Exam 1: Perfusion Flashcards

1
Q

What is the normal conduction pathway? What are each point’s intrinsic rate?

A

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)

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2
Q

What does the normal waveform waves, segments, and intervals indicate?

A

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

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3
Q

What are the steps for interpreting an EKG? What are the normal parameters? What does it indicate if it is outside the normal paramters?

A

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

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4
Q

What is supraventricular tachycardia? Examples? Common causes?

A

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

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5
Q

What is atrial fibrillation? What does the EKG look like? What are complications of it? Types?

A

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

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6
Q

What is atrial flutter? What does the EKG look like? What is the atrial and ventriclar rate?

A

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

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7
Q

What are treatment for atrial fibrillation/flutter?

A

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

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8
Q

What are heart blocks?

A

delay in conduction between AV node and ventricles

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9
Q

What are the EKG characteristics of first degree heart block? What are the symptoms?

A

PR interval is constantly greater than 0.20 with one P for every QRS (slow conduction but reach ventricles)

mild, typically no symptoms

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10
Q

What are the EKG characteristics of second degree heart block? What are the symptoms?

A

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)

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11
Q

What are the EKG characteristics of 3rd degree heart block? Cause?

A

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)

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12
Q

What are ventrical rhythms conduction sequence? Hallmark EKG characteristics? Examples?

A

abnormal ventricular depolarization and retrograde conduction through the system

wide, bizarre QRS complexes

ventricular tachycardia, ventricular fibrillation

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13
Q

What are the EKG characteristics for ventricular fibrillation? Treatment?

A

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

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14
Q

What are the EKG characteristics for ventricular tachycardia? Treatment?

A

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

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15
Q

What are common medications used to treat dysrhythmias? What do they treat? MOA?Examples?

A

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]

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16
Q

What is cardiac resynchronization therapy? Indication? Examples?

A

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)

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17
Q

What are indications for a pacemaker?

A

bradycardia, AV block, MI, cardiomyopathy, HF

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18
Q

What will pacing look like on telemetry?

A

atrial pacing: spike before P wave
ventricle pacing: spike before QRS complex

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19
Q

What is failure to capture? What could cause this?

A

when a pacing stimulus is generated but fails to deliver to myocardial depolarization

could be d/t electrolyte imbalance?

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20
Q

What are indications for ICD?

A

ventricular tachyarrhythmias

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21
Q

What is acute coronary syndrome? What causes it? Types?

A

reduction of blood flow through the coronary arteries

primarily by artherosclerosis

unstable angina, NSTEMI,STEMI

22
Q

What is myocardial ischemia?

A

inadequate oxygen supply to myocardium without damage to myocardial cells, will begin an ACS event

23
Q

What is unstable angina? Cause?

A

chest pain that occurs at rest or with minimal exertion

myocardial ischemia without detectable infarction

24
Q

What is the progression of ACS?

A

myocardial ischemia
unstable angina
myocardial injury
mocardial infarction: NSTEMI to STEMI

25
Q

What is an NSTEMI? What does the EKG look like?

A

non-ST elevation myocardial infarction partial occlusion of coronary blood flow with positive cardiac markers

T-wave inversion and ST depression

26
Q

What is a STEMI? What does the EKG look like?

A

complete occlusion of coronary blood flow causing damage and necrosis with positive cardiac

ST elevation

27
Q

What are clinical manifestations of ACS?

A

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

28
Q

What is troponin? Normal value?

A

protein found in myocardia that is released within 3 to 12 hours following damage to myocardia

<0.03

29
Q

What is the primary diagnostic tool to diagnose ACS? What does it conclude?

A

EKG
the area of the heart is impacted by the blockage

30
Q

What are the assessment changes indicating decreased CO?

A

cardiac: dysrhythmias, HR/rhythm, pulse, edema, angina/pressure

respiratory: crackles, increased respiratory effort

skin: cool, clammy, pale

general appearance: anxious, restless, distress

31
Q

What are the goals of nursing interventions for ACS?

A

increase oxygen delivery: increase diastolic time, coronary vasodilation, O2, revascularize

decrease oxygen consumption: decrease HR (decrease SNS response), decrease pain

32
Q

What is ticagrelor? What is an alternative?

A

PY2 inhibitor, inhibits platelet aggregation

plavix (clopidogrel)

33
Q

What is ventral septal defect? Clinical manifestations?

A

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

34
Q

What is patent ductus arteriosis? Clinical manifestations?

A

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

35
Q

What is indomethicin?

A

medication used to try and close patent ductus arteriosis

36
Q

What can cyanosis cause?

A

high risk of endocarditis, arrhythmias

dizziness, fainting, seizures
delayed growth and development

37
Q

What is tetralogy of fallot? clinical manifestations? What other disorders is this associated with?

A

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

38
Q

What are tet spells? What naturally happens with tet spells? When does it occur?

A

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

39
Q

What is rheumatic fever? Clinical manifestations?

A

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)

40
Q

How can rheumatic disease effect the body long term?

A

rheumatic heart disease: damage to valves

41
Q

What is kawasaki disease? Clinical manifestations per stage?

A

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))

42
Q

What are complications that can be seen during the subacute phase of kawasaki disease?

A

development of coronary artery dilation or aneurysm

43
Q

What is an ischemic stroke? Types?

A

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

44
Q

What is hemorrhagic stroke? Types and their clinical manifestations?

A

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

45
Q

What is a transient ischemic attack?

A

transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain

46
Q

What are risk factors of stroke?

A

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

47
Q

What are right sided brain damage symptoms?

A

left sided hemiplegia and/or neglect
spatial-perceptual defects
deny or minimize problems
rapid performance, short attention span
impulsive
impaired judgement
impaired time concept

48
Q

What are left sided brain damage symptoms?

A

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

49
Q

What is tissue plasminogen activator? When do you give it? When is it contraindicated?

A

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

50
Q

What are symptoms of pulmonary emboli?

A

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

51
Q

What is the treatment for Kawasaki’s disease?

A

high dose ASA and IV immunoglobulin G