Care of the Cardiac Patient Flashcards
problems to right side of the heart lead to X2
generalized edema
decreased perfusion to the body
problems to left side of heart leads to
pulmonary congestion
decreased CO
preload
volume in ventricles at the end of diastole
afterload
resistance left ventricle must overcome to circulate blood
antidote to heparin
protamine sulfate
coumadin antidote
vitamin K
Acute Coronary Syndrome
condition characterized by decreased or blocked blood flow in the heart
3 categories of ACS
unstable angine
NSTEMI
STEMI
unstable angina
chest pain that will go away with treatment and does not cause necrosis
NSTEMI
causes necrosis
lab value changes
STEMI
causes necrosis
lab value changes
is NSTEMI or STEMI worse
STEMI
main objective with ACS
decrease O2 demand and increase O2 supply
first intervention with any cardiac problem
Apply Non-rebreather no matter what
decrease physical activity (wheelchair)
Ca Channel blockers in cardiac
reduces conduction and decreases HR
betablockers in cardiac
affect epi and adrenaline and decreases HR and contractility
Nitrates in cardaic
leaves less blood in ventricles and sends more out to the body
opioids in cardiac
causes coronary artery dilation to decrease workload
opioid of choice in cardiac patients
morphine
what is an MI
death or necrosis of myocardial cells caused by blockage
STEMI
100% blocked - emergent
cath lab immediately
what happens if STEMI is not promptly treated
total necrosis in 4-6 hours
generalized edema
akinesis
no pumping
NSTEMI
partial occlusion/narrowing
still need cath but have more time for imaging
when does hypoxia begin after O2 deprivation
10 seconds
goal for STEMI treatment time
cath lab within 90 minutes
Typical S/S of MI
CHEST PAIN/DISCOMFORT
Hyperglycemia
diaphoresis
tachycardia/pnea
S3/S4 heart sounds
Peripheral Vasoconstriction
SOB
AMS
how are MI Dx X6
elevated cardiac enzymes
elevated CK and CKMB levels
EKG
Stress test
ECHO
Angiogram
what shows early signs of ischemia
EKG
what shows late signs of ischemia
cardiac enzymes
how long does it take troponin to increase
5-7 hours
how soon does troponin return to baseline
10-14 days
baseline CK level
30-170
when does CK return to normal
24-36 hours following injury
why are there false positives for CK
non-specific - working out could falsely elevate it
when does CK begin to elevate
6 hours after injury - peaks at 18 hours
what does CK MB show
myocardial injury - not necessarily MI
when does CKMB elevate
within 2 hours - peaks at 3-15 hours
baseline CKMB
<90
when does CKMB return to normal
12-24 hours post-injury
Chest pain interventions X5
O2 BR Nitro X3 Labs Morphine
when should you hold nitro X2
if systolic <90 and if taken viagra that dayq
mediations for MI X5
nitrates beta blockers antiplatelet anticoagulants thrombolytic therapy
clopidogrel class
antiplatelet agent
HIT
body forms antibodies against heparin
when does HIT usually occur
5-10 days into treatment or <24 hours
when should you suspect HIT
Plt <150K or drop of 50% from baseline + heparin drip
normal Plt value
150-300K
PCI
percutaneous coronary intervention
what is a PCI
catheter is inserted into femoral artery and into heart, clot is sucked out and artery is opened up
allergy CI with PCI
shellfish
post-op risk with PCI
bleeding
how long are you on bedrest after PCI
24 horus
what happens if PCI fails
CABG
cardiogenic shock
inadequate tissue perfusion d/t cardiac dysfunction
cardiogenic shock tx
give them something to make heart pump
what tx should be avoided in cardiogenic shock
fluid infusion - avoid as much as possible
cardiogenic shock classic s/s X2
increased HR and decreased BP
amiodarone class
antidysrhythmics
how to treat hypotension in cardiogenic shock
norepi and dopamine
avoid beta blockers
how to treat fluid overload in cardiogenic shock
diuretics
vasodilators
new medications following MI X4
aspirin
nitro
clopidogrel
Lipitor
how long are you on bedrest post CABG
6 hours
what will you always have after a CABG
chest type
max chest tube drainage/hr
100 mL/hr
what happens if chest tube disconnects from setup
put one inch of tube in sterile water until new setup
aneurysm
artery wall weakens causing it to widen abnormally or balloon out
nonruptured AAA s/s X3
abdominal, back or flank pain
pulsating abdomen
pain or discoloratoin in feet
rupture AAA s/s X3
severe, untreatable pain
hypotension
pulsatile abdominal mass
what happens if an AAA is ruptured
straight to OR
2 surgeries for AAA
open repair
endovascular aneurysm repair (EVAR)
what happens in an EVAR
diseased part of aorta is replaced
AAA interventions
2 large bore IV’s
peripheral pulses
No X-RAY - only CT/contrast or MRI
biggest risk for AAA
hemorrhage and death
cardiac tamponade
pericardial effusion extends the sac beyond its limits
beck’s triad
hypotension
JVD
muffled heart sounds
cardiac tamponade tx
pericardiocentesis
