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N202 > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

risk factors for CAD

A 
high lipid level above 240
over age 65
HTN
smoking
viral ardiomyopathy
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2
Q

cardiac output

A

HR x SV

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3
Q

CI =

A

CO x BMI (includes body mass)

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4
Q

amount of blood pumped out of LV during systole & amount remaining at end of diastole

A

ejection fraction

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5
Q

normal EF

A

60-70 %

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6
Q

O2 demand exceeds ability of coronary arteries to supply heart with O2, (usually insufficiant blood flow)

A

myocardial infarction

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7
Q

what is MI caused by

A

thrombus or spasm (plaque), you have cyanosis in 10 seconds, after minutes, anaerobic metabolism produces lactic acid, stimulates nerves to send pain messages through thoracic cavity = CP

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8
Q

how long are the cells viable for

A

20 minutes, after that they have sustained necrosis, that are of the heart stops beating

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9
Q

what is the leading cause of morbidity and mortality

A

MI

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10
Q

transmural

A

full thickness

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11
Q

subendocardial

A

partial thickness

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12
Q

what will show in the EKG for the zone of infarction

A

develop a Q wave

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13
Q

what will show in the EKG for the zone of injury

A

ST evaluation

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14
Q

what till show in the EKG for the zone of ischemia

A

T wave inversion

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15
Q

what leads will be affected if the anterior part of the heart is injured/ischemic

A

V1-V4

LAD

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16
Q

what leads will be affected if the inferior part of the heart is injured/ischemic

A

II, III, aVf

RCA

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17
Q

what leads will be affected if the lateral part of the heart is injured /ischemic

A

V5, V6, I, aVl

left circumflex

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18
Q

where is the worst place to infarct

A

LAD

*widow maker

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19
Q

when does healing begin after an MI

A

24 hours, leukocytes start working, macrophages remove damaged (necrotic) tissues, tissues are vulnerable for 10-14 days

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20
Q

what happens after injury to the myocardium

A

compensated bby thickening, dialating & remodeling (CHF)

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21
Q

abrupt loss of cerebral blood flow, only 20% of survivors leave the hospital

A

sudden cardiac arrest

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22
Q

Tx for cardiac arrest

A

ICD surgery, low EF is a sign prior to arrest, most have had MIs in the past

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23
Q

management of MI in acute stage, short term goals

A

relieve pain*, control lethal arrhythmias, preserve the myocardium (stop progression of MI)
*primary goal

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24
Q

pain is =

A

cell death

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25
Q

long term goals for management of MI in acute stage

A

cope effectively with anxiety, compliacne with rehab program, modify/alter risk factors

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26
Q

Dx of acute MI

A

H&P
serum enzyme levels CK & troponin*
most indicative (a protein not an enzyme)
12 lead EKG 1 mm ST elevation
CXR, CBC, thyroid, lipid, CRP, CT/PET, Echo, stress test, cardiac cath

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27
Q

ST segment elevation

A

more than 1 mm above or below isoelectric line

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28
Q

why does ST segment elevation occur

A

myocaridal injury, happens over affected area of the ventricle, they return back to the isoelectric line in about 2 weeks

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29
Q

T wave inversion

A

ischemia causes symmetrical inversion of T wave,

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30
Q

Q wave development

A

normal Q wave is 1 mm or less, Q wave develop wen ST segments are elevated, appear several hours/days after MI

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31
Q

what is the greatest sign of ischemia

A

pain

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32
Q

why is morphine sulfate given

A

decrease anxiety, O2 demand, and restlessness

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33
Q

why is nitro given

A

vasodilator used for pain relief, deceases preload & afterload, decreases myocardial O2 demand

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34
Q

side effects of morphine and nitro

A

watch BP, can drop quickly

*assess VS Q5-10 minutes

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35
Q

what are the most common side effects of MI

A

arrhythmias

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36
Q

what is given for PVCs and V tach

A 
lidocaine  give bolus then follow up with drip
administer amiodarone (1st line)
O2
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37
Q

what is given to preserve the myocardium

A

thrombolytics within 30 minutes (if criteria is meet)
O2
stool softeners (decrease risk of straining, decrease the use of valsalva maneuver)
nutrition (low fat diet)

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38
Q

Beta blockers

A

decrease infarct size, decrease preload and afterload, decrease HR/contractility

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39
Q

ACE inhibitors

A

decrease remodeling of ventricle, decrease ventricular dilation, decrease CHF & mortality

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40
Q

Anti coag (Heparin)

A

decrease risk of thrombi, decrease re-occlusion 12-24 hours after thrombolytic therapy

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41
Q

ASA

A

inhibit platelet aggregation rapid antithrombic

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42
Q

Magnesium

A

usually only as an antiarrhythmic (Torsods)

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43
Q

what other interventions can be done for MI

A

HOB elevated, bed rest for 12 hours, reduce stress, rest and comfort, Mild sedative to reduce anxiety, sleeping pills, dietary restrictions (clear liquids to cardiac diet, I & O, daily weights, decrease salt/chol/fat/caffeine, CABG, PTCA, therapeutic hypothermia

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44
Q

PTCA

A

percutaneous transluminal coronary angioplasty

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45
Q

CABG

A

emergency measure for revascularization of myocardium

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46
Q

therapeutic hypothermia

A

proven to improve neurological outcomes following cardiac arrest

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47
Q

what is recommended as first line Tx for MI

A

PTCA, fibrolytic therapy, CABG

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48
Q

plan of care for MI pt

A

perform ongoing assessment, limit energy expenditure, maintain hemodynamic stability (increase CO & tissue perfusion, keep BP and HR increased {not hypotensive}), tx complications, provide emotional support, teach

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49
Q

hypothermia protocol

A

keep temperature between 32-34 degrees, monitor temp with bladder temp probe, keep target temp for 12-24 hours, cooling blankets, ice packs in groin and torso

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50
Q

Signs Sx of possible MI

A

diaphoretic, increase temp, pallor, N/V, confusion, syncope, stroke, CP, EKG changes, JVD, peripheral edema, abnormal heart sounds, SOB, orthopnea, tachypnea, crackles, frothy sputum, decrease UO, anxiety, agitation, denile

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51
Q

what heart sound is common in MI

A

S4 (decrease of LV compliance, atrial gallop)

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52
Q

when is a pericardial friction rub develop in MI pt

A

2-3 days post infarct, inflammation causes loss of function (pericarditis)

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53
Q

what is the most frequent complication of MI

A

arrhythmias (80%)

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54
Q

V fib after MI

A

cause sudden death 2 hours post MI

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55
Q

sinus tach after MI

A

anterior wall MI, need to correct with adenosine to slow the rhythm, need to increase myocardial O2 demand, decrease systemic perfusion

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56
Q

PACs after MI

A

1/2 of all MI pts will have

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57
Q

a fib after MI

A

common with anterior MI, decrease CO, formation of clots

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58
Q

PVC after MI

A

most develop a few hours after MI, need O2, correct any acid imbalance, IV lidocaine, pronestyl, cordarone (amioderone)

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59
Q

2nd degree type 1 after MI

A

inferior MI, temporary pacer, or atropine if hemodynamically significant

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60
Q

2nd degree type 2 after MI

A

anterior MI, need pacemaker

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61
Q

accelerated idioventricular rhythm after MI

A

most common reperfusion rhythm, tolerated well, no Tx

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62
Q

what are the major goals of MI

A

tx the underlying cause, presume CO and tissue perfusion

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63
Q

MI complications are

A

thromboemboli, pericarditis, dresslers syndrome, ventricular septal rupture, ventricular aneurysm, cardiac rupture, papillary muscle rupture

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64
Q

have in deep veins of leg or chambers of the heart, can lead to stroke, pulm. emboli, peripheral arterial occlusion

A

thromboemboli

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65
Q

who is at high risk for emboli

A

severly ill, hx of valvular heart disease, greater than 60 years old, prolonged bed rest, a-fib/a-flutter

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66
Q

Tx for possible thromboemboli

A

heparin, Coumadin, OOB quickly, if have edema (bed rest until it clears)

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67
Q

inflammation of visceral/parietal pericardium or both

A

Pericarditis

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68
Q

causes of pericarditis

A

cardiac compression, decrease ventricular filling, decrease emptying and failure = result in cardiac tamponade

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69
Q

S/Sx of pericarditits

A

CP mild to severe, increase with inspiration, coughing, movement in upper body
sitting forward can relieve the pain

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70
Q

excess fluid in the pericardium causes what

A

tamponade, drained with needle, catheter or surgery

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71
Q

Hallmark sign of pericarditis

A

fricition rub, heard at left sternal boarder

also have fever, dyspnea, cough, EKG have ST segment elevation

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72
Q

Tx for pericarditis

A

Tx of Sx: pain, anxiety, decrease CO

give analgesics, anti-inflammatory, NSAIDs

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73
Q

when is pericardiocentesis used

A

if tamponade develops

look for JVD, listen for rub, assess for CP

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74
Q

Dressler’s syndrome

A

Post MI syndrome, occurs 10 days to 3 months post MI,
pleuritic type CP, hypersensitivity to products of necrotic myocardium
pericarditis with pleural effusion (called late pericarditis, may be an autoimmune response)

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75
Q

S.sx of dresslers syndrome

A

pleuritic pain, fever, increase SED rate & WBC, friction rub audible, left pleural effusion, arthralgia (joint pain)

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76
Q

Tx for dresslers syndrome

A

same as pericarditis, any CP must be Tx as a recurrent ischemic attack
analgesics, anti-inflammatory, NSAIDs

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77
Q

Ventricular septal rupture

A

develop rapidly, usually end in death, rare, when blood is shunted from LV to RV

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78
Q

S/Sx of ventricular septal rupture

A

hear new, loud systolic murmur, progressive dyspnea, tachy, pulm. congestion

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79
Q

Tx for ventricular septal rupture

A

urgent cardiac cath to surgically correct
after load reducers: Nipride
preload reducers: Lasix

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80
Q

non contractile thinned LV wall results in reduction of stroke volume, increase of stress on necrotic portion of LV wall, region bulges out during systole, and a scar forms

A

ventricular aneurysm

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81
Q

where does ventricular aneurysm commonly occur

A

in apical area, may develop in hours or weeks

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82
Q

Dx for ventricular aneurysm

A

palpate ectopic impulses, bulge noted on xray or ECHO

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83
Q

Tx for ventricular aneurysm

A

manage complications, may need surgery

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84
Q

What does prognosis depend on with ventricular aneurysm

A

size of aneurysm, LV function, severity of co existing CAD, rupture of aneurysm is rare

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85
Q

cardiac rupture

A

when you have leukocyte scavenger cells remove necrotic debris causing a thin cardiac wall, important for patients to continue to rest

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86
Q

S/sx of cardiac rupture

A

see sudden neck vein distension, hypotension (not bradycardia), PEA, happens rapidly, usually 5-6 days post MI

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87
Q

papillary muscle rupture

A

95% fatality rate, support the mitral valve, rupture causes mitral valve regurgitation

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88
Q

S.sx of papillary muscle rupture

A

dyspnea, pulmonary edema, decrease CO, increase volume in L atrium, hear systolic murmur

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89
Q

complete rupture of papillary muscle

A

acute mitral regurgitation, cardiogenic shock, high mortality rate

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90
Q

what does partial rupture cause

A

mitral regurgitation but can support need emergency surgery to replace the valve

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91
Q

an abnormal accumulation of fluid in alveoli and interstitial spaces, leads to LV failure and is life threatening, interferes with gas exchange between alveoli & pulmonary capillaries

A

acute pulmonary edema

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92
Q

patho of pulmonary edema

A

increase hydrostatic pressures or decrease colloid oncotic pressure, fluid leaves the pulmonary capillaries & enters interstitial spaces (edema),

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93
Q

common causes of acute pulmonary edema

A

left sided CHF (flash edema)

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94
Q

S/sx of acute pulmonary edema

A

paroxysmal nocturnal dyspnea*, agitation, pale, cyanosis, cool clammy, accessory muscle use, wheezing, coughing with frothy blood tinged sputum, increase of HR, increase or decrease of BP, increase of PaCO2 = acidosis

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95
Q

impaired cardiac function, ventricle is unable to maintain CO sufficient to meet metabolic needs

A

acute congestive heart failure

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96
Q

most at risk for CHF

A

HTN

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97
Q

what compensatory mechanisms are activated with CHF

A

adrenergic system, renin angiotensin aldosterone system, ventricular dilation/ventricular hypertrophy, increase of sympathetic nervous system

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98
Q

adrenergic system

A

release epi

increase PVR, blood is shunted from non vital organs to heart and brain, increases preload

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99
Q

renin angiotensin aldosterone system

A

constriction of renal arterioles

decreases GFR, increases reabsorption of Na, fluid retention = increase of CO

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100
Q

ventricular dilation/ventricular hypertrophy

A

stretches & increases ventricular wall thickness
hypertrophy helps the ventricle overcome the increase of pressure, increases afterload (remodeling)
*give ACE inhibitor

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101
Q

increase of sympathetic nervous system

A

increase of HR and contractility (increases the need for O2)

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102
Q

what do compensatory mechanisms affect

A

HR, preload, afterload, stroke volume, contractility

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103
Q

R sided CHF (cor pulmonale)

A

ineffective RV contractile function

most commonly caused by failure of the left side or blood backing up behind the left ventricle (JVD)

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104
Q

left sided CHF

A

disturbance of contractile function of LV resulting in pulmonary congestion or edema, decrease of CO, most frequently occurs with LV infarcts

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105
Q

acute vs. chronic

A

refers to the rapidity with which syndromes develop and the activation of compensatory mechanisms

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106
Q

S.sx of acute CHF & pulmonary edema

A

resting dyspnea, cachexia (wasting), orthopnea, weight increase, tachy, JVD (with R sided), apical pulse is displaced left and down, hear S3 & S4, crackles, wheeze, edema (symmetrical), cool shiny swollen no hair, brownish color, restless, hepatomegaly (ascities), void @ night increases

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107
Q

Goal of care with CHF

A

reduce edema and cardiac workload, increase CO, manage HTN, decrease afterload

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108
Q

Dx for CHF and pulmonary edema

A

H&P, ABGs, CXRay, hemodynamic monitoring, 12 lead EKG, ECHO (EF), cardiac cath, BNP, D Dimer

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109
Q

BNP

A

b type natriuretic peptide, hormone secreted by ventricular tissue in response to increase of volume and pressure

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110
Q

D Dimer

A

used to rule out blood clotting problems,

monitor Tx if in DIC

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111
Q

goals of therapy for CHF and pulmonary edema

A 
decrease intravascular volume (Lasix)
decrease venous return (preload)
decrease after load (nipride, tridil, morphine)
improve gas exchange
improve cardiac function
reduce anxiety (morphine)
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112
Q

Tx for CHF and pulmonary edema

A

HOB elevated, O2, bed rest, monitor VS, UO, daily weights, possible cardioversion (if hemodynamically unstable tachycardia), intubation, tx underlying cause

113
Q

Medications for CHF and pulmonary edema

A 
ACE inhibitors (1st lind Rx)
Diuretics
positive inotropic agents
phosphodiesterase inhibitors
vasodilators
BB
morphine
natrecor
114
Q

ACE inhibitors

A

(1st lind Rx, suppresses renin, increase CO, limits remodeling), SE: cough, if bad enough put on ARB instead

115
Q

Diuretics

A

decrease preload and workload of heart, assess lung sounds, strict I & O
*if given too fast can cause hearing loss temporarily

116
Q

Positive inotropic agents examples

A

Digoxin and dobutamine and dopamine

117
Q

Digoxin

A

cardiac glycoside, decreases HR, increases muscle contractility, good for A fib A flutter, increases CO and SV
SE: N/V, HA, anorexia, double/blurred vision, confusion

118
Q

Dobutamine and Dopamine

B adrenergic agonists

A

used short term in ICU, increases contractility, blood flow to renal, mesenteric, coronary and cerebral vascular beds
SE: increases ventricular irritability, increases O2 demand by myocardium

119
Q

phosphodiesterase inhibitors

A

Inocar & Primacor
increase CO, promotes vasodilation, decrease SVR and PAWP
SE: arrhythmias, GI and decrease BP, thrombocytopenia
*need frequent assessments of BP

120
Q

Nipride & Nitrates

A

increase cardiac performance, decrease after/preload
Nipride: very potent, have rapid decrease in BP, SE: N/V, confusion, tinnitus, *hypotension, long term can have cyanide poisioning

121
Q

Tridil

A

relieves pain, arterial and venous vasodilation, relieves pulmonary congestion, decrease cardiac workload, decrease cardiac O2 consumption
SE: hypotension, HA

122
Q

morphine

A

drug of choice if anxiety is an issue, causes vasodilation, induces decrease venous return, decreases pain, anxiety, myocardial demand
SE: decrease RR, brady arrhythmias, hypotension

123
Q

natrecor

A

for refractory CHF and pulmonary edema (when not responding to other Rx)
relaxes vascular smooth muscle, inhibits Na and water retention, suppresses renin secretion, decreases aldosterone, decreases PCWP
SE: hypotension, arrhythmias, angina, HA, back pain, anxiety, nausea
IV drip depends on weight, frequent VS & I&O

124
Q

what other therapies can be done for CHF and pulmonary edema

A

biventricular pacing (increases LV performance)
cardiac transplant
intra-aortic balloon pump (IABP)
VAD (bridge to transplant)

125
Q

resynchronization

A

relies on electric leads to correct an arrhythmia, electrically stimulate heart muscle to synchronize contractions of ventricles only when lower chambers beat in harmony can they contract with enough force to push blood caring O2 through the body

126
Q

what teaching can be done for CHF and pulmonary edema

A 
diet: decrease salt (2 gram)
fluid restriction (2000 ml/day)
weigh daily (no more than 2 lbs/day)
rest
follow Tx plan
127
Q

Pump failure, failure to maintain blood supply to the circulatory system and tissues, due to decrease of CO

A

cardiogenic shock

128
Q

Cardiogenic shock is manifested by

A

decrease perfusion, hypotension, decrease or absent UO, change in LOC, sweating, pallor, initially tachy

129
Q

etiology of cardiogenic shock

A

common cause is extensive LV failure with an acute MI, decrease of CO to systemic circulation, blood backs up into the pulmonary vasculature, filing heart tries to pump harder = decrease of CO and BP, decrease of blood to coronary arteries = ischemia (c/o CP, changes on EKG), metabolic acidosis

130
Q

causes of cardiogenic shock

A

papillary muscle rupture, LV free wall rupture, end stage cardiomyopathy, cardiac tamponade, massive pulmonary emboli

131
Q

patho of cardiogenic shock

A

decrease in perfusion of O2, the compensatory mechanism is exceeded (circulatory failure develops), impaired LV compliance, vasoconstriction, shock

132
Q

initial management of cardiogenic shock

A

O2 and inotropic agents (digoxin, dopamine, doubtamine)

133
Q

S.sx of compensation (cardiogenic shock)

A

tachy, increase BP(initial) /PAWP, cool, clammy skin, decrease UP, decrease urine Na, rapid deep respirations (resp. alkalosis { increase pH, decrease PaCO2), altered LOC, decrease bowel sounds, hyperglycemia
compensatory mechanisms eventually fail = decrease Bp, narrow pulse pressure, anaerobic metabolism and lactic acid build up (metabolic acidosis)

134
Q

refractory stage

A

irreversible, all systems have cellular necrosis, Blood clots from DIC, inadequate cerebral perfusion, hypothermia, death

135
Q

Dx of cardiogenic shock

A

H&P

decrease CBC, DIC screen increase, BUN increase, glucose increase, lactate increase, CXR (show ARDS),

136
Q

nursing management for cardiogenic shock

A

control HR, ID and Tx cause, maintain airway, IV fluids (NS, LR, Hespan), Tridil, Nipride, correct any arrhythmias, VAD, heart transplant, nutrition (TPN/protein for wound healing), VS, UO, bowel sounds, hygiene (prevent skin breakdown), emotional support

137
Q

medications for cardiogenic shock

A

vasopressors (dopamine) (maintain BP, increase contractility/CO)
monitor I&O, BP, HR, tissue sloughing
Dobutamine (preferred when no hypotension)
increases CO and SV with minimal increases in HR and BP
Inocor: decreases afterload and preload, relaxes vascular smooth muscle
Levophed (norepi) dilates coronary arteries, need a PA line, peripheral vasoconstrictor

138
Q

stabilizes cardiovascular function, increases coronary and cerebral blood flow, does not correct shock, life saving measure after MI, and while waiting for transplant

A

IABP (intra-aortic balloon pump)

139
Q

IABP

A

sausage shaped polyurethane balloon wrapped around a cath, positioned in the descending thoracic aorta, inserted into the femoral artery, inflated during diastole, deflates just before systole (synchronized with EKG)

140
Q

what are the functions for the IABP

A

relieves the LV workload
forces blood into coronary arteries
decreases afterload

141
Q

the inflation/deflation cycle is called

A

counter pulsation

142
Q

where does the blood below the balloon go

A

propelled forward towards the PV system and enhances renal perfusion

143
Q

what are the hemodynamic effects of IABP

A

increases diastolic pressure, coronary perfusion, O2 to the myocardium, decreases afterload, decreases HR

144
Q

Balloon maintenance

A

catheter in groin must be protected from kinking or dislodgement, assess peripheral pulses, check for infection, HOB elevated 45 degrees or less, log roll, low dose heparin

145
Q

what is a possible risk of IABP

A

thrombocytopenia

the longer the IABP is on, mechanical trauma from inflation/deflation destroys platelets

146
Q

myocardial revascularization, Tx for CAD, use of arteries for bypassing areas of stenosis, done so distal myocardium can receive blood

A

CABG

147
Q

what arteries are used for CABG

A

internal mammery artery (most common)

radial artery and inferior epigastric artery

148
Q

pre op of CABG

A

stop smoking, pre cardiac cath, ECHO, stress, labs, teaching, pre op bath

149
Q

intra op of CABG

A

large bore IV, EKG, central line, foley, NG, intubation, epicardial pacing for bypass, blood is diverted, CPB (cardiopulmonary bypass), once surgery is complete heparin is reversed with protamine sulfate, bypass is removed and heart is restarted

150
Q

CPB (cardiopulmonary bypass)

A

venous cath sits in right atrium, machine oxygenates blood as flows and removes waste, anticoagulated, hypothermic, aorta is clamped, heart is arrested, then surgery is started

151
Q

what do they use to arrest the heart

A

potassium

152
Q

Post op CABG

A

early extubation, hemodynamic stability, pain management, care of 2 surgical sites (chest and leg)

153
Q

complications with CABG

A

loss of appetite, swelling, diff. sleeping, constipation, mood swings/depression, muscle pain in shoulders, temporary muscle loss, fatigue, cardiac tamponade, arrhythmias, emboli, fever, hemorrhage, PE, Stoke, occluded graft, pancreatitis

154
Q

MIDCAB

A

minimally invasive bypass direct coronary artery bypass,
done when have single vessel disease, low risk pt, uncomplicated valve repair, no bypass machine needed, several small incisions made between ribs, harvest L internal mammary artery and anastomose to LAD artery, lateral chest tube or mediastinal tube placed, use video assisted thoracic surgery (VATS)

155
Q

nursing care for MIDCAB

A 
IV nitro (decrease coronary artery ischemia)
pain management, LOS 3 days
156
Q

for pts with inoperable CAD who are not candidate for traditional procedures, create channels between the ventricular cavity and coronary microcirculation, allows for blood flow to ischemic areas, use high energy laser to create 20-40 channels in the myocardial wall

A

transmyocardial revascularization (TMR)

157
Q

what do the new channels allow

A

stimulate new blood vessels to grow or may destroy nerve fibers to the heart
decrease angina

158
Q

complications of TMR

A

murmur, arrhythmias, heart failure, perforation of vessels, bleeding, infection, damage to mitral valve, tamponade

159
Q

most common initial therapy for angina, create or promote blood flow when nitrates cant anymore, cath with balloon inserted in the femoral artery to coronary artery through a sheath, insert cath just past the lesion, balloon is inflated and atherosclerotic plaque is compressed

A

percutaneous transluminal coronary angioplasty (PTCA)

160
Q

what does the PTCA cause

A

angina, bc the vessels are blocked when balloon is inflated, may need to administer nitro

161
Q

advantages of PTCA

A

alt to open heart surgery, performed under local anesthesia, eliminates recovery time, normal activity level in 1 week

162
Q

what can be a complication of PTCA

A

acute coronary occlusion, coronary spasm, bleeding, re stenosis, psuedoaneurysm of femoral artery, arteriovenous fistula at sheath removal site

163
Q

anti Xa goal

A

0.3-0.7

164
Q

glycoprotein IIb/IIa

A

used for increased risk pt such as DM, females, angina, recent MI,

165
Q

similar to PCTA but smaller laser on tip of cath, laser is for plaque ablation/restores blood flow, effective in restenosis of stents, extracting pacer leads and vein graft occulsions

A

laser angioplasty

166
Q

expandable mesh like structure used to maintain patency by compressing the artery wall, resists casoconstriction, may be medicated

A

stents

167
Q

plaque is shaved off using a rotating blade or high speed rotary device, and is then suctioned to prevent emboli, used to debulk lesions,

A

arthrectomy

168
Q

bypasses the affected ventricle and allows the heart to rest, longer term use than IABP, used on left, right or both, battery operated mechanical heart, bridge to transplant

A

VAD (ventricular assist device)

169
Q

LVAD

A

blood is diverted from L atrium, bypasses left ventricle sent to pump and returns via cannulation of ascending aorta

170
Q

RVAD

A

blood is diverted from R atrium, bypasses right ventricle, sent to pump and returns via cannulation of pulmonary artery

171
Q

candidates for VAD include

A

CHF, unable to wean from heart lung machine, awaiting transplant, an MI with cardiogenic shock

172
Q

safety issues with VAD

A

don’t disconnect both cables that connect the controller to its power source at the same time, drink plenty of fluids to maintain blood flow through device

173
Q

weaning criteria for VAD

A

intrinsic MAP of 60 or higher, CI greater than 1.8, may not survive

174
Q

destroys ectopic cells in heart with heat through a cath, used to Tx atrial and ventricular tachycardia, have burning sensation and their heart beating faster after procedure

A

ablation

175
Q

what is the standard practice in acute STEMI/MI , goal is to salvage myocardial muscle /open artery, cause lysis of the thrombus and reopen the obstructed artery (restore blood flow to affected tissue)

A

fibrinolytics

176
Q

how long does it take for entire thickness (transmural MI) to be necrosed

A

4-6 hours

177
Q

criteria for fibrinolytic

A

no more than 12 hours from onset of CP
ST segment elevation or new onset of LBBB
ischemic CP for 30 minute duration
CP unresponsive to nitro
no condition that would cause a predisposition to hemorrhage

178
Q

contraindications of fibrinolytic

A 
recent surgery (within 2 weeks)
pregnancy or recent delivery
Hx of stroke
recent major trauma
bleeding disorders
recent organ biopsy
prolonged CPR
severe advanced illness
severe renal or hepatic disease
179
Q

what is the EO of fibrinolytic

A

coronary artery reopens in 30-90 minutes (increase perfusion, myocardial O2 with relief of Sx, zones of myocardial ischemia/size of infarcted area is limited, ST segment returns to baseline, CPK/CPK-MB will return to normal

180
Q

Nursing management of fibrinolytic

A

Start IV lines, assess continuously, monitor EKG, bleeding, coag studies, avoid IM injections, monitor neuro, reocclusion may occur (watch EKG for St segment changes and dysrhythmias)

181
Q

what evidence will you have if you have reperfusion

A

cessation of CP, reperfusion dysrhythmias (PVC, bradycardia, heart blocks, v tach (rare), ST segment resolution (back to baseline), CPK rises rapidly after reperfusion called washout

182
Q

CPK

A

enzyme released by damaged myocardial cells

183
Q

Ndx for fibrinolytic

A

ineffective cardiopulmonary…
acute pain
anxiety
deficient knowledge

184
Q

what fibrinolytic agents are used

A 
TPA (alteplase)
RPA (reteplase)
TNKase (tenecteplase)
SK (streptokinase)*
APSAC (anistreplase)*
* non clot specific
185
Q

what is used in conjunction with fibrinolytic therapy

A

anticoagulants (heparin) and antiplatelets (asa)

186
Q

battery powered device that provides extrinsic electrical stimuli to cause cardiac contraction when intrinsic cardiac electrical activity is inappropriately slow or absent

A

artificial pacemaker

187
Q

when is temporary emergency pacing needed

A

used for significant/hemodynamically unstable pts, bundle branch blocks, bradycardia with Sx, lyme disease, prolonged PR intervals

188
Q

what will the QRS in the EKG strip look like with a paced beat

A

the QRS may be slightly widened, a paced beat is normally shown as a negative deflections

189
Q

S.sx of a pt that may need a pacemaker

A

syncope, light headedness, fatigue, SOB, angina, hypotension, signs of decreased CO (biventricular pacemaker is needed)

190
Q

fixed rate (asynchronous) pacemaker

A

does not sense, does not see what the heart is doing-fixed rate!, competes with intrinsic rate, used when potential to cardiac arrest

191
Q

demand (synchronous) pacemaker

A

has a sensing circuit, will only fire on demand, senses when the heart rate is low

192
Q

what are the 2 types of demand pacemakers

A

single chamber: most common, I atrium OR ventricle, it senses and paces
Duel chamber: senses and paces the atrium AND ventricle

193
Q

unipolar lead wires

A

loop of conductivity large (larger spike) lead has a negative pole at tip of wire and positive at the generator

194
Q

bipolar lead wires

A

conduction look is smaller, smaller spike, less electro-magnetic interference problems, pacers have both negative and positive poles on end of pacer wire

195
Q

transcutaneous pacer

A

external pacer, quick and easy to use, not meant for long term use

196
Q

transvenous pacer

A

Tx of choice, temporary, used to treat hemodynamically significant bradycardias, not effective in Tx ventricular standstill/PEA

197
Q

goal for temporary pace controls

A

have low # for sensitivity (want it to be sensitive), R on T is biggest risk

198
Q

epicardial pacing

A

electrode end of wire looped through or loosely sutured to epicardial surface of atria or ventricles/Post op CABG

199
Q

permanent pacemakers

A

done with IV conscious sedation under local anesthesia in cath lab, permanent pulse generators powered by lithium batteries life span 10 years

200
Q

what are the 3 basic functions of permanent pacemaker

A

sensing-pulse generator sees intrinsic beats
firing-delivers stimulus to heart
capturing-heart has responded to stimulus

201
Q

pacemaker codes

A 
A-atrium
V-ventricles
D- both atrium and ventricles
I- inhibited
R- rate responsive
M- mulitiprogram
202
Q

inhibited pacer

A

pacer turns off or inhibits output if hearts activity kicked in

203
Q

triggered pacer

A

pacer turns on or fires if preset interval expires

204
Q

VVI codes

A

commonly used, temporary transvenous pacer, ventricular pacing, ventricular sensing, good for afib

205
Q

ventricular capture

A

ventricle responded to pacing stimulus, spike on EKG followed by wide QRS

206
Q

native beat

A

also called intrinsic, represents pts own electrical activity

207
Q

fusion beat

A

pacer fires at same time as intrinsic heart beat occurs, both forces simultaneously depolarize ventricles

208
Q

ICD

A

fires when heart rate increases, has to distinguish if fast rate is sinus tach, SVT, afib, RVR or V tach
has criteria for discharge/shocking

209
Q

tiered therapy

A

ability of ICD to deliver different types of therapy, cardioversion, d fib, antibrday pacing, also records and telemetry

210
Q

active fixation

A

pacing lead with screw, barb, prong, hock or some device affixed to tip of lead embedded in myocardium to ensure stable placement

211
Q

passive fixation

A

a lead not embedded, own tissue will grow around it and keep it in place

212
Q

if a ICD goes off should the pt go to the hospital

A

yes!

213
Q

implanted cardioverter.defibrillator

A

hx of spontaneous sustained v tach, sudden cardiac death,

214
Q

pacemaker malfunctions: failure to capture:

A

ventricles failed to respond to pacing stimulus, EKG shows spike that occurs on time but not followed by QRS, increase stimulation threshold

215
Q

pacemaker malfunctions: failure to sense

A

under-sensing, generator doesn’t sense intrinsic beats, EKG shows spike after QRS but earlier than it should
*if pacer is temporary-turn it off

216
Q

what can happen if pacing occurs at random times

A

can cause v tach…NOT GOOD

217
Q

what do pts with ICDs need to avoid

A

MRIs, TENS, lithotripsy

218
Q

if you are going to cardiovert a pt with a temporary pacer what needs to be done

A

pacer must be turned off

219
Q

forces produced by volume and pressure, which affect circulating blood throughout the body, used for critically ill pts, bedside monitoring

A

hemodynamics

220
Q

why is hemodynamics needed

A

cardiac function, circulating blood volume, physiologic response to Tx

221
Q

what are the indications for hemodynamics

A

critical care pts

  • decrease CO
  • deficient fluid volume or excess fluid volume (CHF)
  • ineffective tissue perfusion
222
Q

invasive catheter with tubing connecting the pt to the transducer, which receives the signal and converts it to electrical energy (monitor), have to flush system to keep patent

A

fluid filled pressurized tubing system

223
Q

what needs to be done at the beginning of every shift

A

must “0” the transducer, the equipment needs to be calibrated to atmospheric pressure
*the transducer is open to air via the 3 way stop cock, and then a “0” will be displaced on the monitor

224
Q

what needs to be monitored with entering the catheter for hemodynamics

A

needs to be monitored by waveform analysis bc it is entering the hearts chambers, threaded into the vena cava into the right side of the heart

225
Q

draw a line from the 4th intercostal space to a midaxillary line on the side of the chest, it is a physical reference point on the patients chest that is used as a baseline for consistent transducer height placement, approximately the level of the atria

A

phlebostatic axis

226
Q

where do you want the transducer located

A

want the air reference stopcock level with the phlebostatic axis, the tip of the catheter should be in line with transducer, to ensure accurate hemodynamic measurements

227
Q

what position does the pt have to be in during hemodynamics

A

HOB needs to be elevated (0-60 degrees), make sure measurements are consistently taken at the same angle

228
Q

what needs to be done with hemodynamics (nursing management)

A

accurately calibrate the equipment, know normal values, est. safe alarm limits, be able to troubleshoot any problems

229
Q

damping

A

distortion of the waveform

230
Q

a thermo dilution catheter capable of measuring cardiac output

A 
Pulmonary artery (PA) monitoring
aka Swan-Ganz catheter
231
Q

the PA catheter can measure include

A
  • pulmonary artery systolic & diastolic pressures
  • pulmonary artery mean pressure
  • pulmonary artery occlusion pressure (PAOP)or wedge (PAWP)
  • cardiac output
  • able to calculate additional measurement
232
Q

measured through distal port, PA pressure reflects left and right sided heart pressures

A

PA and PCWP (pulmonary capillary wedge pressure)

233
Q

the PA systolic pressure is produced b

A

the right ventricle (normal 15-27 mmHg)

Normal PA systolic/diastolic = 25/10

234
Q

wen is increased PA pressure seen

A

atrial or ventricle septal defects, increase pulmonary blood flow as a result of L to R shunt, pulmonary HTN, LF failure, volume over load, ischemia, mitral regurgatatoin

235
Q

indirect measure of LVEDP (left ventricular end diastolic pressure), balloon of the catheter is inflated, wedging in a small branch of the pulmonary artery for less than 15 seconds

A 
Wedge pressure (PCWP)
normal range is 6-12 mmHg
236
Q

abnormal wedge (elevated)

A

an elevated wedge is going to cause decrease CO, this NEEDS priority intervention!
LV failure, ischemia, pericarditis, mitral stenosis or mitral regurg., fluid overload

237
Q

abnormal wedge (decreased)

A

hypovolemia, venous dilating drugs

238
Q

the amount of blood pumped out by a ventricle
HR x SV =

when peripheral tissue needs more O2, the normal healthy heart can augment HR and SV to increase cardiac output

A

cardiac output

239
Q

what is a method to measure cardiac output

A

thermodilution

240
Q

if pt is on PEEP what will happen to your PA pressure

A

will be increased

241
Q

cold or room temperature solution is injected into the right atria part of the PT catheter. There is a thermistor near the end of the catheter that countinusouly measures the temperature of blood flowing past it

A

thermodilution

242
Q

normal CO

A

4-8 l/min

243
Q

normal CI

A

2.2-4.0 l/min/m2

244
Q

what is the best indication for cardiac function

A

CI

245
Q

normal SVR

A

900-1400 dynes/second/cm5

246
Q

normal PVR

A

37-250 dynes/second/cm5

247
Q

causes of decreased CO

A

decrease preload
increase of afterload
MI

248
Q

complications of hemodynamic monitoring

A

infection**

thrombi, cardiac perforation, electrical microshocks, complete heart block, pulmonary infarction (balloon left inflated)

249
Q

what can decrease complications with hemodynamic montioring

A

balloon needs to be completely deflated after a wedge pressure is obtained (pulmonary infarction),
electrical equipment needs to be grounded, less than 1.5ml of air to inflate balloon, need pressure bag on NS drip to maintain patency

250
Q

measured through the proximal port in the right atrium, determines volume status and RV function, guide to overall fluid balance

A

Central venous pressure (CVP)

251
Q

normal CVP

A

2-6 mHg

252
Q

a decrease in CVP is do to

A

hypovolemia, venodilation, venous obstruction (mass) and decrease venous return

253
Q

a increase in CVP is do to

A

increase blood volume, right sided heart failure with vasoconstriction, cardiac tamponade, positive pressure breathing, straining

254
Q

represents the variation in stroke volume during the respiratory cycle, may be a better indicator of volume responsiveness than with a CVP or PCWP, need an A line waveform,

A

Stroke volume variation

255
Q

stroke volume variation is only used in what kind of pt

A

mechanically ventilated patient

256
Q

direct measurement of atrial blood pressure, intra arterial cath located in the radial artery, connect to the electronic monitor and a fluid filled pressurized tubing system

A

intra-arterial monitoring (A-line)

257
Q

A line assessment

“Allen’s test”

A

occlude both ulnar and radial artery, pt needs to clench and unclench their fist, release pressure and observe for return of color to hand, if color returns in 5-7 seconds, circulation is adequate, if color returns in 7-15 seconds, circulation is impaired, longer than 15 seconds means inadequate circulation and the radial artery should NOT be cannulated

258
Q

when is Allen’s test done

A

prior to insertion of intra arterial monitoring line (A-line)

259
Q

complications with A-line

A

infection, accidental blood loss, impaired circulation to the extremity

260
Q

represents perfusion pressure throughout the cardiac cycle, sensed by baroreceptors in the carotid sinuses and the aortic arch, basis for autoregulation by some organ systems

A

MAP (mean arterial pressure)

261
Q

what does the MAP need to be to perfuse the coronary arteries

A

MAP greater than 60
normal is 70-100
ideal is to be able to maintain MAP between 65-75 mmHg

262
Q

calculation of MAP

A

(diastole x 2) + (systole x 1) /3 = MAP

263
Q

provides continuous assessment of the balance between O2 supply and demand

A

Central Venous Oxygen Saturation (ScV2)

264
Q

normal ScVO2

A

75%
*in a critical pt 60-80% is adequate
this indicates adequate balance of O2 supply and demand

265
Q

a ScVO2 of less than 60 % indicates

A

decrease of O2 supply or an increase of demand

266
Q

a ScVO2 of more than 80% indicates

A

a decrease in demand or an increase in supply

267
Q

most people extract 25% of O2 from Hgb, therefore venous return is =

A

75%

268
Q

what pts is hemodynamics good for

A

shock, trauma, pulmonary & cardiac disease or multiple organ dysfunction syndrome (MODS), fluid management, hemodynamically unstable pts

269
Q

Inferior wall infarction involves

A

Occlusion in right coronary artery

270
Q

Anterior wall infarction result from

A

Occlusion of left anterior descending artery

271
Q

Lateral or posterior infarction are caused by

A

Occlusion of left circumflex artery

272
Q

Cardiac output is

A

The volume of blood in liters pumped by the heart in 1 minute

273
Q

Cardiac index is

A

The measurement of CO adjusted for body surface area

274
Q

Systemic vascular resistance

A

Opposition by the left ventricle

275
Q

Pulmonary vascular resistance

A

Opposition encountered by the right ventricle

276
Q

Preload

A

Volume within the ventricle at the end of diastole

277
Q

An increase of PAWP and PAD pressure indicates

A

Heart failure or fluid volume overload

278
Q

A decrease of PAWP indicated

A

Volume depletion

279
Q

Normal cardiac resting output is

A

4-8 liters per minute

N202 (8 decks)

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