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Nursing school level 4 > Nurs 453 test 2 > Flashcards

Nurs 453 test 2 Flashcards

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1
Q

Regulators of our blood

A

valves

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2
Q

Valvular heart disease is defined by

A

Affected valve AND problem

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3
Q

Stenosis:

A

narrowing valve opening

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4
Q

Regurgitation:

A

backward flow of blood into the heart or between heart chambers

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5
Q

Prolapse :

A

“fall out of place”, or valve leaflets move to an area where they are not intended to be

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6
Q

best way to evaluate valve function or dysfunction

A

Transthoracic echocardiogram

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7
Q

mitral valve

A

between the left atrium and the left ventricle

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8
Q

left atrium receives

A

oxygenated blood from the pulmonary veins on the way to systemic circulation

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9
Q

Gold standard for evaluating the severity of MV stenosis

A

Trans-mitral gradient (measured by echocardiogram)

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10
Q

1 cause of MV stenosis

A

congenital heart disease

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11
Q

MV stenosis leads to

A

Obstruction of blood flow
Pressure difference between the LA & LV
↑ of blood volume & pressure in LA causes ↑ risk of atrial fib
Hypertrophy of the pulmonary vessels= ↑ pulmonary HTN

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12
Q

MV Stenosis-Clinical Manifestations

A

Exertional Dyspnea can be accompanied w/ hemoptysis - Caused by reduced lung compliance & lack of ability to move oxygenated blood out of the LV

Palpitations: Atrial fibrillation associated to enlarged RA/RV from fluid overload
fatigue, angina

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13
Q

most cases of MV Regurgitation are caused by

A 
MI
Chronic rheumatic heart disease
MV prolapse
Ischemic papillary muscle dysfunction
Infective Endocarditis (IE)
MI with LV failure ↑ risk for acute MR
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14
Q

acute MV regurgitation clinical manifestations

A

new systolic heart murmur
↑ in pressure transmits to pulmonary bed
pulmonary edema and cardiogenic shock
Thready peripheral pulses, cool, clammy extremities, low cardiac output

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15
Q

chronic MV regurgitation clinical manifestations

A

may be asymptomatic for years

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16
Q

MV Prolapse

A

Structural abnormality allowing MV leaflet to prolapse into LA during systole
Usually benign, but serious complications can occur, including death

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17
Q

MV Prolapse Clinical Manifestations

A

Most pts are asymptomatic for life

but they can have Atypical chest pain, dysrhythmias, Palpitations, SOB, Murmur & clicks

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18
Q

common dysrhythmias with MV prolapse

A 
Ventricular tachycardia (V Tach)
Paroxysmal supraventricular tachycardia (PSVT)
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19
Q

If atypical pain occurs then during MV prolapse

A

Does not respond to Anti-Anginal treatment

Episodes occur in clusters, especially during stress

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20
Q

MV Treatments Stenosis, Regurgitation, Prolapse

A

avoid caffeine and stimulants, Cath lab, mitral valve replacement

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21
Q

aortic valve

A

AV is between the LV and the aorta…key to getting CO!!!

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22
Q

AV stenosis

A

Obstruction of flow from LV to aorta during systole
↑ pressure on LV and ↑ myocardial O2 consumption
↓ CO which leads to Pulmonary HTN and HF (HFpEF and HFrEF)
Can be discovered in childhood, adolescence or young adulthood

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23
Q

cause of AV stenosis

A

Calcification (#1)

Bicuspid AV that calcifies (seen at age 40 to 50)

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24
Q

AV Stenosis Clinical Manifestations

A

Angina
Syncope
Exertional dyspnea

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25
Q

prognosis for AV stenosis

A

Poor prognosis if symptoms and obstruction are not relieved

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26
Q

treatment for AV stenosis

A

Beware of Nitroglyerine: ↓ preload necessary to help open the stiff valve
Anticoagulation: Warfarin (goal 2.0 to 3.5, higher if they have valve replacement)
Aortic Valve Replacement (AVR)

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27
Q

AV regurgitation

A

Blood flows from ascending aorta backs to LV

Happens during diastole and ↑ preload

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28
Q

acute AV regurgitation is a

A

life threatening emergency

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29
Q

cause of acute AV regurgitation

A 
Infective endocarditis (IE)
Rheumatic heart disease
Trauma
Aortic Dissection
Marfans, Lupus
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30
Q

AV Regurgitation Clinical Manifestations

A 
CARDIOVASCULAR COLLAPSE
Abrupt onset of PROFOUND DYSPNEA
Angina…more subtle than in AV stenosis
Diastolic murmur
Hypotension
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31
Q

tricuspid valve

A

Tricuspid valve is between the RA and the RV.

The RA gets its unoxygenated blood from the great veins (superior and inferior vena cava).

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32
Q

TV stenosis

A

RA output becomes obstructed;  the blood volume

RA enlargement, elevated venous pressures

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33
Q

TV stenosis cause

A

Almost always in patients with IV drug use (infective endocarditis)
rheumatic heart disease…patients might also have MV or AV stenosis

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34
Q

TV stenosis treatment

A

valve replacement

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35
Q

Pulmonic Valve (PV)

A 
Pulmonic valve is between the RV and the pulmonary artery… deoxygenated blood.
Pulmonic Valve (PV) disease is very rare
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36
Q

Pulmonic Valve (PV) disease

A

Almost always congenital- may go unnoticed for years if mild

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37
Q

Pulmonic Valve (PV) disease cause

A

RV problems
High pressures in the RV
Hypertrophy of RV

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38
Q

Pulmonic Valve (PV) disease clinical manifestations

A

Fatigue
Cyanosis
JVD
Loud mid-systolic murmur

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39
Q

labs for valve disease

A

CBC w/ diff
May culture if suspicion of infective endocarditis
CMP to see if there is liver, kidney or other organ dysfunction

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40
Q

diagnostics for valve disease

A 
Cardiac echo (thoracic or TEE)
Goals standard best to evaluate valve function or dysfunction
12-lead, cxr
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41
Q

Infective Endocarditis (IE)

A

Infection of the endocardium
Impacts the cardiac valves
Causative agent: staph or strep

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42
Q

patients at risk for infective endocarditis

A

Medical hx of: IV drug use, hospital acquired infections, prior IE
HX within the past 3-6 months:
IV Drug Abuse
Dental, surgical, or GYN procedures (including OB)

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43
Q

Primary lesion of IE

A

Fibrin, leukocytes, platelets, microbes adhere to valve or endocardium
Embolization of portions of vegetation get into circulation
Infarction can occur

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44
Q

sub-acute IE

A

Longer course (months), slower onset
enterococci
Hx of previous valve disease

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45
Q

acute IE

A

Shorter course, rapid onset
strep, staph, viruses, or fungi
Typically have healthy valves prior to infection

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46
Q

infective endocarditis clinical manifestations

A 
Acute: Non specific: symptoms are flu like
Fever in >90% 
New/changing systolic murmur
Sub-acute: more generalized symptoms
Ha, back pains, body ache
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47
Q

infective endocarditis labs

A 
CBC w/ diff
Blood cultures, both aerobic & anaerobic
Electrolytes
Troponins
Coags
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48
Q

infective endocarditis diagnostics

A

12-lead ECG
CXR – look for cardiomegaly
Echocardiogram

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49
Q

Treatment for IE

A

Treat the causative agent may need valve replacement

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50
Q

Modified Duke Infective Endocarditis Criteria

A 
Microorganisms in vegetation
pathological lesions
positive blood cultures
evidence of endocardial involvement
IV drug use
predisposing heart condition
Vascular/ immunologic phenomena
microbiological evidence
Score determines definite, possible or no, and then determines how to treat
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51
Q

pericarditis

A

inflammation of the sac

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52
Q

pericarditis causes

A 
Infectious: 
- bacteria, virus, TB, fungal 
Non-infectious: 
- cancer, MI, trauma, uremia
Autoimmune or Hypersensitivity: 
- rheumatic fever, drug reactions, rheumatoid arthritis, lupus
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53
Q

hall mark finding of pericarditis

A

Pericardial friction rub
also Severe angina, sharp & pleuritic in nature
Worse w/ deep breathing

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54
Q

complications of pericarditis

A

Pericardial effusion: accumulation of excess fluid in the pericardium. Can be rapid or slow.
Cardiac tamponade: effusion increases in volume, compresses the heart.

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55
Q

labs for pericarditis

A 
Pericardiocentesis…culture the fluid
CBC w/diff
CRP/ESR
Troponins
Blood cultures
Coags
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56
Q

diagnostics for pericarditis

A 
ECG-abnormal in 90% of cases (ST elevation)
CXR- look for cardiomegaly
Cardiac Echo
CT/MRI
Pericardiocentesis
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57
Q

leads with pericarditis

A

ST elevation present in all leads

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58
Q

Pericarditis Collaborative management

A

Treatment/Management is based on causative factors
Directed towards identification and tx
Management of pain and anxiety

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59
Q

myocarditis

A

Inflammation of the myocardium leading to cellular damage and necrosis

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60
Q

myocarditis is a common cause of

A

dilated cardiomyopathy

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61
Q

causes of myocarditis

A

Virus, bacteria, fungi

Coxsackie A and B viruses (most common)

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62
Q

myocarditis manifestations

A

Can have a friction rub & pericarditis along w/ myocarditis
flu-like
large range of symptoms

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63
Q

labs for myocarditis

A 
CBC w/diff
Sed rate; c-reactive protein (CRP)
Troponins
Viral titers
tissue and fluid samples
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64
Q

diagnostics for myocarditis

A

12 Lead ECG
Endomyocardial biopsy (w/in first 6 wks most definitive)
Echo
MRI

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65
Q

Treatment for myocarditis

A

Goals: manage associated cardiac symptoms with meds such as digoxin, diuretics, ACE or BB
If severe: consider IABP or heart transplant

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66
Q

nursing diagnosis for Inflammatory Disorders

A

Decreased cardiac outputr/t alterations in afterload and/or preload
Activity intolerancer/tgeneralized weakness, arthralgia, and alteration in O2transport secondary to valvular dysfunction

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67
Q

P wave

A

atrial contraction

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68
Q

PR interval

A

av node conduction should be 0.12-0.2

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69
Q

QRS complex

A

ventricular contraction should be 0.04-0.1

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70
Q

T wave

A

ventricular relaxation

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71
Q

QT interval

A

depolarization should be lass than half of the preceding R-R interval

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72
Q

HFrEF vs HFpEF heart failure

A

left side

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73
Q

Primary risk factors for heart failure

A

HTN and CAD, MI

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74
Q

HF is caused by

A

interference with Preload, Afterload, Myocardial Contractility and Heart Rate (which all regulate CO)

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75
Q

HFrEF

A

Heart Failure with reduced ejection fraction
Systolic Failure…“Failure of systole”
Inability of the heart to pump effectively

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76
Q

hallmark sign of HFrEF

A

Hallmark sign is decreased EF, usually less than 45%

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77
Q

HFpEF

A

Heart Failure with preserved ejection fraction (EF 65% and greater)
Diastolic failure…“Failure of diastole” – failure to fill
Inability of the ventricles to relax and fill during diastole, most commonly r/t hypertension

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78
Q

most common HF

A

left sided

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79
Q

signs of left sided HF

A

pulmonary congestion and edema - back up of blood into the pulmonary veins

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80
Q

primary cause of Right sided HF (for pulmonale)

A

left sided HF

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81
Q

signs of right sided HF

A

Signs: Peripheral edema, JVD, hepatomegaly, splenomegaly because blood is backing up into the systemic venous circulation

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82
Q

Compensatory Mechanisms in HF

A

Aimed at maintaining CO and BP (helps at first!)
Neurohormonal Response – RAAS
SNS stimulation – catecholamine
Dilation – stretch of ventricles/atrium
Hypertrophy - increase of mass & thickness – diuretics, ACEs, ARBs

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83
Q

Counter-regulatory Mechanisms

A 
ANP, BNP (renal, CV, and hormonal effects)
Nitric Oxide (NO)…vasodilation
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84
Q

Cardiac Compensation

A

compensatory mechanisms succeed in maintaining adequate CO to maintain central & local perfusion

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85
Q

Cardiac Decompensation

A

compensatory mechanisms NO longer maintain adequate CO and inadequate perfusion results

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86
Q

what happens during Acute Decompensated Heart Failure

A

Engorgement of the pulmonary vascular system, as this increases, alveolar lining cells disrupted – RBCs leak w/ fluid

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87
Q

s/s of Acute Decompensated Heart Failure

A

Tachypnea, dyspnea and orthopnea (RR>30) – increased pulmonary congestion
Worsening ABGs – ↓ PaO2, possibly ↑ PaCO2 & progressive acidosis
Anxious, pale  cyanotic, clammy, cold skin
Bilateral crackles, possibly wheezes, copious frothy, pink sputum (due increased pressure and RBC crossing the membrane)
Tachycardia – compensating
↑ BP initially – but then drops

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88
Q

meds for Acute decompensated HF

A

Diuretics, Vasodilators, morphine, positive inotropes

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89
Q

Diuretics

A

Mainstay of treatment for volume overload

Reduces preload

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90
Q

Vasodilators

A

Reduces preload & afterload

Type depends on if we are treating preload or afterload

91
Q

morphine

A

Reduces preload and afterload
Improves gas exchange
Reduces anxiety and can reduce dyspnea

92
Q

positive inotropes

A 
Increases myocardial contractility and CO
Includes dobutamine (preferred), milrinone, and digoxin
93
Q

meds for chronic HF

A

diuretics, ACE, ARB, vasodilator, Beta blocker, positive inotropes, antiarrythmic, anticoagulant

94
Q

beta blockers

A

Metoprolol, carvedilol (preferred)- assists with blocking ventricular remodeling
Can help with rate control

95
Q

anticoagulant during HF

A

due to pooling of blood

Warfarin, DOACs, ASA

96
Q

diagnostics during acute decompensation

A

Cardiac echo (must have…prior to discharge), 12 lead

97
Q

labs during acute decompensation

A

BNP, CMP, CBC, ABGs

98
Q

managing acute decompensation

A

Assess, Assess, Assess!
High flow O2, consider CPAP or intubation
Cardiac monitor, IV x2, positioning (high folwers)
Daily weights, strict I&Os, Na/H2O diet/fluid restriction

99
Q

assessment with heart failure

A

1st complete a history & physical exam; determine underlying cause of the HF. get BNP, troponin, cardiac echo, 12 lead, and possible Cath

100
Q

complications of HF

A

pleural effusions, dysrhythmias, thrombus, hepatomegaly, renal failure

101
Q

women and MI

A

SOB and fatigue are common presenting factors
Present w/ general fatigue, flu like symptoms, n/v or GI upset…
they often don’t think they are having an MI

102
Q

cause of ACS

A 
Occlusion of coronary artery…#1 cause
   Endothelial damage occurs
   Atherosclerotic plaque disruption “rupture”
   Platelet aggregation
   Thrombus formation
103
Q

N-STEMI

A

Non-ST-segment-elevation myocardial infarction

will have positive trops

104
Q

Management of N-STEMI and unstable angina is

A

identical

105
Q

STEMI

A

ST-segment-elevation myocardial infarction
Manifests w/ signs and symptoms of dyspnea, diaphoresis & change in ECG
will have positive trops

106
Q

troponins

A

show cardiac ischemia!

107
Q

chest pain work up

A

trop, 12 lead EKG, H&P, cardiac monitor, O2, pain relief, ASA, fibrolytics

108
Q

STEMI management

A

Get the artery open ASAP, immediate cath lab

Fibrolytics (NO cath lab available)

109
Q

NSTEMI management

A

ASA, heparin, monitor and Cath lab later

110
Q

door to needle

A

less than 30 minutes

111
Q

door to balloon

A

less than 90 minutes

112
Q

MD responsibility during chest pain

A

Interprets ECG w/in 10 min, interprets labs, gives antiplatelet therapy, β-blockers w/in 24 hr, determines STEMI vs NSTEMI, Chest Pain or
Ischemic Symptoms

113
Q

if no Cath lab is available

A

Percutaneous Catheter (PCI) or fibrinolytic agent (if cath lab not immediately available) for STEMI

114
Q

H&P with chest pain

A

Assess pain – PQRST or OLDCARTS

Assess age, race, co-morbidities, risk factors, family history, recent drug use

115
Q

does a normal ECG rule out ACS/AMI

A

no

116
Q

primary identifier of STEMI

A

ST segment elevation in 2 or more consecutive leads

117
Q

what differentiates old MIs from acute process

A

T-wave inversions and pathologic Q-waves develop after an MI

118
Q

ST elevation

A

infarction

119
Q

ST depression

A

Ischemia

120
Q

Lateral leads

A

CIR - I, AVL, V5, V6

121
Q

anterior leads

A

LAD (left anterior descending artery) - V1, V2, V3

122
Q

Inferior leads

A

RCA - II, III, AVF

123
Q

which STEMI carries the worst prognosis

A

anterior - Due to larger infarct size; feeds a majority of the LV
Infarct in the left coronary artery will see septal, anterior and lateral changes…left coronary artery

124
Q

Inferior MI

A

Right Coronary Artery RCA

ST elevation in leads II, III and aVF

125
Q

nitroglycerin is a concern with

A

right sided MI decreases preload!!!

126
Q

pharm management with ACS/AMI

A

MONA (aspirin is key), atorvastatin

127
Q

High Sensitivity Troponin T levels

A 
Negative = 6
Positive = 20
NSTEMI = 52
Critical = 100
higher trop means more myocardial damage
128
Q

when to get troponin

A

BASELINE, then at minimum x 2 hours for three times (hour 0, hour 2, hour 14)
Chest pain centers may obtain every 4 hours, Positive is > or = 0.04

129
Q

other cardiac markers

A

CK-MB
Myoglobin - Sensitive, but not specific…
Elevations occur in 1-2 hours after onset of symptoms
neither of these are specific for cardiac injury

130
Q

Other Causes of Elevated Troponins

A

Sepsis
Burns
Extreme Exertion

131
Q

Criteria for stress test:

A

Chest pain present
2 negative Troponins
No significant 12 lead ECG changes (pt may have abnormal but not STEMI)
Need some form of direct evaluation of the heart (prior to discharge)

132
Q

two type fo stress test

A

exercise and nuclear (pharmacology)

133
Q

exercise limitations

A

Women- ↑ false +

βBlockers blunt maximum HR & maximum work so ↓ sensitivity

134
Q

Cardiac Nuclear Stress Tests

A

Uses dobutamine, adenosine, or dypridamole which:
↑ myocardial work load in pts unable to exercise
Adenosine & dypridamole are contraindicated in patients w/ bronchospasm or high grade AV block

135
Q

what can decrease the effectiveness of Cardiac Nuclear Stress Tests

A

Theophylline & caffeine decrease the effectiveness of the test
Also beta blockers or drugs that speed up or slow down the heart can effect the test

136
Q

What would make us want to immediately stop a stress test?

A

Substernal chest pain, ST elevation on ECG or lethal rhythm

137
Q

coronary angiography also called

A

Cath lab - gives direct visualization of coronary arteries

138
Q

who gets immediate Cath lab

A

STEMI pt

139
Q

shock state primary problem

A

perfusion

140
Q

What do we need to maintain perfusion? what if these things are altered

A

Adequate cardiac pump
Adequate vasculature or circulatory system
Sufficient blood volume
When these are severely altered…shock states occur!!!

141
Q

shock is characterized by

A

ineffective tissue perfusion
decrease tissue perfusion
acute circulatory failure
impaired cellular metabolism – cellular level move in to anaerobic metabolism

142
Q

shock leads to

A

imbalance between the supply and demand for oxygen/nutrients

143
Q

4 stages of shock

A

initial, compensatory, progressive and refractory

144
Q

Initial stage of shock

A

Begins at cellular level, not clinically apparent
Oxygen to cells impacted by  perfusion
decrease cardiac output
Metabolism changing from aerobic to anaerobic

145
Q

Anaerobic Metabolism =

A

lactic acid buildup

146
Q

Compensatory Stage of Shock

A

Activation of compensatory mechanisms
Goal: maintain homeostasis
Neural: ↑ HR, contractility, arterial/venous congestion, shunting of blood to vital organs
Hormonal: activation of RAAS-causes vasocontraction, ADH and ACTH
Drop in BP
Immediate response of baroreceptors activating SNS
increase HR & vasoconstriction (most common)

147
Q

Compensatory stageClinical manifestations

A 
Oriented x 3 (restless, apprehensive)
Shunting of blood to heart and brain
↑ contractility and HR
↓ BP
↑ renin, aldosterone and ADH
↓ blood flow to lungs
↓ GI blood supply
↓ renal blood flow
148
Q

Progressive Stage

A

Compensatory mechanisms fail
Trying to prevent multiple organ dysfunction syndrome
Continued ↓ in cellular perfusion
↓ cerebral perfusion = ↓ responsiveness
↑ cap permeability
Critical dysfunction first seen in lungs (ARDS)
First signs of MODS

149
Q

Progressive StageClinical Manifestations

A

Cardiovascular collapse – ↓ perfusion
Worsening of metabolic acidosis
Renal: ARF,AKI – increased BUN = decreased perfusion to the kidney
GI: Dysfunction – (bleeding, impaired absorption) – obstruction (ileus) , decreased bowel sounds
Liver: ↑ LFTs, altered drug/waste metabolism – decreased perfusion to liver
DIC (Disseminated intravascular coagulation)
Seen more in sepsis
Clotting and bleeding at the same time – seen in shock states

150
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

Generalized inflammation in organs remote from the initial insult

151
Q

Multisystem organ dysfunction syndrome

A

Failure of 2 or more separate organ systems
Acute illness
Homeostasis cannot be maintained without interventions

152
Q

clinical manifestations of Multisystem organ dysfunction syndrome

A

Clinical manifestations…Depends on the organ

153
Q

DIC

A

Bleeding and Clotting disorder
ALWAYS a complication of another disorder
Massive trauma (hemorrhagic shock)
Sepsis

154
Q

what happens in DIC

A

Pro-inflammatory cytokines activates clotting cascade causing microclots forming in capillaries = widespread microvascular coagulation
Systemic Clotting factors are being used up at microvascular level
No clotting factors left = bleeding everywhere!

155
Q

LABS that will be decrease for DIC

A 
Decreased:
Hgb/Hct - bleeding
Platelets (key…rapid decline) 
Fibrinogen 
aPTT (early DIC)
156
Q

LABS that will be increased for DIC

A

PT/INR
aPTT (late DIC)
D-dimer
Fibrin degradation products

157
Q

Nursing Interventions for DIC

A 
ABCs, ongoing assessment, I/Os
Administer:
Crystalloids
Blood products as needed:
PRBCs
FFP, cryoprecipitate, platelets 
Heparin (may be given)
158
Q

Refractory Stage

A

↓ perfusion from peripheral vasoconstriction & ↓ CO exacerbate anaerobic metabolism  Low BP
Lactic acid leads to cap permeability and loss of vascular fluid  Edema
As decrease perfusion and hypoxic state continues, organs fail
MODS
Profound hypotension & hypoxemia
Ischemic gut, Anuria, progression of DIC
Hypothermia

159
Q

cold shock is

A

dead shock

160
Q

Goals of Care for Shock patients

A

Improvement and preservation of tissue perfusion

161
Q

Labs for shock

A 
depends on the type fo shock but should have stuff like 
RBCs/H/H
WBCs
Troponin
CPK
DIC screen 
electrolytes
BUN/Creat
Liver enzymes 
Lactate
162
Q

Cardiogenic Shock

A

Impaired ability of ventricle to pump blood forward

163
Q

Cardiogenic Shock manifestations

A

Early presentation similar to decompensated HF
Increased: HR, SVR, pulmonary pressures
Decreased: B/P, cardiac output/index, urine output
Chest pain, tachypnea, crackles, cyanosis, anxiety

164
Q

mortality rate of Cardiogenic Shock

A

60% despite aggressive RX

165
Q

cause of cardiogenic shock

A

Acute MI – most common cause of systolic dysfunction
Cardiopulmonary arrest, acute decompensated HF
Trauma, Septic or hemorrhagic shock

166
Q

care for cardiogenic shock

A

Restore blood flow to the heart through Cardiac Cath w/ angioplasty or stent or Thrombolytic Therapy (tPA, streptokinase) if cath unavailable
Pulmonary Artery Catheter, IABP or VAD

167
Q

meds for cardiogenic shock

A

inotropes, vasopressor, diuretics, vasodilators, antidysrhythmic agents

168
Q

what is the issue with cardiogenic shock

A

Hypovolemia is generally NOT an issue
Think the patient is in extreme PUMP FAILURE…
Afterload and Preload issues

169
Q

dobutamine

A

inotrope - commonly used for acute HF or cardiogenic shock
it stimulates beta receptors in the heart
beta 1 - increases contractility, HR, and CO
beta 2 - decreases SVR and after load (vasodilation)

170
Q

Intra aortic balloon pump (IABP)

A

balloon that sits in the aorta to decrease after load

171
Q

Left Ventricular Assist Device (LVAD)

A

Used to stabilize patients awaiting heart transplantation

Pulls blood from the LV and sends out to the aorta

172
Q

Hypovolemic Shock

A

Loss of intravascular fluid volume

173
Q

Hypovolemic Shock manifestations

A

Decreased: B/P, CVP, preload, SV, UO, cap refill; Hgb/Hct
Increased: HR, SVR, RR
Pallor, anxiety, confusion, agitation
Depends on severity of volume depletion - how much and how fast is volume lost

174
Q

Interventions with Hypovolemic Shock

A

ABCs
2 large bore IVs
fluid resuscitation

175
Q

diagnostics with Hypovolemic Shock

A

imaging

labs: type and cross, CBC w/ diff, CMP

176
Q

treatment with Hypovolemic Shock

A

stop hemorrhage or prevent fluid loss
Surgery
IR

177
Q

How will we know when our interventions are successful?

A

↑ in BP…don’t forget to look at MAP

↓ in HR

178
Q

Obstructive Shock

A

Physical obstruction impeding the filling/outflow of blood flow occurs resulting in ↓ CO

179
Q

causes of Obstructive Shock

A

Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, massive pulmonary embolism

180
Q

Anaphylactic Shock

A

Acute life-threatening hypersensitivity reaction to a sensitizing substance

181
Q

manifestations of Anaphylactic Shock

A

↓B/P, ↑ HR, massively decreased SVR

swelling of the lips and tongue (angioedema), laryngospasm, wheezing, stridor, rhinitis, urticaria

182
Q

types of distributive shock

A

sepsis and anaphylactic

183
Q

medications for Anaphylactic Shock

A

Epinephrine, Benadryl, Bronchodilators, fluids, Corticosteroids, H2 Blockers

184
Q

epinephrine

A

good in crisis - typically used for severe sepsis or anaphylaxis. triggers beta 1 in the heart to increase inotropy, HR, and CO. triggers beta 2 to bronchodilate and alpha 1 to increase SVR and BP

185
Q

Leading cause of inpatient death in non-coronary adult ICUs in the US

A

septic shock

186
Q

most common cause of shock

A

sepsis

187
Q

sepsis

A

systemic inflammatory and coagulopathic response to infection- Life-threatening organ dysfunction caused by dysregulated host response to infection

188
Q

septic shock

A

Persisting BP requiring vasopressors to maintain MAP ≥65 and LA >2 despite adequate volume resuscitation. (Surviving Sepsis Campaign)

189
Q

3 major pathophysiologic effects of septic shock

A

Vasodilation
Maldistribution of blood flow
Myocardial depression

190
Q

infection leads to

A

an immune response that releases immune mediators from WBC and vascular endothelium. This leads to increase in inflammation, endothelial damage and coagulation/ decrease in fibrinolysis.

191
Q

who’s at risk for sepsis

A

over 65, neonates, immunocompromised, invasive procedures, specific types of infections, prior antibiotics, critically ill, genetic predisposition

192
Q

1 hour bundle

A

for sepsis

  • measure lactate level
  • rapidly administer 30 mL/kg cystalloid for hypotension or lactate greater than or equal to 4 mmol/L
  • apply vasopressors after fluids - Norepinephrine (Levophed) is first, then others
193
Q

levophed (norepinephrine)

A

common first line pressor for sepsis, cardiogenic shock, or nuerogenic shock. stimulates beta 1 heart receptor which increases HR and CO. and stimulates alpha 1 - increases SVR and BP (vasoconstriction) and beta 2 - protects blood flow to organs

194
Q

phenylephrine (neosynephrine)

A

peripheral pusher - alpha 1- increase SVR and BP but can cause reflex bradycardia

195
Q

vasopressin (ADH)

A

commonly used as an adjunct to norepinephrine - vasoconstriction and increases volume by increasing H20 reabsorption

196
Q

signs of sepsis

A

increase temp, tachypnea, warm and flushed skin, respiratory alkalosis

197
Q

septic shock signs

A

cool and mottles (cold shock is dead shock), respiratory failure, GI bleed or paralytic ileus, myocardial dysfunction

198
Q

septic shock care

A

assess! ABCs, fluids, vasopressors, lactate levels, antibiotics, hemodynamic monitoring

199
Q

nursing diagnosis for cardiogenic shock

A

Decreased CO r/t alterations in contractility, HR

200
Q

nursing diagnosis for anaphylactic shock

A

Deficient fluid volume r/t relative loss

Decreased CO r/t alterations in preload

201
Q

nursing diagnosis for hypovolemic shock

A

Deficient fluid volume r/t active blood loss

202
Q

Thrombolytic/Fibrinolytic Therapy

A

When no access to cardiac cath lab or patient to unstable to transfer.
Advantages:
Widely Available
Rapidly administered

203
Q

indications for Thrombolytic/Fibrinolytic Therapy

A

Chest pain typical of MI ≤ 6 hours
+ ECG
PCI not available or to far away.

204
Q

contraindications for Thrombolytic/Fibrinolytic Therapy

A

Active Internal Bleeding; Hx Cerebral aneurysm, stroke and more

205
Q

labs needed for Thrombolytic/Fibrinolytic Therapy

A 
Need rainbow of labs: 
Troponin
H/H
Pt/Ptt
CBC
Type and cross
206
Q

what else do you need besides labs for Thrombolytic/Fibrinolytic Therapy

A

2-3 IV lines and neuro assessment (assess for brain bleed)

207
Q

The Gold Standard of Treatment for someone having a MI

A

Percutaneous Cardiac Intervention (PCI )

208
Q

Cardiac Catheterization aka PCI

A

Venous and arterial access to the right and left side of the heart.

209
Q

what do you need to do before Cardiac Catheterization

A 
Medication Hx & Allergies
assess pulses! 
Check Labs (Which Ones & Why?)
	Pt/Ptt/INR – need to know clotting 
	kidney function labs 
IV assess
pt understands procedure and consent
210
Q

Takotsubo

A

broken heart syndrome - Chest pain, ST elevation, mildly elevate troponins - caused by stress

211
Q

post Cardiac Catheterization

A

position leg straight, monitor for reclusion- s/s ischemia, thrombosis, bleeding and Trops will go up first then down. monitor pulses

212
Q

concerns post cardiac cath

A

Decreased LOC
Hypotension & Tachycardia
bleeding

213
Q

Cardiac Mapping/Ablation

A

Provides information about SA and AV nodes

Determine the origins of a dysrhythmia

214
Q

CORONARY ARTERY BYPASS GRAFT (CABG)

A

A procedure in which the patient’s diseased coronary arteries are bypassed with the patient’s own venous (saphenous vein) or arterial (internal mammary artery [most common]) vessels.

215
Q

who is a CABG for

A

Failed Medical Mgt

Have Left Main or 3 diseased vessels with significant blockage.

216
Q

who is not a candidate for CABG

A

Failed PCI
Newly added criteria
Diabetes Mellitus
Expected longer term benefits/outcomes

217
Q

Alpha 1

A

vasoconstriction

218
Q

alpha 2

A

blocks sympathetic activity

219
Q

beta 1

A

increase contractility HR and renin

220
Q

beta 2

A

dilation of bronchioles

221
Q

vasoconstrictors/vasopressors

A

epinephrine, norepinephrine, phenylephrine, vasopressin

222
Q

inotropes

A

DOBUTAMINE, DOPAMINE

223
Q

dopamine

A

(hulk)- squeeze! - vasoconstriction

Nursing school level 4 (6 decks)

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