Special Populations Flashcards

1
Q

At rest, how much does the myocardium consume of the oxygen that is delivered to it?

A

70%

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2
Q

When the oxygen demand in the heart is increased, can the heart meaningfully increase its extraction ratio?

A

NO

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3
Q

What must increase when the heart requires more O2?

A

Coronary blood flow and/or CaO2 must increase

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4
Q

What causes decreased oxygen delivery?

A

Decreased coronary flow:
- tachycardia
-decreased aortic pressure
-decreased vessel diameter
-increased LVEDP

Decreased CaO2:
-Hypoxemia
-Anemia

Decreased Oxygen extraction :
- left shift of Hgb curve (decreased P50
- decreased capillary distention

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5
Q

What increased oxygen demand?

A

-tachycardia
-HTN
-SNS stimulation
-Increased wall tension
-Increased LVEDV
-Increased afterload
-Increased contractility

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6
Q

What is the definition of heart failure?

A

Complex physiologic process that causes a clinical syndrome characterized by the hearts inability to fill or eject blood in a sufficient quantity to meet tissue requirements

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7
Q

What does the ventricle not do well in systolic heart failure?

A

Ventricle doesn’t empty well (problem with ejection)

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8
Q

What is the hallmark of systolic heart failure?

A

Decreased EF with and increased EDV

since the heart can’t squeeze well, a greater amount of blood remains in the ventricle after each contraction

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9
Q

What kind of hypertrophy does systolic heart failure create?

A

Eccentric

becomes more spherical shaped

chamber size increases in an attempt to preserve stroke volume

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10
Q

What is the degree of systolic dysfunction expressed as?

A

ejection fraction (EF)

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11
Q

How is EF calculated?

A

SV/EDV

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12
Q

what is a normal EF?

A

> 55%

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13
Q

What is considered a mild EF?

A

45-54%

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14
Q

What is considered moderate dysfunction in terms of EF?

A

30-44%

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15
Q

What is considered severe dysfunction in terms of EF?

A

<30%

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16
Q

What are the causes of systolic HF?

A

CAD/myocardial ischemia

Volume overload (d/t valve insufficiency

Dilated cardiomyopathy

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17
Q

What is the compensatory mechanism in systolic HF?

A

When SV is reduced, the body compensates by activating SNS to raise the resting HR in an effort to maintain CO

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18
Q

What should you do to the preload in systolic HF?

A

already high

avoid overload, give diuretics if too high

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19
Q

What should you do to the afterload in systolic HF?

A

decrease- to reduce myocardial workload

  • coronary perfusion pressure must be maintained
    -SNP works well if volume is adequate
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20
Q

What should you do to the contractility in systolic HF?

A

May be reduced, augment w inotropes as needed
- avoid agents that cause reduced contractility

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21
Q

What should you do to the HR in systolic HF?

A

Usually high d/t sympathetic activation
- if EF is low, higher HR is needed to preserve CO

Fast, full, forward

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22
Q

What is the problem in diastolic HF?

A

Filling problem

Slow, full, constricted

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23
Q

Whats the hallmark of diastolic HF?

A

HFpEF

Diastolic failure occurs when the heart is unable to relax and accept the incoming volume.

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24
Q

What kind of hypertrophy happens in diastolic HF?

A

Concentric hypertrophy

-chronic pressure overload causes the myocardium to thicken

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25
Q

What are the causes of diastolic HF?

A

demand ischemia from chronic pressure overload

-myocardial ischemia
-stenotic heart valves
-hypertrophic cardiomyopathy
-chronic HTN
-cor pulmonale
-obesity

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26
Q

What is a preserved EF considered?

A

> 40%

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27
Q

What should you do to preload in diastolic HF?

A

volume is required to stretch the non-compliant ventricle

  • LVEDP does not correlate with LVEDV
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28
Q

What should you do to afterload in diastolic HF?

A

Usually already elevated

  • if not, need to keep elevated to perfuse thick myocardium

-phenylephrine

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29
Q

What should you do to contractility in diastolic HF?

A

Usually normal

  • caution w agents that depress function
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30
Q

What should you do to HR in diastolic HF?

A

Slow/normal to maximize diastolic time for coronary perfusion and decrease MVO2

-maintain SR, dependent on atrial kick

** The LV with concentric hypertrophy is prone to ischemia, Maintenace of a high MAP and slow normal HR is crucial. Hypotension should be treated promptly with phenylephrine!

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31
Q

What is the most common cause of right heart failure?

A

left heart failure

also caused by pulmonary HTN, and right-sided MI

the right heart is thinner, more compliant, and weaker than the left heart

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32
Q

What does right sided HR cause?

A

systemic congestion, hepatomegaly, peripheral edema

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33
Q

What are things that can increase PVR (which can impair RV function?)

A

hypoxemia
hypercarbia
acidosis
N2o
desflurane

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34
Q

What is the treatment for right ventricular failure?

A

Main goal is to improve contractility which reduces right heart afterload

inotropes and decreased PVR

Management of right sided HF can be more difficult than left sided HF because fewer options exist for unloading and supporting the right ventricle

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35
Q

What is ventricular remodeling?

A

Compensatory mechanism in response to abnormal pressure or volume loads

Failing heart changes size, shape, function in attempts to preserve C.O.

Remodeling can be reversed by Ace Inhibitors/ aldosterone inhibitors

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36
Q

what BP is considered Pre-HTN?

A

120-129 / < 80

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37
Q

What is stage 1 HTN?

A

130-139/ 80-90

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38
Q

What is stage 2 HTN?

A

> 140 / > 90

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39
Q

What is considered HTN crisis?

A

> 180 / > 120

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40
Q

What are the secondary causes of HTN?

A

Coarctation of the aorta
Renovascular disease
Cushing syndrome
Conn’s syndrome
Pheochromocytoma
Pregnancy-induced HTN

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41
Q

What are the complications of HTN?

A

Left ventricular hypertrophy
Ischemic heart disease
Congestive heart failure
Arterial aneurysm (aorta, cerebral)
Stroke
ESRD

A high afterload increases myocardial work and an elevated arterial driving pressure damages nearly every organ in the body

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42
Q

Chronic HTN shifts the cerebral autoregulation curve which way?

A

RIGHT

This helps the brain tolerate a higher range of blood pressures
However, it can not tolerate lower blood pressures

43
Q

What does the cerebral autoregulation curve describe?

A

the range of blood pressures where cerebral perfusion remains constant

44
Q

blood pressure past the range of autoregulation is dependent on what?

A

pressure

Malignant HTN –> hemorrhagic stroke/cerebral edema
Hypotension –> cerebral hypoperfusion

45
Q

What is the patho of constrictive pericarditis?

A

Fibrosis or any condition where the pericardium becomes thicker

During diastole, ventricles cannot relax fully, which reduces compliance and limits filling, which leads to ventricular pressure increases and creates a back pressure on peripheral circulation

Ventricles adapt by increasing myocardial mass

46
Q

What is the cause of constrictive pericarditis?

A

Cancer (radiation)

cardiac surgery

rheumatoid arthritis

TB

Uremia

47
Q

What are the signs and symptoms of Constrictive pericarditis?

A

Kussmaul’s sign: JVD during inspiration

Pulsus Paradoxes- decreased SBP by 10mmHg during inspiration.

Increased venous pressure- distended neck veins, hepatomegaly, ascites, peripheral edema

Atrial dysrhythmias

pericardial shock

48
Q

What is the visceral layer attached to?

A

myocardium

49
Q

what is the parietal layer attached to?

A

mediastinum

50
Q

How much fluid separates the visceral and parietal layer?

A

10-15 mL

51
Q

What is the treatment for constrictive pericarditis?

A

Pericardiotomy

  • hemorrhage and dysrhythmias common
52
Q

What is the management for constrictive pericarditis?

A

CO is dependent on HR= avoid bradycardia

Preserve HR and contractility= pancuronium and ketamine are good
- opioids, benzos, etomidate are ok
-caution w volatile anesthetics

Maintain afterload

53
Q

What the pathophys of acute pericarditis?

A

Results from inflammation

Does NOT impair diastolic filling unless inflammation leads to constrictive pericarditis or tamponade

54
Q

What are the causes of acute pericarditis?

A

Infection (viral most common)

Dressler’s syndrome (inflammation from necrotic myocardium s/p MI)

SLE

Scleroderma

Trauma

Cancer (radiation)

55
Q

What are the signs and symptoms of acute pericarditis?

A

Acute chest pain w pleural component
- increased w inspiration and postural changes
-pain relieved by leaning forward

Pericardial friction rub

ST elevation w normal enzymes

Fever

56
Q

What is the treatment for acute pericarditis?

A

Usually resolves spontaneously

57
Q

What are the best drugs to manage Acute pericarditis?

A

Salicylates

Oral analgesics

corticosteroids

58
Q

What is the management for acute pericarditis?

A

None, non-surgical

59
Q

What is cardiac tamponade?

A

Accumulation of fluid inside the pericardium = pericardial pressure high enough to compress the myocardium, which interferes with the heart’s ability to fill and act like a pump

60
Q

What pressures will equalize in tamponade?

A

As ventricular compliance deteriorates, left and right diastolic pressure (CVP & PAOP) begins to equalize

Increased pericardial pressure compresses heart= increased LV pressure

Decreased ventricular volume = decreased SV, decreased CO, increased HR

61
Q

What is Beck’s Triad?

A

HoTN

JVD

Muffled heart sounds

62
Q

What are the S/S of cardiac tamponade?

A

Beck’s triad

Pulsus paradoxes ( decreased SBP by 10 mmhg during inspiration)

Kussmaul’s sign (increased CVP and JVD during inspiration

Reduced EKG voltage

Compression of heart, lungs, trachea, and esophagus d/t mass effect

63
Q

What kind of anesthesia is preferred for cardiac tamponade?

A

LA preferred for pericardiocentesis

If general GA: primary goal is preserve myocardial function

(Stroke volume is severely decreased but increased SNS tone (increased contractility and afterload) provide compensation
-Any drug that depressed the myocardium or reduces afterload can precipitate CV collapse)

64
Q

What drugs should be avoided in cardiac tamponade?

A

-Halogenated agents
-Propofol
-thiopental
-high dose opioids
-neuraxial anesthesia

65
Q

What drugs are safer for tamponade?

A

Ketamine–> activation of SNS= best choice
Nitrous oxide
benzodiazepines
opioids

66
Q

What do you want to do the HR for tamponade?

A

Maintain

67
Q

What do you want to do to the rhythm for tamponade?

A

NSR

68
Q

What do you want to do to the preload in tamponade?

A

Maintain/increase

69
Q

What are the other names for obstructive hypertrophic cardiomyopathy?

A

-Hypertrophic obstructive cardiomyopathy
-Asymmetrical hypertrophy
-Idiopathic hypertrophic subaortic stenosis

70
Q

Whats the pathophys of obstructive hypertrophic cardiomyopathy?

A

LVOT obstruction caused by:
- congenital hypertrophy of intraventricular septum
-systolic anterior motion (SAM) of the anterior leaflet of mitral valve
-When the ventricle contracts forcefully or quickly –> greater tendency of the anterior leaflet of the mitral valve to reduce flow through or completely obstruct the LVOT

  • occurs during SYSTOLE

-problem is proximal to aortic valve, not the valve itself

71
Q

What is the most common cause of sudden cardiac death in young adults?

A

Obstructive Hypertrophic cardiomyopathy
(thickened ventricular septum= small left ventricle)

72
Q

What causes SAM?

A

Likely caused by the venturi effect as blood rapidly flows over the LVOT (velocity increases over the point of constriction)

-Easily diagnosed by TEE
Can occur following mitral valve REPAIR (not replacement)

73
Q

Conditions that distend the LVOT=

A

GOOD!
Increased systolic volume (increased preload, decreased HR)

Decreased contractility

increased transmural pressure gradient (increased Ao pressure)

increased afterload

74
Q

Conditions that narrow the LVOT=

A

BAD!!

Decreased systolic volume (decreased preload or increased HR)

increased contractility

decreased Ao pressure

75
Q

What is infective endocarditis?

A

Bacteria enters the blood stream and finds their way to a heart valve, chamber or blood vessel

76
Q

Who should receive pre-op antibiotics?

A

-Previous infective endocarditis

-Prosthetic heart valve

-Unrepaired cyanotic congenital heart disease
Repair congenital heart defect if repair < 6 months old

-Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site

77
Q

When are antibiotics not required?

A

CABG

Coronary stent placement

unrepaired cardiac valve disease (including mitral valve prolapse)

78
Q

Which surgical procedures have an increased risk of infective endocarditis?

A
  • Dental procedures involving gingival manipulation and/or damage to the mucosal lining

-respiratory procedures that perforate the mucosal lining

Biopsy of infected lesion on skin or muscle

79
Q

Are antibiotics required for GI endoscopic procedures w/o infection and GU procedures w/o infection?

A

NO

80
Q

What is associated w the highest risk for perioperative MI?

A

Unstable angina

81
Q

High risk procedures:

A

aortic surgery
major vascular
peripheral vascular
long lenght

82
Q

Intermediate risk procedures:

A

Carotid endarterectomy
Peripheral artery angioplasty
Endovascular aneurysm repair
Head and neck surgery
Major neurologic/orthopedic
Intrathoracic
Intraperitoneal
Major urologic
Transplant

83
Q

Low risk procedures:

A

Breast
Dental
Endoscopic
Superficial
Endocrine
Cataract
Gynecologic
Reconstructive
Minor orthopedic
Minor urologic

84
Q

ACC/AHA recommend waiting _______ after MI before patient undergoes elective surgery

A

at least 60 days

85
Q

If reinfarction does occur, mortality rate is approx:

A

50%

86
Q

1 MET:

A

Self-care
Eating, dressing, using the toilet
Walking indoors and around the house
Walking one to two blocks on level ground at 2-3 mph

87
Q

4 METs

A

Light housework
Climbing a flight of stairs without stopping, or walking up a hill longer than 1 to 2 blocks
Walking on level ground at 4 mph
Running a short distance
Golf, dancing, throwing a baseball

88
Q

What valvular disorder poses the greatest pt risk for noncardiac surgery?

A

Severe aortic stenosis

89
Q

pacemaker should be interrogated within ______ months of elective surgery

A

12

90
Q

ICD should be interrogated within ____ months

A

6

91
Q

Electromagnetic interference risk is low if the device is less than_____ years old and bipolar cautery is greater than _____cm from the device lead or generator

A

10 years

greater than 15 cm

92
Q

When is a cardiac cath indicated?

A

NYHA class 3 or 4

provides definitive info about distribution and severity of CAD

93
Q

what is considered the gold standard for diagnosis of cardiac pathology before most open heart surgeries and for definition of lesions of the coronary vessels

A

cardiac cath

94
Q

What is considered significant narrowing of vessel diameter?

A

Lesions that reduce diameter by greater than 50%, reducing cross-sectional area by greater than 70%

95
Q

meds for stents:

A

ASA: continue indefinitely
clopidogrel: continue for a minimum of 6 months to prevent restenosis

96
Q

Elective non-cardiac surgery should NOT be scedules within_____ of bare metal stent and within ____months of DES

A

BMS: 1 month
DES: 6 months

97
Q

beta blockers:

A

Restore the oxygen supply/demand mismatch
Reduce perioperative ischemia
Redistribute coronary blood flow to subendocardium
Stabilizes plaques
Increases** v-fib threshold- makes it harder for v.fib to occur

98
Q

statins:

A

Enhance endothelial function
Improve atherosclerotic plaque stability
Reduce vascular inflammation

99
Q

ACEI:

A

** we routinely have ACE inhibitors held for 1-2 days prior to surgery due to the extreme refractory hypotension that can be associated with ACE inhibitors and volatile anesthetics

100
Q

how long should you hold ASA?

A

7-10 days

101
Q

how long to hold plavix/brillinta:

A

5 days

102
Q

how long to hold effient:

A

7 days

103
Q

How long to hold pradaxa, Xarelto, eliquis:

A

1-2 days