Exam 1: Perfusion

Question 1

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

Answer 1

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)

Question 2

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

Answer 2

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

Question 3

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

Answer 3

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

Question 4

What is supraventricular tachycardia? Examples? Common causes?

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

What are treatment for atrial fibrillation/flutter?

Answer 7

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

Question 8

What are heart blocks?

Answer 8

delay in conduction between AV node and ventricles

Question 9

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

Answer 9

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

mild, typically no symptoms

Question 10

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

Answer 10

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)

Question 11

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

Answer 11

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)

Question 12

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

Answer 12

abnormal ventricular depolarization and retrograde conduction through the system

wide, bizarre QRS complexes

ventricular tachycardia, ventricular fibrillation

Question 13

What are the EKG characteristics for ventricular fibrillation? Treatment?

Answer 13

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

Question 14

What are the EKG characteristics for ventricular tachycardia? Treatment?

Answer 14

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

Question 15

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

Answer 15

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]

Question 16

What is cardiac resynchronization therapy? Indication? Examples?

Answer 16

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)

Question 17

What are indications for a pacemaker?

Answer 17

bradycardia, AV block, MI, cardiomyopathy, HF

Question 18

What will pacing look like on telemetry?

Answer 18

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

Question 19

What is failure to capture? What could cause this?

Answer 19

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

could be d/t electrolyte imbalance?

Question 20

What are indications for ICD?

Answer 20

ventricular tachyarrhythmias

Question 21

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

Answer 21

reduction of blood flow through the coronary arteries

primarily by artherosclerosis

unstable angina, NSTEMI,STEMI

Question 22

What is myocardial ischemia?

Answer 22

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

Question 23

What is unstable angina? Cause?

Answer 23

chest pain that occurs at rest or with minimal exertion

myocardial ischemia without detectable infarction

Question 24

What is the progression of ACS?

Answer 24

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

Question 25

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

Answer 25

non-ST elevation myocardial infarction partial occlusion of coronary blood flow with positive cardiac markers T-wave inversion and ST depression

Question 26

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

Answer 26

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

Question 27

What are clinical manifestations of ACS?

Answer 27

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

Question 28

What is troponin? Normal value?

Answer 28

protein found in myocardia that is released within 3 to 12 hours following damage to myocardia <0.03

Question 29

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

Answer 29

EKG the area of the heart is impacted by the blockage

Question 30

What are the assessment changes indicating decreased CO?

Answer 30

cardiac: dysrhythmias, HR/rhythm, pulse, edema, angina/pressure respiratory: crackles, increased respiratory effort skin: cool, clammy, pale general appearance: anxious, restless, distress

Question 31

What are the goals of nursing interventions for ACS?

Answer 31

increase oxygen delivery: increase diastolic time, coronary vasodilation, O2, revascularize decrease oxygen consumption: decrease HR (decrease SNS response), decrease pain

Question 32

What is ticagrelor? What is an alternative?

Answer 32

PY2 inhibitor, inhibits platelet aggregation plavix (clopidogrel)

Question 33

What is ventral septal defect? Clinical manifestations?

Answer 33

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

Question 34

What is patent ductus arteriosis? Clinical manifestations?

Answer 34

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

Question 35

What is indomethicin?

Answer 35

medication used to try and close patent ductus arteriosis

Question 36

What can cyanosis cause?

Answer 36

high risk of endocarditis, arrhythmias dizziness, fainting, seizures delayed growth and development

Question 37

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

Answer 37

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

Question 38

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

Answer 38

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

Question 39

What is rheumatic fever? Clinical manifestations?

Answer 39

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)

Question 40

How can rheumatic disease effect the body long term?

Answer 40

rheumatic heart disease: damage to valves

Question 41

What is kawasaki disease? Clinical manifestations per stage?

Answer 41

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))

Question 42

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

Answer 42

development of coronary artery dilation or aneurysm

Question 43

What is an ischemic stroke? Types?

Answer 43

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

Question 44

What is hemorrhagic stroke? Types and their clinical manifestations?

Answer 44

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

Question 45

What is a transient ischemic attack?

Answer 45

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

Question 46

What are risk factors of stroke?

Answer 46

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

Question 47

What are right sided brain damage symptoms?

Answer 47

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

Question 48

What are left sided brain damage symptoms?

Answer 48

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

Question 49

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

Answer 49

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

Question 50

What are symptoms of pulmonary emboli?

Answer 50

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

Question 51

What is the treatment for Kawasaki's disease?

Answer 51

high dose ASA and IV immunoglobulin G