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NSG 478 > EKG interp, Ventricular dysrhythmias, AV blocks and med mgmt > Flashcards

EKG interp, Ventricular dysrhythmias, AV blocks and med mgmt Flashcards

1
Q

Atrioventricular Blocks (AV blocks)

A
  • A delay or failed conduction of impulses from atria to ventricles
  • Can occur in the AV node, Bundles of HIS and the bundle branches
  • QRS will be normal at or above the bundles of his
  • It is common to see rabbit ears in these patients: LBBB, can have a notching, or second peak of the R wave
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2
Q

Normal QT interval

A

0.4-0.43 sec

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3
Q

Normal R-R interval

A

0.6-1.0 seconds
60-100 bpm

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4
Q

AV blocks: Left bundle branch block

A
  • Notching of the R wave can hide a STEMI
  • Treat as if they have ACS unless proven otherwise
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5
Q

First degree block

A
  • Signals are delayed in the AV node but are conducted to the ventricles
  • PR interval over 0.2 seconds, consistent
  • QRS is normal (0.1 or less)
  • Atrial and ventricular rate is the same
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6
Q

Second degree block

A
  • Mobitz I and Mobitz II, some impulses are conducted to the ventricles and some are blocked
    *
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7
Q

Third degree AV block

A

All impulses are blocked and non are conducted to the ventricles
* P wave and QRS are independent of each other
* P waves appear across the rhythm strip hiding in QRS, ST or T wave, Consistent across the strip
* Inconsistent PR interval
* Atria rate higher than ventricular rate
* regular atrial and ventricular rhythm, just not together

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8
Q

How to determine the AV block

A
  1. Look for the P waves: (Is there one for each QRS or is there more than one?)
  2. Measure the regularity of the atrial rhythm (P-P interval) and the ventricular rhythm (R-R interval)
  3. Measure the PR interval (is it consistent?)
    3.5 The PR is key to identifying the type of block
  4. Measure the QRS complex
    • Is it narrow or wide
    • The lower the block in the conduction system, the wider the QRS and the slower the rate
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9
Q

How do you manage a first degree block

A
  • You don’t, you just watch them to make sure they dont get worse, note in the chart
  • Make sure the pt is stable
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10
Q

Second degree AV block: Mobitz I

A
  • longer, longer, longer, drop now you have a wenckebach
  • Each impulse has increasing difficulty passing through the AV node, until one impulse does not pass through and is blocked (PR interval increases more and more until a QRS complex is dropped)
  • P wave is regular and occurs on schedule
  • After a beat is dropped, the cycle repeated
  • Ventricular rhythm is irregular due to the beat being dropped
  • AV block is conducted through the AV node so QRS duration is normal
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11
Q

Mobitiz I mgmt

A
  • If stable, no treatment
  • Seen as intermittent benign rhythm
  • Usually temp and resolves spontaneously
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12
Q

Causes of Mobitz I

A
  • Acute inferior wall MI: From ischemia of the AV node
  • Meds affecting rate and rhythm (CCB, BB, Dig)
  • Hyperkalemia
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13
Q

Second Degree AV block: Mobitz II

A
  • Failure of some SA impulses to be conducted through the AV node to the ventricles
  • More than one P wave for each QRS complex
  • PR ratio is the consistent however some impulses do not conduct resulting in more than one P wave per QRS complex
  • Conduction disorder may be located in bundles of his or bundle branches

The PR ratio is huge

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14
Q

Mobitz II: Block is located in bundles of His

A

QRS complex is normal duration

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15
Q

Mobitz II: Block is located in the bundle branches

A

QRS is wide

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16
Q

Complications of Mobitz II

A

Potential to progress to third degree AV block or ventricular standstill with little to no warning

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17
Q

Causes of Mobitz II

A
  • Anterior wall MI
  • Acute myocarditis
  • Degeneration of electrical conduction system occurring with aging
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18
Q

Mgmt of Mobitz II

A
  • Address reversible causes first
  • Pacemaker therapy, due to this block often being perm and its progression to third degree AV block
  • External pacing is done for symptomatic Mobitz II until transversal pacing can be done

Atropine is not recommended especially if the QRS complexes are wide as it can further slow down rate

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19
Q

Reversible causes of nodal blocks: Mobitz II

A
  • Medications: Dig, beta adrenergic blockers, CCB
  • Electrolyte imbalances (hyperkalemia
  • AV block due to a heart condition would make you adress the heart condition
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20
Q

Atropine

A
  • Works on the SA node to increase HR in bradycardic patients
  • Does not work on Mobitz II and below with the bundle branches , as it can worsen heart blocks
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21
Q

Third Degree AV Block: Block is located in the AV node or bundles of His

A
  • QRS will be narrow
  • Ventricular rate between 40-60
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22
Q

Third Degree AV Block: Block is located in the R/L bundle branches

A
  • QRS is wide
  • Ventricular rate less than 40

Atropine is not recommended

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23
Q

mgmt of third degree heart block

A
  • External pacing can be used for Temp treatment of symptomatic complete heart block until transvenous pacing
  • Perm pacemaker may be required for unresolved third degree AV block (due to anterior wall MI)
  • Atropine is not recommended for a complete heart block with wide QRS complexes, can slow ventricular rate down further
  • Vasopressors may be used to treat hypotension
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24
Q

Inferior MI: Third Degree AV block

A
  • Can resolve on it own
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25
Anterior MI: Third degree block
May require perm pacemaking
26
Causes of third degree AV block
* MI * Lyme disease * Dig tox * Aging
27
Supraventricular arrhythmias
* Originates above the ventricles * Above the bundle branches * Sinus, atrial and junctional rhythms * Simultaneous depolarization of left and right ventricles occur, resulting in a narrow QRS complex Atrial dysrhythmia
28
Ventricular arrhythmias
* **Below bundle of His** in the ventricles * Async depolarization of left and right ventricle occur, resulting in a **wide QRS** * More dangerous, **potential to limit cardiac out put Severely** Premature ventricular contraction (PVC) V-Tach V-Fib Ventricular standstill
29
Premature ventricular contraction (PVC)
* Premature, beat originating in an **ectopic site** in the ventricles * The premature beat (PVC) occurs in **addition to a basic underlying rhythm** * Characterized by **wide QRS, ST segment and T wave** which **slope in the direction opposite** the main QRS deflection * **P wave** is not associated with PVC * Occurs on a rhythm, with it occuring after x amount of beats (Can occur every 2, 3, 4 beats) | Essentially it looks like the heart skipped a beat
30
PVC: look the same on the same lead
Unifocal PVC: only one focal point
31
PVC: look different on the same lead
Multifocal PVC: Coming from multiple ectopic sites
32
Causes of PVC
* May occur following reperfusion procedures * Thrombolytic therapy or angioplasty * Basically anything that causes irritation to the heart (Abnormal K, Hypoxia, Low EF) * May occur in individuals with a healthy heart but are more common in people with heart disease
33
Mgmt of PVC
* If infrequent, without symptoms, **No treatment** * 6 or more PVC per min (Significant) , multifocal paired **R-on T** runs of three or more should be treated with**Antiarrhythmic meds** especially after cardiac surg * Increased risk of V-tach or V fib * Make sure Mg and K levels are normal
34
V-Tach
* Originates in an ectopic pacemaker site in the ventricles at a rate of 140-250 * Impulse originates in the ventricles, meaning **no p wave and Qrs is wide** * VT occurs as a continuous rhythm or intermittently in short runs of 3 or more beats * **3 or more CONSECUTIVE PVC** is considered to be V-tach. Rhythm is usually reg by may be slightly irreg * VT may be **precipitated** by PVC
35
What is V-tach precipitated by
It can be significant runs of PVC
36
Causes of V-Tach
* **Underlying heart disease** * Electrolyte imbalances and hypoxia * following stimulation of the endocardium during invasive cardiac procedures (Pacing lead insertion or swan cath) * Following **reperfusion** procedures (PCI and thrombolytics)
37
Why is sustained V-tach life threatening
* Rapid ventricular rate and loss of atrial kick significantly reduces CO * Sustained V-tach has the potential to be come v-fib or asystole
38
Treatment of V-tach: Stable monomorphic V-tach
* Amiodarone bolus, followed by amiodarone drip * Synchronized cardioversion: once completed maintenance amiodarone infusion is started
39
Treatment of V-tach: Unstable monomorphic V-tach
* **Immediate synchronized cardioversion**: once there is a rhythm we give a maintenance dose of **amiodarone**, and an oral after acute period
40
V-fib
* Disorganized chaotic electrical focus that originates in the ventricles * No, P or QRS, no contraction * Ventricles quivers, irregular chaotic waves that have no pattern * Shockable
41
V-fib: With large fib waves
Coarse V-fib, usually more irregular and distinctive than fine V-fib waves
42
V-fib:with small fib waves
Fine V-fib: can resemble asystole, should be confirmed in 2 leads
43
Most common cause of cardiac death in pt with acute MI
V-fib
44
What precedes V-fib
* Significant PVC, V-tach * Can occur spontaneously without any precipitating rhythms
45
Causes of V-fib
* PVC/V-tach * Myocardial ischemia * Hypoxia * Electrolyte imbalances * Stimulation of the endocardium during invasive cardiac procedures (Pacing leads and swan cath) * Following reperfusion procedures (Thrombolytic therapy and angio)
46
Pt in V-fib is unresponsive, apneic and pulseless
Death is imminent without treatment
47
Mgmt of V-fib:
* Attach monitor, check responsiveness and pulse * If no pulse and pt is unresponsive defib once at highest energy level * Start CPR, Establish IV line, intubate * Admin EPI * Continue CPR for 5 cycles (Circulate drug) and then defib at highest energy level * Admin amiodarone or lidocaine * Continue CPR for 5 cycles to circulate drug and defib at highest energy level * Continue Drug,CPR,shock until rhythm resolves or a decision is made to stop
48
Mgmt of V-fib: Arrest is unwitnessed
Perform CPR for 5 cycles before initial shock
49
P waves without QRS
Asystole
50
Ventricular standstill
* Asystole * Absence of all electrical activity in the ventricles * When the ventricles are inactive there is no QRS, but there can be electrical activity in the atria, producing P waves
51
Two presentations of Asystole
* P waves without QRS * Straight line
52
What precedes asystole
* Mobitz II * Third degree heart block (complete) * V-tach * V-fib * Defib or cardioversion procedures * myocardial ischemia or infarction * electrolyte imbalances * hypoxia * Drug overdose * Cardiac trauma
53
How to determine asystole from fine V-fib at the bedside without cardiac monitoring
You cant, death is immediate without treatment
54
Asystole prognosis
Extremely poor despite resuscitation efforts
55
Amiodarone
* Class 3 antiarrhythmic, acting on K channels * During arrest this can be given 2 times in adult * 1st dose is 300mg * 2nd is 150 mg * V tach with pulse * 150 mg bolus given over ten min * Followed by a continuous drip of 1mg/hr for 6hr followed by 0.5 mg for 18hr
56
Amiodarone side effects
* It has an extremly long half life * worsening AV Blocks * Pulmonary fibrosis * Increased liver enzymes Better to have these side effects than dead
57
Epi
* Catecholamine which acts to support vascular tone and increase HR * Acts on Alpha and beta receptors * Used during complete asystole * 1mg q 3-5 min
58
Mgmt of Asystole
CPR, until a smidge of electrical activity is returned then defib * Start CPR, call a code * Attach monitor * Check responsiveness and pulse * Establish IV lines and intubate * Admin epi * Consider causes of rhythm * Continue CPR and epi unti rhythm is resolved or decision is made to stop
59
Bradycardia med mgmt
* None if not symptomatic * If symptomatic * Atropine * Dopamine or Epi if atropine does not work
60
A-Fib med mgmt
* Amiodarone * Adenosine
61
SVT med mgmt
* Amiodarone * Adenosine
62
V-tach, with pulse med mgmt
* Amiodarone * Adenosine
63
V-tach without pulse, med mgmt
* Amiodarone * Lidocaine * Epi
64
V-fib med mgmt
* Amiodarone * Lidocaine * Epi

NSG 478 (23 decks)

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