cardiac Flashcards
blood flow of heart
superior and inferior vena cava (deoxygenated)–R atrium–R ventricle–pulmonary artery–goes to lungs and becomes oxygenated–pulmonary veins (oxygenated now)– L atrium–L ventricle–aorta– body
preload
blood returning to the R side of the heart muscle stretch (strength) that the volume causes ANP released during stretch
increased preload = increased strength (workload)
afterload
pressure in aorta and PERIPHERAL arteries that the L ventricle has to pump against to get blood out
aka resistance
high afterload = low cardiac output and low forward flow
stroke volume
amount of blood pumped out of the ventricles with each beat
cardia output
HR x SV
tissue perfusion is dependent on adequate CO
CO changes according to body’s needs
factors that affect CO
HR
arrhythmia (brady and tachy)
blood volume (less volume = less CO) (more volume = more CO)
decreased contractility
meds that affect preload
vasodilator/diurese to decrease preload
diuretics (furosemide)
nitrates (nitroglycerin)
meds that affect afterload
vasodilator to decrease afterload
ACE inhibitors (enalapril) “pril”
ARBS (losartan) “sartan”
hydralazine
nitrates (nitroglycerin)
meds that improve contractility
inotropes (dopamine) “amine”
meds that control rate
beta blockers (propranolol) "olol" calcium channel blockers (diltiazem, verapamil, amlodipine) digoxin
meds that control rhythm
antiarrhythmics (amiodarone)
patho of low CO
will not perfuse properly LOC goes down chest pain crackles SOB cold and clammy urine output goes down weak peripheral pulses
arrhythmias that are always a big deal
pulseless vtach
vfib
asystole
coronary artery disease
broad term
chronic stable angina
acute coronary syndrome
chronic stable angina patho
intermittent decreased blood flow
ischemia so pain/pressure in chest
low O2 r/t exertion
rest or nitro to relieve pain/pressure
chronic stable angina treatment
nitroglycerin
beta blockers
calcium channel blockers
acetylsalicylic acid (aspirin)
nitroglycerin
causes venous and arterial dilation
decreased preload and afterload
dilation of coronary arteries which increases blood flow to the heart muscle (myocardium)
take 1 q 5min x 3doses
DONT SWALLOW keep in dark, glass bottle, dry, cool will get a headache renew every 6 months renew spray every 2 years
BP drops so make them sit when taking
beta blockers
prevention of angina
check BP and pulse before giving
“olol”
decrease BP, pulse, and myocardial contractility
decreases workload of heart
CO decreases
calcium channel blockers
prevention of angina
"pine" nifedipine verapamil amlodipine diltiazem
decrease BP
vasodilate arterial system
dilate coronary arteries
decrease afterload and increase O2 to the heart muscle
acetylsalicylic acid
aka aspirin
dose determined by provider
teaching for chronic stable angina
rest avoid overeating avoid excess caffeine avoid drugs that increase HR wait 2 hours after eating to exercise dress warm in cold weather nitro prophylactically smoking cessation weight loss isometric exercise reduce stress *****do everything you can to decrease the workload of the heart
cardiac catheterization
ask if they are allergic to iodine or shellfish
check kidney function because dye is excreted through the kidneys
hot shot (warm, flush, sweaty)
palpitations are normal
get baseline VS and 5Ps
after:
monitor VS
watch puncture site **for bleeding and hematoma formation
assess extremity distal to puncture site (5 Ps)
puleslessness
pallor
pain
paresthesia
paralysis
temp CRT
bedrest– flat, extremity straight x4-6hours
***major complication is bleeding/hemorrhage
report pain ASAP
hold metformin 48hours after
unstable chronic angina
impending MI
acute coronary syndrome patho
aka MI
aka unstable angina
decreased blood flow to myocardium– ischemia and necrosis
can happen at any time
rest and nitro do NOT relieve pain
acute coronary syndrome symptoms
pain (crushing)
pressure radiating to the L arm and L jaw
N/V
pain between shoulder blades
women: GI s/s epigastric discomfort pain between shoulders aching jaw or choking sensation unusual fatigue inability to catch a breath
****SOB is the number one sign for elderly cold, clammy BP drops CO down ECG changes vomiting
labs for troponin isomers
troponin T <0.10
troponin I <0.03
stemi vs nstemi
*****worry about stemi client
stemi:
ST segment elevation myocardial infarction
having a heart attack
get them to cath lab for PCI (percutaneous coronary intervention) in less than 90min
nstemi:
non-st segment elevation myocardial infarction
less worrisome
labs for acute coronary syndrome
CPK-MB
cardiac specific isoenzyme
high w/ damage to cardiac cells
elevates within 3-6hours and peaks in 12-24 hours
troponin:
cardiac biomarker w/ high specificity to myocardial damage
elevates within 3-4 hours and remains elevated for up to 3 weeks
myoglobin:
increases with 1 hour and peaks in 12 hours
negative results are a good thing
troponin is the most sensitive for an MI or delays seeking care
untreated arrhythmia that can kill
pulseless vtach
vfib
asystole
vfib
treatment:
defibrillate
epinephrine or vasopressor
amiodarone or lidocaine
lidocaine toxicity
neuro changes
amiodarone
anti-arrhythmic of choice
SE: hypotension
meds used for chest pain in ED
O2 if less than 90
aspirin (chewable)
nitro
morphine
Head up to decrease workload and increase CO
thromboyltics
used to dissolve a clot that is blocking blood flow to the heart muscle and decrease the size of the infarction
alteplase
tenecteplase
reteplase
streptokinase
should be given within 6-8 hours after onset of pain
**bleeding is a major complication
obtain bleeding hx
bleeding precautions during and after administration
draw blood when starting IVs to decrease pokes
do not do ABGs r/t high risk for bleeding
common meds that require bleeding precautions
abciximab acetaminophen acetylsalicyclic acid apixaban clopidogrel dabigatran enoxaparin sodium eptifibatide heparin rivaroxaban warfarin
PCI (percutaneous coronary intervention)
percutaneous transluminal coronary angioplasty
stents
angioplasty complication: MI
if any problems– surgery
chest pain after procedure– call provider r/t reoccluding
antiplatelet meds
acetylsalicylic acid clopidogrel prasugrel abciximab eptifibatide
coronary artery bypass graft
aka open heart surgery
used for multiple vessel disease or coronary artery occlusion
L main coronary artery supplies the entire L ventricle
**L main coronary artery occlusion– think sudden death or widow maker
cardiac rehab
smoking cessation stepped care plan (increase activity gradually) low fat low salt low cholesterol no isometric exercise no valsalva no straining no suppository sex resumed 7-10days safest time for sex is 8-9am walk teach s/s of HF (weight gain, ankle edema, SOB, confusion)
heart failure causes
complication from cardiomyopathy valvular heart disease endocarditis acute MI *****hypertension
left sided heart failure s/s
blood not moving forward into aorta and go back into lungs
pulmonary congestion dyspnea cough blood tinged frothy sputum restlessness s-3 orthopnea nocturnal dyspnea
R sided heart failure s/s
not moving into lungs
back into venous system
causes: normally a disease in lungs (PE, COPD)
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
heart failure diagnosis
BNP:
sensitive indicator
if on Nesiritide turn off for 2hr prior to drawing
secreted by ventricular tissues in the heart when ventricular volumes and pressures are increased
CXR:
enlarged heart
pulmonary infiltrates (fluid/edema)
echocardiogram:
looks at pumping action or ejection fraction of heart
New York Heart association functional classification of persons with HF: class 4 is the worse "can they complete activities of daily living test"
meds for HF
ace inhibitors: drug of choice suppress RAS prevent conversion of angiotensin 1 to 2 results in arterial dilation and high SV SE: dry, naggy cough
ARBs:
block angiotensin 2 receptors
cause low arterial resistance and low BP
beta blockers: first line therapy relax vessels decrease BP decrease afterload decrease workload of heart
ACE and ARBs both block aldosterone so we lose Na and H2O and retain K
most likely sent home on ace inhibitor and/or beta blocker because they decrease workload on the heart and prevent vasoconstriction to increase CO and keep blood going forward
digoxin
monitor for toxicity
sinus rhythm or afib and has accompanying chronic HF
makes contractions stronger
slows HR (gibes ventricles more time to fill with blood)
high CO
high kidney perfusion
good to diurese r/t HF pts cannot handle extra fluid
**HF pts should not get whole blood– only give what they need (RBCs, platelets)
diuretics: furosemide hydrochlorothiazide bumetanide spironolaction decreases preload give in AM
severe HF:
IV inotropes (milrinone, dobutamine)
vasodilators (nitroprusside, nesiritide, nitroglycerin)
digoxin nursing considerations
good to diuresis working when CO goes up s/s of toxicity: early-- anorexia, N/V late-- arrhythmias and vision changes (yellow halos)
check apical pulse (5th ICS mid clavicular line) before giving
monitor electrolytes (hypokalemia + dig = toxicity)
normal dig levels
0.5-2
toxicity if over 2
other treatment for heart failure
low Na diet:
decreases fluid retention and helps decrease preload
watch salt substitutes (contain excess K)
elevate HOB
daily weight (report 2-3lbs)
s/s of recurring failure
pacemaker
pacemaker
“natural” = SA node or sinus node
sends impulses to make heart contract
used to increase HR with symptomatic bradycardia
**always worry if HR drops below set rate
demand pacemaker sets in only when they need it
fixed rate fire at a fixed rate constantly
rate should never decrease–okay to increase
post procedure
monitor incision
common complication: electrode displacement
immobilize arm
assisted passive ROM to prevent frozen shoulder
don’t raise arm higher than shoulder
s/s of malfunction capture: no contraction follows stimulus sense: fires at inappropriate times may not be programmed right electrodes can dislodge battery may be dead watch for s/s of low CO or low HR
teaching: check pulse daily ID card/bracelet avoid electromagnetic fields avoid MRIs
pulmonary edema patho
risk factors:
IV fluid fast
young/old
hx of heart or kidney disease
fluid backing into the lungs
heart cannot move the volume forward
usually occurs at night during bed
pulmonary edema s/s
sudden onset breathless restless/anxious hypoxia productive cough
pulmonary edema treatment
O2– keep above 90
upright position
legs down
improves CO
promotes pooling in lower extremities
prevention:
lung sounds
avoid FVE
meds for pulmonary edema
diuretics:
furosemide
diuresis & vasodilate and traps more blood out in the arms and legs and reduces preload
nitroglycerin:
vasodilation
decrease afterload = increase CO because heart is pumping again less pressure and more blood moved forward
morphine
decrease preload and afterload
nesiritide
IV infusion
short term– no more than 48hours
vasodilates veins and arteries and has a diuretic effect
turn off infusion 2 hours before drawing BNP
cardiac tamponade patho
blood, fluid or exudates leak into pericardial sac results in compression of the heart
cardiac tamponade s/s
low CO (ventricle is being squeezed) *****high CVP *****low BP muffled or distant heart sounds distended neck veins pressure in all 4 chambers shock narrowed pulse pressure (difference between systolic and diastolic reading)
narrow vs wide pulse pressure
narrow: cardiac tamponade
wide: increased ICP
cardiac tamponade treatment
pericardioentesis to remove blood from the heart
surgery
arterial disorders patho
if you have atherosclerosis in one place you have it everywhere
medical emergency if occluded numbness and pain cold extremity no palpable pulse more symptomatic in lower extremities ****intermittent claudication (arteries only) arterial blood isn't getting to the tissue--> coldness, numbness, ***Decreased peripheral pulses, atrophy, bruit, skin/nail changes, and ulcerations pain at rest means severe obstruction
***artery issues = something is not getting O2
arterial disorder treatment
pain will increase if you elevate legs
angioplasty
endarterectomy
venous disorders
**arteries carry oxygenated blood
**veins carry deoxygenated blood
inflammation and chronic ulcers can occur
could develop a DVT
V: elevate veins
A: dangle arteries
chronic arteria insufficiency s/s
intermittent claudication pain (pain progresses at rest)
decrease or absent pulses
pale when elevated
red with lowering of leg
cool
mild or absent edema
thin, shiny, loss of hair over foot/toes, nail thickening
ulceration if present will involve toes or areas of trauma on feet (painful)
gangrene may develop
don’t use compressions
chronic venous insufficiency s/s
none to aching pain normal pulses (may be hard to palpate r/t edema) normal color (may see petechiae or brown pigmentation with chronic) normal temp edema brown pigmentation around ankles possible thickening of skin scarring ulceration if present on sides of ankles no gangrene compression
