final Flashcards
1
Q
cardiac pacemaker vs automatic implanted cardiac defibrillator
A
- cardiac pacemaker- rate and rhythm
- AICD- rhythm and shock -> previous ventricular fibrillation MI
2
Q
AMI versus aortic aneurysm
A
AMI -gradual, with additional symptoms -tightness or pressure -increases with time -may max and wane -substernal; back is rarely involved -peripheral pulses equal DISSECTING ANEURYSM -abrupt, without additional symptoms -sharp or tearing pain -maximal pain from the outset -does not abate once it has started -back possible involved, between the shoulder bladed -blood pressure discrepancy between arms or decrease in a femoral or carotid pulse
3
Q
congestive heart failure
A
- left heart failure
- often occurs a few days following heart attack
- increased heart rate and enlargement of left ventricle no longer make up for decreased heart function
- lungs become congested with fluid
- may cause dependent edema -> right sided
4
Q
3 serious consequences of AMI
A
- sudden death -> resulting from cardiac arrest
- cardiogenic shock
- CHF
5
Q
angina pectoris
A
- occurs when the hearts need for oxygen exceeds supply
- crushing or squeezing pain
- does not usually lead to death or permanent heart damage
- should be taken as a serious warning sign
- treat angina patients like AMI patients
- unstable angina- in response to fewer stimuli than normal
- usually after exertion
6
Q
junctional rhythms
A
-40-60
-rhythm- irregular in single occurrence, regular in escape rhythm
-pacemaker site- AV junction
-p waves inverted before QRS- atria contract from bottom up bc it comes from AV
-p waves buried in the QRS
-p waves inverted after the QRS
-PRI < .12
The rhythm originates from the AV node and is regular
7
Q
junctional escape complexes and rhythms: etiology, clinical significance, treatment
A
- Etiology- Results when the AV node becomes the pacemaker.
- Results from increased vagal tone, pathologically slow SA discharges, or heart block.
- Clinical Significance- Slow rate may decrease cardiac output, precipitating angina and other problems.
- Treatment- None if the patient remains asymptomatic.
- treat symptomatic episodes with ATROPINE or pacing as indicated
8
Q
accelerated junctional rhythm
A
- 60-100
- Etiology- Results from increased automaticity in the AV junction.
- Often occurs due to ISCHEMIA of the AV junction.
- Clinical Significance- Usually well tolerated but monitor for other dysrhythmias.
- treatment- None generally required in the prehospital setting
9
Q
(Paroxysmal) junctional tachycardia
A
- rate- > 100-180
- Etiology- Rapid AV junction depolarization overrides the SA node.
- Occurs with or without heart disease.
- May be precipitated by stress, overexertion, smoking, or caffeine ingestion.
- Clinical Significance- May be well tolerated for brief periods.
- Decreased cardiac output will result from prolonged episodes, which may precipitate angina, hypotension, or congestive heart failure
10
Q
prolonged episodes of junctional tachycardia may lead to hypotension
A
true
11
Q
locations of AV blocks
A
- at the AV node
- at the bundle of His
- below the bundle of his
12
Q
first degree heart block
A
- PR interval is longer than its supposed to be*
- PRI is > .2 seconds ***
- PR intervals are equal and R to R is equal*
- you must name the underlying rhythm when identifying first degree heart block (ex. regular, brady, tachy)
- etiology- delay in the conduction of an impulse through the AV node
- may occur in healthy hearts, but often indicative of ISCHEMIA at the AV junction
- avoid drugs that may further slow AV conduction
13
Q
type 1 second degree block (Mobitz I, or Wenckebach)
A
- pacemaker site is SA node or atrial
- PRI- increases until QRS is dropped, then repeats**
- PR intervals and R to R are not equal*
- Indicative of ischemia at the AV junction.
- cardiac compromise.
- Avoid drugs that may further slow AV conduction.
- Treat symptomatic bradycardia.
14
Q
type 2 second degree block (Mobitz II or infranodal)
A
- slight more dangerous bc its dropping beats randomly
- pacemaker site is SA node or atrial
- PR intervals are equal, R to R is not equal
- Usually associated with MI or septal necrosis
- Clinical Significance- May compromise CO and is indicative of MI*
- Often develops into full AV blocks
- Treatment- Avoid drugs that may further slow AV conduction.
- Treat symptomatic bradycardia.
- Consider transcutaneous pacing
15
Q
third degree block
A
- ventricular = 40-60
- pacemaker site is SA node and AV junction or ventricle
- P waves- normal with no correlation to QRS
- atria and ventricle are doing their own thing with no correlation
- PR intervals are not equal, R to R is equal
- Etiology- Absence of conduction between the atria and the ventricles.
- Results from AMI, digitalis toxicity, or degeneration of the conductive system.
- Severely compromised CO
- Treatment- Transcutaneous pacing for acutely symptomatic patients.
- Treat symptomatic bradycardia.
- Avoid drugs that may further slow AV conduction.
16
Q
ventricular escape complexes and idioventricular rhythms
A
- rate- 15-40
- pacemaker site- ventricle
- QRS- >.12 seconds -> bizarre
- etiology- safety mechanism to prevent cardiac standstill
- results from failure of other foci or high degree AV block
- clinical significance- decrease CO, possibly to life threatening levels
- treatment- for perfusing rhythms, administer atropine and/or TCP (preferred)
17
Q
accelerated idioventricular rhythm: etiology, clinical significance, treatment
A
- etiology- a subtype of ventricular escape rhythm that frequently occurs with MI
- ventricular escape rhythm with a rate of 60-100
- clinical significance- may cause decreased cardiac output if the rate slows
- treatment- does not usually require treatment unless the patient becomes hemodynamically unstable
- primary goal is to treat the underling MI
18
Q
premature ventricular contractions
A
- rate is underlying rhythm
- QRS: > .12 s -> bizarre
- single ectopic impulse resulting from an irritable focus in either ventricle
- causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, electrolyte imbalances, or as normal variation of the ECG
- bigeminy* (every other is a PVC), trigeminy (two normal beats than a PVC -> every three), or quadrigeminy (three normal beats than a PVC -> every 4)
- couplet (two in a row) and triplets (3 PVCs in a row -> really just called ventricular tachycardia)
- malignant PVCs
- significant when there are a lot of them
- more than 6/minute
- R on T phenomenon- r wave of the next complex lands on the T wave before it -> can throw you into ventricular fibrillation
- multifocal PVCs- PVCs that look different from each other
- PVCs associated with chest pain
- ventricles do not adequately fill, causing decrease cardiac output (CO)
19
Q
ventricular tachycardia
A
- rate- 101-250+
- QRS- >.12 s -> bizarre
- 3 or more ventricular complexes in succession at a rate of > 100
- causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, or electrolyte imbalances
- VT may appear monomorphic (all look alike) or polymorphic (look different)
- decreased cardiac output, possibly life threatening levels
- may deteriorate into ventricular fibrillation
20
Q
torsades de pointes
A
- Polymorphic VT.
- Caused by the use of certain antidysrhythmic drugs.
- Exacerbated by coadministration of antihistamines; azole antifungal agents and macrolide antibiotics; erythromycin, azithromycin, and clarithromycin
- caused by hypomagnesemia - not enough magnesium
- typical occurs in non-sustained bursts
- prolonged QT interval during “breaks”
- QRS rates from 166-300
- RR interval highly variable
21
Q
ventricular fibrillation
A
- rate- no organized rhythm
- rhythm- no organized rhythm
- pacemaker site- numerous ventricular foci
- lethal -> no CO
- Etiology- Wide variety of causes, often resulting from advanced coronary artery disease.
- Clinical Significance- Lethal dysrhythmia with no cardiac output and no organized electrical pattern
22
Q
asystole
A
- rate- no electrical activity
- rhythm- no electrical activity
- pacemaker- no electrical activity
- p waves- none
- PRI- none
- QRS- none
- Etiology- Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis.
- Final outcome of ventricular fibrillation.
- Clinical Significance- Asystole results in cardiac arrest.
- Poor prognosis for resuscitation.
23
Q
sinus bradycardia
A
may result in decreased CO, hypotension, angina, or CNS symptoms
24
Q
sinus tachycardia
A
- exercise, fever, anxiety, hypovolemia, anemia, pump failure, increased sympathetic tone, hypoxia, or hyperthyroidism
- decreased CO for rates > 140
- > 140- ventricles arnt filling enough -> stroke volume is too low
- very rapid rates -> ischemia or infarct
- Treat underlying cause
25
Q
sinus arrest
A
- sinus node fails to discharge
- may result from ischemia of the SA node, digitalis toxicity, excessive vagal tone, or degenerative fibrotic disease
- decrease CO and cause syncope
- may result in escape rhythms- AV node may fire (back up plans)
26
Q
wandering atrial pacemaker
A
- irregular rhythm
- SA node, atrial tissue, or AV junction
- P waves are variable or absent**
- natural phenomenon in the very young or old
- may be caused by ischemic heart disease or atrial dilation
27
Q
multifocal atrial tachycardia
A
- > 100
- irregular
- Pacemaker- ectopic sites in the atria
- P waves - organized, non sinus P waves -> at least 3 forms
- WAP but tachycardic
- Often in acutely ill patients
- may result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery, COPD
- often indicates a serious underlying illness -> treat
28
Q
premature atrial tachycardia
A
- pacemaker site is ectopic sites in atria
- P wave early
- p waves and t waves are combining and colliding
- single electrical impulse originating outside the SA node
- caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic
- administering high flow, high concentration oxygen and establishing IV access
29
Q
paroxysmal supraventricular tachycardia
A
- 150-250
- combo of the p and t wave
- rapid atrial depolarization overrides the SA node
- Stress, overexertion, smoking, caffeine
- reduction in CO -> angina, hypotension, or congestive heart failure
30
Q
atrial flutter
A
- 250-350
- P waves -> F waves
- when AV node cant conduct all the impulses
- congestive heart failure (rarely seen with MI)
- compromise CO and result in symptoms
31
Q
atrial fibrillation
A
- most common!
- 350-750
- P waves- nondiscernible
- Results from multiple ectopic foci
- associated with underlying heart disease
- decrease CO
32
Q
Ventricular contraction begins at the apex of the heart.
A
true
33
Q
The absolute refractory period is from the peak of the t wave back to the isoelectric line.
A
false
- absolute refractory- onset of QRS to the peak of T wave
- relative refractory- peak of T to end of T (ex. PVC into VT -> premature and strong)
34
Q
normal PR and QRS
A
PR interval- .12-.2
QRS- .08- .12
35
Q
t wave
A
ventricular repolarization
36
Q
BLS
A
- check pulse for no more than 10s
- breaths are over 1s
- rescue breath- 1 breath every 6 seconds
- recheck pulse every 2 minutes
- advanced airway- 1 breath every 6s never stopping compression
37
Q
layers of the heart
A
- Fibrous pericardium
- Serous pericardium of layers (2) & (3)
- Parietal layer of serous pericardium
- Visceral layer of serous pericardium = 1. epicardium
- myocardium
- endocardium
38
Q
S1 and S2
A
- S1 is the closing of AV (Mitral and Tricuspid) valves at the start of ventricular systole
- S2 is the closing of the semilunar (Aortic and Pulmonic) valves at the end of ventricular systole
39
Q
afterload
A
- pressure left in the system that the left ventricle has to overcome
- high number -> bad
- makes it harder for blood to get back into circulation
40
Q
chronotropy, inotropy, dromotropy
A
- chronotropy- heart rate
- inotropy- force of contraction
- dromotropy- makes impulse easier to be conducted through the heart -> initiates heart beats
41
Q
single lead
A
- rate and regularity
- time to conduct an impulse
42
Q
ECG paper
A
- 5 big boxes- 1 second
- one small box- .04s
43
Q
6 second method
A
- 30 big boxes
- peaks in 6s x 10
44
Q
immediate general treatment: MOAN
A
- oxygen- maintain oxygen saturation 94-99%
- aspirin 160 to 325 mg
- nitroglycerin SL or spray- pain relief
- morphine IV (if pain not relieved with nitroglycerin)- pain and anxiety relief
- MOAN
45
Q
oxygen used in acute coronary syndromes
A
- why- increases supply of oxygen to ischemic tissue
- lack of circulation and oxygen
- when- always when AMI is suspected
- how- start with nasal cannula at 4 L/min
- maintain oxygen saturation 94-99%
- remember one word- oxygen-IV-monitor
- WATCH OUT!- rarely COPD patients with hypoxic ventilatory drive will hypoventilate
46
Q
nitroglycerin
A
- increases venous dilation
- decreases venous blood return to heart -> heart works less hard
- decreases preload and cardiac oxygen consumption
- dilates coronary arteries
- increases cardiac collateral flow**
- the result: decreases pain of ischemia*
- sublingual (under the tongue) -> into circulation quickly
- .4mg; repeat every 5 minutes
47
Q
nitroglycerin precautions
A
- use extreme caution if systolic BP <90 mm Hg
- use extreme caution in right ventricular infarction -> you may lose more preload
- suspect RV infarction with inferior ST changes
- limit BP drop to 10% if patient is normotensive
- limit BP drop to 30% if patient is hypertensive
- watch for headache, drop in BP, syncope, tachycardia -> (from the drop in preload)
- tell patient to sit or lie down during administration
48
Q
morphine
A
-or pentanol
-reduce pain of ischemia
-reduce anxiety
-reduce extension of ischemia by reducing oxygen demands
-use if:
-continuing pain
-evidence of vascular congestion (acute pulmonary edema)
-systolic blood pressure >90 mmHg
-no hypovolemia
2-4 mg titrated to effect
49
Q
morphine precautions
A
- drop in BP, especially in pts with volume depletion, increased systemic resistance, RV infarction*
- depression of ventilation
- nausea and vomiting (common)
- bradycardia
- itching and bronchospasm (uncommon)
50
Q
aspirin
A
- blocks formation of thromboxane A2 (thromboxane A2 causes platelets to aggregate and arteries to constrict)
- prevents more clots from happening -> does nothing for clots that are already there
- reduce:
- overall mortality from AMI
- nonfatal reinfarction
- nonfatal stroke
- ASAP
- for all patients with new pain suggestive of AMI
- 160-325 mg
51
Q
aspirin precautions
A
- active peptic ulcer disease
- asthma
- aspirin hypersensitivity
- bleeding disorders
- severe hepatic disease
52
Q
SALI
A
- septal- V1 and V2
- anterior- V3 and V4
- lateral- V5, V6, lead 1, aVL
- inferior- lead 2, lead 3, aVF
- STEMI- complete occlusion of blood to part of the myocardium
