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Med-Surg II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

what ventricular wall of the heart is how much thicker

A

left, 2-3x

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2
Q

cardiac valves connected by what

A

chordae tendineae

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3
Q

QRS

A

depolarization from AV node through ventricles (heartbeat)

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4
Q

heart block in ECG

A

long time between isoelectric and QRS (PR interval >0.20)

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5
Q

effective and relative refractory period

A

nothing happens, cells let 3 major electrolytes in and out

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6
Q

normal CO

A

4-8 L/min

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7
Q

cardiac index and normal number

A

CO / body surface area
normal is 2.8-4.2 L/min/m^2)

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8
Q

3 factors that affect cardiac output

A

preload
contractility
afterload

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9
Q

afterload

A

the amount of pressure that the heart needs to eject blood during ventricular contraction
THINK OF BP

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10
Q

A patient is receiving a drug that decreases afterload. To evaluate the patient’s response to this drug, what is most important for the nurse to assess?
HR, lung sounds, BP, JVD

A

BP

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11
Q

HR influenced by what 3 things

A

acidosis
certain meds
hypoxemia

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12
Q

frank-starling law

A

r/t preload
cardiac and muscle cells can only stretch so far

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12
Q

afterload affected by

A

systemic and pulmonary vascular resistance

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12
Q

HR and adrenal gland

A

tumor can cause secretion of hormones like cortisol, epinephrine, and adrenaline

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12
Q

common symptoms of MI

A

chest pain/discomfort (neck and shoulder in women)
SOB/dyspnea
peripheral edema, weight gain, abd distention
palpitations
unusual fatigue, dizziness, syncope, change in LOC

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12
Q

peripheral edema upon waking

A

NOT NORMAL
except with ACE or calcium channel blockers
can actually be present in abdomen

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13
Q

C-reactive protein

A

elevated in heart problems, viral infection, lupus, RA

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14
Q

troponin and drawn how often?

A

cardiac muscle damage
drawn in series of 3 q8h

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15
Q

lab tests for cardiac

A

Cardiac biomarkers
Blood chemistry, hematology, coagulation
Lipid profile
Brain (B-type) natriuretic peptide
C-reactive protein
Homocysteine
TROPONIN

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16
Q

point of maximal impulse

A

at the apex
midclav, 5th intercostal space

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17
Q

pharm stress test

A

vasodilators given

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18
Q

echocardiography

A

measures EF
examine size, shape, and motion of cardiac structures

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19
Q

transthoracic

A

like an ultrasound

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20
Q

transesophageal

A

like an endoscopy

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21
Q

nuclear cardiology 2 tests

A

MUGA
stress perfusion imaging

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22
Q

CT angiography

A

calcium screening
looks for HARD calcium not soft

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23
Q

right heart cath

A

pulmonary artery pressure, O2 sats, and myocardial tissue biopsy may be obtained

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24
Q

left heart cath

A

uses contrast agent unless kidney failure

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25
Q

bed rest after cardiac cath

A

2-6 hours

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26
Q

some blocked arteries, what procedure?

A

coronary artery bypass

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27
Q

major blockage, what procedure

A

stent

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28
Q

what to know about insertion site

A

lots of pressure
can leak under skin and form hematoma (pt c/o pressure)
check pulse below insertion site

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29
Q

hemodynamic monitoring

A

central venous pressure
pulmonary artery pressure
intra-arterial BP monitoring
minimally invasive CO monitoring devices

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30
Q

5 factors of normal sinus rhythm

A

regular
60-100 BPM
P waves normal and precede QRS complex
PR 0.12-0.20
QRS <0.12

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31
Q

sinus tachy

A

100-160 BPM

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32
Q

sinus arrythmia

A

irregular rate
normal or brady
associated w respirations, NORMAL! tell pt to relax

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33
Q

premature atrial contractions causes and where is the focus

A

alcohol, drugs, stress
SA node

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34
Q

atrial flutter

A

reg or irreg
atrial rate 250-400
ventricular varies on # of impulses to AV node (less than atrial)
SAW TOOTH PATTERN
normal QRS but PR not measurable

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35
Q

afib

A

rapid irregular
atrial rate >400 (not measurable)
ventricular rate varies on # of impulses to AV node
P waves waving deflections entire baseline
PR and QRS not measurable

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36
Q

3 vfib causes

A

accident, drowning, electrocution

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37
Q

blood pathway (right side)

A

Blood enters the heart through two large veins, the inferior and superior vena cava, emptying the oxygen-poor blood from the body into the right atrium.

As the atrium contracts, blood flows from the right atrium into the right ventricle through the open tricuspid valve

When the right ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts.

As the right ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs where it is oxygenated.

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38
Q

blood pathway (left)

A

The pulmonary vein empties oxygen-rich blood from the lungs into the left atrium of the heart.

As the left atrium contracts, blood flows from the left atrium into the left ventricle through the open mitral valve.

When the left ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts

As the left ventricle contracts, oxygen-enriched blood leaves the heart through the aortic valve, into the aorta and to the arteries and eventually into veins to complete blood circulation in your body.

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39
Q

tertiary pacemaker of heart

A

his-purkinje fibers (20-40)

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40
Q

lead 1

A

right side, 5th intercostal space

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41
Q

lead 2

A

left sternum, 4th intercostal space

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42
Q

lead 4

A

midclavicular, 5th intercostal space

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43
Q

costochondritis

A

mimics pain of MI, inflammation of cartilage that joins ribs to sternum

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44
Q

what 3 things can mimic cardiac disease

A

GERD
hiatal hernia
pregnancy

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45
Q

PR interval

A

time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)

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46
Q

QT interval

A

duration of ventricular depolarization and repolarization

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47
Q

manifestations of sinus brady (7)

A

Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
SOB
Can be normal during sleep!

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48
Q

sinus tachy caused by vagal __________ or sympathetic ________

A

INHIBITION!!! STIMULATION!!!
valsalva maneuver (bearing down) stimulates vagus nerve, fixes sinus tach

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49
Q

4 manifestations of sinus tachy

A

dizziness (not getting enough oxygenated blood whether brady or tachy)
dyspnea
hypotension
angina in pts with CAD

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50
Q

PAC

A

-Contraction originating from ectopic focus in atrium in location other than SA node
-Travels across atria by abnormal pathway, creating distorted P wave
-May be stopped, delayed, or conducted normally at the AV node

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51
Q

8 causes of PAC

A

Stress
Fatigue
Caffeine
Tobacco
Alcohol (depletes electrolytes)
Hypoxia
Electrolyte imbalance
Disease states

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52
Q

2 manifestations of PAC

A

palpitations
heart skips a beat

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53
Q

3 treatments for PAC

A

monitor for more serious dysrhythmias
withhold sources of stimulation
beta blockers

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54
Q

aflutter

A

associated with disease
symptoms from high ventricular rate and loss of atrial “kick” (decreased CO –> risk of HF)
increases risk of CVA

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55
Q

3 treatments for aflutter

A

-Pharmacologic agent
-Electrical cardioversion
-Radiofrequency ablation (if someone has ectopic focus, wire gets threaded thru right atrium and gives meds to stimulate dysrhythmia so they can see it [can cause new dysrhythmia]. Ablated with high frequency or freezing)

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56
Q

afib

A

paroxysmal or persistent
most common in people over 65
in pts with underlying heart dx
can occur in other disease states

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57
Q

5 treatments for afib

A

-Drugs to convert ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common)
-Electrical cardioversion
-Anticoagulation (work on platelet aggregation, careful with ppl with high or low platelets)
-Radiofrequency ablation
-Maze procedure (also done thru angiogram, different technique) with cryoablation

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58
Q

PSVT causes

A

Overexertion
stress
deep inspiration
stimulants
disease
digitalis toxicity (N/V, loss of appetite)

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59
Q

digoxin toxicity

A

N/V, loss of appetite

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60
Q

reentrant phenomenon

A

PAC triggers a run of repeated premature beats

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61
Q

manifestations of PSVT

A

HR 150-220
HR >180 leads to decreased CO and SV
hypotension
dyspnea
angina

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62
Q

6 treatments for PSVT

A

Vagal stimulation
IV adenosine
IV beta blockers
Calcium channel blockers
Amiodarone
DC cardioversion

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63
Q

vtach

A

-SA node nonfunctional
-Ectopic foci take over as pacemaker
-Monomorphic (all same shape), polymorphic (many), sustained, and nonsustained
-Considered life-threatening because of decreased cardiac output and the possibility of deterioration to v-fib

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64
Q

vtach- torsades de pointes associated with what

A

Associated with heart disease, electrolyte imbalances, drugs, CNS disorder (GBS, parkinsons, spinal cord injury)

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65
Q

manifestations of vtach

A

Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest

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66
Q

treatment for STABLE vtach

A

antidysrhythmics or cardioversion

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67
Q

treatment for UNSTABLE vtach

A

CPR and rapid defibrillation

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68
Q

vfib associated with?

A

MI, ischemia, disease states, procedures
unresponsive, pulseless, and apneic

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69
Q

vfib treatment

A

CPR and ACLS (defibrillation and drug therapy including epinephrine, vasopressin [-pressors bring BP up], anything to restore blood flow

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70
Q

asystole is a result of what

A

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

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71
Q

treatment for asystole

A

immediate CPR and ACLS measures
Epinephrine and/or vasopressin
Intubation

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72
Q

PEA

A

weak electrical activity shown in ECG, no pulse
NONSHOCKABLE

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73
Q

6 Hs of PEA

A

HYPOvolemia
HYPOxia
Hydrogen ion (acidosis)
HYPER/HYPOkalemia
HYPOglycemia
HYPOthermia

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74
Q

5 Ts of PEA

A

Toxins
Tamponade
Thrombosis (MI and pulmonary)
Tension pneumothorax
trauma

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75
Q

treatment of PEA

A

CPR followed by intubation and IV epinephrine
Correct the underlying cause

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76
Q

SCD (sudden cardiac death)

A

death from cardiac cause
majority from ventricular dysrhythmias (vtach and vfib)
prolonged QT

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77
Q

defibrillation

A

treatment of choice for vfib and pulseless VT
most effective within 2 mins of dysrhythmia
passage of shock through heart to depolarize myocardial cells
allows SA node to become pacemaker
output in joules/watts per second

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78
Q

monophasic and biphasic defibrillators

A

mono: deliver energy in one direction
bi: 2 directions, lower energies, fewer post-shock abnormalities

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79
Q

recommended energy for initial shocks in defibrillation

A

bi: 120-200 joules
mono: 360
START CPR AFTER FIRST SHOCK

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80
Q

8 steps to defibrillation

A

-start CPR and set up defibrillator
-turn on and select energy
-turn off sync button
-gel pads
-charge
-position paddles firmly on chest
-all clear!
-deliver charge

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81
Q

steps to synchronized cardioversion and initial energies

A

same but make sure sync is ON
initial energy 70-75 (bi) or 100 (mono)
if pt stable, sedate prior
if pt pulseless, turn sync button off and defib

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82
Q

synchronized cardioversion rhythms

A

VT with a pulse or supraventricular tachydysrhythmias

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83
Q

how does synchronized cardioversion work

A

delivers a countershock on the R wave of the QRS complex of the ECG

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84
Q

ICDs (who are they for and how do they work)

A

for pts who:
-have survived SCD
-have spontaneous sustained VT
-syncope w inducible vtach/fib during EPS
-high risk for LT dysrhythmias
lead system in subclavian vein to endocardium
delivers 25 joules when dysrhythmia detected
CHECK FOR BLEEDING AND HEMATOMA
includes antitachy/antibrady pacemakers
-overdrive for tachy
-backup for brady

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85
Q

pre and postop care for ICDs

A

same as pacemaker
fear of body image change and recurrent dysrhythmias
expectation of pain w discharge
anxiety about going home
SUPPORT GROUP

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86
Q

pt teaching for ICD

A

-Follow-up appointments
-Incision care (check site for drainage, heat, redness, swelling)
-Arm restrictions (don’t lift that arm above head for 6 weeks and don’t lift anything above 5 lbs on that side)
-Sexual activity (not that forbidden unless symptoms)
-Driving
-Avoid direct blows
-Avoid large magnets, MRI (newer ones [2 years] are usually compatible)
-Air travel (don’t use wand over site)
-Avoid anti theft devices (can disarm mechanics)
-What to do if ICD fires
-Medic alert ID
-ICD identification card (defibrillator brand, serial number, etc)
-Caregivers to learn CPR

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87
Q

pacing circuit consists of

A

-Programmable pulse generator (power source)
-One or more conducting (pacing) leads to myocardium
goes in the same way as ICD but 2 wires

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88
Q

3 temporary pacemakers

A

outside of the body:
transvenous
epicardial
transcutaneous

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89
Q

epicardial pacing

A

-leads placed on epicardium during heart surgery
-passed through chest wall and attached to external power source

90
Q

transcutaneous pacing

A

-For emergent pacing needs
-Noninvasive
-Bridge until transvenous pacer can be inserted
-Use lowest current that will “capture”
-Pt may need analgesia/sedation

91
Q

fail to sense and capture in pacemaker

A

fail to sense causes inappropriate firing
failure to capture causes lack of pacing when needed (leading to brady or asystole)

92
Q

5 complications of pacemaker placement

A

infection
hematoma
pneumothorax
atrial or ventricular septum perforation
lead misplacement

93
Q

postop care for pacemaker

A

OOB once stable
limit arm and shoulder activity
monitor insertion site

94
Q

pacemaker pt teaching

A

Follow-up appointments for pacemaker function checks
Incision care
Arm restrictions
Avoid direct blows
Avoid high-output generator
No MRIs unless pacer approved
Microwaves OK
Avoid anti theft devices
Air travel
Monitor pulse
Pacemaker ID card
Medic Alert ID

95
Q

ECG changes with ACS

A

ischemia
-ST depression (1 mm below isoelectric line) or T wave inversion
-changes reverse once adequate blood flow is restored

96
Q

injury (cell death) in ECG

A

ST elevation (1 mm above isoelectric)
QUICK treatment to prevent infarction
absence of serum markers shows no infarction

97
Q

infarction in ECG

A

pathologic Q wave (deep and >0.03 seconds in duration)

98
Q

5 noncardiovascular causes for syncope

A

Stress
Hypoglycemia
Dehydration
Stroke
Seizure

99
Q

5 cardiovascular causes for syncope

A

Cardiogenic or “vasovagal” syncope (Carotid sinus sensitivity)
Dysrhythmias (tachy/brady)
Prosthetic valve malfunction
Pulmonary emboli
HF

100
Q

4 diagnostic tests for syncope

A

Echocardiography
Stress test
EPS (internal rhythm of heart)
Head-up, tilt test

101
Q

C-reactive protein

A

Nonspecific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol (like a pt with a viral problem that doesn’t go away, autoimmune)

102
Q

manifestations of CAD

A

symptoms caused by MI
symptoms and complications related to location and degree of obstruction
angina pectoris!!
epigastric distress, pain that radiates to jaw or left arm, SOB, atypical symptoms in women
HF
sudden cardiac death

103
Q

risk factors for CAD

A

cholesterol abnormalities, tobacco use, HTN, and diabetes**
LDLs are primary target in meds
framingham risk calculator
metabolic syndrome
hs-CRP (high sensitivity CRP)

104
Q

6 lipid lowering agents

A

HMG-CoA (statins, NO GRAPEFRUIT AND RHABDO)
nicotinic acids (facial flushing and hot flashes)
fibric acids
bile acid sequestrants (resins, cause diarrhea)
cholesterol absorption inhibitors
omega-3 acid ethyl esters (some benefit but dose causes increased bleeding)

105
Q

Gerontologic considerations for CAD

A

Diminished pain transition that occurs with aging may affect presentation of symptoms
“Silent” CAD
Teach older adults to recognize their “chest pain–like” symptoms (i.e., weakness or heaviness, may miss symptoms because they take so many meds)
Pharmacologic stress testing; cardiac catheterization
Medications should be used cautiously!
Start low and go slow
Liver or kidney dysfunction

106
Q

treatment for CAD

A

decrease oxygen demand and increase supply

107
Q

meds for CAD

A

-Nitroglycerin (potent vasodilator, may give migraines bc they dilate temporal vessels)
-Beta blockers (watch HR and blood sugar, may go up from some beta blockers)
-Calcium channel blockers (may cause tachycardia and pedal edema)
-Aspirin (antiplatelet)
-Clopidogrel and ticlopidine
-Anticoags like heparin
-Glycoprotein IIb/IIIa agents

108
Q

Angina pectoris

A

A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow
Physical exertion or emotional stress increases myocardial oxygen demand, and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand

109
Q

intractable or refractory angina

A

severe incapacitating pain

110
Q

variant (prinzmetal’s) angina

A

pain at rest w reversible ST elevation, caused by coronary artery vasospasm

111
Q

assessment of angina

A

May be described as tightness, choking, or a heavy sensation
Frequently retrosternal (behind sternum, deep pain) and may radiate to neck, jaw, shoulders, back or arms (usually left)
Anxiety frequently accompanies the pain
Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting

112
Q

NTG and angina

A

Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG.
requires medical intervention!

113
Q

7 collaborative problems of angina

A

ACS
MI
both of the above
dysrhythmias
cardiac arrest
HF
cardiogenic shock (collapse of CV system, BP plummets, pulse pressure widens)

114
Q

nursing priorities for treating angina

A

pt should stop activity and rest in semi fowlers
assess
with VS, assess for resp distress and pain assessment
ECG
oxygen 2L/min nasal cannula

115
Q

pt teaching for angina

A

avoid OTC meds that increase HR or BP
low fat high fiber diet
NTG AWAY FROM SUN AND KIDS
maintain normal BP and glucose

116
Q

treatment for stable angina

A

medication and interventional treatment (procedures to open or bypass narrowed coronary arteries)

117
Q

3 forms of ACS

A

unstable angina
STEMI
NSTEMI

118
Q

unstable angina diagnostics

A

manifestations of coronary ischemia, ECG & biomarkers show no evidence of acute MI

119
Q

STEMI diagnostics

A

ECG evidence of acute MI, characteristic changes in two contiguous leads on a 12-lead ECG. There is significant damage to the myocardium

120
Q

NSTEMI diagnostics

A

Elevated cardiac biomarkers (e.g., troponin, no definite ECG evidence of acute MI. There may be less damage to the myocardium

121
Q

myocardial infarction treatment MONA

A

morphine
oxygen
nitrates
aspirin

122
Q

myocardial infarction priorities VOMIT

A

vitals
oxygen
monitor
IV access
time to decision (when did this happen? clot busters if within a few hours)

123
Q

assessment of ACS

A

chest pain: sudden, SOB, C/O indigestion, nausea, anxiety, cool pale skin, increased HR and RR
ECG changes: ST elevation in 2 contiguous leads
lab studies: troponin, creatinine kinase (muscle damage), myoglobin, BNP

124
Q

collaborative problems with ACS

A

Acute pulmonary edema
HF
Cardiogenic shock
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade

125
Q

7 symptoms of MI in women

A

sweating (like stress sweat, not exercise)
SOB
fatigue
chest pain (not limited to left)
pain in arms, back, neck, or jaw (gradual or sudden)
nausea (flu-like, days before MI)
stomach pain (heartburn to severe abd pressure)

126
Q

5 risk factors women and heart

A

anemia
metabolic syndrome
sleep apnea
BC
preeclampsia

127
Q

nursing management ACS/MI

A

Oxygen and medication therapy
Frequent VS assessment
Physical rest in bed with head of bed elevated
Relief of pain helps decrease workload of heart
Monitor I&O and tissue perfusion
Frequent position changes to prevent respiratory complications
Report changes in patient’s condition
Evaluate interventions!

128
Q

4 invasive coronary artery surgeries

A

percutaneous transluminal coronary angioplasty (PTCA) (opening vessels and putting stent or CABG
coronary artery stent
coronary artery bypass graft (CABG)
cardiac surgery

129
Q

vasovagal response is an overstimulation of _______

A

parasympathetic nervous system (vagus nerve)

130
Q

3 types of bypass grafts

A

internal thoracic arteries
radial artery
saphenous veins

131
Q

internal thoracic artery bypass

A

under the left and right sides of the breast bone. They are not fully removed from their original position.
Least invasive and little scar, often collapse and stent is needed later

132
Q

radial artery bypass graft

A

Radial arteries are taken from the inner forearm. Long-term outcome is almost equivalent to that of the internal thoracic artery.
Good!

133
Q

saphenous vein bypass graft

A

taken from the leg (calf or thigh). Narrowing (stenosis) of the vein graft due to changes that are similar to those of a coronary artery is a major problem with saphenous vein grafts.
Great except for pt with diminished circulation, they are at risk for infection so watch donor and incision site

134
Q

10 potential complications from CABG

A

Bleeding during or after the surgery
Blood clots
Infection at incision site
Pneumonia
Breathing problems
Pancreatitis
Kidney failure
Abnormal heart rhythms
Failure of the graft
Death

135
Q

rheumatic endocarditis can be from what infection

A

unresolved strep-A

136
Q

adhesive vs malignant pericarditis

A

adhesive: forming scar tissue and sticking to other parts of the body
malignant: leads to more complicated problems

137
Q

causes of pericarditis

A

connective tissue disorders (SLE, arthritis, scleroderma)
hypersensitivity
disorders of adjacent structures
neoplastic (cancer)
trauma

138
Q

nursing management of pericarditis

A

pain management w analgesics
positioning
psych support
gradual increase of activity
enhance immune system
be alert for cardiac tamponade and HF

139
Q

nursing assessment of pericarditis

A

Substernal (underneath breast bone), precordial pain (in front of heart, hurts w deep breathing, coughing, and swallowing), can radiate to left neck, shoulder, and back
Increases with breathing, coughing, swallowing
Pericardial friction rub
Distinguish between acute and chronic restrictive pericarditis
Treatment depends on type

140
Q

acute pericarditis

A

elevated WBC
St-T wave elevation (looks like MI)
fever

141
Q

treatment for acute pericarditis

A

NSAIDS (GI effects, not for cardiac pts)
corticosteroids (glucose!)
abx (blood culture bc systemic)
rest

142
Q

chronic restrictive pericarditis

A

right sided HF
pericardial thickening on echo and CT
inverted or flat T wave
chronic afib

143
Q

chronic restrictive pericarditis treatment

A

Surgical excision of the pericardium (pericardiectomy or pericardial window)

144
Q

complications of pericarditis

A

Pericardial effusion
Cardiac tamponade
Failure to identify and treat can lead to death

145
Q

endocarditis

A

Can start with valve disease
Can become incompetent
Can happen as a result of many illnesses, including viral

146
Q

endocarditis treatment

A

Spironolactone can cause gynecomastia (large boobs) in men and women
Use eplerenone instead
Empagliflozin is best bc less hospital revisits

147
Q

class 1 HF

A

The patient does not display symptoms (fatigue or shortness of breath) with regular activity; no limitation of physical activity is needed

148
Q

class 2 HF

A

The patient may display some symptoms with activity but is comfortable when resting; slight limitation of physical activity is required.

149
Q

class 3 HF

A

The patient displays symptoms with minor activity but is comfortable when at rest; increased limitation of activity is required

150
Q

class 4 HF

A

The patient displays symptoms with any activity and also while at rest; severe limitation of activity is required

151
Q

Causes of sinus brady

A

in response to carotid sinus massage, valsalva maneuver, hypothermia, increased ICP, vagal stimulation, certain drugs (beta-adrenergic blockers, ca+ channel blockers)
Hypothyroidism, hypoglycemia, inferior MI

152
Q

ventricular heart rate classifications

A

sinus tachy: 100-160
160+: SVT
180+: beats no longer productive

153
Q

sinus tachy pharm causes

A

Drugs like epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine. albuterol, pseudoephedrine

154
Q

PAC ECG

A

distorted P waves
normal PR, QRS

155
Q

atrial rate with aflutter

A

200-350

156
Q

atrial rate in afib

A

350-600

157
Q

afib with a rapid or uncontrolled ventricular response

A

afib with ventricular rate above 100

158
Q

PVC

A

unifocal or multifocal
bigeminy
trigeminy
quadrigeminy

159
Q

vtach and PVCs

A

3+ PVCs means vtach

160
Q

insurance and hospital admission with HF

A

need an IV, diuretics, and echo (IN FIRST 2 DAYS OR ELSE INSURANCE DOESN’T COVER)
INSURANCE CAN CONTEST PAYING IF PT COMES BACK IN 30 DAYS

161
Q

right sided HF

A

Viscera (near abdominal area, ASCITES) and peripheral congestion
JVD
Dependent edema
Hepatomegaly
Weight gain

162
Q

left sided HF

A

Pulmonary congestion, crackles
S3 or ventricular gallop (happens with HTN, right after S2, S4 is right before S1)
Dyspnea on exertion (DOE)
Activity level before you feel out of breath, diet, how many pillows
Low O2 sat
Dry, nonproductive cough initially (Ace inhibitors, arbs taken instead)
Oliguria

163
Q

patho of SYSTOLIC HF

A

caused by:
-impaired contraction (like scar tissue from MI)
-increased afterload
-cardiomyopathy (hypertrophic and dilated)
-mechanical abnormalities
-DECREASED EF (<45%, 5-10%=transplant)

164
Q

patho of DIASTOLIC HF

A

can’t relax and fill causing decreased SV and CO
normal EF
result of left ventricular hypertrophy from HTN, MI, valve disease, or cardiomyopathy

165
Q

patho of MIXED HF

A

seen in disease states like cardiomyopathy
poor EF (<35%)
high pulmonary pressure
biventricular failure (both dilated and poor emptying/filling)

166
Q

patho of general HF

A

ventricular failure leads to:
-Low BP
-Low CO
-poor renal perfusion
abrupt or subtle
end of viral infection
compensatory (adrenal) mechanisms to maintain adequate CO

167
Q

5 compensatory mechanisms for HF

A

-SNS activation (epi and norepi, increases HR, myocardial contractility, peripheral vasoconstriction, helps then hurts)
-neurohormonal responses (kidneys release renin and initiate RAAS, pos pituitary releases ADH, endothelin released, proinflammatory cytokines (CRP, homocysteine like MI)
-ventricular remodeling (hypertrophy of ventricular myocytes, larger but less effective, can cause dysrhythmias and SCD (get implantable defib)
-dilation (enlargement of chambers when pressure in left ventricle is elevated, later inadequate and CO drops)
-hypertrophy (increases muscle mass and wall thickness, effective but then leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for ventricular dysrhythmias)

168
Q

pulmonary edema clini manifestations

A

Anxious, pale, cyanotic
Cool and clammy skin
Dyspnea
Orthopnea
Tachypnea
Use of accessory muscles
Cough with frothy, blood-tinged sputum (small capillaries in the lungs are breaking, red specks)
Crackles, wheezes, rhonchi
Tachycardia
Hypotension or hypertension

169
Q

chronic HF clini manifestations

A

depends on age, underlying type and extent of heart disease, and affected ventricle

170
Q

FACES clini manifestations chronic HF

A

Fatigue
Activity intolerance
Chest congestion/cough
Edema
Shortness of breath

also syncope

171
Q

anasarca

A

seen in chronic HF
entire body having a pitting edema, skin is weeping (fluid comes from pores of skin, soaking bed thru skin, end stage 🙁)
Pt can’t be comfy, given morphine

172
Q

acute decompensated HF

A

meds work and then suddenly don’t work
sudden weight gain 3lbs in 2 days
exacerbation of chronic HF

173
Q

chronic HF nursing assessment

A

frothy, blood tinged sputum, electrolytes, NT-proBNP or BNP
chest xray for displacement of the heart
echo

174
Q

HF complications

A

pleural effusion
dysrhythmias
left ventricular thrombus
hepatomegaly
renal failure (bad)

175
Q

meds for HF

A

-ACE inhibitors (vasodilation, diuresis, decreases afterload, monitor for hypotension, hyperkalemia, and altered renal function; COUGH
-angiotensin II receptors (alternative for ACE)
-hydralazine and isosorbide (alternative for ACE)
-BB (in addition to ACE, takes weeks to see effects, careful in asthmatic pts)
-diuretics (decreases fluid volume, watch electrolytes)
-digitalis (improves contractility, TOXIC ESP IF HYPOKALEMIC)
-IV meds (for hospitalized pts with ADHF [milrinone and dobutamine])

176
Q

milrinone

A

for ADHF
decreases pre/afterload
causes hypotension and increased risk for dysrhythmias

177
Q

dobutamine

A

for ADHF
used for pts with left ventricular dysfunction
increases contractility and renal perfusion

178
Q

what electrolyte to check for in chronic HF

A

potassium!

179
Q

gerontologic considerations HF

A

atypical signs like fatigue and somnolence
resistance to diuretics and more sensitive to volume changes
watch for bladder distention caused by enlarged prostate gland

180
Q

chronic HF management

A

oxygen therapy
rest
structured exercise program

181
Q

chronic HF nursing intervention

A

treatment plans and quality of life
restrict salt and water
conserve energy
maintain support systems

182
Q

chronic HF activity intolerance

A

bed rest for acute exacerbations
30-45 mins regular activity
2 hrs after eating for activity
avoid activities in hot and cold
elevate HOB and support arms

183
Q

pulmonary edema and LV failure

A

acute event results in LV failure
when LV fails, blood backs up in pulmonary circulation, causing pulmonary interstitial edema
hypoxemia!!

184
Q

manifestations of pulmonary edema

A

restlessness, anxiety, dyspnea, cool and clammy skin, cyanosis, weak and rapid pulse, cough, lung congestion (moist, noisy respirations), increased sputum production (sputum may be frothy and blood tinged), decreased LOC

185
Q

management of pulmonary edema

A

easier to prevent than treat
monitor lung sounds and signs of decreased activity tolerance and increased fluid retention
minimize exertion and stress
nonrebreather
diuretics and vasodilators

186
Q

nursing management of pulmonary edema

A

upright w legs dangling
fowler’s or semi
psychological support
I&O

187
Q

cardiogenic shock

A

decreased CO leads to inadequate tissue perfusion and initiation of shock syndrome

188
Q

cardiogenic shock clini manifestations

A

symprtoms of HF, shock state, and hypoxia

189
Q

cardiogenic shock treatment

A

reduce preload and afterload to decrease cardiac workload
improve oxygenation and restore perfusion
monitor hemodynamic parameters
fluid status, and adjust meds
diuretics, positive inotropic agents, and vasopressors
intra-aortic balloon pump does work for the heart (temporary)

190
Q

thromboembolism S&S

A

dyspnea, pleuritic chest pain, tachypnea, cough

191
Q

thromboembolism treatment

A

anticoag therapy
unfractionated heparin (low weight)
fondaparinux (arixtra) or rivaroxaban (xarelto)
FALL RISK!!!

192
Q

clini manifestations of pericardial effusion

A

ill-defined chest pain or fullness, pulsus paradoxus, engorged neck veins, labile or low BP, shortness of breath

193
Q

4 cardinal signs of cardiac tamponade

A

falling systolic BP, narrowing pulse pressure, rising venous pressure, distant heart sounds (bc behind fluid)

194
Q

medical management of pericardial effusion and cardiac tamponade

A

Pericardiocentesis: Puncture of the pericardial sac to aspirate pericardial fluid
Pericardiotomy: Under general anesthesia, a portion of the pericardium is excised to permit the exudative pericardial fluid to drain into the lymphatic system

195
Q

emergency management: cardiopulmonary resuscitation (ABCD of priority)

A

airway
breathing
circulation
defib for VT and VF

196
Q

cardiac transplantation

A

for pts with refractory end-stage HF, inoperable CAD, and cardiomyopathy
candidate goes under physical, diagnostic, and psychological eval
stable pts wait at home
unstable pts stay in hospital for intensive therapy

197
Q

steps of cardiac transplantation

A

retrieve heart
remove recipient heart except portions of atria and venous connections
implant donor heart

anticoags for rate control

198
Q

paroxysmal, persistent, long-standing persistent, and permanent afib

A

paroxysmal: terminates with no intervention within 7 dats
persistent: 7+ days
long-standing: 12+ months
permanent: persists beside all efforts, no further attempts made

199
Q

management of afib (8) mostly lifestyle

A

-obesity (BMI >30), reduce weight by 10%, 150 min mod exercise or 75 vigorous
-HTN (BP >140/90) reg physical activity 2-3 days/week
-obstructive sleep apnea (use CPAP)
-diabetes (reg testing, activity, quit smoking, nutrition)
-smoking (vasoconstriction and workload)
-alcohol (decreases effectiveness of meds, 2 drinks per day for men, 1.5 for women)
-caffeine (moderate!)
-surgery (monitor pain, electrolytes, stressors, may need BB)

200
Q

4 meds of choice to achieve target HR

A

target HR <110
-BB (rapid onset, better than digitalis, can be combined w amiodarone and digitalis, NOT FOR PTS WITH ACUTE HF OR BRONCHOSPASM)
-calcium channel blockers (verapamil, diltiazem, for COPD and asthma pts, HTN and HF with good EF)
-digitalis (lower dose or with BB and calcium channel)
-amiodarone (with BB and digoxin for reduced EF)

201
Q

when is rhythm control indicated with afib

A

when pt has persistent symptoms and poor quality of life

202
Q

how to assess for atrial thrombus

A

transesophageal echo
IF PRESENT, CARDIOVERSION CONTRAINDICATED

203
Q

electrical cardioversion (npo for how long and what 2 meds given)

A

patient NPO for 6 hours
pt sedated with midazolam and propofol

204
Q

pharmacologic cardioversion

A

antidysrhythmics (amiodarone, sotalol, flecainide) for pt with afib in past 7 days
monitor HR, BP, K+, 12-lead EKG for QT prolongation
contraindicated in digitalis toxicity, multifocal atrial tachy, and sub-optimal coag

205
Q

catheter ablation

A

catheter in femoral vein into heart releasing radiofrequency energy targeting pulmonary vein in left atrium to ablate abnormal current

206
Q

surgical ablation (maze proceure)

A

sternotomy or mini-thoracotomy to restore NSR by creating scar tissue w cryotherapy or radiofrequency. For pts with failed pharm or catheter ablation, or during mitral valve repair

207
Q

what med preferred in pts w mechanical heart valves and what to watch

A

warfarin
fequent INR
watch vitamin K

208
Q

anticoags for thromboembolism prevention

A

apixaban, dabigatran, edoxaban, and rivaroxaban
don’t require blood draws

209
Q

what to do if pt can’t tolerate long-term anticoags

A

left atrial appendage obliteration for CVA prevention bc this is where thrombi form

210
Q

complications of afib

A

risk of stroke, MI, and cognitive decline (from micro thrombi and hypoperfusion)
depression
KEEP PT AT CENTER OF CARE
education to adhere to plan and lifestyle mods

211
Q

palliative care

A

philosophy of and system for delivering care that expands on traditional medical care for serious, progressive illness to include a focus on quality of life, function, decision making, and opportunities for personal growth

212
Q

hospice and international considerations

A

a coordinated program of interdisciplinary care and services for terminally ill patients and their families that in the United States is provided primarily in the home

If person is not from the US, what is their perception of what should happen now?

213
Q

grief

A

feelings

214
Q

mourning

A

behaviors and expressions

215
Q

assisted suicide

A

DOCTORS ONLY NOT NURSES

216
Q

palliative vs hospice

A

All hospice care is palliative care; not all palliative care is hospice care
Palliative care can start the second the pt gets the diagnosis, hospice is once the pt has 6 months or less to live
Pts don’t have to stay in hospice!! They can come off it by choice or by medical reasons!

217
Q

eligibility for hospice

A

Serious, progressive illness
Limited life expectancy
Informed choice of palliative care over cure-focused treatment
-Teach back method used so you know pt understands

218
Q

last sense to disappear when dying

A

hearing

219
Q

vision at EOL

A

blurry
no blinking
half open eyes

220
Q

skin at EOL

A

waxy, looks wet

221
Q

HR at EOL

A

fast then slow and weak
move to IV and transdermal drugs

222
Q

how long does fentanyl patch last

A

72h

223
Q

bereavement

A

time which grief is experienced and mourning occurs

224
Q

dysfunctional grief

A

denial of loss for 6 months +

225
Q

can we euthanize and what is it

A

hastening of death on purpose and NO

226
Q

who decides to withhold nutrition and hydration

A

pts and healthcare team

227
Q

Rule for mcg/kg/min

A

Dose ordered x mL/mg x conversion factor x 60 min x kg = ml/hr

Med-Surg II (5 decks)

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