cardiac Flashcards
preload
amount of blood returning to the right side of the heat and the muscle stretch that the volume causes
- ANP released upon stretch
afterload
pressure in the aorta and peripheral arteries that the left ventricle has to pump against to get blood out
- referred to as resistance
stroke volume
amount of blood pumped out of ventricles with each beat
factors that affect cardiac output x3
heart rate, certain arrhythmias
blood volume
contractility
decreased cardiac output: impact on brain
LOC down
decreased cardiac output: impact on heart
chest pain
decreased cardiac output: impact on lungs
short of breath, wet sounds
decreased cardiac output: impact on skin
cold and clammy
decreased cardiac output: impact on kidneys
uop down
decreased cardiac output: impact on peripheral pulses
weaker
LESS VOLUME LESS PRESSURE
arrhythmias are no big deal until
they impact your cardiac output
3 arrhythmias that are always a big deal
pulseless v tach
v fib
asystole
CPR ASAP
coronary artery disease includes x2
chronic stable angina
acute coronary syndrome
chronic stable angina
decreased blood flow to myocardium = ischemia = temporary pain/pressure in chest
what brings on pain of chronic stable angina?
low O2 usually due to exertion
what relieves pain of chronic stable angina?
rest and/or nitro
single largest killer of americans
coronary artery disease
chronic stable angina tx: meds
nitro
beta blockers
Ca channel blockers
aspirin
nitroglycerin (Nitrostat)
causes venous and arterial dilation resulting in decreased preload and afterload
- includes dilation of coronary arteries therefore increasing blood flow to myocardium
for chronic stable angina
beta blockers
block beta cells aka receptor sites for catecholamines = decrease BP, HR, contractility = decrease workload of the heart
for prevention of angina
Ca channel blockers
vasodilate arterial system (increase oxygen to heart) = decrease BP
- includes coronary arteries
decreased arterial resistance (afterload) = decreased workload of left ventricle
for prevention of angina
aspirin
for angina is for platelet aggregation, not pain
most common type of cardiovascular disease
cad
prior to cardiac catheterization
check for iodine, shellfish allergy
(iodine based dye used)
check kidney function
(renal excretion of dye)
normal responses to injection of cardiac cath dye
“hot shot”
palpitations
post heart cath, monitor
vitals, puncture site for bleeding or hematoma
post-heart cath assessment - where & what
assess extremity distal to puncture site p ulse p allor p ain p aresthesia p aralysis
post-heart cath bed rest - how & how long
flat, leg straight
4-6 hours
major complication post heart cath
bleeding
hold what medication post-heart cath, how long, why?
glucophage (Metformin) - renal excretion and dye = eye on kidney function
47 hours post procedure
associate unstable chronic angina with
impending MI
acute coronary syndrome
disorder including unstable angina and acute myocardial infarction - results from obstruction of coronary artery by ruptured atherosclerotic plaque
- plaque = platelet aggregation, thrombus formation, vasoconstriction
acute coronary syndrome: ischemia or necrosis?
BOTH
acute coronary syndrome: pain!
described as crushing
pressure radiating to left arm and left jaw
n/v
pain between shoulder blades
acute coronary syndrome: pain version xx
typically present with GI issues epigastric complaints pain between shoulders aching jaw choking sensation
what is the #1 sign of MI in the elderly?
SOB
acute coronary syndrome: s/s
pain cold, clammy, BP drops cardiac output going down EKG changes (heart irritated - PVCs, v tach) vomiting
STEMI
ST-Segment Elevation Myocardial Infarction: indicates the client is having a heart attack
goal: get to catch lab for PCI in under 90 minutes
NSTEMI
Non-Elevation ST Segment Myocardial Infarction: usually less worrisome
acute coronary syndrome: diagnostic lab work
CPK-MB
troponin
myoglobin
CPK-MB
cardiac specific isoenzyme that increases with damage to myocardium
elevates within 3-12 hours, peaks in 24 hours
diagnostic lab for acute coronary syndrome
troponin
cardiac biomarker with highest specificity to myocardial damage
elevates within 3-4 hours and remains elevated for up to 3 weeks
diagnostic lab for acute coronary syndrome
myoglobin
not very specific to myocardial damage: negative results are a good thing
increases within 1 hour and peaks in 12 hours
diagnostic lab for acute coronary syndrome
which cardiac biomarker is the most sensitive indicator for an MI?
tropnonin
which enzymes or markers are most helpful when the client delays seeking care?
troponin
what untreated arrhythmias will put the acute coronary syndrome client at risk for sudden death?
pulseless v tach
v fib
asystole
post-MI bradycardia
priority treatment for v fib?
defib the v fib!
no AED? CPR until one is available.
if first shock doesn’t work and client remains in v fib, what is the first vasopressor given?
epi
v fib and pulseless v tach: treatment then back up if resistant to treatment
treatment: epi, defibrillation
back up: amiodarone (anti-arrhythmic)
amiodarone (Cordarone)
anti-arrhythmic
- given when v fib and pulseless v tach not responsive to treatment
- also given for fast arrhythmias
what anti-arrhythmic drugs are continuously given to prevent a second episode of v fib?
amiodarone (first choice)
lidocaine (not really used as much but still on ACLS protocol)
lidocaine toxicity looks like
any neuro changes
important side effect of amiodarone
hypotension - can lead to further arrhythmias
ED treatment for chest pain in order of least to most invasive
oxygen
aspirin (chewable)
nitro
morphine (IV)
after MONA, patient with chest pain in head up position - why?
decreases workload on heart and increases cardiac output
fibrinolytics
use for acute coronary syndrome: dissolve clot blocking blood flow to heart muscle; this decreases the size of the infarction
the sooner the better - door to drug ideally 30 minutes or less
acute coronary syndrome: treatment
ED drugs (MONA) fibrinolytics (ASAP if cath unavailable) percutaneous coronary intervention (PCI) coronary artery bypass graft (CABG) cardiac rehab
how soon after onset of myocardial pain should fibrinolytics be administered?
within 6 to 8 hours
major complication of fibrinolytics
bleeding
absolute contraindications for fibrinolytic use
intracranial neoplasm
intracranial bleed
suspected aortic dissection
internal bleeding
massive hemmorhage could result!
fibrinolytic follow up therapy: class and examples
anti-platelet meds
- acetylsalicylic acid (aspirin)
- clopidogrel (Plavix)
- abciximab (ReoPro IV - continuous infusion to inhibit platelet aggregation)
percutaneous coronary intervention (PCI)
treatment for acute coronary syndrome
includes all interventions such as angioplasty and stents
major complication of angioplasty is
MI
but also important: client may bleed from heart cath site or reocclude
any problems: go to OR ASAP
eptifibatide (Integrilin IV)
abciximab (ReoPro IV)
in context of PCI, given why?
for high risk clients who have been stented to keep artery open
also for clients waiting to go to cath lab
coronary artery bypass graft
occluded coronary arteries bypassed with client’s own venous or arterial blood vessels
- saphenous vein, internal mammary artery, others
performed when client does not respond to medical management of coronary artery disease or when vessels are severely occluded
the widowmaker and why
left main coronary artery occlusion
left main coronary artery supplies the entire left ventricle
why teach acute coronary syndrome client about s/s heart failure (and what are they)
post unstable angina or AMI, heart is in weakened state so heart failure is always a potential
s/s: weight gain, ankle edema, shortness of breath, confusion
heart failure
complication that can result from problems such as cardiomyopathy, valvular heart disease, endocarditis, acute MI, and hypertension (leading cause)
left sided heart failure
looks very pulmonary in nature
blood not moving forward into aorta and out into body - it goes backwards into lungs
systolic vs diastolic
left sided heart failure: s/s
pulmonary congestion dyspnea, orthopnea, cough, blood tinged frothy sputum, nocturnal dyspnea restlessness tachycardia S3
right sided heart failure
blood is not moving forward into lungs - it moves backwards into the venous system
PS. cor pulmonale
right sided heart failure: s/s
distended neck veins edema enlarged organs weight gain ascites
systolic heart failure
heart can’t contract and eject
diastolic heart failure
ventricles can’t relax and fill
SBP / DBP mnemonic for heart failure
SBP = contraction = ejection = depolarize DBP = relaxation = filling = repolarize
cor pulmonale
abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels
heart failure: diagnostics
B-type natriuretic peptide
CXR (enlarged heart, pulm infiltrates)
Echocardiogram
New York Heart Association Functional Classification of Persons with HF
BNP
b-type natriuretic peptide; secreted by ventricles when ventricular volumes/pressures increased
pacemaker
increase heart rate with symptomatic bradycardia
depolarize myocardium = contraction
HR drops below 60, cardiac output…?
decreases
pacemakers: always worry if…?
HR drops below set rate
rate increase okay
most common post-op complication of pacemaker
electrode displacement
keep client from raising arm higher than shoulder height
before giving digoxin check
apical pulse
implantable cardiac device
can be used to pace
OR
defibrillate v-fib
pulmonary edema: at risk patients
- receiving IVF very fast
- very young, very old
- hx of kidney or heart disease
pulmonary edema
fluid backing up into lungs; usually occurs at night abruptly (bedtime)
pulmonary edema priority nursing intervention
administer high flow O2, titrate to keep above 90%
pulmonary edema tx
VASODILATION!!!
diuretics (furosemide, bumetanide)
nitro, morphine, nesiritide (Natrecore)
cardiac tamponade
blood, fluid, or exudates have leaked into pericardial sac resulting in compression of the heart (as little as 20-50mL!!)
causes: MVA, RV biopsy, MI, pericarditis, hemorrhage post CABG
cardiac tamponade: hallmark signs
increased CVP
decreased BP
an arterial problem is a ? problem
O2
if you have atherosclerosis in one place…
you have it EVERYWHERE
acute arterial occlusion
MEDICAL EMERGENCY!
numb, pain, cold, no pulse - intermittent claudication
pain at rest means SEVERE obstruction
intermittent claudication
hallmark sign of acute arterial occlusion - pain!!