Exam 1 Flashcards
1
Q
are arteries in the heart deoxygenated or oxygenated?
A
deoxygenated (in the body they are usually oxygenated)
2
Q
are veins in the heart oxygenated or deoxygenated?
A
oxygenated (in the body they are usually deoxygenated
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)
4
Q
systole
A
contraction of myocardium
5
Q
diastole
A
relaxation of myocardium
6
Q
preload
A
volume of blood in the ventricle at the end of diastole (what’s already in there)
7
Q
afterload
A
peripheral resistance the left ventricle must pump against
8
Q
baroreceptors location
A
aortic arch, carotid sinus; sensitive to pressure
9
Q
formula for CO
A
CO = HR x SV
10
Q
formula for BP
A
BP = CO x systemic vascular resistance (SVR)
11
Q
pulse pressure
A
difference between SBP and DBP
12
Q
normal pulse pressure
A
approximately 1/3 of SBP ~ about 40-60
13
Q
mean arterial pressure (MAP)
A
the pressure/perfusion the organs actually feel
14
Q
normal MAP
A
greater than 60
15
Q
MAP formula
A
MAP = (SBP + 2DBP)/3
16
Q
postprandial hypotension
A
decrease 20 mm Hg within 75 minutes after eating
17
Q
triglycerides
A
main storage form of lipids
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)
19
Q
contributing risk factors to HF
A
- advanced age
- diabetes
- tobacco use (vasoconstrictor)
- obesity
- high serum cholesterol
20
Q
what can hypertrophy of the heart lead to?
A
overtime leads to poor contractility, increased O2 needs, and risk for dysrhythmias
21
Q
what is pulmonary edema?
A
- life-threatening situation (alveoli fill with fluid)
- most commonly associated with left-sided HF
22
Q
pulmonary edema treatment
A
LMNOP
Lasix
Morphine
Nitrates (NTG)
Oxygen
Position upright
23
Q
clinical manifestations of chronic HF
A
- fatigue
- dyspnea
- orthopnea
- paroxysmal nocturnal dyspnea
- tachycardia
- edema
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!
25
normal ejection fraction
greater than 50%
26
what position is best for a patient in HF?
high-fowlers
27
normal BNP (beta natriuretic peptide)
below 100
28
where does an impulse begin in the heart?
in the SA node
29
how does vagus nerve stimulation play a role in the heart?
works through the parasympathetic NS, vagus nerve stimulation decreases firing which decreases HR
30
what should come first in CAB?
compressions!
31
manifestations of sinus bradycardia
* think decreased CO
- hypotension
- pale, cool skin
- weakness
- angina
- dizziness or syncope
- confusion or disorientation
- SOB
32
atropine
takes HR up
33
adenosine
HR down
34
treatment of sinus bradycardia
- check O2 sat and correct as needed
- give atropine
- transcutaneous pacemaker
- stop offending drugs (digoxin, beta-blockers, ACE inhibitors)
35
treatment of sinus tachycardia
- 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)
36
SVT
originates above the ventricles but not from the sinus node
37
atrial fibrillation
chaotic atrial activity
38
atrial flutter
- more organized than a. fib.
- sawtooth pattern
39
what can SVT be associated with?
overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity
40
treatment of SVT
- vagal stimulation, carotid massage, coughing
- IV adenosine (pushed fast)
- IV beta-blockers
- calcium channel blockers
- amiodarone
- DC cardioversion (last resort)
- ablation (last resort)
41
most common dysrhythmia
atrial fib.
42
in a. fib. what does prevalence increase with?
age
43
what are you at an increased risk for with a. fib.
- stroke
- MONITOR FOR STROKE
- CALL STROKE ALERT or 911
44
treatment for a. fib.
- 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
45
what does a. flutter put you at risk for?
increased risk of stroke
46
treatment of a. flutter
- calcium channel or beta blockers
- electrical cardioversion
radiofrequency ablation
47
treatment of a third-degree AV block
pacemaker
48
what should you do for a third-degree AV block while waiting for a pacemake?
drugs to increase HR if needed
49
what does a PVC do?
interrupts regularity
50
with a PVC, what is important to assess?
apical-radial pulse deficit
51
why is v. tach. considered life threatening?
because of decreased CO and the possibility of deterioration to v. fib.
52
treatment for v. tach. with a pulse
- IV magnesium sulfate
- other antidysrhythmics
- cardioversion
53
treatment for v. tach. without a pulse
- CPR
- rapid defibrillation
54
what can v. fib. be associated with?
MI, ischemia, disease states, procedures
55
what does a patient look like who is in v. fib.?
unresponsive, pulseless, apneic
56
if v. fib. is not treated rapidly, what can happen?
death
57
treatment of v. fib.
immediate CPR, defibrillation, epinephrine, vasopressin
58
what can asystole be a result of?
advanced cardiac disease, severe conduction disturbance, or end-stage HF
59
treatment of asystole
immediate CPR, epinephrine, intubation (poor prognosis)
60
PEA
- patient has no pulse
- prognosis is poor unless underlying cause quickly identified and treated
61
Hs and Ts pneumonic
- hypovolemia hypoxia, hydrogen ion (acidosis), hyper-/hypokalemia, hypoglycemia, hypothermia
- toxins, tamponade (cardiac), thrombosis (MI and pulmonary), tension pneumothorax, trauma
62
treatment of PEA
CPR followed by intubation and IV epinephrine
63
when do we give CPR and epi.?
PEA and asystole
64
when do we defibrillate and CPR?
pulseless v. tach. or v. fib.
65
when would we do a cardioversion?
*less severe
a. fib., a. flutter., v. tach. with a pulse, SVT
66
when is defibrillation most effective?
when completed within 2 minutes of dysrhythmia onset
67
monophasic vs. biphasic defibrillation
- monophasic deliver energy in one direction
- biphasic deliver energy in two directions and uses lower energies
68
what kind of defibrillator is the better of the two?
biphasic (BETTER)
69
why is a biphasic defibrillator better?
- uses lower energies
- fewer postshock ECG abnormalities
70
synchronized cardioversion
- 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
if patient becomes pulseless during a cardioversion, what should you do?
turn sync button off and defibrillate
72
what would an inverted T wave mean?
ischemia, lack of O2
73
what would ST elevation mean?
zone of injury
74
what would abnormal Q mean?
zone of necrosis
75
major cause of CAD
atherosclerosis
76
what is considered a high cholesterol level that we can modify?
>200 mg/dL
77
what is considered high triglycerides that we can modify?
>150 mg/dL
78
other modifiable risk factors for CAD
- HTN
- tobacco use
- physical inactivity
- obesity
- diabetes
- metabolic syndrome-insulin resistance
- psychological stress
- substance abuse
79
clinical manifestations of angina pain
- pressure/ache
- squeezing, heavy, choking, or suffocating sensation
- rarely sharp or stabbing
- indigestion or burning
- various locations
80
what does chronic stable angina look like on an ECG?
ST segment depression and/or T-wave inversion (heart not getting O2)
81
goal of treating chronic stable angine
decrease O2 demand and/or increase O2 supply
82
how do short-acting nitrates work for the heart?
- 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
what other drugs help with chronic stable angina?
- ACE inhibitors
- beta-blockers
- calcium channel blockers
84
what kind of studies should be performed with chronic stable angina?
- chest x-ray
- cardiac biomarkers, lipids, CRP
- 12-lead ECG
- echocardiogram
- exercise stress test
- CT, angiography
85
what procedure is the GOLD STANDARD to localize CAD?
cardiac catheterization/coronary angiography
86
clinical manifestations of unstable angina
- new in onset
- occurs at rest
- worsening pattern
- increase in frequency
- unpredictable
- medical emergency
- symptoms in women may be more vague
87
if someone has an MI, how long until necrosis occurs?
necrosis of entire thickness of myocardium takes 4-6 hours
88
symptoms of MI
- 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
most common complication of an MI
dysrhythmias (occurs in 80% of MI patients
90
other complications of an MI
- HF
- cardiogenic shock
- acute pericarditis
91
what is the protocol when someone has ACS?
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
MONA acronym for treatment of MI
Morphine
Oxygen
Nitroglycerine
ASA
93
treatment of choice for confirmed MI
emergent PCI
94
what is the goal after someone has an MI to get them to the cath. lab?
90 minutes from door to cath. lab
95
when PCI isn't available what should you do?
- thrombolytic therapy
- stops infarction process by dissolving thrombus
- ideally within 30 minutes
- like tPa
96
after giving thrombolytic therapy for an MI, what do you want to watch for?
- monitor for signs of bleeding
- assess for signs of reperfusion (return of ST segment to baseline best marker)
- IV heparin to prevent reocclusion
97
what can PVCs lead to?
v. tach. which can lead to v. fib. which can lead to asystole
98
most common causative organism for infective endocarditis
bacteria ~ streptococcus viridans and staphylococcus aureus
99
what is it called when parts break off and enter circulation
embolism
100
what kind of lab tests do we want to get with infective endocarditis?
- blood culture
- CBC with differential
- ESR, CRP
101
how to treat infective endocarditis?
IV antibiotics (long-term, for 4-6 weeks) ~ teach importance of adherence to treatment regimen
102
how often will HF occur in patients who have infective endocarditis?
HF occurs in up to 80% of patients with aortic valve endocarditis and in approximately 50% of patients with mitral valve endocarditis
103
patient teaching with infective endocarditis
- need to avoid infectious people
- avoid stress and fatigue
- rest
- hygiene
- prophylactic antibiotics
- drug rehabilitation
- monitor body temperature
- S/S of complications
104
what virus is most commonly identified with acute pericarditis?
coxsackie
105
hallmark clinical manifestation of acute pericarditis
pericardial friction rub
106
treatment of acute pericarditis
- treat underlying cause
- antibiotics if bacteria
- NSAIDs (monitor bleeding and kidney function)
- pericardiocentesis if needed
- pericardial window if necessary
107
how do most patients recover from myocarditis?
most recover spontaneously but some may develop dilated cardiomyopathy
108
main cause of rheumatic heart
complication following group a strep infection
109
main treatment of rheumatic heart
steroids
110
classic symptom of PAD
intermittent claudication
111
intermittent claudication
- ischemic muscle pain that is cause by a constant level of exercise
- resolves within 10 minutes or less with rest
- reproducible
112
arterial manifestations of PAD
- 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
what can PAD lead to in worse cases?
nonhealing arterial ulcers and gangrene are most serious complications that may result in amputation
114
what is a risk factor modification for PAD concerning diabetes?
Glycosylated Hgb. <7.0%
115
what drugs do we give for PAD?
ACE inhibitors (ramipril)
- decreases CV morbidity
- decreases mortality
- increases peripheral blood flow
- increases ABI
- increases walking distance
antiplatelet agents: aspirin and clopidogrel (plavix)
116
drug alert concerning prilosec and clopidogrel
prilosec decreases clopidogrel in half so there is more of a risk for clots, strokes, DVT, etc.
117
most effective exercise for claudication
walking for 30-60 minutes daily, 3 times/week
118
what is a good IR procedure for PAD?
atherectomy: removal of the obstructing plaque
119
what is the most common surgical approach for PAD?
- 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
aortic aneurysm
outpouching or dilation of the arterial wall
121
what population is more prone to aortic aneurysms?
- men more than women
- incidence increases with age
122
thoracic aortic aneurysm most common manifestation
- often asymptomatic
- deep diffuse chest pain that may extend to the scapular area
123
clinical manifestations of ascending aorta/aortic arch aneurysm
- angina
- hoarseness
- if pressure is on SVC, decreased venous return so distended neck veins and edema of face and arms
124
if an AAA spontaneously embolizes a plaque, what can happen?
"blue toe syndrome": patchy mottling of feet/toes with presence of palpable pedal pulses
125
serious complication of aortic aneurysm
rupture
126
clinical manifestations of an aneurysm rupture
- severe back pain
- may/may not have back/flank ecchymosis
127
most accurate test to determine an aortic aneurysm
CT scan
128
if an aneurysm ruptures, what needs to happen?
emergent surgical intervention ~ 90% mortality with ruptured AAAs
129
indications of aortic aneurysm rupture
- diaphoresis
- pallor
- weakness
- tachycardia
- hypotension
- abdominal, back, groin, or periumbilical pain
- changes in LOC
- pulsating abdominal mass
130
what is an aortic dissection often misnamed?
dissecting aneurysm ~ it is not a type of aneurysm
131
clinical manifestations of aortic dissection
- 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
complications of aortic dissection
aorta may rupture leading to exsanguination and death
133
initial goal in an aortic dissection
- decrease BP and myocardial contractility to diminish pulsatile forces within aorta
- HR less than 60 and SBP less than 100-110
134
If a patient comes in with chest pain what do we do?
- EKG
- O2
- troponin lab
- ask what they were doing
- MONA: Morphine, oxygen, nitroglycerine, aspirin
- sit them up
135
atherosclerosis
plaque in the vessels
136
why would someone be on heparin?
prevents clots
137
why would someone be on tPA (thrombolytics)?
dissolves clots
138
what do we want to do in an MI, dissolve a clot or prevent clots?
dissolve them
139
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?
ST should go back to normal (shows perfusion)
140
patient has a stent what would you assess?
- bleeding
- pulses
141
if a patient has chest pain after a stent is placed what should you do?
CALL STROKE ALERT
142
patient teaching for aneurysm regarding meds
compliance with HTN meds and antianeurysm meds
143
what should we teach our PAD patient to stop doing
smoking
144
can nurses stop a beta-blockers order?
no not without an MD approval
145
important labs for kidney function
- creatinine
- >30 mL/hr
146
patient comes in with the "worst pain" of their life and abdominal tearing sensation in stomach, what do you think it is?
aortic rupture
147
after an abdominal aorta repair, the patient's food is white and there is no pulse, what should you do?
call MD
148
important labs with heparin?
clotting factor, PTT, INR
149
reversal of heparin
protamine sulfate
150
how does adenosine work in the heart?
it stops the heart and resets it
151
if after giving adenosine the heart doesn't reset and the patient goes into v. fib. what do you do?
defibrillate/CPR
152
if a patient has any arrhythmia, what do we assess?
patient's pulse and airway
153
normal potassium levels
3.5-5.0
154
important assessment with digoxin
assess apical HR for at least one minute, if HR is 45 BPM call provider
155
before giving nitroglycerin, what do you want to ensure about your patient's home meds?
if they are on viagra
156
rule for when the patient can return to sexual activity after heart problems
if they can climb two flights of stairs
157
what will you hear in HF?
S3 S4
158
what will you hear with pericarditis?
friction rub
159
what will you hear with cardiac tamponade?
muffled
