Exam 1 Flashcards

(231 cards)

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
nuclear cardiology 2 tests
MUGA stress perfusion imaging
22
CT angiography
calcium screening looks for HARD calcium not soft
23
right heart cath
pulmonary artery pressure, O2 sats, and myocardial tissue biopsy may be obtained
24
left heart cath
uses contrast agent unless kidney failure
25
bed rest after cardiac cath
2-6 hours
26
some blocked arteries, what procedure?
coronary artery bypass
27
major blockage, what procedure
stent
28
what to know about insertion site
lots of pressure can leak under skin and form hematoma (pt c/o pressure) check pulse below insertion site
29
hemodynamic monitoring
central venous pressure pulmonary artery pressure intra-arterial BP monitoring minimally invasive CO monitoring devices
30
5 factors of normal sinus rhythm
regular 60-100 BPM P waves normal and precede QRS complex PR 0.12-0.20 QRS <0.12
31
sinus tachy
100-160 BPM
32
sinus arrythmia
irregular rate normal or brady associated w respirations, NORMAL! tell pt to relax
33
premature atrial contractions causes and where is the focus
alcohol, drugs, stress SA node
34
atrial flutter
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
35
afib
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
36
3 vfib causes
accident, drowning, electrocution
37
blood pathway (right side)
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.
38
blood pathway (left)
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.
39
tertiary pacemaker of heart
his-purkinje fibers (20-40)
40
lead 1
right side, 5th intercostal space
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lead 2
left sternum, 4th intercostal space
42
lead 4
midclavicular, 5th intercostal space
43
costochondritis
mimics pain of MI, inflammation of cartilage that joins ribs to sternum
44
what 3 things can mimic cardiac disease
GERD hiatal hernia pregnancy
45
PR interval
time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
46
QT interval
duration of ventricular depolarization and repolarization
47
manifestations of sinus brady (7)
Hypotension Pale, cool skin Weakness Angina Dizziness or syncope Confusion or disorientation SOB Can be normal during sleep!
48
sinus tachy caused by vagal __________ or sympathetic ________
INHIBITION!!! STIMULATION!!! valsalva maneuver (bearing down) stimulates vagus nerve, fixes sinus tach
49
4 manifestations of sinus tachy
dizziness (not getting enough oxygenated blood whether brady or tachy) dyspnea hypotension angina in pts with CAD
50
PAC
-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
51
8 causes of PAC
Stress Fatigue Caffeine Tobacco Alcohol (depletes electrolytes) Hypoxia Electrolyte imbalance Disease states
52
2 manifestations of PAC
palpitations heart skips a beat
53
3 treatments for PAC
monitor for more serious dysrhythmias withhold sources of stimulation beta blockers
54
aflutter
associated with disease symptoms from high ventricular rate and loss of atrial "kick" (decreased CO --> risk of HF) increases risk of CVA
55
3 treatments for aflutter
-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)
56
afib
paroxysmal or persistent most common in people over 65 in pts with underlying heart dx can occur in other disease states
57
5 treatments for afib
-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
58
PSVT causes
Overexertion stress deep inspiration stimulants disease digitalis toxicity (N/V, loss of appetite)
59
digoxin toxicity
N/V, loss of appetite
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reentrant phenomenon
PAC triggers a run of repeated premature beats
61
manifestations of PSVT
HR 150-220 HR >180 leads to decreased CO and SV hypotension dyspnea angina
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6 treatments for PSVT
Vagal stimulation IV adenosine IV beta blockers Calcium channel blockers Amiodarone DC cardioversion
63
vtach
-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
64
vtach- torsades de pointes associated with what
Associated with heart disease, electrolyte imbalances, drugs, CNS disorder (GBS, parkinsons, spinal cord injury)
65
manifestations of vtach
Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest
66
treatment for STABLE vtach
antidysrhythmics or cardioversion
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treatment for UNSTABLE vtach
CPR and rapid defibrillation
68
vfib associated with?
MI, ischemia, disease states, procedures unresponsive, pulseless, and apneic
69
vfib treatment
CPR and ACLS (defibrillation and drug therapy including epinephrine, vasopressin [-pressors bring BP up], anything to restore blood flow
70
asystole is a result of what
advanced cardiac disease, severe conduction disturbance, or end-stage HF
71
treatment for asystole
immediate CPR and ACLS measures Epinephrine and/or vasopressin Intubation
72
PEA
weak electrical activity shown in ECG, no pulse NONSHOCKABLE
73
6 Hs of PEA
HYPOvolemia HYPOxia Hydrogen ion (acidosis) HYPER/HYPOkalemia HYPOglycemia HYPOthermia
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5 Ts of PEA
Toxins Tamponade Thrombosis (MI and pulmonary) Tension pneumothorax trauma
75
treatment of PEA
CPR followed by intubation and IV epinephrine Correct the underlying cause
76
SCD (sudden cardiac death)
death from cardiac cause majority from ventricular dysrhythmias (vtach and vfib) prolonged QT
77
defibrillation
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
78
monophasic and biphasic defibrillators
mono: deliver energy in one direction bi: 2 directions, lower energies, fewer post-shock abnormalities
79
recommended energy for initial shocks in defibrillation
bi: 120-200 joules mono: 360 START CPR AFTER FIRST SHOCK
80
8 steps to defibrillation
-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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steps to synchronized cardioversion and initial energies
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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synchronized cardioversion rhythms
VT with a pulse or supraventricular tachydysrhythmias
83
how does synchronized cardioversion work
delivers a countershock on the R wave of the QRS complex of the ECG
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ICDs (who are they for and how do they work)
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
85
pre and postop care for ICDs
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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pt teaching for ICD
-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
87
pacing circuit consists of
-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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3 temporary pacemakers
outside of the body: transvenous epicardial transcutaneous
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epicardial pacing
-leads placed on epicardium during heart surgery -passed through chest wall and attached to external power source
90
transcutaneous pacing
-For emergent pacing needs -Noninvasive -Bridge until transvenous pacer can be inserted -Use lowest current that will “capture” -Pt may need analgesia/sedation
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fail to sense and capture in pacemaker
fail to sense causes inappropriate firing failure to capture causes lack of pacing when needed (leading to brady or asystole)
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5 complications of pacemaker placement
infection hematoma pneumothorax atrial or ventricular septum perforation lead misplacement
93
postop care for pacemaker
OOB once stable limit arm and shoulder activity monitor insertion site
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pacemaker pt teaching
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
ECG changes with ACS
ischemia -ST depression (1 mm below isoelectric line) or T wave inversion -changes reverse once adequate blood flow is restored
96
injury (cell death) in ECG
ST elevation (1 mm above isoelectric) QUICK treatment to prevent infarction absence of serum markers shows no infarction
97
infarction in ECG
pathologic Q wave (deep and >0.03 seconds in duration)
98
5 noncardiovascular causes for syncope
Stress Hypoglycemia Dehydration Stroke Seizure
99
5 cardiovascular causes for syncope
Cardiogenic or “vasovagal” syncope (Carotid sinus sensitivity) Dysrhythmias (tachy/brady) Prosthetic valve malfunction Pulmonary emboli HF
100
4 diagnostic tests for syncope
Echocardiography Stress test EPS (internal rhythm of heart) Head-up, tilt test
101
C-reactive protein
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
manifestations of CAD
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
risk factors for CAD
cholesterol abnormalities, tobacco use, HTN, and diabetes** LDLs are primary target in meds framingham risk calculator metabolic syndrome hs-CRP (high sensitivity CRP)
104
6 lipid lowering agents
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
Gerontologic considerations for CAD
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
treatment for CAD
decrease oxygen demand and increase supply
107
meds for CAD
-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
Angina pectoris
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
intractable or refractory angina
severe incapacitating pain
110
variant (prinzmetal's) angina
pain at rest w reversible ST elevation, caused by coronary artery vasospasm
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assessment of angina
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
NTG and angina
Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. requires medical intervention!
113
7 collaborative problems of angina
ACS MI both of the above dysrhythmias cardiac arrest HF cardiogenic shock (collapse of CV system, BP plummets, pulse pressure widens)
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nursing priorities for treating angina
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
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pt teaching for angina
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
treatment for stable angina
medication and interventional treatment (procedures to open or bypass narrowed coronary arteries)
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3 forms of ACS
unstable angina STEMI NSTEMI
118
unstable angina diagnostics
manifestations of coronary ischemia, ECG & biomarkers show no evidence of acute MI
119
STEMI diagnostics
ECG evidence of acute MI, characteristic changes in two contiguous leads on a 12-lead ECG. There is significant damage to the myocardium
120
NSTEMI diagnostics
Elevated cardiac biomarkers (e.g., troponin, no definite ECG evidence of acute MI. There may be less damage to the myocardium
121
myocardial infarction treatment MONA
morphine oxygen nitrates aspirin
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myocardial infarction priorities VOMIT
vitals oxygen monitor IV access time to decision (when did this happen? clot busters if within a few hours)
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assessment of ACS
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
collaborative problems with ACS
Acute pulmonary edema HF Cardiogenic shock Dysrhythmias and cardiac arrest Pericardial effusion and cardiac tamponade
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7 symptoms of MI in women
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
5 risk factors women and heart
anemia metabolic syndrome sleep apnea BC preeclampsia
127
nursing management ACS/MI
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
4 invasive coronary artery surgeries
percutaneous transluminal coronary angioplasty (PTCA) (opening vessels and putting stent or CABG coronary artery stent coronary artery bypass graft (CABG) cardiac surgery
129
vasovagal response is an overstimulation of _______
parasympathetic nervous system (vagus nerve)
130
3 types of bypass grafts
internal thoracic arteries radial artery saphenous veins
131
internal thoracic artery bypass
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
radial artery bypass graft
Radial arteries are taken from the inner forearm. Long-term outcome is almost equivalent to that of the internal thoracic artery. Good!
133
saphenous vein bypass graft
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
10 potential complications from CABG
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
rheumatic endocarditis can be from what infection
unresolved strep-A
136
adhesive vs malignant pericarditis
adhesive: forming scar tissue and sticking to other parts of the body malignant: leads to more complicated problems
137
causes of pericarditis
connective tissue disorders (SLE, arthritis, scleroderma) hypersensitivity disorders of adjacent structures neoplastic (cancer) trauma
138
nursing management of pericarditis
pain management w analgesics positioning psych support gradual increase of activity enhance immune system be alert for cardiac tamponade and HF
139
nursing assessment of pericarditis
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
acute pericarditis
elevated WBC St-T wave elevation (looks like MI) fever
141
treatment for acute pericarditis
NSAIDS (GI effects, not for cardiac pts) corticosteroids (glucose!) abx (blood culture bc systemic) rest
142
chronic restrictive pericarditis
right sided HF pericardial thickening on echo and CT inverted or flat T wave chronic afib
143
chronic restrictive pericarditis treatment
Surgical excision of the pericardium (pericardiectomy or pericardial window)
144
complications of pericarditis
Pericardial effusion Cardiac tamponade Failure to identify and treat can lead to death
145
endocarditis
Can start with valve disease Can become incompetent Can happen as a result of many illnesses, including viral
146
endocarditis treatment
Spironolactone can cause gynecomastia (large boobs) in men and women Use eplerenone instead Empagliflozin is best bc less hospital revisits
147
class 1 HF
The patient does not display symptoms (fatigue or shortness of breath) with regular activity; no limitation of physical activity is needed
148
class 2 HF
The patient may display some symptoms with activity but is comfortable when resting; slight limitation of physical activity is required.
149
class 3 HF
The patient displays symptoms with minor activity but is comfortable when at rest; increased limitation of activity is required
150
class 4 HF
The patient displays symptoms with any activity and also while at rest; severe limitation of activity is required
151
Causes of sinus brady
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
ventricular heart rate classifications
sinus tachy: 100-160 160+: SVT 180+: beats no longer productive
153
sinus tachy pharm causes
Drugs like epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine. albuterol, pseudoephedrine
154
PAC ECG
distorted P waves normal PR, QRS
155
atrial rate with aflutter
200-350
156
atrial rate in afib
350-600
157
afib with a rapid or uncontrolled ventricular response
afib with ventricular rate above 100
158
PVC
unifocal or multifocal bigeminy trigeminy quadrigeminy
159
vtach and PVCs
3+ PVCs means vtach
160
insurance and hospital admission with HF
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
right sided HF
Viscera (near abdominal area, ASCITES) and peripheral congestion JVD Dependent edema Hepatomegaly Weight gain
162
left sided HF
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
patho of SYSTOLIC HF
caused by: -impaired contraction (like scar tissue from MI) -increased afterload -cardiomyopathy (hypertrophic and dilated) -mechanical abnormalities -DECREASED EF (<45%, 5-10%=transplant)
164
patho of DIASTOLIC HF
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
patho of MIXED HF
seen in disease states like cardiomyopathy poor EF (<35%) high pulmonary pressure biventricular failure (both dilated and poor emptying/filling)
166
patho of general HF
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
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5 compensatory mechanisms for HF
-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
pulmonary edema clini manifestations
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
chronic HF clini manifestations
depends on age, underlying type and extent of heart disease, and affected ventricle
170
FACES clini manifestations chronic HF
Fatigue Activity intolerance Chest congestion/cough Edema Shortness of breath also syncope
171
anasarca
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
acute decompensated HF
meds work and then suddenly don't work sudden weight gain 3lbs in 2 days exacerbation of chronic HF
173
chronic HF nursing assessment
frothy, blood tinged sputum, electrolytes, NT-proBNP or BNP chest xray for displacement of the heart echo
174
HF complications
pleural effusion dysrhythmias left ventricular thrombus hepatomegaly renal failure (bad)
175
meds for HF
-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])
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milrinone
for ADHF decreases pre/afterload causes hypotension and increased risk for dysrhythmias
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dobutamine
for ADHF used for pts with left ventricular dysfunction increases contractility and renal perfusion
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what electrolyte to check for in chronic HF
potassium!
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gerontologic considerations HF
atypical signs like fatigue and somnolence resistance to diuretics and more sensitive to volume changes watch for bladder distention caused by enlarged prostate gland
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chronic HF management
oxygen therapy rest structured exercise program
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chronic HF nursing intervention
treatment plans and quality of life restrict salt and water conserve energy maintain support systems
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chronic HF activity intolerance
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
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pulmonary edema and LV failure
acute event results in LV failure when LV fails, blood backs up in pulmonary circulation, causing pulmonary interstitial edema hypoxemia!!
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manifestations of pulmonary edema
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
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management of pulmonary edema
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
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nursing management of pulmonary edema
upright w legs dangling fowler's or semi psychological support I&O
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cardiogenic shock
decreased CO leads to inadequate tissue perfusion and initiation of shock syndrome
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cardiogenic shock clini manifestations
symprtoms of HF, shock state, and hypoxia
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cardiogenic shock treatment
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)
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thromboembolism S&S
dyspnea, pleuritic chest pain, tachypnea, cough
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thromboembolism treatment
anticoag therapy unfractionated heparin (low weight) fondaparinux (arixtra) or rivaroxaban (xarelto) FALL RISK!!!
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clini manifestations of pericardial effusion
ill-defined chest pain or fullness, pulsus paradoxus, engorged neck veins, labile or low BP, shortness of breath
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4 cardinal signs of cardiac tamponade
falling systolic BP, narrowing pulse pressure, rising venous pressure, distant heart sounds (bc behind fluid)
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medical management of pericardial effusion and cardiac tamponade
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
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emergency management: cardiopulmonary resuscitation (ABCD of priority)
airway breathing circulation defib for VT and VF
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cardiac transplantation
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
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steps of cardiac transplantation
retrieve heart remove recipient heart except portions of atria and venous connections implant donor heart anticoags for rate control
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paroxysmal, persistent, long-standing persistent, and permanent afib
paroxysmal: terminates with no intervention within 7 dats persistent: 7+ days long-standing: 12+ months permanent: persists beside all efforts, no further attempts made
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management of afib (8) mostly lifestyle
-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)
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4 meds of choice to achieve target HR
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)
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when is rhythm control indicated with afib
when pt has persistent symptoms and poor quality of life
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how to assess for atrial thrombus
transesophageal echo IF PRESENT, CARDIOVERSION CONTRAINDICATED
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electrical cardioversion (npo for how long and what 2 meds given)
patient NPO for 6 hours pt sedated with midazolam and propofol
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pharmacologic cardioversion
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
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catheter ablation
catheter in femoral vein into heart releasing radiofrequency energy targeting pulmonary vein in left atrium to ablate abnormal current
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surgical ablation (maze proceure)
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
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what med preferred in pts w mechanical heart valves and what to watch
warfarin fequent INR watch vitamin K
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anticoags for thromboembolism prevention
apixaban, dabigatran, edoxaban, and rivaroxaban don't require blood draws
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what to do if pt can't tolerate long-term anticoags
left atrial appendage obliteration for CVA prevention bc this is where thrombi form
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complications of afib
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
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palliative care
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
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hospice and international considerations
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?
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grief
feelings
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mourning
behaviors and expressions
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assisted suicide
DOCTORS ONLY NOT NURSES
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palliative vs hospice
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!
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eligibility for hospice
Serious, progressive illness Limited life expectancy Informed choice of palliative care over cure-focused treatment -Teach back method used so you know pt understands
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last sense to disappear when dying
hearing
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vision at EOL
blurry no blinking half open eyes
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skin at EOL
waxy, looks wet
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HR at EOL
fast then slow and weak move to IV and transdermal drugs
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how long does fentanyl patch last
72h
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bereavement
time which grief is experienced and mourning occurs
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dysfunctional grief
denial of loss for 6 months +
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can we euthanize and what is it
hastening of death on purpose and NO
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who decides to withhold nutrition and hydration
pts and healthcare team
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Rule for mcg/kg/min
Dose ordered x mL/mg x conversion factor x 60 min x kg = ml/hr