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932 Pathophysiology > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Emptying problems include

A

SHF, dilated cardiomyopathy, aortic stenosis, pulmonic stenosis

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2
Q

Considerations for SHF & DCM include:

A
  1. ) optimize inotropy (balance w/ causing increased MVO2)
  2. ) decrease afterload (as long as it doesn’t cause drop in BP)
  3. Maintain NSR to allow for atrial kick
  4. Don’t fluid overload
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3
Q

Systolic heart failure (pathophys)

A

an emptying problem that is triggered by volume overload causing eccentric remodeling
known as heart failure with reduced ejection fraction

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4
Q

Systolic heart failure characteristics include

A

decreased LVEF, Increased LV chamber size, volume overload, LV hypertrophy on ECG, S3 gallop, compliant, eccentric remodeling

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5
Q

Heart failure is

A

reduce forward flow

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6
Q

Causes for the heart to fail include:

A

volume overload, pressure overload (two most common), myocardial contractile impairment d/t ischemia or infarct), restrictive filling (pericarditis, tamponade), idiopathic remodeling of sarcomeric or extracellular matrix proteins, myocardial inflammation

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7
Q

Chronic vs. acute heart failure

A

chronic: stable where BP is maintained b/c of physiological compensations
Acute: sudden decrease in CO resulting in hypotension; medical emergency and can turn into flash pulmonary edema

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8
Q

Acute heart failure can occur due to

A

worsening chronic HF, new onset HF (i.e. valve or septal wall rupture, MI, or severe HTN crisis)

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9
Q

NYHA Class 1

A

no symptoms and no limitation in ordinary physical exercise

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10
Q

NYHA Class 2

A

mild symptoms (mild SOB and/or angina) and slight limitation during ordinary activity

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11
Q

NYHA Class 3

A

Marked limitation in activity d/t symptoms even during less than ordinary activity; comfortable only at rest

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12
Q

NYHA Class 4

A

Severe limitations; experiences symptoms even while at rest; mostly bedbound patients

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13
Q

Describe differences between left versus right sided heart failure

A

Left side: pulmonary congestion, dyspnea, increased LVEDP, pulmonary edema, dyspnea
Right side: increased RVEDP, systemic congestion, hepatomegaly

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14
Q

Most common causes of left heart failure include

A

HTN, CAD, MI, valvular disease

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15
Q

Most common causes of right heart failure include

A

Left-sided heart failure

may also be caused by pulmonary arterial hypertension or MI of right ventricle

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16
Q

Describe low output vs. high-output heart failure

A

Both are d/t heart being unable to pump enough blood to meet oxygen demand of tissues
low-output: filling or emptying problem; CO can be normal but only b/c of compensation
High-output: not a filling or emptying problem; problem is metabolic demand and/or SVR; cardiac output can be normal or above normal but CO is insufficient to meet global metabolic demands

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17
Q

Causes of low-output HF

A

CAD, chronic HTN, cardiomyopathy, valvular disease, pericardial disease

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18
Q

Causes of High-output HF

A

Anemia, septicemia, hyperthyroidism

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19
Q

Common causes of HF include:

A

pressure overload, volume overload, MI, idiopathy cardiomyopathy, hypertrophy/cardiac remodeling

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20
Q

Increased catecholamines cause cardiotoxicity and promote

A

cardiac remodeling

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21
Q

ANP & BNP promote

A

diuresis, natriuresis, inhibition of RAAS and SNS, vasodilation, and INHIBIT REMODELING

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22
Q

Concentric remodeling is

A

caused by increased pressure and results in sarcomeres being laid down in parallel; smaller chamber radius and thicker/less compliant chamber wall
Results in a filling problem
associated with DHF

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23
Q

Eccentric remodeling is

A

caused by volume overload resulting in sarcomeres being laid down in series; larger chamber radius and more compliant chamber wall
results in an emptying problem
associated with SHF

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24
Q

diastolic heart failure is

A

a filling problem (occurs L>R)
triggered by pressure overload
stiff/non-compliant ventricles impair filling
heart failure with preserved EF

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25
Q

Diastolic heart failure characteristics include

A

normal LVEF, decreased chamber size, pressure overload, LV hypertrophy on EKG, S4 gallop, decreased compliance, concentric ventricular remodeling

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26
Q

In patients who develop acute heart failure during surgery, the immediate goal is to

A

increase CO and decrease LVEDP

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27
Q

Heart failure responses include

A

increased SNS, increased RAAS, increased humoral and biochemical, increased remodeling

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28
Q

The key difference between SHF & DCM is

A

etiology!

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29
Q

DCM risk factors include

A

African American Men (Dark Dads- DDD)

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30
Q

Cardiomyopathy is a

A

chronic disease of the heart
heart muscle is structurally and functionally abnormal in the absence of CAD, HTN, valvular disease, & congenital heart disease
associated with mechanical and/or electrical abnormality

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31
Q

Etiology of cardiomyopathies (in general):

A

are genetic, genetic/non-genetic (mixed), or acquired
not caused by other CV diseases
Are not congenital diseases
Can include metabolic, inflammatory or toxic

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32
Q

Etiology of HCM

A

Genetic

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33
Q

Etiology of DCM & RCM

A

mixed genetic/non-genetic

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34
Q

Causes of DCM include

A

caused by genetic & non-genetic factors
non-genetic factors include: alcoholism, cocaine, infection, thyroid disease, pheochromocytoma, chemotherapy or radiation

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35
Q

Dilated cardiomyopathy pathophysiology

A

increased cardiomyocyte apoptosis, increased sarcomeric proteins in eccentric pattern resulting in eccentric remodeling of the chamber–> emptying problem
Sarcomeric protein changes that reduce contractile filament senstivity to Ca2+ and decrease force generation
Remodeling can lead to conduction abnormalities
s/s consistent with SHF

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36
Q

Signs/symptoms of DCM include

A

mimic angina pectoris, chamber is hypokinetic and dilated so increased thrombus risk, valve regurgitation possible d/t dilated ventricles, dysrhythmias

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37
Q

Diagnosis of DCM is via

A

Echo or chest XR that shows LV dilation

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38
Q

The anesthetic goals for DCM & SHF:

A

Prevent acute drop in CO and increase in LVEDP

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39
Q

Restrictive cardiomyopathy is

A

rare but lethal
has changes to sarcomeric proteins that impair relaxation and infiltrations/deposits stiffen ventricle
no concentric or eccentric remodeling
a filling problem

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40
Q

RCM etiology

A

caused by genetic and non-genetic factors

non-genetic causes: infection, chemo or radiation, diseases of infiltration like amyloidosis, sarcoidosis

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41
Q

The pathophysiology of RCM includes:

A

1) ventricular stiffness
2) impaired relaxation d/t altered Ca2+ cycling
3) system diseases that cause ventricular infiltration w/ substances that stiffen the ventricle
Results in high LVEDP, reduced filling, reduced SV, and reduced CO
can progress to DHF

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42
Q

Signs and symptoms of RCM include

A

same as those for DHF- congestion in pulmonary or systemic systems, decreased CO to tissues–> syncope, decreased myocardial contractility
conduction abnormalities d/t deposition of infiltrative substances

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43
Q

Diagnosis of RCM

A

Echo- diastolic dysfunction, atria enlarged not ventricles

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44
Q

The quintessential for DHF & restrictive cardiomyopathy:

A

SV limited: maintain HR in NSR, do not decrease afterload
Need their preload (titrate carefully so as not to fluid overload)
Have inotropy- maintain
Ischemia- avoid hypotension b/c CorrPP is at risk since can’t increase SV to compensate

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45
Q

Etiology of HCM:

A

caused in whole or part by genetic abnormality

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46
Q

Pathophysiology of HCM:

A

excessive growth of left ventricular muscle for no apparent reason
usually concentric remodeling which can result in obstruction of LVOT and mitral regurgitation
LVOT is primary cause of HCM clinical manifestations

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47
Q

Describe LVOT:

A

left ventricle hypertrophy w/ unfavorable mitral valve anatomy results in obstruction of the LVOT
decreased forward blood flow d/t:
narrowed tract & leaflet of the mitral valve obstructs LVOT

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48
Q

The most common cardiomyopathy is

A

HCM: 1 in 500

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49
Q

S/S of HCM include:

A

vary widely but similar to SHF (d/t outflow obstruction) and DHF (d/t prolonged relaxation and decreased ventricular compliance)
angina, fatigue, syncope, tachydysrhythmias, HF

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50
Q

Positioning is important in this cardiomyopathy:

A

HCM- supine reduces LVOTO

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51
Q

Diagnosis of HCM:

A

Echo & ECG: looking for LV hypertrophy

Cardiac cath to measure increased LVEDP

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52
Q

Anesthetic considerations for HCM:

A

Avoid acute HF by minimizing decreased LVOTO

  • Avoid increased contractility- makes LVOTO worse
  • Avoid decreased afterload- makes LVOTO worse d/t venturi affect
  • Avoid tachycardia- does not allow for filling time
  • Maintain adequate preload b/c they need filling
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53
Q

With regional anesthesia there is a risk for

A

decreased SVR and venodilation which causes decreases afterload

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54
Q

Describe DHF from triggering event to response:

A

Pressure load–> concentric remodeling–> collagen stiffness–> reduced compliance–> decreased filling–> DHF–> diastolic dysfunction

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55
Q

Describe restrictive cardiomyopathy from triggering event to response:

A

Genetic/acquired–> sarcomeric proteins–> impaired relaxation–> decreased filling–> diastolic dysfunction

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56
Q

Describe HCM from triggering event to response:

A

Genetic–> LVH–> obstruct LVOT–> emptying–> SHF–> systolic dysfunction
Genetic–> collagen, sarcomeric proteins–> decreased compliance and decreased relaxation–> decreased filling–> DHF & RCM–> diastolic dysfunction

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57
Q

Describe DCM from triggering event to response:

A

genetic/acquired–> eccentric–> increased chamber size–> decreased Ca2+ sensitivity–> decreased force–> decreased emptying–> systolic dysfunction

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58
Q

Describe systolic HF from triggering event to response:

A

Volume load–> eccentric–> increased chamber size–> increased L to W ratio–> decreased force–> decreased emptying–> SHF–> systolic dysfunction

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59
Q

What is acute pericarditis?

A

inflammation of the pericardium

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60
Q

How much fluid can the pericardial space contain?

A

15 to 50 mL

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61
Q

How many layers surround the heart?

A

3 layers:

outermost: fibrous pericardium
middle: parietal pericardium
inner: visceral pericardium

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62
Q

Where is the pericardial cavity or pericardial space located?

A

between the parietal and visceral pericardial layers

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63
Q

Common causes of acute pericarditis:

A

viral infection or MI

Result: benign unless pericardial effusion occurs

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64
Q

S/s of acute pericarditis

A

no change in cardiac function unless there is an associated pericardial effusion

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65
Q

Diagnosis of acute pericarditis:

A

more often in men commonly between 20-50 years
chest pain
ECG changes d/t inflammation of superficial myocardium
friction rub

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66
Q

Tx of acute pericarditis:

A

Salicylates, NSAIDs, and corticosteroids to treat inflammation
Corticosteroids are second line b/c withdrawal is associated with increased incidence of pericarditis relapse

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67
Q

Describe pericardial effusion

A

collection of fluid in the pericardial space that may occur with or without pericardial inflammation

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68
Q

Describe cardiac tamponade

A

Collection of fluid in the pericardial sac sufficient to cause increased pericardial pressure that results in reduced cardiac filling

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69
Q

Describe the pathophysiology of cardiac tamponade:

A

pressure reduces ventricular dilation, diastolic filling and increases RAP
depends on how rapidly the fluid collection occurs- slow chronic stretch dissipates the pressure
Result: FILLING PROBLEM

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70
Q

Filling and emptying problems include:

A

HCM w/ LVOTO

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71
Q

Filling problems include:

A

cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, DHF, mitral valve stenosis, tricuspid valve stenosis

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72
Q

What is the difference between transudative & exudative?

A

transudative: a filtrate of the blood; it accumulates in tissues outside the blood
Exudative: any fluid that filters from the circulatory system into lesions or areas of inflammation

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73
Q

Common causes of pleural effusion/cardiac tamponade include:

A

fluid in pericardial space d/t disease (cancer, TB, etc.), trauma (implantation of pacemaker or CVC), exposure to radiation

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74
Q

Describe the difference between acute and chronic pericardial effusion.

A

chronic- the effusion develops overtime so the pericardium has time to stretch & no increase in intrapericardial pressure
acute- occurs rapidly and the pericardium is unable to stretch and thus increase intrapericardial pressure and symptoms occur

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75
Q

Beck’s triad includes:

A

hypotension, increased JV pressure, distant heart sounds (pericardial fluid muffles)- s/s of cardiac tamponade

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76
Q

S/S of cardiac tamponade include

A

Increased RAP, BP normal if compensated or hypotensive, CVP elevated, compression of adjacent intrathoracic structures leading to anorexia, cough, hoarseness, dyspnea, chest pain, & hiccup
Beck’s triad: hypotension, increased JV pressure, distant heart sounds
ultimately decrease in CO
PULSUS PARODOXUS is classic

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77
Q

What is pulsus paradoxus?

A

decrease in systolic BP > 10 mmHg during inspiration (more common if the tamponade is acute rather than chronic)
Inhibition of RV into pericardial space on inspiration and thus it moves toward the LV and impairs filling –> decreased LVEDV–> decreased SV–> decreased SBP

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78
Q

Diagnosis of cardiac tamponade:

A

echo

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79
Q

Anesthetic implications of cardiac tamponade:

A

Goal: relieve pressure before surgery
During: maintain CO & BP
Optimize volume, give catecholamines, avoid decreased HR, decreased SVR, decreased VR

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80
Q

An issue when tamponade is relieved is

A

significant hypertension

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81
Q

Quintessential of cardiac tamponade:

A 
avoid decreased HR because SV limited
avoid decreased afterload b/c SV limited
Maximize preload to engage F/S & avoid anything that impacts VR (PEEP, coughing)
high risk of ischemia d/t high LVEDP
maintain contractility
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82
Q

What is constrictive pericarditis?

A

constriction of the heart due to changes in the pericardial sac

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83
Q

What is the difference between chronic constrictive pericarditis & subacute constrictive pericarditis?

A

Chronic: fibrous scarring and adhesions that create a rigid shell
Subacute: fibroelastic, more common & less serious

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84
Q

The pathophysiology of constrictive pericarditis:

A

pericardium scarring and adhesions–> decreased compliance of sac–> decreased diastolic filling
Thickening of pericardial space—> constricts heart–> increased intrapericardial pressure
FILLING problem

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85
Q

Causes of constrictive pericarditis:

A

usually idiopathic

can be caused by: radiation, TB, aberrant wound repair of myocardium d/t trauma or surgery

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86
Q

The s/s of constrictive pericarditis:

A

similar to right-sided HF: increased RVP leads to back up of blood, atrial dysrhythmia d/t compression and remodeling of SA node, reduced cardiac filling leads to decreased VR, decreased F/S, decreased SV, and decreased CO
Kussmaul’s sign

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87
Q

What is Kussmaul’s sign?

A

Increase in JV distension during inspiration

RV unable to expand normally during inspiration so increased VR d/t abdominal compression on inspiration goes to JV

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88
Q

How is constrictive pericarditis diagnosed?

A

increased CVP w/ other signs of heart disease
pericardial thickening on ECHO
ECG may or may not display minor abnormalities

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89
Q

Anesthetic implications of constrictive pericarditis?

A

Avoid decrease in VR as this reduces cardiac filling
Avoid increased HR as this reduces cardiac filling
avoid decreased SVR since heart cannot compensate (SV LIMITED)
Optimize preload

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90
Q

Common themes with filling disorders:

A

Stroke volume limited so maintain HR and do not decrease afterload; careful titration of preload b/c need volume to fill but do not overload

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91
Q

What factors increase MVO2?

A

Preload, HR, inotropy, afterload

CO is work and works is proportional to MVO2

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92
Q

What factor increases MVO2 the least?

A

preload

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93
Q

The afterload equation:

A

Afterload= (LVP x chamber radius )/Wall thickness

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94
Q

What factors cause an increase in LVEDP?

A

increased volume–> increases LVEDV and thus LVEDP

Increased elastance of ventricle or poor relaxation

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95
Q

What type of hypertrophy reduces afterload?

A

concentric hypertrophy

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96
Q

When we say heart rate is a double whammy we are referring to the idea that

A

heart rate affects both supply and demand- increased heart rate increases the MVO2 demand and decreases the supply (less time in diastole= less coronary perfusion time)

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97
Q

Coronary perfusion pressure is equal to

A

CorrPP=aortic DP-LVEDP

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98
Q

Coronary perfusion pressure is

A

diastolic dependent
depends on time in diastole (HR)
Diastolic BP (hypotension)
LV pressures during diastole (diastolic dysfunction)

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99
Q

Any kind of internal or external pressures squeezes the arteries which means

A

resistance goes up and supply goes down

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100
Q

Factors that affect coronary vascular resistance include:

A

Cardiac work output, cardiac extravascular compressive forces, neurohumoral and endothelial factors

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101
Q

Supply is affected by

A

coronary blood flow and O2 carrying capacity

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102
Q

Neurohumoral regulation of coronary VSMC tone:

A

vasodilation: adenosine, hypoxia, nitric oxide, PSNS stimulation, SNS stimulation (B2)
Vasoconstriction: SNS stimulation (a1), Ang II, endothelin (also PSNS acts on endothelin receptors)

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103
Q

Coronary blood flow is directly proportional to

A

CorrPP/coronary resistance

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104
Q

Blood flow to the coronaries occurs mainly during

A

diastole

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105
Q

Myocardial ischemia occurs when

A

O2 supply cannot keep pace with O2 demand

106
Q

Ischemic heart disease is

A

insufficient coronary blood flow to meet the metabolic demands of the cardiomyocytes

107
Q

The two major components of cardiac ischemia are

A

metabolism in cardiomyocytes (demand) & delivery of O2 and nutrients to cardiomyocytes (supply)

108
Q

Most ischemic heart disease results from

A

coronary artery disease which can be atherosclerotic or non-atherosclerotic

109
Q

Atherosclerosis is

A

abnormal deposition of a plaque in the artery wall–> arterial narrowing–> increased resistance–> decreased blood flow

110
Q

Non-atherosclerotic decreased coronary blood flow can result from

A

coronary artery dissection, coronary artery spasm, coronary artery embolism and congenital abnormalities of the heart

111
Q

CAD is a problem at

A

the level of the coronary arteries

112
Q

The two most common reasons for myocardial ischemia:

A

coronary artery narrowing (atherosclerosis) & occlusion (thrombus)

113
Q

Coronary microvascular disease affects

A

women more than men and it affects the tiny arteries in the heart muscle (can occur with or without CAD)

114
Q

Risks associated with ischemic heart disease include:

A

increased risk for periop CV events including MI, HF, and death
recent UA or MI further increase the risk

115
Q

What is stable angina?

A

chest pain or discomfort due to CAD
Stable means frequency and severity of symptoms consistent for >2 months
usually occur on exertion so demand is what is changing

116
Q

S/S of stable angina include

A

chest pain, pressure, or heaviness; may or may not radiate to neck, arms, shoulder or jaw
epigastric discomfort
pain characterized by crescendo-decrescendo
lasts several minutes

117
Q

Diagnosis of stable angina:

A

induced by physical exertion, emotional tension, or cold

ECG changes coincide with chest pain- ST segment depression or T wave inversion

118
Q

Acute coronary syndrome includes:

A

unstable angina, NSTEMI, and STEMI
SA is NOT an ACS
occurs when atherosclerotic coronary plaque becomes unstable, leading to a series of events that eventually results in partial or total thrombotic occlusion of a coronary artery

119
Q

STEMI definition

A

MI caused by complete blockage of coronary artery

120
Q

Pathophysiology of STEMI

A

ischemia–> injury–> death

121
Q

S/S of STEMI include:

A

same as for NSTEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, sudden weakness, fatigue

122
Q

STEMI is characterized by

A

ST elevation on more than one EKG
Cardiac biomarkers
imaging may show abnormal ventricular wall motion

123
Q

STEMI is treated with

A

TPA because it can get at fibrin to break it down

may need PCI or CABG

124
Q

NSTEMI definition:

A

MI caused by a partially blocked coronary artery

125
Q

NSTEMI is characterized by

A

ECG showing absence of elevated ST segment (transient ST elevation, T wave inversion, ST depression), elevated cardiac biomarkers

126
Q

S/S of NSTEMI:

A

same as those for STEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, fatigue

127
Q

Definition of unstable angina:

A

chest pain or discomfort due to coronary artery disease that occurs randomly and unpredictably without any of the obvious triggers (physical exertion, emotional stress, or cold)

128
Q

Causes of unstable angina include:

A

decreased myocardial oxygen supply (vasospasm, worse narrowing, inflammation) or increased myocardial oxygen demand

129
Q

Descriptive pathology of unstable angina:

A

angina at rest, angina of new onset, increase in the severity or frequency of previously stable angina, no elevation of cardiac biomarkers

130
Q

Unstable angina treatment

A

still needs to be treated like a medical emergency
Reduce myocardial O2 consumption
Rest, increased FIO2, analgesia, BB, Ca2+ inhibitor, NO, anticoagulant

131
Q

Diagnosis of unstable angina:

A

no elevation of ST segment (other EKG changes)

no elevation of cardiac biomarkers

132
Q

Management of patients with IHD:

A

take a thorough cardiac history of patients with suspected
avoid triggering SNS elevation during intubation or laryngoscopy (increased SNS increases demand)
monitor for ischemia- continuous ECG w/ ST analysis, cardiac biomarkers, TEE monitoring

133
Q

The goals for patients with IHD are

A

avoid ischemia, monitor ischemia, treat ischemia

134
Q

Perioperative MI has a ____ risk of death

A

20% which occurs 24-48 hours post surgery

135
Q

Risk of periop MI is increased if:

A

history of IHD, high-risk vascular surgery, emergency surgery

136
Q

Diagnosis of periop MI is difficult because

A

hemodynamic instability is common post-op, post-op analgesia may mask MI pain, measure cardiac troponin to understand duration of ischemia

137
Q

For patients getting a PCI and stents:

A

if PCI was recent then patient will be on anti-platelet therapy
monitor patient closely for MI or infarct

138
Q

Volume overload problems include:

A

AVR & MVR

139
Q

High ischemia risks patients include:

A

HCM-LVOTO, Cardiac tamponade, AS, AVR

140
Q

Patients with baseline elevated afterload include

A

AS, SHF

141
Q

Patients with elevated inotropy include:

A

Constrictive pericarditis, cardiac tamponade, Tricuspid valve stenosis, aortic stenosis, pulmonic stenosis

142
Q

Any of the diastolic/filling problems can advance

A

to DHF

143
Q

Any of the emptying problems can advance to

A

SHF

144
Q

Regional anesthesia will decrease

A

SVR

145
Q

Hypotension is defined as

A

systolic blood pressure < 90 mmHg

146
Q

Neuraxial anesthesia can lead to

A

hypotension and bradycardia d/t anesthesia of spinal sympathetic nerve fibers

147
Q

Patients with preexisting hypertension are at higher risk for

A

intraoperative hypotension

& increased risk of mortality and/or MI

148
Q

The duration of hypotension

A

increases risk

149
Q

Hypotensive effects may occur at

A

normal BP in patients with uncontrolled hypertension (autoregulatory adaptation to higher pressures)

150
Q

Hypotension can result from:

A

arterial vasodilation, myocardial depression, venodilation, bradycardia, volume: hemorrhage or third space (starling forces)

151
Q

Causes of intra-operative hypotension includes:

A

hypovolemia, induction of general anesthesia, sympathectomy due to neuraxial block, inhibition of RAAS, periop MI or acute HF causing hypotension

152
Q

For severe or refractory hypotension (treatment):

A

infusion of a short-acting vasopressor/inotropic agent, aggressive treatment

153
Q

Acute post-operative hypotension is defined by

A

systolic BP <90 mmHg, mean BP <65 mmHg, or relative decrease in BP 20% below baseline

154
Q

Post-op hypotension may occur due to:

A

chronic or recent administration of hypertensive agents, inadequate intraoperative fluid replacement, blood loss, residual anesthetic effects, allergic drug reactions, adrenal insufficiency, myocardial ischemia or acute congestive heart failure

155
Q

Hypertension is defined by

A

BP >130/80 mmHg or higher

1/3rd of non-cardiac patients will be hypertensive & 2/3rds of cardiac patients will be hypertensive

156
Q

Patients with chronic HTN are at significant risk for

A

IHD, HF, CVA, arterial aneurysm, and ESRD

157
Q

Even short durations of MAP <65 was associated with

A

increased overall mortality, AKI, myocardial injury and stroke

158
Q

Anesthetic implications for hypertensive patients:

A

prevent end-organ damage, reduce periop risk of adverse events (vessel injury)

159
Q

Isolated systolic hypertension is primarily a result of

A

stiffening of the arteries

suspect in patients >65 years

160
Q

Widening pulse pressure is better than

A

SBP alone as diagnostic for intraoperative hemodynamic instability and adverse postoperative outcomes

161
Q

Distinguish hypertensive urgency from emergency:

A

presence of end organ damage: emergency

162
Q

Hypertensive crisis is defined as

A

BP >180/120 mmHg

163
Q

The cause of hypertensive emergency is

A

pheochromocytoma

164
Q

S/S of hypertensive urgency:

A

HA, epistaxis, anxiety

165
Q

Chronic HTN patients are more likely to experience a hypertensive

A

urgency than emergency

166
Q

S/S of hypertensive emergency:

A

acute CV emergency (ACS, acute decomp. HF, pulm edema, dissecting aortic aneurysm), acute RF, postop complications exacerbated by the elevated BP (hemorrhage, increased ICP), neurologic s/s

167
Q

Treatment of hypertensive emergency includes:

A

using short-acting vasodilators such as nitroprusside (need to bring SVR down)

168
Q

Pheochromocytoma is

A

adrenal gland chromaffin cell tumor that has NE release greater than Epi release

169
Q

S/S of pheochromocytoma:

A

tachycardia, diaphoresis, HA, paroxysmal HTN, HTN, hyperglycemia

170
Q

For patients diagnosed with pheochromocytoma

A

pre-treat to inhibit alpha 1 adrenergic

2 in 1 million patients have undiagnosed pheochromocytoma

171
Q

Define stenosis:

A

abnormal narrowing of a passage or orifice

valve stenosis thickens and stiffens the valve and increases resistance to blood flow through the orifice

172
Q

Mitral valve stenosis is

A

a narrowing of the mitral valve resulting in a LV filling problem

173
Q

Pathology of mitral valve stenosis:

A

increased resistance to blood flow through the mitral valve–> reduced LV filling–> decreased SV–> decreased CO
back up of blood in the LA results in increased LAP
when LAP >25 mmHg then blood is backed up into pulmonary circulation

174
Q

S/S of mitral valve stenosis begin when

A

orifice narrowing is >50%

heart murmur, pulm arterial HTN, 1/3rd of patients have afib

175
Q

Diagnosis of mitral valve stenosis:

A

Echo, increased transvalvular pressure gradient, LA hypertrophy

176
Q

Treatment of mitral valve stenosis:

A

goal is to decrease LAP

diuretics, control a-fib (thrombus risk), surgery to repair leaflet

177
Q

Anesthetic implications of mitral valve stenosis:

A

Goal: avoid pulm edema or decreased CO
avoid increased HR- causes reduced LV filling time and ultimately decreased CO
Careful fluid balance to avoid hypotension but prevent fluid overload
Avoid increased pulmonary vascular resistance–> may lead to RHF

178
Q

Causes of aortic valve stenosis:

A

calcification of aortic valve leaflet occurs with increasing age
infective endocarditis
rheumatic fever
risk factors: HTN, hypercholesterolemia

179
Q

Aortic valve stenosis is:

A

a narrowing of the aortic valve resulting in an obstruction to the flow of blood from the left ventricle to the aorta
results in an LV emptying problem

180
Q

In advanced stages of aortic valve stenosis,

A

concentric remodeling may occur resulting in a LV filling problem

181
Q

Pathology of aortic valve stenosis

A

Myocardial oxygen demand problem: increased LVSP, increased LVEDP, increased afterload
Myocardial oxygen supply problem: increased afterload: emptying is not complete and increased LVEDV and LVEDP leads to compression of coronary arteries

182
Q

S/S of aortic valve stenosis:

A

systolic murmur, exercise intolerance, syncope, LV hypertrophy, can lead to LH failure

183
Q

Diagnosis of aortic valve stenosis:

A

ECG LV hypertrophy, Echo/doppler shows decreased aortic valve area, increased transvalvular pressure gradient increases

184
Q

Treatment of aortic valve stenosis:

A

surgical valve replacement

185
Q

Anesthetic implications of aortic valve stenosis:

A

goal is to maintain CO and decrease risk of myocardial ischemia/infarct
AVOID HYPOTENSION AND KEEP HR NORMAL
avoid hypotension b/c decreased coronary perfusion
keep NS b/c need atrial kick to improve SV via F/S

186
Q

Tricuspid valve stenosis is

A

a narrowing of the tricuspid valve opening resulting in an obstruction to the flow of blood from the RA to the RV
results in a RV filling problem

187
Q

Tricuspid valve stenosis the the result of

A

rheumatic fever

188
Q

S/S of tricuspid valve stenosis include:

A

systemic venous congestion with JVD, ascites, and peripheral edema; decreased CO, abdominal discomfort d/t hepatomegaly, Kussmaul’s sign, NO pulmonary congestion unless have mitral valve stenosis

189
Q

Diagnosis of tricuspid valve stenosis:

A

echo

differential diagnosis: r/o other causes of systemic venous HTN

190
Q

Treatment of tricuspid valve stenosis includes:

A

diuretics to avoid congestion

191
Q

Anesthetic implications of tricuspid valve stenosis:

A

balance fluids so that decreased CO is avoided but that systemic congestion is not exacerbated

192
Q

Normal HR for infants:

A

113-145 bpm

193
Q

Normal HR for child:

A

75-113 bpm

194
Q

Normal HR for adult:

A

60-90 bpm

195
Q

MHR declines with

A

age- normal MHR for older adult ~73 bpm

196
Q

Cardiac dysrhythmia is a

A

cardiac rhythm that displays abnormal rate, interval length or conduction path

197
Q

Tachydysrhythmias can result in

A

HTN increased CO & IHD (decreased supply/ increased demand)

198
Q

Sinus tachycardia is defined as

A

HR: 100-160

tolerable unless history of cardiac disease

199
Q

Supraventricular tachycardia is defined as

A

HR 160-180 initiated at or sustained by tissue at or above the AV node
more common Young>old, women>men

200
Q

Ventricular tachycardia is defined as

A

HR>170 + 3 or more PVCs

common after MI, cardiac infection

201
Q

Atrial fibrillation is defined as

A

no ECG P wave

multiple areas of the atrium continuously depolarize, quivering atrial wall

202
Q

Big risk with atrial fibrillation is

A

blood clots

203
Q

Atrial flutter differs from atrial fibrillation because

A

atrial to ventricular beat rate is 1:2

204
Q

Ventricular fibrillation is defined by

A

no pulse or BP
most common cause of sudden cardiac death
common in IHD, risk declines with statins, ACEi, beta-blockers

205
Q

Sinus bradycardia is defined by

A

HR <60 (athletes, sleeping)

206
Q

Premature ventricular contractions

A

arise from single or multiple foci below the AV node
s/s: palpitations, syncope, near syncope
management: keep defib handy, rule out acid-base or electrolyte triggers

207
Q

Heart blocks can be precipitated by:

A

MI, myocarditis, lyme disease, rheumatic fever, infiltrative disease, mononucleosis, overdose of beta blockers or Ca2+ channel blockers

208
Q

1st degree AV block is defined by

A

PR interval >200msec (slow conduction through AV node)

inconsequential except increased risk for a-fib

209
Q

2nd degree heart block is defined by

A

impaired conduction in “conduction fibers” (MI, fibrosis, calcification, infiltration, inflammation)
P wave and no corresponding QRS
may require atropine or pacing

210
Q

3rd degree heart block is defined by

A

“complete heart block” atrial electrical system disconnected from ventricular
MI, aged, or diseased heart
treatment: pace, beta-agonists

211
Q

Bundle branch blocks are defined as

A

conduction error in conducting fibers
RBBB- ASD, IHD, valve disease, DCM
LBBB- IHD, valve disease, HTN, cardiomyopathy

212
Q

The goal of cardioversion is to

A

re-coordinate the electrical pathways

213
Q

Defibrillation creates

A

a fire risk in the OR b/c it arcs electricity

electrical discharge to correct dysrhythmias when cardioversion is not possible (no R wave or no pulse)

214
Q

Aneurysm is

A

dilation of all three layers of the artery wall (intima, media, and adventitia)
rupture is a medical emergency

215
Q

Dissection is

A

when blood enters the medial wall layer d/t intimal layer tear

216
Q

Risk factors for aortic aneurysm:

A

HTN, family history, smoking, atherosclerosis, male, older age, Marfan’s syndrome (dissecting aneurysm, atherosclerosis

217
Q

Factors that precipitate dissection:

A

deceleration injuries, crack cocaine, pregnancy, aortic cannulation/clamping, aortic valve replacement

218
Q

S/S of thoracic aortic aneurysm:

A

usually asymptomatic, stridor, hoarseness, dysphagia, superior vena cava edema, aortic valve incompetence–> aortic regurgitation–> HF

219
Q

S/S of aneurysm dissection:

A

severe sharp pain in chest, neck, shoulder blades, progress to high SVR, shock, absence of peripheral pulses, myocardial ischemia, ischemic stroke

220
Q

When the thoracic aortic is cross-clamped–>

A

there is an increased blood flow to the brain and reduced blood flow to the spinal cord
release of the clamp can result in hypotension (severe)

221
Q

Surgical considerations for aortic aneurysm:

A

increased risk for: high blood loss, hypoperfusion of end organs

222
Q

Peripheral arterial disease is defined by

A

atherosclortic plaque deposition in peripheral artery, narrowed artery, reduced blood flow (chronic); embolism (acute); or vasculitis (inflammation)- rare

223
Q

Risk factors for peripheral arterial disease include

A

smoking, age, family history, DM, HTN, obesity, dyslipidemia

224
Q

Diagnosis of PAD includes:

A

ankle to brachial index <0.9

SBP is reduced at ankle in PAD

225
Q

S/S of PAD include:

A

intermittent claudication (muscle pain/cramps), leg coolness, pallor, atrophy, hair loss, leg symptoms worse when supine, absent or decreased peripheral arterial pulse

226
Q

Anesthetic considerations for PAD

A

similar to that for surgical repair of AAA b/c aortic clamping occurs
issues revolve around hypotension with unclamping

227
Q

PVD formation is promoted by

A

Virchow’s triad: venous stasis (immobility), hypercoagulability, and injury to vascular endothelium

228
Q

Congenital heart disease is

A

a defective heart structure
gene-environmental interactions account for 90% of cardiac congenital abnormalities
single or multi-gene abnormalities account for 10%

229
Q

Atrial septal defect results in

A

RH and pulm circulatory volume overload
septal wall between right and left atria is defective
allows blood flow through the septum
decreased systemic blood flow because LA kick is reduced

230
Q

Atrial septal defect accounts for

A

1/3rd of all cardiac congenital defects

more likely in females

231
Q

With septal defects the goal is to avoid

A

increased shunt volume or right to left shunt (can lead to hypoxemia)
Decreased SVR will increase right to left shunt and increased PVR will increase right to left shunt

232
Q

Ventricular septal defect is

A

the most common cardiac congenital defect

pulm circulation and left heart volume overload (volume overload in pulm circulation transmitted to left heart)

233
Q

Pulmonic valve stenosis is

A

a narrowing of the pulmonic valve resulting in an obstruction to the flow of blood from the right ventricle to the pulmonary artery

234
Q

Prevalence of pulmonic valve stenosis:

A

accounts for 10% of all congenital heart disease; acquired is rare, PVS usually discovered in childhood

235
Q

Cause of pulmonic valve stenosis:

A

congenital»> rheumatic heart disease, infective endocarditis, carcinoid heart disease, iatrogenic causes (radiation or chemo)

236
Q

Pulmonic valve stenosis results in

A

a RV emptying problem, increased MVO2

237
Q

With pulmonic valve stenosis, right ventricle

A

outflow tract can also be obstructed

238
Q

In pulmonic valve stenosis, RV pressures become elevated d/t increased

A

pulmonic valve resistance and RVOT obstruction–> RV hypertrophy–> RV diastolic dysfunction occurs

239
Q

S/S of pulmonic valve stenosis include

A

Mild disease: asymptomatic, good long term survival
Severe disease: present during childhood–> RV failure and cyanosis
adult: exertional dyspnea, fatigue RV hypertrophy, RV failure

240
Q

Diagnosis of pulmonic valve stenosis:

A

echo

a systolic ejection murmur

241
Q

Treatment of aortic valve stenosis:

A

valve surgery

balloon pulmonary valvuloplasty

242
Q

Anesthetic implications of pulmonic valve stenosis:

A

goal is to maintain CO & avoid RV decompensation
volume needs to be sufficient but don’t overload
inotropes may be necessary

243
Q

Aortic valve regurgitation is defined by:

A

during diastole a portion of the SV moves backwards from aorta into the LV
results: decreased CO, LV volume overload, Increased LVEDV & LVEDP, and decreased coronary perfusion

244
Q

Aortic valve regurgitation is a

A

volume overload and ischemia problem

245
Q

Chronic aortic regurgitation is due to

A

rheumatic fever, idiopathic, Marphan’s syndrome, Rheumatoid arthritis

246
Q

Acute aortic regurgitation is due to

A

infective endocarditis, aortic dissection

247
Q

Rapid deterioration in LV function results in (aortic valve regurgitation)

A

LHF; coronary ischemia

248
Q

S/S of aortic valve regurgitation

A

patients may be asymptomatic for decades; initial symptoms are exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea

249
Q

Descriptive pathology of aortic valve regurgitation:

A

regurgitant flow increased LVEDV, LV remodeling–> eventually LHF

250
Q

With aortic valve regurgitation, volume regurgitated is

A

directly proportional to duration of diastole, directly proportional to the pressure across the valve, directly proportional to size of aortic valve orifice

251
Q

Diagnosis of aortic valve regurgitation

A

diastolic murmur, decrease DBP d/t backflow, enlarged LV on ECHo
acute s/s include CV collapse

252
Q

Treatment of aortic valve regurgitation:

A

surgically replace valve

253
Q

Anesthetic management of aortic valve regurgitation:

A

Maintain LV forward flow & CO
Summary: desire slight increase in HR and slight decrease in SVR, adequate volume
Heart rate- Increase >80 bpm; decreased duration in diastole and increased CO
Preload: need preload for F/S and SV/CO
Afterload: decreased afterload favors forward flow; avoid increased SVR

254
Q

Mitral valve regurgitation is

A

during systole a portion of the SV moves backwards from LV into the LA

255
Q

Mitral valve regurgitation is a

A

Volume overload problem

256
Q

Causes of chronic mitral regurgitation include

A

rheumatic fever, incompetent valve

257
Q

Causes acute mitral regurgiation include

A

myocardial ischemia/infarct, infective endocarditis, chest trauma

258
Q

Descriptive pathology of mitral valve regurgitation:

A

decreased forward flow, regurgitation into LA, increased LAP, pulmonary congestion

259
Q

Diagnosis of mitral valve regurgiation:

A

murmur, echo, ECG atrial or ventricular hypertophy

260
Q

Treatment of mitral valve regurgitation

A

surgery

261
Q

Anesthetic management of mitral valve regurgitation:

A

avoid increased CO
HR- normal or slight increase
preload: need preload for F/S and SV but overload increases pulmonary congestion
use inotropes to improve forward flow and decrease LV volume
Summary: inotropes increase SV, vasodilators decrease SVR, titrate volume

932 Pathophysiology (8 decks)

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