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
