Exam 2 Cardiac Flashcards
mitral stenosis
narrowing of the mitral valve (left side of heart) reducing blood flow to the left ventricle
effects of mitral valve stenosis
reduced blood flow to left ventricle; reduced cardiac output; increased pressure in left atrium; left atrium hypertrophy and pulmonary congestion
mitral valve regurgitation
allows blood flow from the left ventricle back into the left atria; causes decrease in cardiac output and left ventricular hypertrophy as it tries to pump harder
aortic stenosis
narrowing of the aortic valve causing left ventricle hypertrophy
aortic regurgitation
blood travels back into the left ventricle from the aorta and causes reduced blood flow out through the aorta
pulmonary hypertension
can be caused by mitral stenosis
clinical manifestations of pulmonary hypertension
shortness of breath, fatigue, racing heart, decreased appetite, right abdominal pain
interventions for pulmonary hypertension
meds consist of sildenafil and veletri
mitral valve prolapse
part of one or both valve leaflets collapse back into the left atrium
clinical manifestations of mitral valve prolapse
palpitations, chest pain, fatigue, dizziness, shortness of breath
valvuloplasty
valve repair and reconstruction; minimally invasive procedure
types of valvular replacement
replacements done when unable to do valvuloplasty prosthetic consist of mechanical, biological, homograft
mechanical valve replacement
long term disability; risk for thrombi and emboli; risk for infection; requires life-long anticoagulation
biologic valve replacement
durability of <10 years
homograft valve replacement
comes from deceased human valve; limited availability
purpose of hemodynamic monitoring…
early detection, identification, and treatment of life threatening conditions such as HF or cardiac tamponade; used to evaluate pt immediate response to medications; used to evaluate cardiovascular function like cardiac index and output
arterial line
IV pressure catheter in an artery (radial or femoral); continuous BP monitoring; transducer has to be at phelbostatic axis (midaxillary line or 4th intercostal space)
indications for arterial line
intubation to monitor ABG and have lab access; shock; critical patients on vasopressor medications
central venous pressure
measures preload because it is influenced by venous return
indications for central venous pressure
assess the circulating blood volume and allows for a guide for fluid therapy; allows assess right ventricular function and venous blood return
central venous pressure limitations
does not always reflect true fluid volume; not a reliable indicator of left ventricular function or preload of the left side of heart
pulmonary artery catheter
measures the only artery that carries blood away from the heart and is deoxygenated; normal pressure is 30/15; travels in the superior vena cava and through the RA then RV then through pulmonary valve to artery; aka Swan ganz catheter
pulmonary wedge
when the pulmonary artery catheter is advanced and balloon is inflated; we then measure a wedge pressure which is the inadvertent pressure of the left side of heart; wedge pressure usually 12
commissures
repair of stenosed mitral valve; fused commissures are incised
assessment valvular disorders
decreased cardiac output and cerebral perfusion; syncope with exertion; pulmonary edema (crackles), dyspnea and tachypnea; tachycardia; chest pain
risks of valve replacement
bleeding, stroke, perforation, infective endocarditis
new meds after valve replacement
aspirin- antiplatelet; clopidogrel (plavix)- antiplatelet; warfarin (coumadin)- vitamin k antagonist; heparin- thrombin inactivater
central line
IV in large vein such as internal jugular vein, subclavian vein; catheter is advanced into cavoatrial junction; can provide continuous central venous pressure monitoring
angina
cardiac pain caused by imbalance of O2 demand and O2 supply; stble is predictable. unstable is preinfarction; prinzmetal is coronary artery spasm
stable angina
predictable; occurs with exertion
unstable angina
preinfarction state; occurs at rest and more frequently
prinzmetal/variant angina
pain at rest with reversible ST elevation
medications for angina
nitrates, beta blockers, calcium channel blockers, antiplatelet, oxygen, morphine
calcium channel blockers
S1 heart sound
tricuspid and mitral valves closing; “lub”; beginning of systole; ventricles are contracting; best heard at the apex
S2 heart sound
aortic and pulmonic valves are closing; beginning of diastole; “dub”; best auscultated at bases
S3 heart sound
heard just after S2; low pitched sound that is best heard with the bell; caused by rapid filling of ventricle likely due to HF
S4 heart sound
4th heart sound heard at end of diastole; low pitched that is best heard with the bell; produced during atrial contraction; caused by decreased ventricular compliance
electrical conduction through the heart
begins in SA node (primary) in right atrium which initiates atrial activation; then moves to AV node (backup) which causes atria depolarization and slows the impulse; then atrial contraction begins and traves to heart apex; then bundle of his and bundle branches (going down septum); then to purkinje fibers through the ventricular myocardium which then causes ventricular contraction
depolarization on 12 lead
negative to positive; moving from the top of the heart down to the apex; heart goes from negative at rest to positive as it depolarizes (creates positive deflection)
acute coronary syndrome
caused by blocked or decreased blood flow to the heart muscle angina-warning but no damage results; unstable warning occurs at rest; NSTEMI is a partial occlusion that is reversible; STEMI is a complete occlusion that is irreversible
signs and symptoms of acute coronary syndrome
chest pain is most common; arm shoulder jaw back or upper abdominal pain; other symptoms are SOB, cool clammy skin, nausea, lightheadedness, anxiety, indigestion
difference between STEMI and NSTEMI
STEMI shows EKG changes associated with the infarction whereas NSTEMI does not show EKG changes
management of acute coronary syndrome
morphine to decrease pain and cardiac workload by vasodilating; oxygen to increase PaO2 in blood and reach ischemic tissue; nitrates to dilate vessels; aspirin as an antiplatelet
why nitrates used during angina or acute coronary syndrome
vasodilation of veins and large arteries to increase O2; dilates coronary arteries; improves blood flow to heart muscle and decreases workload which decreases O2 demand; decreases preload and afterload; can admin up to 3 doses 5 min apart as long as BP is adequate
side effects of nitrate use
headache, dizziness, weakness, hypotension, flushing, pallor, increased perspiration, tachycardia, nausea
prior to administering nitrates… (contraindications)
hepatic/renal disease, hypotension, hypovolemia, increased cranial pressure, ED medication within past 24 hours
chest pain protocol
VS, height, weight, cardiac monitor; EKG and call cath lab; portable CXR; start 2 IVs and draw labs (troponin, glucose, INR, rainbow); undress shave pt, allens test; assess pain using OPQRST, PMH allergies and meds; drug or alcohol use, admin meds (NS, pain meds, zofran, pressors, atropine/amio, electrolytes)
cardiac catheterization
coronary angiography to view where occlusion is and open up; stent is placed
cardiac cath complications
bleeding, hemorrhage, hematoma, retroperitoneal bleed, thrombus/emboli, LOC changes, arrythmia, tamponade, MI, restenosis, reaction to dye used, infection, pulmonary edema, infection
coronary artery bypass graft (CABG)
can be schedule or be emergent; indications are angina not controlled by medication and data from cath lab
complications caused by pump during cardiac surgery
neuro-cognitive changes, ischemic hypo perfusion, micro-emboli, renal failure, renal hypo perfusion, arrhythmias, coagulopathy
indications for cardiac transplant
severe disease that would result in death in a year if untreated; cardiomyopathy; end stage cardiac disease
P wave
atrial contraction; depolarization;
PR segment
movement of electrical activity from atria to ventricles; isoelectric or flat line from P wave to q wave is electricity being held in AV node; from end of P wave to beginning of QRS
QRS complex
ventricle contraction; depolarization; positive deflection; 0.06-0.12s; from beginning of Q wave to end of S wave
ST segment
time between ventricular depolarization and repolarization; end of S wave to beginning of T wave
QT interval
from beginning of Q wave to end of T wave; start of ventricular contraction to repolarization; < 0.40s
T wave
ventricle relaxing (repolarizing)
TP interval
time from end of T wave to beginning of next P wave
measuring EKG strips
each strip is 6 seconds; each small box is 0.04s; each large box is 0.20s; 5 large boxes are 1.0s
interpreting EKG 8 step process
measure rate; examine R-R interval ad decipher if regular or irregular; examine P wave and identify if upright, constant, and one for every QRS; measure P-R interval to decide if prolonged; is the p followed by QRS complex; examine and measure QRS complex; measure QT interval; identify the rhythm
sinus bradycardia
rate of 60 or below; R-R interval is regular; P wave is regular, upright, and matches all QRS; P-R interval is 0.18-0.2; P preceds QRS; QRS complex is 0.08; QT interval is 0.40; Sinus bradycardia
treatment of sinus bradycardia
atropine 0.5mg and dopamine; pacemaker
Sinus tachycardia
rate 100-140; R-R interval is regular; P wave is regular upright and matching
treating cause of sinus tachycardia
fluids, O2, fever, pain, rest; treat with meds BB; antianxieties, antipyretics, CCB, BB, vagal stim, carotid artery massage, pain relief
Sinus rhythm
60-100; R-R interval is regular; P wave is upright and precedes each QRS
Atrial fibrillation
atrial rate is unable to be calculated; R-R interval is irregular; P wave is undistinguishable; PR interval cannot be calculated; cannot identify if a P wave precedes each QRS
concern with atrial fibrillation
loss of atrial kick and blood stasis; increased risk for blood clots; increased risk of hypotension; increased or decreased rate; decreased CO; need blood thinners for life
atrial fibrillation RVR
atrial fibrillation with a ventricular rate above 110
atrial fibrillation medications to convert
beta blockers, calcium channel blockers, digoxin all used to slow conduction from SA node to AV node; amiodarone not as commonly used; cardioversion
atrial flutter
one spot of atria is misfiring; can see sawtooth P wave with regular R-R interval; cannot distinguish P wave due to sawtooth; PR interval cannot be calculated
concerns with atrial flutter
loss of atrial kick; blood stasis; NOT as dangerous as Afib due to ore regularity
Supraventricular tachycardia
fast and skinny; cannot distinguish between P and T waves (p and t smushed together); R-R regular; cannot calculate PR interval; cannot distinguish if P wave precedes each QRS;
treatment of SVT
want to convert and slow; use vagal maneuver, meds to slow rates, cardioversion, adenosine
adenosine
1st line med used to convert SVT to sinus rhythm when vagal is ineffective; pushed rapidly over 1-2s; temporarily inhibits AV node conduction and blocks retry leading to reset HR
premature atrial contraction (PAC)
feels like a palpitation; temporarily lose cardiac output; Pr interval may be normal or prolonged with normal QRS
treatment of PAC
may not be treated if asymptomatic; reduce caffeine, alcohol, smoking; give beta blocking meds
treatment of atrial flutter
beta blocker, calcium channel blocker, cardioversion
ventricular tachycardia
can have a pulse or be pulseless; very wide QRS complex; unable to identify atrial rate; regular R-R interval; undistinguishable P wave; no P-R interval; no p wave preceding each QRS
treating Vtach with a pulse
oxygen, antiarrhythmics such as amiodarone, synchronized cardioversion
synchronized cardioversion
shock delivered in sync with QRS complex
treating unstable Vtach (pulseless)
CPR, follow ACLS protocol for defibrillation, intubation, drug therapy like epi, vaso, and amiodarone
ventricular fibrillation
no pulse present; complete loss of contraction; no atrial rate or ventricular rate; R-R interval is undeterminable; no P wave present; P-R interval is undistinguishable; no P wave before QRS
treating Vfib
CPR, then defibrillate, meds such as epi and amiodarone; no cardiac output present
asystole
complete cessation of electrical impulses in the heart; unconscious and pulseless
treating asystole
CPR and meds such as epi, bicarb; cannot shock due to no electrical activity present
Pulseless electrical activity (PEA)
electrical activity on EKG but no pulse is present
treatment of PEA
CPR, treat underlying causes, administer meds like epinephrine
etiology of PEA
H’s and T’s; hypovolemia, hypoxia, hydrogen ion (acidosis), hypo or hyperkalemia, hypoglycemia, toxins, tamponade, tension pneumo., thrombosis (coronary or pulmonary), trauma
premature ventricular contraction
3 in a row is considered vtach; can be completely normal; can be electrical or actual contraction but does not add to cardiac output; no p wave present before QRS
cardioversion
administration of electrical current synchronized with patients heart rhythm to treat SVT, AF, Aflutter, Vtach with pulse; beware of R on T phenomenon
R on T phenomenon
cardioverting on T wave instead of QRS which can cause lethal arrhythmia
nursing considerations for cardioversion
informed consent with pt timeout, sedation (propofol), ACLS equip., 12 lead to confirm rhythm, NPO, electrolyte in normal limits, pt connected to pads, TEE done prior to assess for clot, anticoagulated (INR > 2); successful 12 lead and gag reflex prior to transfer
defibrillation
used to treat vfib or vtach without a pulse; unsynchronized shock of 360 joules for example; CPR, pads applied, “all clear”, resume CPR after shock, assess for rhythm, admin epi
transcutaneous pacing
antidysrhythmic classes
- sodium channel blockers (lidocaine) to slow impulses in atria ventricles and bundle of his (used for ventricular arrhythmias; 2. beta blockers; 3. potassium channel blockers; 4. calcium channel blockers; 5. non classed drugs
class 2. beta blockers like metoprolol
used to treat SVT and PVCs; decreases HR, cardiac excitability, and cardiac output); slows conduction through AV node and prolongs AV node repolarization
side effects of beta blockers
hypotension, bradycardia, AV block, bronchospasm, dyspnea, loss of libido, decreased exercise tolerance
class 3. potassium channel blocker
first line management for vfib; prolongs electrical impulses in all heart cells; blocks potassium channels and slow outward movement of K during phase 3 of action potential and prolongs; example is amiodaronesi
side effects of potassium channel blockers
decreased HR, lung damage, visual impairment
class 4. calcium channel blockers
ex. verapamil and diltiazem; slows SA node automaticity, delays AV conduction, reduces myocardial contractility; block calcium ions across the cell membrane and depresses generation of action potentials
side effects of calcium channel blockers
decreased HR, AV block, HF, hypotension, constipation
digoxin
inotropic effect meaning squeezes harder; inhibits NA-K ATPase and calcium accumulates in myocytes, competes with K for binding sites; negative dromotropic effects; meaning it slows AV node impulses; negative chronotropic effects meaning beats slower
parameters of blood pressure
transcutaneous pacing
electrical shocks to increase HR if goes below certain amount; done via placing pads; temporary; sedate because pt will be getting shocks
