitation

142
Q

criteria for systemic htn

A

≥ 140/90 mmHg

143
Q

Risk Factors of Primary/Essential HTN:

A 
•	Risk factors
	↑Age
	Obesity
	High-sodium diet
	DM
	Smoking
	Genetics
	Black>White>Asian
144
Q

what is the racial order of primary htn predominance

A

Black>White > Asians

145
Q

Primary HTN may present with these features:

A

o Retinal changes (copper wires, AV nicking)
o Systolic click
o Loud S2
o S4; may

146
Q

retinal changes (nicking, etc) is often associated with what CV disease?

A

Primary HTN

147
Q

The cause of Secondary HTN? TX?

A
  • Renal Vascular Disease
  • Renal Artery Stenosis
  • PO BC
  • Pheochromocytoma
  • Cushing’s syndrome
  • Primary Hyperaldosteronism (Conn’s Syndrome) - hypokalemia/ elevated aldo
  • Hyperthyroidism
  • Drugs, steroids, cocaine

Tx: ACE inhibitors, CCB’s, Diuretics, Alpha/beta blockers; lifestyle modification

148
Q

HTN can predispose one to what disease/processes?

A 
o	Atherosclerosis
o	LVH --> subendocardial ischemia 
o	Loss of cerebral and coronary blood flow autoregulation 
o	Stroke
o	CHF
o	RF
o	Retinopathy
o	Aortic dissection
149
Q

extremely high blood pressure is known as:

A

malignant HTN

150
Q

malignant HTN can lead to what if not treated?

A

o Progressive renal failure and/or encephalopathy plus papilledema

151
Q

tx for malignant htn

A

IV nitroprusside and diuretics

152
Q

to decrease HR during intubation anesthesia provider would give:

A

Beta blocker (esmolol)

153
Q

volatile agents lower what?

A

BP

154
Q

to control HTN during general anesthesia, what do you do?

A
  • deepen anesthesia
  • Phentolamine (alpha 1 antagonist)
  • Nitroprusside
155
Q

antihypertensive choice for African American Men:

A

Diuretics

Beta blockers not effective

156
Q

antihypertensive choice in diabetics with renal insufficiency/CHF:

A

ACE inhibitors

157
Q

antihypertensive choice in exertional angina:

A

beta blocker

158
Q

beta blockers are ineffective in:

A

“beta blockers bad in black men”

159
Q

antihypertensive drugs to avoid in elderly are:

A

clonidine (alpha 2 agonist)
prazosin (alpha 1 antagonist)

cause orthostatics = falls

160
Q

antihypertensive drugs to avoid in smokers, COPD:

A

beta blockers

161
Q

antihypertensive drugs to avoid in renal insufficiency:

A

beta blockers and diuretics

162
Q

antihypertensive drugs to avoid in diabetes, gout

A

thiazide diuretics

163
Q

isolated right heart failure due to pulmonary disease (pulmonary HTN). It is characterized by RVH and eventually RVF. this defines

A

cor pulmonale

164
Q

MCC of chronic cor pulmonale is

A

COPD

165
Q

acute cor pulmonale is due to

A

extensive PE

alveolar hypoxia results from vasoconstriction of pulmonary vasculature.

166
Q

clinical features of cor pulmonale include:

A
  • Peripheral edema, liver enlargement and distended neck veins
  • Loud P2 (normally A2 is louder) suggest pulmonary hypertension
  • Low Sat.
  • EKG shows right axis deviation
  • High mean pulmonary artery pressure
167
Q

tx for cor pulmonale

A

O2 to keep > 90%
diuretics
heart-lung transplant

168
Q

right axis deviation on ekg is associated with

A

cor pulmonale

169
Q

Primary pulmonary HTN is associated with a mean PA pressure of

A

> 25mmHg in absence of cardiac/lung dx

  • poor prognosis
  • unknown cause
170
Q

Normal mean PA pressures are

A

12-16mmHg

171
Q

Secondary Pulmonary HTN is more common. It’s frequently associated with:

A
  • COPD (d/t SMOKING!)
  • congenital Right to left shunt of pulm BF
  • Increased resistance w/in pulm circulation d/t PE or hypoxic vasoconstriction
  • polycythemia (increased blood viscosity)
  • collagen diseases (SLE, Scleroderma)
172
Q

secondary pulmonary HTN often leads to

A

right ventricular hypertorphy

173
Q

secondary pulmonary HTN is associated with what phenomenon? what %?

A

10% with Raynaud’s Phenomenon

174
Q

Acute pericarditis has many associated causes; however there is one cause secondary to MI. What is it and what happens?

A

Dressler’s Syndrome

-immune reaction against necrotic myocardium

175
Q

Clinical and diagnostic findings with pericarditis:

A 
o	Pleuritic chest pain
o	Pericardial friction rub that occurs in systole and diastole
o	Pain often positional
o	Tachycardia
o	Diffuse ST segment elevation
176
Q

the hallmark finding of pericarditis:

A

diffuse ST-segment elevation

177
Q

tx for pericarditis includes:

A

o NSAID
o Ketorolac
o Codeine
o Steroid for non-responders

178
Q

exudative pericardial effusion is always the result of

A

infection

179
Q

the fluid of a pericardial effusion in cancer and TB will be

A

bloody

180
Q

“bag of fluid” is a description of distant heart sounds heard in this disease

A

pericardial effusion

181
Q

is there friction rub in pericardial effusions?

A

no - two pericardial layers are no longer opposed

182
Q

CXR of pericardial effusion will show

A

globular shaped heart

183
Q

Water Bottle Heart on CXR is diagnostic of

A

cardiac tamponade

184
Q

pathophysiology of cardiac tamponade:

Cardiac ____ d/t increased pressure from _____ ___.

A

o Cardiac compression due to Increased pressure from pericardial fluid

o Impaired left ventricular filling (preload) and decrease in SV and CO
o Equalization of pressures (Swan) because all four chambers are subjected to the external pressure

185
Q

Kussmaul’s sign and pulsus paradoxus are PE’s of this cardiac disease process

A

cardiac tamponade

  • as well as diminished heart sounds
  • hypotension
  • JVP
  • tachycardia
  • hepatomegaly
  • edema
186
Q

Anesthetic considerations for surgical mgmt of cardiac tamponade:

A

Ketamine induction
increased IVF’s
avoid vasodilation and cardiac depression

187
Q

“Heart in Shell” is the nickname for what cardiac condition?

A

constrictive pericarditis

-the heart becomes encased in a rigid, chronically inflamed, calcified pericardium

188
Q

Kussmal’s sign =

A

is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart dysfunction.

189
Q

pericardial knock manifests with constrictive pericarditis. describe the cause of pericardial knock:

A

o As the ventricles fill, the distending ventricles “knocks” against the pericardium

190
Q

treatment of constrictive pericarditis is

A

surgical stripping of pericardial shell

191
Q

Type A aneurysms involve:

A

ascending aorta

Type B aneurysms do not.

192
Q

MCC associated with AAA is

A

atherosclerosis

Other causes: genetics, HTN, injury, inflammation, Marfan’s, Ehlers-Danlos

193
Q

Pulsatile abdominal mass, bruits, and sometimes hypotension are physical exam findings for

A

Abdominalaortic Aneurysm (AAA)

194
Q

AAA rupture is associated with what s/s:

A

Grey turner’s sign
Cullen’s sign
CV Collapse –> emergent laparotomy

195
Q

general repair measurement guidelines for AAA

A

repair if diameter > 5cm

b/c rupture risk 30% in 3 yrs

196
Q

dissecting thoracicaortic aneurysms start from a tear in the

A

intima

-blood then seeps in between layers of vessels leading to medial layer destruction and the Double Barrel Aorta

197
Q

Atherosclerosis is a disease of elastic arteries and

A

large and medium sized muscular arteries

198
Q

name 4 risk factors of atherosclerosis:

A
  1. smoking
  2. DM
  3. HTN
  4. Hyperlipidemia
199
Q

tell me the progression of atherosclerosis

A

“FPC”

Fatty streak (young age) –> proliferative plaque –> Complex Atheroma (middle age to elderly)

200
Q

tell me location of atherosclerosis:

A

AA.CPCa

Abdominal Aorta> coronary artery > popliteal artery > carotid artery

201
Q

Takayasu Arteritis

  • vessels affected
  • is
  • highest at risk
  • symptoms
A
  • LARGE Vessel vasculitis
  • Inflammation of aorta and major vessels; causes weak pulse
  • Young, Asian women at highest risk

Symptoms:
pain in arm (carrying bags), angina/CHF, absent pulses, arterial bruits, BP different in each arm

202
Q

Temporal Arteritits

  • vessels affected
  • is
  • highest at risk
  • symptoms
A
  • LARGE vessel vasculitis
  • Pathologically identical to Takayasu Arteritis; occurs in Temporal artery
  • Over age of 50

Symptoms:
unilateral H/A, visual disturbance, jaw claudication (“sore”); may have tenderness over temporal artery and elevated ESR (>50mm//hr)

203
Q

tx for temporal arteritis is

A

steroids

to prevent blindness

204
Q

increased ESR (>50mm/hr) is associated with what systemic vasculitis?

A

temporal arterititis

205
Q

this vasculitis is known as “smokers disease”

A

Buerger’s disease / “thromboangititis Obliterans”

206
Q

Buerger’s disease (also known as thromboangiitis obliterans) affects blood vessels in the body, most commonly in the arms and legs. Blood vessels swell, which can prevent blood flow, causing clots to form. This can lead to pain, tissue damage, and even gangrene (the death or decay of body tissues).

This vasculitis effects what size arteries?

A

medium and small

207
Q

Known as a triad of upper and lower airway and renal disease - glumerulonephritis.

what is this form of vasculitis? what size vessels are affected?

A

Wegner’s granulomatosis

small/ micro vessels

Granulomatosis with polyangiitis is an uncommon disorder that causes inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener’s granulomatosis, this condition is one of a group of blood vessel disorders called vasculitis. It slows blood flow to some of your organs

208
Q

Methotrexate, cyclophosphamide, and/or steroids may be used to treat this vessel disorder

A

wegner’s granulomatosis

209
Q

Polyarteritis nodosa involves arteries of the:

A

Medium sized arteries in the:
Kidneys
Gut
SKin

**Microaneurysms on angiogram

210
Q

common s/s of polyarteritis nodosa include:

A 
fever, 
weight loss, 
malaise, 
abdominal pain,
melena, 
headache, 
myalgia, 
hypertension and cutaneous erruption

TX with cyclophosphamide, and/or steroids

211
Q

Kawasaki Disease
signature s/s =
affects =
Tx =

A

acute, self-limiting necrotizing vasculitis

  • ASAIN population; Infants/Children
  • Fever, conjunctivitis, “strawberry tongue”, desqumative rash

TX ASA and Immunoglobulins

212
Q

DVT facts

A

arise from lower limbs
may –> PE
tx - anticoagulants; thrombolytic therapy

213
Q

Protein C & S deficiency may put someone at risk for

A

DVT

“natural anticoagulants”

214
Q

CAD is also known as

A

Ischemic Heart Disease

o Ischemia is defined as the state of insufficient O2 supply
o Supply can’t meet demand  inadequate perfusion of heart

215
Q

stable vs unstable angina

A

unstable - pain at rest (or without provoking cause)

new dramatic onset

216
Q

in diabetic patients, how does CAD manifest?

A

silent ischemia - w/o pain in diabetics

217
Q

third heart sound in CAD

A

bad sign

shows global ischemia

218
Q

Cannon “a’ wave” is evidence of

A

arrhythmia

219
Q

Diagnostics of CAD/ ischemia.

What is the gold standard in the first 6hrs?
blood test of choice during/after ischemia?

A
  • gold standard = EKG
  • Cardiac Troponin-I first 4hour to 7-10 days; CK-MB is test of choice in first 24 hrs POST MI

-LDH is elevated 2-7days post MI

220
Q

ST Elevation on EKG =

A

transmural ischemia

221
Q

Q waves on EKG =

A

transmural infarct

222
Q

indications for cardiac cath include:

A

 Suspicion of severe or extensive CAD
 Marked positive stress test
 Failure to respond to medical management

223
Q

differential diagnosis for angina - CV related:

A
  • aortic stenosis
  • pericarditis
  • Aortic dissection
224
Q

differential diagnosis for angina - NON- CV related:

A

 Esophageal disease e.g. reflux
 PUD
 Biliary disease e.g. gall stones
 Musculoskeletal disease e.g. costochondritis
 Pleurisy
 Pulmonary infarction
 Pneumothorax–> diminished breath sounds

225
Q

treatment for unstable angina:

A

 Hospitalization “ ROMI”
 IV Nitroglycerine
 Aspirin and anti-platelet therapy to prevent thrombus
 Patients who don’t stabilize with medical therapy should undergo cardiac cath for revascularization

226
Q

angina at rest that is associated with ST Segment elevation (hallmark) secondary to coronary artery spasm is known as:

A

Prinzmetal’s angina

TX with nitrates and CCB’s to tx vasospasm

227
Q

this form of angina is associated with raynauds disease?

A

prinzmental’s angina

both associated with vasospasm

228
Q

silent ischemia usually seen in

A

diabetics

– nitrates and CCB’s

229
Q

• Nitrates relieve angina by

A

venodilation which decreases cardiac wall tension

230
Q

• Ca++ channel blockers relieve angina by

A

decreasing afterload, HR and contractility

231
Q

the most potent CCB in lowering HR and decreasing contractility

A

o Verapamil is

o Verapamil > Diltiazem>Nifedipine

232
Q

What medication for tx of CAD

↓ HR, ↓BP, ↓contractility resulting ↓ O2 consumption

A

• Beta blockers:

o Most effective, useful in exercise induced ischemia. Avoid in bronchial spasm, CHF or bradycardia

233
Q

what two medications reduce myocardial O2 demand

A

• Diuretics and ACE inhibitors

234
Q

what reduces the risk of MI?

A

Low dose ASA

235
Q

• Coronary revascularization—CABG improves survival in patient with (3)

A

o Left main coronary disease –>Left main=OR
o Triple vessel disease
o EF < 50%

236
Q

success rate of angioplasty is what %?

A

80-90%

237
Q

Acute MI clinical presentation:

A
  • severe, persistent anginal pain > 30 mins
  • associated symptoms : jaw/arm pain, SOB, fatigue, adrenergic symptoms

hypotension d/t HF
increased JVP
arrhythmias
S3 - Volume Overload = significant LV dysfunction

238
Q

Tachycardia in the presentation of AMI may be due to

A

anxiety
pericarditis
pump failure

239
Q

Bradycardia in the presentation of AMI may be due to

A

Inferior wall ischemia (RCA)

or Increased Vagal Tone

240
Q

acute management of AMI is

A

“BOOMAR”

Bed rest, 
Oxygen, 
Opiate, (morphine)
Monitoring, 
Anticoagulation, (thrombolysis)
Reduce clot size
241
Q

therapy required for first degree HB

A

rarely required

242
Q

therapy required for second degree HB - mobitz type 1

A

Mobitz type I associated with ischemia at or ABOVE AV node and occurs with INFERIOR wall MI, rarely progresses to complete block.

Pacemaker is not indicated

243
Q

therapy required for second degree HB - mobitz type 2

A

Mobitz type II due to ischemia BELOW the AV node; associated with ANTERIOR wall MI and often progresses to complete AV block.

Pacemaker is indicated.

244
Q

Temporary pacemaker for

A

both RBBB & LBBB

245
Q

Pacemaker for

A

Alternating bundle branch block

Bundle branch block with AV block / MOBITZ II

246
Q

MCC of death (90%)

A

cardiac arrhythmia

247
Q

Complications associated with AMI:

A
  • cardiac arrhythmia
  • post infarct ischemia (mc after non-Q wave MI)
  • Pump Failure
  • Cardiogenic shock (low BP; large infart - large risk of mortality)
  • Rupture of ventricular free wall
  • Papillary muscle rupture
  • Fibrinous Pericarditis
  • Dressler’s Syndrome
  • LV mural thrombus
  • RV infraction
248
Q

rupture of ventricular free wall is a complication associated with MI. this results in:

A

interventricular septum rupture === Left to Right shunting

  • occurs 4-10days post MI
  • results in SHOCK and Cardiac Tamponade
249
Q

*** Dressler’s Syndrome is an autoimmune phenomenon resulting in fibrinous pericarditis.

  • what’s the timeframe of occurance?
  • tx?
A
  • 2-6weeks post MI
  • low fever
  • Tx: NSAIDS
250
Q

RV Infarction occurs with ______ , due to occlusion of ___.

  • should be suspected in patient with?
  • TX?
A

Occurs w/ INFERIOR wall MI; due to occlusion of RCA.

-suspected in pt with INFERIOR wall MI that is HYPOtensive, increased JVP and CLEAR Lungs; ST elevation.

TX hypotension with FLUIDS to maintain right sided filling pressures

251
Q

dilated cardiomyopathy associated with:

A

*MC form

  • Low EF
  • Ischemia (mcc)
  • alcoholism / BeriBeri
  • chemo agents
  • LVH
  • Nonspecific ST or T abn
  • Sequellae (HIGH risk of PE, arrhythmias, MV or Tricuspid regurgitation)
252
Q

“holiday heart syndrome”

A

alcohol acutely diminishes LV function

-5-10 yrs of heavy drinking

253
Q

Peripartum cardiomypathy develops

A
  • most cases are reversible
  • just before and 3 mos after delivery
  • is Autoimmune
254
Q

diastolic dysfunction is the “hallmark” of

A

Restrictive Cardiomyopathy [MYOCARDIUM}

255
Q

amyloidosis, hemochromoatosis “Iron Heart” are diseases that can cause what kind of cardiomyopathy?

A

restrictive cardiomyopathy

256
Q

with restrictive cardiomyopathy; what happens to heart:

A
  • stiff ventricle –> restrict ventricular filling = to hallmark of DIASTOLIC DYSFUNCTION
  • cardiac size and fxn are normal
  • atrial arrhythmias or AVB may occur

TX - CCB increase diastolic relaxaction and allow better filling

257
Q

Hypertrophic Cardiomyopathy (aka: Idiopathic Hyptertrophic Subaortic Stenosis -IHSS)

Features:

A
  • asymmetric Ventricular concentric hypertrophy with LV outflow Obstruction (b/w hypertorphied septum and MV leaflet)
  • Diastolic dysfunctions d/t hypertrophied and stiff ventricles
  • Increased LVEDP
258
Q

IHSS effect on decreasing and increasing the obstruction

A

conditions enlarge the LV – increase in Preload and afterload seperate the septum and anterior leaflet of teh MV and DECREASE the obstruction

conditions that make the ventricle smaller; increases velocity of blood flow (dehydration; + ve inotrops) INCREASE obstruction

259
Q

Factor increasing outflow obstruction (IHSS):

A
  • increased contractility
  • Increase HR
  • DECREASE Preload (vol) or afterload
260
Q

MCC of sudden death in young athletes is

A

IHSS / cardiomyopathy

261
Q

preferred tx for IHSS

A

Beta blockers
CCB
Surgical excision of hypertrophied septum

262
Q

spinal and epidural considerations for IHSS patients

A

o Spinal and epidural blocks are CONTRAINDICATED– will decrease preload and afterload

263
Q

anesthesia considerations for IHSS:

A
  • GIVE FLUID! avoid hypovolumia “FULL, FULL, FULL” increase PRELOAD
  • Neo and alpha stimulants are ideal b/c they increase SVR w/out increasing contractility “UP, UP, UP” (increase afterload)
  • reduce LV - aortic systolic pressure gradient
  • Avoid decrease in LV afterload
  • beta blockers to decrease contractility
  • halothane is ideal gas - direct myocardial depressant but doesn’t decrease SVR
264
Q

would you use fentanyl for pt with IHSS?

A

no use; does not depress myocardium or increase SVR

265
Q

IHSS and Bernoulli’s theorem

A

-in regards to increased afterload (b/c a decrease in afterload worsens the obstruction)

Bernoulli’s principle: Within a horizontal flow of fluid, points of higher fluid speed will have less pressure than points of slower fluid speed.

Fall'20 A&P III (13 decks)

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