Download supraventricular dysrhythmias

Source: http://www.rnceus.com/ekg/ekghowto.html
Dysrhythmias
• Identified by pattern and origin
• Supraventricular
• Atrial
• Junctional
• Ventricular
• Manifestations?
Fast Channel Action Potential
Slow Channel Action Potential
Goals of Dysrhythmic Therapies
• Decrease symptoms
• Prolong survival
Achieved by
Slowing rate of conduction
Decreasing automaticity
Increasing refractory period
Classes of Dysrhythmic Drugs
•
•
•
•
Class I—Sodium Channel Blockers
Class II—Beta Blockers
Class III—Potassium Channel Blockers
Class IV—Calcium Channel Blockers
Class I
Sodium Channel Blockers
•
•
•
•
•
•
Depress phase 0
Block sodium through fast channel
Slow conduction velocity (SA to AV nodes)
Prolong refractory period
Reduce automaticity
Subclasses based on action in refractory
period
Sodium Channel Blocker
Procainamide (Procan, Procanbid, Pronestyl)
• MOA: blocks sodium channels in myocardial cells, reducing
automaticity and slowing conduction
• Indications: acute/chronic atrial and ventricular dysrhythmias
• Contraindications: AV block, severe CHF, blood dyscrasias,
MG; caution in hepatotoxicity
• Side Effects: n/v, HA, abdominal/joint pains (lupus-like
syndrome); significant anticholinergic effects
• Assessment/Monitoring: EKG, VS, drug levels, weight,
edema, I/O, CBC, electrolytes, BUN/Cr, LFTs, bowel/bladder status,
eye pain
• Education: give NSAIDs for joint pains; report weight increase,
edema, SOB, fever, syncope, jaundice, eye pain, sxs of stroke,
increase fluid/fiber intake; no ETOH or stimulants; don’t skip dose
Other Class I Drugs
• Ia—Quinidine (Diarrhea, tinnitus)
• Ib
• Lidocaine* (DOC for ventricular dysrhythmias)
• Mexiletine (Mexitil)
• Phenytoin (Dilantin)—for Digoxin toxicity
• Ic—most likely to CAUSE arrhythmias
• Flecanide (Tambocor)
• Propafenone (Rhythmol)
Can local lidocaine given as an
anesthetic affect the heart?
Class II
Beta Adrenergic Blockers
Class II
Beta Blockers
• Decrease automaticity, HR
• Decrease input to sinus node
• Block epinephrine, NE in CNS
• Decrease polarization through Purkinge fibers
• Increase refractory period
• Decrease risk of sudden cardiac death
• Primarily supraventricular dysrhythmias
Beta Blocker
Propranolol (Inderal)
• MOA: blocks epi, NE at beta-1 & 2 receptors, reducing HR,
conduction, velocity; lowers BP
• Indications: primarily SVT, or stress-induced, HTN, angina,
prevention of MI, hypermetabolic states; glaucoma, migraines
• Contraindications: cardiogenic shock, bradycardia, heart blocks,
heart failure, asthma, COPD; caution in DM
• Side Effects: hypotension, bradycardia, fatigue, depression,
sexual dysfunction, hypoglycemia (DM)
• Assessment/Monitoring: VS, EKG, weight, I/O, mood,
glucose, lungs, safety
• Education: check HR, BP, weight, report SOB, chest pain, weight
gain, edema, syncope (safety), sxs of stroke, depression or ED, DO
NOT DISCONTINUE
Class III
Potassium Channel Blockers
Class III
Potassium Channel Blockers
•
•
•
•
•
•
Prolongs phase 3 of FA potential
Slows repolarization
Reduce automaticity
Used in life-threatening arrhythmias
Most likely to cause arrhythmias
Less ventricular fibrillation than Class I
Potassium Channel Blocker
Amiodarone (Cordarone)
• MOA: block potassium channels, prolongs refractory period, slows
repolarization; also blocks sodium channels
• Indications: resistant, life-threatening V tach
• Contraindications: severe bradycardia, cardiogenic shock, heart
blocks; caution in heart failure, hepatic disease
• Side Effects: ARDS, thyroid disorders, blurred vision, n/v,
anorexia, fatigue, syncope; skin discoloration
• Assessment/Monitoring: VS, EKG, lungs/CXR/PFTs, TFTs,
digoxin and warfarin levels
• Education: hold for HR < 60; report chest pain, palpitations,
syncope, SOB, sxs of thyroid dx: monitor weight, I/O, edema, sxs of
hepatotoxicity; take with food; wear sun-screen
Additional Class III
•
•
•
•
Bretyllium (Bertylol)
Dofetilide (Tikosyn)
Ibutilide (Covert)
Sotolol (Betapace)
Class IV
Calcium Channel Blockers
Class IV
Calcium Channel Blockers
• Slow automaticity in SA node
• Slowed impulse conduction through AV
node
• Prolonged refractory period
• Only for supraventricular dysrhythmias
Calcium Channel Blocker
Verapamil (Calan)
• MOA: slows calcium ions in myocardial cells and vascular smooth
muscle; slows conduction velocity
•
•
•
•
Indications: HTN, angina, supraventricular dysrhythmias
Contraindications: hypotension, heart block, bradycardia
Side Effects: hypotension, bradycardia, HA, constipation
Assessment/Monitoring: VS, BP, EKG, weight, I/O, sxs of
HF, bowel status
• Education: hold for syncope or HR < 60; report SOB, chest pain,
weight gain, edema, syncope (safety), sxs of stroke; don’t take with
GF juice; do not break/chew SR tablets, increase fiber, DO NOT
DISCONTINUE
Additional Calcium Channel
Blockers
• Diltiazem (Cardizem)
• Adenosine (Adenocard)—PSVT
• Nifedipine (Procardia)—selective for
vasculature
Nursing Implications with
Antidysrhythmic Drugs
• Any drug that prevents or corrects
a dysrhythmia is capable of
causing a dysrhythmia.
• Patients, especially on Class I and
Class III need to be closely
monitored.
RB is a 74 yo male with recent CABG x 3.
During the post-op period he developed
PVCs and A fib. He is started on a lidocaine
drip to control PVCs. What should you
monitor?
While receiving IV lidocaine, RB’s HR
decreases to 52 with continued PVCs.
What should you do?
RB is now in NSR. The MD prescribes
amiodarone 200 mg po daily. Why is he
getting this drug and what should be
monitored?
RB needs more instruction regarding
amiodarone when stating
1. “I will take 2 tablets, if I
miss a dose.”
2. “I will report fatigue.”
3. “I will check my pulse
before taking the pills.”
4. “I should use decaffeinated
coffee.”
Additional Dysrhythmic Drugs
• Digoxin (Lanoxin)
• Decreases automaticity in SA node
• Slows conduction through AV node
• Supraventricular dysrhythmias
• Phenytoin (Dilantin); for Digoxin toxicity
• Magnesium sulfate (torsades de pointes)
How do we know these drugs
are working?
How do we know if they aren’t?
Nursing Intervention
•
•
•
•
•
•
•
•
•
Screening?
What will will monitor?
Monitor which organs?
Monitor which electrolytes?
Interactions?
Signs of success?
Signs of failure?
Side-effects?
Safety?
All of the following indicate improvement in cardiac
status, except
1. Decreased pulse
deficit
2. Syncope
3. Weight loss
4. Lungs CTA
Causes of Shock
•
•
•
•
•
Hypovolemic
Neurogenic
Cardiogenic
Anaphylactic
Septic
Initial Key Steps
•
•
•
•
•
•
•
Lay flat with feet elevated
Keep warm
Get help
Call physician
Initiate IVFs
Oxygen
Prepare for code
IV Fluid Replacement
• Crystalloids
• Normal Saline (NS)
• Lactated Ringer’s Solution (LR)
• Plasmalyte
• Colloids
•
•
•
•
Albumin
Hetastarch
Dextran
Plasma Protein Fraction
Colloidal Fluid Replacement
Albumin (Albuinar, Albutein, Buminate, Plasbumin)
• MOA: maintains plasma oncotic pressure in vasculature
• Indications: restore plasma volume in hypovolemic shock or
restore proteins in hypoproteinemia
• Contraindications: severe heart failure
• Side Effects: allergy, fluid overload
• Assessment/Monitoring: VS/PO, lungs, I/O, weight, edema,
sxs of anaphylaxis
• Education: report SOB, wheezing, palpitations, edema
Additional Colloids
• Plasma Protein Fraction (Plasmanate)
• Dextran 40 (Gentran, Macrodex)
• Hetastarch (Hespan)
The client at greatest risk from fluid
overload is...
1.
2.
3.
4.
36 yo with sepsis
68 yo with CHF
70 yo with HTN
70 yo with CRF
Vasoconstrictor (Sympathomimetic)
Norepinephrine (Levarterenol, Levophed)
• MOA: alpha-1* and beta-1 agonist
• Indications: acute shock (septic) and cardiac arrest
• Contraindications: hypovolemic shock; caution in ischemic
disease
• Side Effects: HTN, reflex bradycardia, dysrhythmias, organ
ischemia
• Assessment/Monitoring: VS, EKG, organ fx, glaucoma, IV
patency, HA, CRT
• Education: report chest pain, palpitations, SOB, eye pain, IV pain,
HA
Other Vasoconstrictors
• Isoproterenol (Isuprel); alpha & beta*
• Phenylephrine (Neosynephrine); alpha
• Mephentermine (Wyamine); alpha & beta
The priority nursing action for a client about
to receive Levophed for hypovolemic shock
is...
1. Evaluate IV access
2. Measure baseline
HR & BP
3. Measure urine
output
4. Obtain weight
Perfusion can be evaluated by all, except
1.
2.
3.
4.
Vital signs
Weight
Output
CRT
The nurse knows that all are true,
relating to NE, except
1. NE should be stopped
immediately after BP
stabilizes
2. NE may cause organ failure
3. NE requires telemetry
4. NE may aggravate glaucoma
Inotropic Agent
Dopamine (Dopastat, Inotropin)
• MOA: stimulates dopamine receptors in kidney (activates
renin/angiotensin); beta 1 agonist at moderate doses; alpha 1 at high
doses
•
•
•
•
Indications: maintain renal perfusion, increase CO, shock
Contraindications: pheochromocytoma, ventricular fibrillation
Side Effects: dysrhythmia, HTN, tissue necrosis at IV site
Assessment/Monitoring: VS, EKG, I/O, weight, edema, sxs
of HF, CRT, HA, IV site
• Education: report chest pain, palpitations, SOB, pain at IV site,
cold/numb extremeties, HA; ICU protocols
Other Inotropic Agents
• Digoxin (Lanoxin)
• Dobutamine (Dobutrex); beta 1
The treatment for dopamine
extravasation is...
1.
2.
3.
4.
Atropine
Narcan
Neostigmine
Regitine
Anaphylaxis Drug (Sympathomimetic)
Epinephrine (Adrenalin)
• MOA: non-selective sympathomimetic
• Indications: anaphylaxis
• Contraindications: caution in HTN, CVA, CAD, glaucoma,
dysrhythmias, organ ischemia, hyperthyroidism
• Side Effects: HTN, dysrhythmias, organ ischemia
• Assessment/Monitoring: VS, EKG, lungs, I/O, CRT, organ
perfusion, MS
• Education: report SOB, chest pain, palpitations, cold/numb
extremities, anxiety; ICU protocols; injection techniques, reasons for
test doses
Additional Drugs for
Anaphylaxis
• Antihistamines (-amines)
• Beta 2 agonists (-terols)
• Steroids (-sones)
Key Points for Shock
• Correct hypovolemia before using
•
•
•
•
•
vasoconstrictors or inotropics
All drugs given on infusion pumps
Telemetry required
Almost all drugs have short ½ life (x digoxin)
Most have potential to cause tissue damage if
extravasation occurs
All can compromise organ function