↑↓Dysrhythmias pt.1, pt.2, drugs

Dysrhythmias— problem with impulse formation or conduction → ↓ CO (primary problem) and poor perfusion

Nsg priority: identify cause and treat underlying problem.

What causes Dysrhythmias:

1. MI: when the heart tissue dies → irritates/block normal conduction

2. electrolyte imbalance

   1. K: Resets each beat (repo)

      1.  ↓K → ↑ cadiotox → PVC—extra heartbeats in the lower chambers of the heart

   2. Mg: maintain steady heartbeat

   3. Ca: SA node fire; AV node speed; Allows for the heart muscles to contract AKA for Squeezing

3. hypoxia (starve the heart of energy it needs to contact) & hypovolemia (force the heart to beat abnormally fast)

4. Hormonal changes (thyroid and stress hormones): ↑ stress = ↑ SA node firing

5. Meds, caffince, nicotine, alcohol are stimulants → interferes in timing, irritates heart muscle → extra or misplaced beats

Contributing Factors:

S/S:

¡SA (pacemaker) à RA & LA à AV node (gatekeeper) à HIS Bundle à R & L Bundle Branches

Sinus Tachycardia: HR > 100

Key feature: Normal rhythm, just fast (SA node firing rapidly)

Why: 1. pain, fever, anxiety: release of stress hormones → forces SA node to fire quickly

         2. Hypovolemia: force the heart to beat faster when blood volume is low

Trx. 1. treat underlying cause

meds: 1. Beta blockers (Propranolol): ↓ firing of SA node + ↓ contractility

           2. Calcium channel blockers (Verapamil + diltiazem): slows SA node + delay electrical signals as they passed through the heart

Nursing priorities: monitor vital signs and EKG

1. Assess perfusion (↑ HR, ↓ BP): pale skin, decrease U/O

2. Labs and electrolyte imbalance: mg, ca, k

Sinus Bradycardia HR <60

key feature: normal for athletes, but medical concern when symptomatic:

1. dizziness (indication of ↓ CO)

2. weakness

3. hypotension → fewer squeezes per minute → less pressure in the arteries to push blood through the systemic circulation

Trx:

1. non symptomatic: O2: address hypoxia

2. symptomatic PRIMARY TRX.: Atropine: block the “brakes” of the heart → ↑ HR

   1. IN ATROPINE FAILURE use Dopamine or epinephrine

3. Temp pacing if needed

Nsg priorities: monitor EKG + vitals for poor signs of perfusion

Supraventricular Tachycardia (SVT) rapid ATRIA rhythm 100-280 bpm

key feature: fast atrial HR w/ no P waves (heart is beating so fast that there is very little time in between beats so it get hidden in the T wave)

Trx.

1. Vagal maneuvers- natural way of stimulating the vagal nerve—acts as brakes to help it slow down → ↓HR

2. Adenosine: chemical rest button that has a short life span of 1.5-10 sec sos it must be injected close to the heart to slow down electrical signal as the pass through the AV node

3. Recurrent SVT long term treatment: radiofrequency catheter ablation

   1. most effective for SVT

   2. Identifies using EPS and destroys the cardiac tissue cause the SVT by using radiofrequency waves to destroy irritable focus

   3. complication: damage to the normal conduction or cause heart blocks

4. UNSTABLE MEDICAL EMERGENCY( signs of poor perfusion—↓BP, LOC): Cardioversion: shocking heart

Nursing priorities: ↓ CO: when the heart beats this fast it doesn’t have enough time to fill w/ blood in btwn beats → ↓Bp & s/s of poor perfusion

Atrial fibrillation CHAOTIC ATRIAL activity 350-600 bpm

key feature: most common dysrhythmias where the Atria quivers from receiving hundreds of electrical signal instead of 1→ failure to pump blood effectively to the ventricles → blood pools in chambers causing clots that travel to the brain → stroke

Trx: to control rate: BB,CCB, digoxin: Block chemical signals from reaching the AV node

1. PREVENTION: Anticoag

2. EMERGENCY: cardioversion or ablation

nursing priorities: Antidysrhythmic Meds

• monitor signs of poor perfusion or clot related complications (stroke symptoms)

• monitor K due to digoxin or amiodarone → hypokalemia → digoxin toxicity

Premature Ventricular Complexes (PVCS)

key feature: early ventricular beat for irritable focus (sends out a signal before it is supposed to) → heart has less time to fill with blood → weak beat → ↓ amt of total volume being pumped to the rest of the body aka ↓ CO

Trx. correct underlying cause: caffeine, nicotine, alcohol, stress

1. Replace K or Mg because they act as electrical stabilizers so when it is low its not stable and contribute to excess firing

2. FREQUENT: BB (propranolol): ↓ firing and ↓ irritability

Nursing priorities: Identify cause

• monitor poor perfusion (↓ BP or dizziness) → ↓CO

Ventricular Tachycardia Rapid VENTRICULAR rhythm >140 bmp

Key feature: electrolyte imbalances of K & Mg → Chambers don't have enough time to fill with blood between beats → dangerous drop in CO → cardiac arrest

•     This is serious because regular rhythm can quickly turn into ventricular fibrillation (VFib)—state of total electrical chaos where there is no organized beat and provides NO BLOOD FLOW to the body

Trx:

1. elective cardioversion if stable (no signs of severe poor perfusion yet)

2. Amiodarone: delay, the reset button on repolarization of the heart cells

3. MEDICAL EMERGENCY IF pulseless: Defibrillation: delivers high energy shock to stop the electrical chaos

Nursing priorities: Assess for pulse

1. Monitor vitals + electrolytes (K, Mg)

Ventricular fibrillation: MOST DANGEROUS

Key features: electrical chaos ventricles, where instead of one organized signal telling hard to beat hundreds of disorganized impulses fire at once → ventricle quivers → total failure of the hearts pumping system—no pulse and 0 CO due to organize contraction

Trx: immediate defibrillation — give SA node opportunity to take back control

• CPR while waiting for dfib

• Epinephrine: stimulate the heart to reset

• antidysrhythmic med (amiodarone/lidocaine): stabilize a hearts electrical system, and prevents chaotic rhythm from occurring

Nursing priorities:

1. Call for help and start CPR immediately while preparing for D fib

2. Once stabilized long-term therapy such as implantable cardioverter defibrillator (ICD) will be used to shock the heart if Vfib happens again

• One or more episodes of spontaneous sustained VT or VF (not caused by a MI)

• Education: avoid magnets & sources of electromagnetic interference, cell phones, sit/lie down if dizzy

Heart block: imparied conduction through the AV Node or conduction system

Firstdegree AV block PR > .2 sec (five small boxes)

Key feature impulse that has difficulty moving through the AV NODE

Trx:

• Check medication

• On going monitoring

Second-degree AV block Mobitz type I (wenkeback) —WARNING PR

progressively length until a ventricle beat is skipped

Key features: not all of the atrial poses are conducted through to the ventricles

Trx:

ASYMPTOMATIC: ongoing monitoring

SYMPTOMATIC: atropine .5 mg to max three

Second-degree AV block Mobitz type II — RAPIDLY PROGRESS TO COMPLETE HEART BLOCK not all atrial pulses are conducted to the ventricles

Key features: PR intervals are the same (fixed) vs type I has prolongation

Trx:

• Pacing (transcutaneous/trans Venus): until permanent base can be placed

• Consider epinephrine or dopamine infusion to maintain BP until the pacing is started

Third- degree AV block (complete heart block)

Key features: complete block of the AV node, the bundle of his or the branches → disassociation of impulse between atria and ventricles → ventricles fire independently at a slower rate

Trx:

• Temporary facing until you can get a permanent one

• Dopamine and epinephrine to accelerate ventricular rhythm

• Atropine is not effective because the block is below the AV node

Pacemakers

• for symptomatic bradycardia or heart block to pace and sense

Types:

1. Temporary (non surgical) — electrical stimulus spread throughout the heart to depolarize the cells

   1. transvenous

      1. Invasive (subclavial) and inserted in an emergency

   2. transcutaneous—used as an emergency measure until invasive pacing can be used or until HR returns to normal

      1. Non-invasive and external electrodes that electrical impulses→ stimulate ventricular depolarization when HR is lower than the set heart rate on the base maker

1. Permanent implanted pacemaker

Pacemaker Malfunctions:

1. failure to sense

   1. oversensing: The pacemaker incorrectly detects non-cardiac electrical signals (like muscle movement or outside interference) as actual heartbeats. Because it "thinks" the heart is beating fine, it stays quiet, resulting in not enough paced beats

   2. undersensing: The pacemaker fails to see the heart's natural beats. Because it doesn't know the heart has already fired, it sends out its own signal anyway, leading to extra, unneeded paced beats

1. failure to capture: You will see the pacemaker’s electrical spike, but it is not followed by a P wave or a QRS complex. The signal happened, but the heart did not contract.

1. failure to pace: no impulse initiated (no pacer spikes) during a time when the heart rate is slower than the pacemaker's set limit

   • causes: hardware or power issue: broken lead, battery failure, a displaced lead, or a total generator failure

Nursing focus: monitor rhythm and device function

• possibly monitor for poor sign of perfusion

  • Dizziness, weakness, and ↓ HR are the primary signs of battery or device failure

Nursing edu:

• Lifting restrictions (4 weeks) so leads won’t dislodge

• Teach pulse taking: ONE FULL MIN + REPORT ANY PULSE LOWER THAN THE SET

• Learn symptoms of battery failure (Bradycardia, dizziness, weakness)

• Avoid MRI, ESWL, therapeutic radiation; Large magnets & motors, TENS; Close contact with cell phone; Antitheft devices in stores

Antidysrhythmic drugs