Exam 1: Perfusion Flashcards
What is the normal conduction pathway? What are each point’s intrinsic rate?
begins at the sinoatrial node (60-100) in the right atrium then moves down to the atriventricular bundle (40-60) found in the septum and travels down the purkinje fibers (20-40)
What does the normal waveform waves, segments, and intervals indicate?
P: atrial contraction (depolarization)
Upright, constant, rounded
QRS: ventricular contraction (depolarization)
Atrial repolarization also occurs here but is masked
T: wave ventricular relaxation (repolarization)
Isoelectric line: return to baseline during waveform
PR interval is beginning of P wave to beginning of QRS: Important for blocks
QRS complex: begins at Q and ends when it goes back to isoelectric line: indicates how long it take for ventricle electrical activity
QT interval is beginning of QRS and ends where T returns to isoelectric line: If prolonged could lead to ventricular dysrhythmias
What are the steps for interpreting an EKG? What are the normal parameters? What does it indicate if it is outside the normal paramters?
Rate: count # of R waves in a six second strip
NSR=60-100
Regularity: measure distance between R to R
Assess for P waves
If upright and rounded = rhythm starts in SA node
Measure PR interval
Should be: 0.12-0.20
If greater than 0.2 think AV block
QRS duration
Should be: 0.06-0.12
If greater than 0.12 think of BBB
What is supraventricular tachycardia? Examples? Common causes?
narrow QRS complex with a rate >100
signal originates at or above AV node
atrial fibrillation
atrial flutter
HTN, DM, HF, ischemic heart disease, hyperthyroidism, moderate to heavy alcohol usage, heart valve disease, congenital heart disease, heart surgery
What is atrial fibrillation? What does the EKG look like? What are complications of it? Types?
electrical signal scrambled within the atria causing an atrial rate of 300-600bpm
no distinct p wave, wavy isoelectric line with irregular QRS complexes
blood pooling, blood clots, pulse deficit
controlled: rate<100bpm and usually well tolerated
uncontrolled: rate>100bpm, aka: rapid ventricular response, typically symptomatic and need intervention
What is atrial flutter? What does the EKG look like? What is the atrial and ventriclar rate?
ectopic foci sending irregular signals to atria causing them to circulate within the atria (causes the saw tooth pattern in EKG)
multiple p waves, QRS complexes are usually regular with saw tooth pattern between
atrial: 200-350
ventricular: 150
What are treatment for atrial fibrillation/flutter?
rate control: beta blockers, calcium channel blockers
anticoagulation: to reduce risk of stroke includes warfarin, non-vitamin k anticoagulants (apixaban, rivaroxaban)
synchronized cardioversion
radiofrequency ablation
What are heart blocks?
delay in conduction between AV node and ventricles
What are the EKG characteristics of first degree heart block? What are the symptoms?
PR interval is constantly greater than 0.20 with one P for every QRS (slow conduction but reach ventricles)
mild, typically no symptoms
What are the EKG characteristics of second degree heart block? What are the symptoms?
Type 1: Wenckebach - there are more P waves than QRS, PR interval gets longer until the QRS is dropped; benign that rarely causes hemodynamic instability but symptomatic patients will require a pacemaker (longer, longer, longer, drop, then you have a wenckebach)
Type 2: there are more P waves than QRS (no conduction to ventricles), PR interval is constant (if the PR stays normal and QRS quits then you have a type 2 mobitz)
What are the EKG characteristics of 3rd degree heart block? Cause?
there are more P waves than QRS complexes, PR interval is always changing (If P and QRS beat independently then it must be a complete third degree)
there are no electrical signals reaching the ventricles, THIS IS A LETHAL RHYTHM, the perfusing rhythm is maintained by junctional (QRS narrow 40-60bpm) or ventricular escape rhythm (QRS broad, 20-40bpm)
What are ventrical rhythms conduction sequence? Hallmark EKG characteristics? Examples?
abnormal ventricular depolarization and retrograde conduction through the system
wide, bizarre QRS complexes
ventricular tachycardia, ventricular fibrillation
What are the EKG characteristics for ventricular fibrillation? Treatment?
no P waves, no consistent QRS complexes, ventricular rate is accelerated at 150-250bpm
THIS IS A LETHAL RHYTHM
continue with CPR until defibrillator arrives
What are the EKG characteristics for ventricular tachycardia? Treatment?
no P waves, QRS complexes are wide and bizarre (may start with “runs” of 2 ro3 wide QRS periodically), ventricular rate is accelerated 150-200bpm
THIS IS A LETHAL RHYTHM
if w/ pulse and stable: synchronized cardioversion
if pulseless: early defibrillation
if good bp: IV adenosine
What are common medications used to treat dysrhythmias? What do they treat? MOA?Examples?
potassium channel blockers/class III anti arrhythmic: treats VT/VF Afib/SVT; inhibits adrenergic stimulation to prolong action potential and repolarization and decreases AV conduction and sinus node function; amiodarone, dofetilide
calcium channel blockers: Afib/flutter/SVT; inhibits extracellular calcium influx across membrane of myocardial cells and vascular smooth muscle resulting in inhibitory effects on cardiac conduction system and acts on AV and sinus node; diltiazem
adenosine: SVT; slows conduction through AV node and interrupts AV reentry pathways to restore normal sinus rhythm (chemical cardioversion) [pt needs to be educated on brief asystole, chest pain, tightness, and flushing]
beta blockers: Afib; decreases automaticity of SA node to reduce atrial and ventricular contractility
atropine: for symptomatic bradycardia; blocks effect of vagus nerve on heart [NOT effective for mobitz type 2 or third degree AVB or if pt has had a heart transplant]
What is cardiac resynchronization therapy? Indication? Examples?
sends signals to upper and lower chambers of heart to help beat in a more synchronized pattern
HF with LVEF<35%
pacemaker (CRT-P), defibrillator (CRT-D)
What are indications for a pacemaker?
bradycardia, AV block, MI, cardiomyopathy, HF
What will pacing look like on telemetry?
atrial pacing: spike before P wave
ventricle pacing: spike before QRS complex
What is failure to capture? What could cause this?
when a pacing stimulus is generated but fails to deliver to myocardial depolarization
could be d/t electrolyte imbalance?
What are indications for ICD?
ventricular tachyarrhythmias
What is acute coronary syndrome? What causes it? Types?
reduction of blood flow through the coronary arteries
primarily by artherosclerosis
unstable angina, NSTEMI,STEMI
What is myocardial ischemia?
inadequate oxygen supply to myocardium without damage to myocardial cells, will begin an ACS event
What is unstable angina? Cause?
chest pain that occurs at rest or with minimal exertion
myocardial ischemia without detectable infarction
What is the progression of ACS?
myocardial ischemia
unstable angina
myocardial injury
mocardial infarction: NSTEMI to STEMI
What is an NSTEMI? What does the EKG look like?
non-ST elevation myocardial infarction partial occlusion of coronary blood flow with positive cardiac markers
T-wave inversion and ST depression
What is a STEMI? What does the EKG look like?
complete occlusion of coronary blood flow causing damage and necrosis with positive cardiac
ST elevation
What are clinical manifestations of ACS?
pain: chest (substernal, epigastric), described as a heavy pressure, tightness, crushing feeling, lasting more than 20 minutes, may radiate to back, neck, jaw, arm
nausea, indigestion, fatigue (atypical in women, diabetics, geriatrics)
Hyper/hypotension
tachy/bradycardia
SOB
diaphoresis
What is troponin? Normal value?
protein found in myocardia that is released within 3 to 12 hours following damage to myocardia
<0.03
What is the primary diagnostic tool to diagnose ACS? What does it conclude?
EKG
the area of the heart is impacted by the blockage
What are the assessment changes indicating decreased CO?
cardiac: dysrhythmias, HR/rhythm, pulse, edema, angina/pressure
respiratory: crackles, increased respiratory effort
skin: cool, clammy, pale
general appearance: anxious, restless, distress
What are the goals of nursing interventions for ACS?
increase oxygen delivery: increase diastolic time, coronary vasodilation, O2, revascularize
decrease oxygen consumption: decrease HR (decrease SNS response), decrease pain
What is ticagrelor? What is an alternative?
PY2 inhibitor, inhibits platelet aggregation
plavix (clopidogrel)
What is ventral septal defect? Clinical manifestations?
hole between ventricles (may close naturally within 1st year of life) causing increased pulmonary blood flow
may be asymptomatic, may have failure to thrive, dysrhythmia, loud harsh murmur that starts 4-6wks of age
What is patent ductus arteriosis? Clinical manifestations?
ductus arteriosis does not close within first weeks of life causing blood flow from aorta to pulmonary artery and an increased pulmonary blood flow
murmur, enlargement of LV, wide pulse pressure, bounding pulse, tachypnea
What is indomethicin?
medication used to try and close patent ductus arteriosis
What can cyanosis cause?
high risk of endocarditis, arrhythmias
dizziness, fainting, seizures
delayed growth and development
What is tetralogy of fallot? clinical manifestations? What other disorders is this associated with?
4 anomalies: ventricular septal defect, overriding aorta (aortic valve sits over VSD and over septum taking mixed blood), pulmonary artery stenosis, RV hypertrophy
murmur, growth retardation, polycythemia (to increase oxygen carrying ability but can increase risk of clots), cyanosis
down’s and D. George syndrome
What are tet spells? What naturally happens with tet spells? When does it occur?
rapid drop of oxygenation in blood causing cyanosis, SOB, increased RR, fainting
child will squat to increase pressure and blood flow to lungs, infants will draw knees to chest
children: with activity
infants: crying or after feeding
What is rheumatic fever? Clinical manifestations?
delayed inflammatory disease occurring after infection of group A beta-hemolytic streptococcal pharyngitis (at risk 2 to 6 weeks after untreated strep throat)
effects joints, skin, brain, serous surfaces, and heart
cardiac: tachy, cardiomegaly, new murmur, pericardial friction rub, muffled heart sounds, angina, subcutaneous nodules (esp over joints), polyarthritis, rash, chorea (jerky mvts in shoulders, hip, face)
How can rheumatic disease effect the body long term?
rheumatic heart disease: damage to valves
What is kawasaki disease? Clinical manifestations per stage?
acute systemic vasculitis of an unknown cause
acute phase: high fever (min 5 days), red eyes (no drainage), red chapped lips, strawberry tongue, red palms and soles, joint pain, myocarditis, decreased LV function, pericardial effusion, mitral regurgitation
subacute phase (end of fever through end of clinical manifestations): peeling skin, irritability
convalescent phase (end of clinical manifestations to when lab values return to normal (6-8wks))
What are complications that can be seen during the subacute phase of kawasaki disease?
development of coronary artery dilation or aneurysm
What is an ischemic stroke? Types?
inadequate blood flow to part of brain due to a blockage of a blood vessel
thrombotic: blood clot forms in brain, the progression is slow
embolic: blood clot or debris travels to brain from body, onset is sudden and occurs during activity
What is hemorrhagic stroke? Types and their clinical manifestations?
bleeding into brain that results in death of brain cells
intracerebral: bleeding within brain tissue itself; worst headache of their life
subarachnoid: hemorrhage into subarachnoid space, sudden usually d/t head trauma; headache
What is a transient ischemic attack?
transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain
What are risk factors of stroke?
non modifiable: gender (men, but women die more), ethnicity/race (AA, hispanics, NA, Asian americans), genetics (screen if two first degree relatives w/ hx of subarachnoid hemorrhage), age (doubles each decade after 55yr, 2/3 of strokes are 65yr)
modifiable: HTN, heart disease, DM, smoking, obesity, drugs (cocaine), and alcohol
What are right sided brain damage symptoms?
left sided hemiplegia and/or neglect
spatial-perceptual defects
deny or minimize problems
rapid performance, short attention span
impulsive
impaired judgement
impaired time concept
What are left sided brain damage symptoms?
right sided hemiplegia and/or neglect
impaird speech (aphasias)
impaired right-left discrimination
slow performance, cautious
aware of deficits (causes depression, anxiety)
impaired comprehension related to language, math
visual field defect
What is tissue plasminogen activator? When do you give it? When is it contraindicated?
clot busting, digests fibrin
0-4.5 hrs from symptom onset of: ischemic stroke causing neuro deficits
hx of intracranial or subarachnoid hemorrhage
active internal bleeding
recent (w/in 3 mo) head trauma or potential for head bleed
excessive bleeding
current severe uncontrolled HTN >185/110
>80yo
severe stroke
hx of DM or stroke
taking anticoagulants
What are symptoms of pulmonary emboli?
may be nonspecific and transient
most common: dyspnea, angina, cough
hypoxemia, tachypnea, hemoptysis, crackles and/or wheezing, fever, loud pulmonic heart sound, tachycardia, syncope, sweating, leg pain or swelling
What is the treatment for Kawasaki’s disease?
high dose ASA and IV immunoglobulin G
