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NSG 420 Caring for Adult II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

are arteries in the heart deoxygenated or oxygenated?

A

deoxygenated (in the body they are usually oxygenated)

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2
Q

are veins in the heart oxygenated or deoxygenated?

A

oxygenated (in the body they are usually deoxygenated

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3
Q

what ventricle is bigger and by how much?

A

the left ventricular wall is 2-3 times thicker than the right (because it pumps to the whole body)

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4
Q

systole

A

contraction of myocardium

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5
Q

diastole

A

relaxation of myocardium

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6
Q

preload

A

volume of blood in the ventricle at the end of diastole (what’s already in there)

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7
Q

afterload

A

peripheral resistance the left ventricle must pump against

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8
Q

baroreceptors location

A

aortic arch, carotid sinus; sensitive to pressure

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9
Q

formula for CO

A

CO = HR x SV

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10
Q

formula for BP

A

BP = CO x systemic vascular resistance (SVR)

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11
Q

pulse pressure

A

difference between SBP and DBP

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12
Q

normal pulse pressure

A

approximately 1/3 of SBP ~ about 40-60

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13
Q

mean arterial pressure (MAP)

A

the pressure/perfusion the organs actually feel

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14
Q

normal MAP

A

greater than 60

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15
Q

MAP formula

A

MAP = (SBP + 2DBP)/3

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16
Q

postprandial hypotension

A

decrease 20 mm Hg within 75 minutes after eating

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17
Q

triglycerides

A

main storage form of lipids

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18
Q

anytime a dye is injected in a (-graphy), what is important to assess for?

A
  • allergies
  • metformin use
  • kidney function (> 30 mL/hr)
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19
Q

contributing risk factors to HF

A
  • advanced age
  • diabetes
  • tobacco use (vasoconstrictor)
  • obesity
  • high serum cholesterol
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20
Q

what can hypertrophy of the heart lead to?

A

overtime leads to poor contractility, increased O2 needs, and risk for dysrhythmias

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21
Q

what is pulmonary edema?

A
  • life-threatening situation (alveoli fill with fluid)
  • most commonly associated with left-sided HF
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22
Q

pulmonary edema treatment

A

LMNOP
Lasix
Morphine
Nitrates (NTG)
Oxygen
Position upright

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23
Q

clinical manifestations of chronic HF

A
  • fatigue
  • dyspnea
  • orthopnea
  • paroxysmal nocturnal dyspnea
  • tachycardia
  • edema
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24
Q

in someone with HF who has edema, what do we want them to do everyday?

A

sudden weight gain of > 3 lbs (1.4 kg) in 2 days may indicate worsening, so have them weigh themselves every day!

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25
Q

normal ejection fraction

A

greater than 50%

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26
Q

what position is best for a patient in HF?

A

high-fowlers

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27
Q

normal BNP (beta natriuretic peptide)

A

below 100

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28
Q

where does an impulse begin in the heart?

A

in the SA node

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29
Q

how does vagus nerve stimulation play a role in the heart?

A

works through the parasympathetic NS, vagus nerve stimulation decreases firing which decreases HR

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30
Q

what should come first in CAB?

A

compressions!

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31
Q

manifestations of sinus bradycardia

A
  • think decreased CO
  • hypotension
  • pale, cool skin
  • weakness
  • angina
  • dizziness or syncope
  • confusion or disorientation
  • SOB
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32
Q

atropine

A

takes HR up

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33
Q

adenosine

A

HR down

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34
Q

treatment of sinus bradycardia

A
  • check O2 sat and correct as needed
  • give atropine
  • transcutaneous pacemaker
  • stop offending drugs (digoxin, beta-blockers, ACE inhibitors)
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35
Q

treatment of sinus tachycardia

A
  • guided by cause
  • vagal maneuver (bearing down like having a BM, blowing into something, cold water to the face)
  • beta-blockers (metoprolol/lopressor - reduce HR and decrease myocardial oxygen consumption)
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36
Q

SVT

A

originates above the ventricles but not from the sinus node

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37
Q

atrial fibrillation

A

chaotic atrial activity

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38
Q

atrial flutter

A
  • more organized than a. fib.
  • sawtooth pattern
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39
Q

what can SVT be associated with?

A

overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity

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40
Q

treatment of SVT

A
  • vagal stimulation, carotid massage, coughing
  • IV adenosine (pushed fast)
  • IV beta-blockers
  • calcium channel blockers
  • amiodarone
  • DC cardioversion (last resort)
  • ablation (last resort)
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41
Q

most common dysrhythmia

A

atrial fib.

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42
Q

in a. fib. what does prevalence increase with?

A

age

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43
Q

what are you at an increased risk for with a. fib.

A
  • stroke
  • MONITOR FOR STROKE
  • CALL STROKE ALERT or 911
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44
Q

treatment for a. fib.

A
  • drugs to control ventricular rate and/or convert to sinus rhythm (beta-blockers, digoxin, ca channel, amiodarone
  • electrical cardioversion
  • anticoagulation
  • radiofrequency ablation
  • maze procedure with cryoablation
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45
Q

what does a. flutter put you at risk for?

A

increased risk of stroke

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46
Q

treatment of a. flutter

A
  • calcium channel or beta blockers
  • electrical cardioversion
    radiofrequency ablation
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47
Q

treatment of a third-degree AV block

A

pacemaker

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48
Q

what should you do for a third-degree AV block while waiting for a pacemake?

A

drugs to increase HR if needed

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49
Q

what does a PVC do?

A

interrupts regularity

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50
Q

with a PVC, what is important to assess?

A

apical-radial pulse deficit

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51
Q

why is v. tach. considered life threatening?

A

because of decreased CO and the possibility of deterioration to v. fib.

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52
Q

treatment for v. tach. with a pulse

A
  • IV magnesium sulfate
  • other antidysrhythmics
  • cardioversion
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53
Q

treatment for v. tach. without a pulse

A
  • CPR
  • rapid defibrillation
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54
Q

what can v. fib. be associated with?

A

MI, ischemia, disease states, procedures

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55
Q

what does a patient look like who is in v. fib.?

A

unresponsive, pulseless, apneic

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56
Q

if v. fib. is not treated rapidly, what can happen?

A

death

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57
Q

treatment of v. fib.

A

immediate CPR, defibrillation, epinephrine, vasopressin

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58
Q

what can asystole be a result of?

A

advanced cardiac disease, severe conduction disturbance, or end-stage HF

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59
Q

treatment of asystole

A

immediate CPR, epinephrine, intubation (poor prognosis)

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60
Q

PEA

A
  • patient has no pulse
  • prognosis is poor unless underlying cause quickly identified and treated
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61
Q

Hs and Ts pneumonic

A
  • hypovolemia hypoxia, hydrogen ion (acidosis), hyper-/hypokalemia, hypoglycemia, hypothermia
  • toxins, tamponade (cardiac), thrombosis (MI and pulmonary), tension pneumothorax, trauma
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62
Q

treatment of PEA

A

CPR followed by intubation and IV epinephrine

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63
Q

when do we give CPR and epi.?

A

PEA and asystole

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64
Q

when do we defibrillate and CPR?

A

pulseless v. tach. or v. fib.

65
Q

when would we do a cardioversion?

A

*less severe
a. fib., a. flutter., v. tach. with a pulse, SVT

66
Q

when is defibrillation most effective?

A

when completed within 2 minutes of dysrhythmia onset

67
Q

monophasic vs. biphasic defibrillation

A
  • monophasic deliver energy in one direction
  • biphasic deliver energy in two directions and uses lower energies
68
Q

what kind of defibrillator is the better of the two?

A

biphasic (BETTER)

69
Q

why is a biphasic defibrillator better?

A
  • uses lower energies
  • fewer postshock ECG abnormalities
70
Q

synchronized cardioversion

A
  • choice of therapy for v. tach. with a pulse or SVT
  • synchronized circuit delivers a countershock on the R wave of QRS complex of ECG
    *syncs on R
  • similar to defibrillation except sync button turned ON
71
Q

if patient becomes pulseless during a cardioversion, what should you do?

A

turn sync button off and defibrillate

72
Q

what would an inverted T wave mean?

A

ischemia, lack of O2

73
Q

what would ST elevation mean?

A

zone of injury

74
Q

what would abnormal Q mean?

A

zone of necrosis

75
Q

major cause of CAD

A

atherosclerosis

76
Q

what is considered a high cholesterol level that we can modify?

A

> 200 mg/dL

77
Q

what is considered high triglycerides that we can modify?

A

> 150 mg/dL

78
Q

other modifiable risk factors for CAD

A
  • HTN
  • tobacco use
  • physical inactivity
  • obesity
  • diabetes
  • metabolic syndrome-insulin resistance
  • psychological stress
  • substance abuse
79
Q

clinical manifestations of angina pain

A
  • pressure/ache
  • squeezing, heavy, choking, or suffocating sensation
  • rarely sharp or stabbing
  • indigestion or burning
  • various locations
80
Q

what does chronic stable angina look like on an ECG?

A

ST segment depression and/or T-wave inversion (heart not getting O2)

81
Q

goal of treating chronic stable angine

A

decrease O2 demand and/or increase O2 supply

82
Q

how do short-acting nitrates work for the heart?

A
  • dilates peripheral and coronary blood vessels
  • give SL tablet or by spray
  • if no relief in 5 minutes, call EMS
  • can use prophylactically
  • check other medications taken
  • cardiac biomarkers
83
Q

what other drugs help with chronic stable angina?

A
  • ACE inhibitors
  • beta-blockers
  • calcium channel blockers
84
Q

what kind of studies should be performed with chronic stable angina?

A
  • chest x-ray
  • cardiac biomarkers, lipids, CRP
  • 12-lead ECG
  • echocardiogram
  • exercise stress test
  • CT, angiography
85
Q

what procedure is the GOLD STANDARD to localize CAD?

A

cardiac catheterization/coronary angiography

86
Q

clinical manifestations of unstable angina

A
  • new in onset
  • occurs at rest
  • worsening pattern
  • increase in frequency
  • unpredictable
  • medical emergency
  • symptoms in women may be more vague
87
Q

if someone has an MI, how long until necrosis occurs?

A

necrosis of entire thickness of myocardium takes 4-6 hours

88
Q

symptoms of MI

A
  • pain that is severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
  • heaviness, pressure, tightness, burning, constriction, crushing
  • substernal, retrosternal, epigastric
  • more common in AM
  • atypical in women, elderly
  • no pain if cardiac neuropathy (diabetes)
  • sweaty and clammy skin
  • initially HR and BP increase, then BP decreases due to decrease in CO
  • crackles
  • JVD
  • abnormal heart sounds (S3, S4, murmur)
  • N/V
  • fever
89
Q

most common complication of an MI

A

dysrhythmias (occurs in 80% of MI patients

90
Q

other complications of an MI

A
  • HF
  • cardiogenic shock
  • acute pericarditis
91
Q

what is the protocol when someone has ACS?

A
  1. semi-fowlers position
  2. O2 (NRB 100%)
  3. 12-lead ECG
  4. NTG (SL) and ASA (chewable)
  5. IV access
  6. morphine
  7. statin
92
Q

MONA acronym for treatment of MI

A

Morphine
Oxygen
Nitroglycerine
ASA

93
Q

treatment of choice for confirmed MI

A

emergent PCI

94
Q

what is the goal after someone has an MI to get them to the cath. lab?

A

90 minutes from door to cath. lab

95
Q

when PCI isn’t available what should you do?

A
  • thrombolytic therapy
  • stops infarction process by dissolving thrombus
  • ideally within 30 minutes
  • like tPa
96
Q

after giving thrombolytic therapy for an MI, what do you want to watch for?

A
  • monitor for signs of bleeding
  • assess for signs of reperfusion (return of ST segment to baseline best marker)
  • IV heparin to prevent reocclusion
97
Q

what can PVCs lead to?

A

v. tach. which can lead to v. fib. which can lead to asystole

98
Q

most common causative organism for infective endocarditis

A

bacteria ~ streptococcus viridans and staphylococcus aureus

99
Q

what is it called when parts break off and enter circulation

A

embolism

100
Q

what kind of lab tests do we want to get with infective endocarditis?

A
  • blood culture
  • CBC with differential
  • ESR, CRP
101
Q

how to treat infective endocarditis?

A

IV antibiotics (long-term, for 4-6 weeks) ~ teach importance of adherence to treatment regimen

102
Q

how often will HF occur in patients who have infective endocarditis?

A

HF occurs in up to 80% of patients with aortic valve endocarditis and in approximately 50% of patients with mitral valve endocarditis

103
Q

patient teaching with infective endocarditis

A
  • need to avoid infectious people
  • avoid stress and fatigue
  • rest
  • hygiene
  • prophylactic antibiotics
  • drug rehabilitation
  • monitor body temperature
  • S/S of complications
104
Q

what virus is most commonly identified with acute pericarditis?

A

coxsackie

105
Q

hallmark clinical manifestation of acute pericarditis

A

pericardial friction rub

106
Q

treatment of acute pericarditis

A
  • treat underlying cause
  • antibiotics if bacteria
  • NSAIDs (monitor bleeding and kidney function)
  • pericardiocentesis if needed
  • pericardial window if necessary
107
Q

how do most patients recover from myocarditis?

A

most recover spontaneously but some may develop dilated cardiomyopathy

108
Q

main cause of rheumatic heart

A

complication following group a strep infection

109
Q

main treatment of rheumatic heart

A

steroids

110
Q

classic symptom of PAD

A

intermittent claudication

111
Q

intermittent claudication

A
  • ischemic muscle pain that is cause by a constant level of exercise
  • resolves within 10 minutes or less with rest
  • reproducible
112
Q

arterial manifestations of PAD

A
  • thin, shiny, and taut skin
  • loss of hair on lower legs
  • diminished or absent pedal, popliteal, or femoral pulses
  • pallor of foot with leg elevation
  • reactive hyperemia of foot with dependent position
113
Q

what can PAD lead to in worse cases?

A

nonhealing arterial ulcers and gangrene are most serious complications that may result in amputation

114
Q

what is a risk factor modification for PAD concerning diabetes?

A

Glycosylated Hgb. <7.0%

115
Q

what drugs do we give for PAD?

A

ACE inhibitors (ramipril)
- decreases CV morbidity
- decreases mortality
- increases peripheral blood flow
- increases ABI
- increases walking distance

antiplatelet agents: aspirin and clopidogrel (plavix)

116
Q

drug alert concerning prilosec and clopidogrel

A

prilosec decreases clopidogrel in half so there is more of a risk for clots, strokes, DVT, etc.

117
Q

most effective exercise for claudication

A

walking for 30-60 minutes daily, 3 times/week

118
Q

what is a good IR procedure for PAD?

A

atherectomy: removal of the obstructing plaque

119
Q

what is the most common surgical approach for PAD?

A
  • a peripheral artery bypass surgery with autogenous vein or synthetic graft to bypass blood around the lesion
  • PTA with stenting may also be used in combination
120
Q

aortic aneurysm

A

outpouching or dilation of the arterial wall

121
Q

what population is more prone to aortic aneurysms?

A
  • men more than women
  • incidence increases with age
122
Q

thoracic aortic aneurysm most common manifestation

A
  • often asymptomatic
  • deep diffuse chest pain that may extend to the scapular area
123
Q

clinical manifestations of ascending aorta/aortic arch aneurysm

A
  • angina
  • hoarseness
  • if pressure is on SVC, decreased venous return so distended neck veins and edema of face and arms
124
Q

if an AAA spontaneously embolizes a plaque, what can happen?

A

“blue toe syndrome”: patchy mottling of feet/toes with presence of palpable pedal pulses

125
Q

serious complication of aortic aneurysm

A

rupture

126
Q

clinical manifestations of an aneurysm rupture

A
  • severe back pain
  • may/may not have back/flank ecchymosis
127
Q

most accurate test to determine an aortic aneurysm

A

CT scan

128
Q

if an aneurysm ruptures, what needs to happen?

A

emergent surgical intervention ~ 90% mortality with ruptured AAAs

129
Q

indications of aortic aneurysm rupture

A
  • diaphoresis
  • pallor
  • weakness
  • tachycardia
  • hypotension
  • abdominal, back, groin, or periumbilical pain
  • changes in LOC
  • pulsating abdominal mass
130
Q

what is an aortic dissection often misnamed?

A

dissecting aneurysm ~ it is not a type of aneurysm

131
Q

clinical manifestations of aortic dissection

A
  • pain that is sudden, severe in anterior part of chest, or scapular pain radiating down spine to abdomen or legs
  • described ad “sharp” and “worst ever”
  • may mimic that of MI
  • neuro deficiencies
132
Q

complications of aortic dissection

A

aorta may rupture leading to exsanguination and death

133
Q

initial goal in an aortic dissection

A
  • decrease BP and myocardial contractility to diminish pulsatile forces within aorta
  • HR less than 60 and SBP less than 100-110
134
Q

If a patient comes in with chest pain what do we do?

A
  • EKG
  • O2
  • troponin lab
  • ask what they were doing
  • MONA: Morphine, oxygen, nitroglycerine, aspirin
  • sit them up
135
Q

atherosclerosis

A

plaque in the vessels

136
Q

why would someone be on heparin?

A

prevents clots

137
Q

why would someone be on tPA (thrombolytics)?

A

dissolves clots

138
Q

what do we want to do in an MI, dissolve a clot or prevent clots?

A

dissolve them

139
Q

a patient comes in with possible MI and is rushed to the cath lab. what tells you on the EKG that it was a STEMI?

A

ST should go back to normal (shows perfusion)

140
Q

patient has a stent what would you assess?

A
  • bleeding
  • pulses
141
Q

if a patient has chest pain after a stent is placed what should you do?

A

CALL STROKE ALERT

142
Q

patient teaching for aneurysm regarding meds

A

compliance with HTN meds and antianeurysm meds

143
Q

what should we teach our PAD patient to stop doing

A

smoking

144
Q

can nurses stop a beta-blockers order?

A

no not without an MD approval

145
Q

important labs for kidney function

A
  • creatinine
  • > 30 mL/hr
146
Q

patient comes in with the “worst pain” of their life and abdominal tearing sensation in stomach, what do you think it is?

A

aortic rupture

147
Q

after an abdominal aorta repair, the patient’s food is white and there is no pulse, what should you do?

A

call MD

148
Q

important labs with heparin?

A

clotting factor, PTT, INR

149
Q

reversal of heparin

A

protamine sulfate

150
Q

how does adenosine work in the heart?

A

it stops the heart and resets it

151
Q

if after giving adenosine the heart doesn’t reset and the patient goes into v. fib. what do you do?

A

defibrillate/CPR

152
Q

if a patient has any arrhythmia, what do we assess?

A

patient’s pulse and airway

153
Q

normal potassium levels

A

3.5-5.0

154
Q

important assessment with digoxin

A

assess apical HR for at least one minute, if HR is 45 BPM call provider

155
Q

before giving nitroglycerin, what do you want to ensure about your patient’s home meds?

A

if they are on viagra

156
Q

rule for when the patient can return to sexual activity after heart problems

A

if they can climb two flights of stairs

157
Q

what will you hear in HF?

A

S3 S4

158
Q

what will you hear with pericarditis?

A

friction rub

159
Q

what will you hear with cardiac tamponade?

A

muffled

NSG 420 Caring for Adult II (4 decks)

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