Cardiac Flashcards
Preload
The amount of blood returning to the RIGHT side of the heart and the muscle stretch that the volume causes. ANP is released when we have this stretch
Afterload
The pressure in the aorta and peripheral arteries that the left ventricle has to pump against to get blood out
This pressure is referred to as resistance
With hypertension there is even more resistance to pump against thats why HTN can eventually lead to HF and pulmonary edema, because high afterload decreases cardiac output and decreases the forward flow, in addition to wearing out your heart.
Stroke volume
The volume of blood pumped out of the ventricles with each beat
Cardiac Output
Tissue perfusion is dependent on an adequate cardiac output. Cardiac output changes according to the body’s needs
Factors that affect Cardiac Output
Heart rate and arrhythmia’s such as A.fib, Tachycardia and Bradycardia.
Blood Loss = Less volume, Less pressure (less perfusion). More volume, more pressure.
Ineffective contractility due to MI, cardiac muscle disease , medication
Angiotensin- converting Enzyme (ACE) Inhibitors
Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril, Prinivil), Moexipril (Univasc), Ramipril (Altace)
Commonly used for Heart failure, HTN and MI
PO/IV
1-2 hours/ 15-30 minutes
Interactions: Hyperkalemia can result if takein in combination with potassium sparing diuretics or eating salt substances
MoA:Suppress the Renin Angiotensin System (RAS). Prevents the conversion of Angiotensin I to Angiotensin II. This results in arterial dilation (decreasing the afterload) and increased stroke volume. ACE inhibitors block aldosterone so the client loses sodium and water and retains potassium. ACE inhibitors improve lung function by increasing alveolar-capillaries membrane diffusing capacity and pulmonary function in patients with HF.
Advantages: Effective in treating heart failure
Disadvantages: African Americans and older adults do not respond to ACE inhibitors with the desired reduction in blood pressure without the addition of a diuretic
Side effects: Dizziness Hyperkalemia Hypermagnesemia Fatigue Headache Dry, nonproductive cough
Adverse effects: Angioedema, Orthostatic hypotension
Interventions:
Monitor BP and HR.
Monitor potassium and magnesium levels.
Initiate safety precautions.
Education:
Rise slowly from lying or sitting to standing position.
Safety precautions.
Can be administered with food (EXCEPT: Moexipril)
Do not use salt substitutes with potassium.
Angiotensin 2 Receptor Blockers (ARBS) - Decrease After load
Losartan (Cozaar),
Olmesartan (Benicar),
Valsartan (Diovan)
Common Uses: HTN and HF
PO/ 2 Hours
Intercations: MAOIs, alcohol, diuretics may increase hypotensive effects. ACE inhibitors and ASA may increase hyperkalemia and renal dysfunction
MoA: Prevent the release of aldosterone. They act on the renin-angiotensin system (RAS). ARBS block angiotensin II from the
angiotensin I receptors found in tissue. Potent vasodilator. Decreases peripheral resistance. Decrease the workload of the heart by decreasing afterload. This will increase cardiac output and keep blood moving forward out of the heart.
Advantages: Do not cause the constant, irritating dry
cough that ACE inhibitors do.
Disadvantages:Less effective for treating hypertension in
African-American clients.
Side Effects: Headache Dizziness Drowsiness GI complaints Fatigue
Adverse Effects: Orthostatic hypotension Hypoglycemia Hyperkalemia Renal dysfunction Angioedema
Interventions: Monitor BP and Heart rate, AST, ALT, BUN and creatinine.
Education: Rise slowly from lying and sitting position to standing position. Safety precautions. Can be taken on empty or full stomach. Do not use salt substitutes.
Antianginal/ Nitrates
Nitroglycerin - Decreases the preload and Afterload
Common use: Angina, MU and pulmonary Edema
Contraindications: Pre-existing Hypertension Head trauma Increased ICP Pericardial tamponade
SL - 1 every 5 min. up to 3 doses. (1 - 3 minutes) Tablet - 20 - 30 mins Spray Ointment: 20 - 60 mins Transdermal- 30 - 60 mins
Interactions: Enhance hypotensive effects: Beta blockers, Calcium channel blockers, Vasodilators, Alcohol, Erectile dysfunction meds
May antagonize effects of
Heparin: IV nitroglycerin
MoA: Acts directly on the smooth muscle of venous and arterial blood vessels, causing relaxation and dilation. Dilates coronary arteries. Sublingual administration rapidly absorbs into the internal jugular vein and right atrium. IV nitroglycerin vasodilates the client to decrease afterload which increases cardiac output, so that more blood can be pumped forward
Advantages:
Decreases preload, afterload, and workload of the heart
Increases blood flow to heart muscle
Reduces myocardial oxygen demand
Side Effects: Headache Faintness/Syncope Nausea/vomiting Dizziness Flushing Palpitations Diaphoresis Tolerance Contact dermatitis with topical
ADVERSE EFFECTS: Hypotension Reflex Tachycardia Paradoxical Bradycardia Circulatory Collapse
Interventions: Monitor Blood pressure. Do not leave client until BP stabilizes. Assess cardiac output. Evaluate pain relief. Safety precautions. Maintain adequate hydration. IV: Use a pump; hold for systolic BP < 100
Education:
Activate EMS if pain unrelieved after taking 1 tab SL or spray.
Do not swallow SL nitro.
Keep in dark, glass bottle.
Do not mix medications in bottle with nitroglycerin.
Do not open bottle frequently.
Keep dry and cool.
May or may not burn or fizz in mouth.
Renew every 3-5 months; 2 years of spray.
Antidysrhythmic Class 3 /Amiodarone
Commonly used when V-fib and pulseless V-tach are resistant to a vasopressor and defibrillation. Fast arrhythmias.
Contraindications: Cardiogenic shock 2nd degree heart block 3rd degree heart block Iodine allergy
IV/PO/Rapid
Interactions: MAOIs-hyperpyretic crisis, seizures.
MoA: Prolongs duration of action potential and refractory period to decrease heart rate. Decreases peripheral vascular resistance and
increases PR and QT intervals. First antiarrhythmic of choice.
Advantages:
Very little negative inotropic activity making it advantageous for use in clients with heart failure.
Disadvantages:
Potentially serious side effects requiring careful monitoring. Has lots of iodine in it - can affect thyroid function.
Side Effects: Photophobia Weakness Skin discoloration Tremors Impaired thinking/reactions
Adverse Effects: Hypotension Bradycardia Difficulty breathing Wheezing Chest pain Light-headed Vision loss Jaundice
Interventions:
IV: Continuous ECG monitoring and BP monitoring
PO: Assess BP lying, standing. If systolic BP drops 20 mmHg, hold.
Monitor Hepatic studies: AST, ALT, bilirubin.
Education:
Do not skip a dose or discontinue abruptly.
Do not take with grapefruit juice.
Use sunscreen or stay out of sun to prevent burns.
Dark glasses may be needed for photophobia.
Lidocaine
Common Uses:
Frequent PVCs
Ventricular tachycardia
Alternative antiarrhythmic agent to amiodarone in the treatment of cardiac
arrest secondary to VF or pulseless VT resistant to CPR, cardioversion (after 2 to 3 shocks) and a vasopressor (epinephrine)
Contraindications: Adam-Stokes Syndrome and Heart block
IV/ 45 to 90 seconds
Interactions: Lidocaine toxicity – cimetidine, beta blockers. Increase lidocaine effects – barbiturates, ciprofloxacin
MoA:Decreases irritability of the heart muscle. Increases electrical stimulation threshold of ventricles, which stabilizes cardiac
membrane and decreases automaticity.
Side Effects: Headache Dizziness Drowsiness Blurred vision Phlebitis
Adverse: Heart block Seizures CNS depression Respiratory depression Malignant hyperthermia Lidocaine toxicity
Interventions:
Administer IVP at a rate of 25-50 mg/minute. Monitor lidocaine blood levels.
Continuous ECG monitoring. Observe for prolonged PR interval and QRS
complex.
Have resuscitative equipment readily available.
Watch for malignant hyperthermia: tachypnea, tachycardia, changes in BP,
increased temperature.
Monitor for signs of toxicity (hearing impairment, muscle twitching, confusion,
seizures).
Education:
About the use of lidocaine.
Report signs of toxicity (hearing impairment,
muscle twitching, confusion)
Lidocaine Toxicity
Lidocaine toxicity (and all local anesthetic toxicity) can cause circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech, and tonic-clonic seizures. Local anesthetics are actually CNS depressants, thus tonic-clonic seizures are thought to be caused by depression of inhibitory pathways.
Circumoral and/or tongue numbness. Metallic taste. Lightheadedness. Dizziness. Visual and auditory disturbances (difficulty focusing and tinnitus) Disorientation. Drowsiness.
Beta blockers
RATE CONTROL Atenolol (Tenormin) Metoprolol (Lopressor) Propranolol (Inderal) Carvedilol (Coreg)
Commonly used for HTN, Angina, dysrhythimias, MI, migraines, Tachycardia due to stage fright
Contraindications:
2nd and 3rd degree heart Block, Cardiogenic Shock, Hypotension, AHF, Sinus Bradycardia
PO/IV
Interactions: Digitalis worsens bradycardia. Other antihypertensives and alcohol worsen HTN. NSAIDS, Licorice, ma-haung, ephedra decrease effect of beta blockers causing hypertension. Black cohosh, Hawthorn, Parsley, Goldenseal increase hypotensive effect.
MoA: Blocks beta receptor cells (catecholamines) to decrease vascular resistance, decrease BP, decrease HR, decrease myocardial
contractility, decrease workload of the heart, decrease cardiac output, decrease renin release.
Advantages: Well tolerated in low doses
Side Effects: Blurred vision Mental changes Nasal stuffiness Photosensitivity Sexual dysfunction Fatigue Weakness Dizziness Lethargy Nausea/ Vomiting Diarrhea Headache Depression Insomnia
Adverse Effects: Bradycardia Hypotension 2nd & 3rd degree Heart block Thrombocytopenia Bronchospasm Wheezing
Interventions:
Monitor for increased BUN, Creatinine, AST, LDH, Glucose.
Do not discontinue abruptly: Rebound HTN, angina, dysrhythmias, MI
can result.
Monitor BP & pulse.
Hold for HR < 60 / min.
Education:
Teach how to take radial pulse and BP.
Rise slowly to prevent postural hypotension.
May cause sexual dysfunction.
Report constipation: Eat foods high in fiber
Calcium Channel Blockers
RATE CONTROL Amlodipine (Norvasc), Diltiazem (Cardizem), Ranolazine (Ranexa)
Common Uses: Angina, HTN, Dysrhythmias, Migraines and Raynauds Disease
Contraindications: Heart Block, Hypotension, Severe Heart Failure
PO (10 - 30 mins )/ IV (3mins)
Interactions: Increased levels of digitalis, theophylline. Decreased effects of lithium. Increased hypotensive effects with grapefruit juice
MoA: Blocks the calcium channel in the vascular smooth muscle cells. This causes vasodilation of the arterial system to decrease arterial resistance and decrease blood pressure. This decreases afterload, which decreases the workload of the heart. These medications dilate the coronary arteries so more oxygen reaches the heart muscle
Advantages: Decreases afterload and increases
oxygen to the heart muscle.
Decreases BP better in African
Americans than drugs in other categories
Disadvantages: Need to reduce dose with known liver disease
Side Effects: GI upset Ankle edema Dermatitis Flushing Headache Dizziness
Adverse Effects: Bradycardia Reflex Tachycardia Heart Block Hypotension Dyspnea Wheezing
Interventions:
Taper dose: Do not discontinue abruptly.
Monitor BP, HR – Notify PHCP for HR < 50 or Systolic BP < 90.
Monitor for increased AST, ALT, Alk phosphatase, BUN, Creatinine, and cholesterol.
Education: Do not stop taking abruptly. Rise slowly.
Increase fluids and fiber to counteract constipation.
Teach how to take pulse and BP.
Avoid hazardous activities until dizziness is no longer a
problem.
Avoid grapefruit products.
Report chest pain, palpitations, irregular heart rate, swelling of extremities, tremor
Digoxin
RATE CONTROL
Used in heart failure and atrial fibrillation
Contraindicated in Ventricular dysrhythmias and Heart blocks
PO/IV
Interactions: Loop diuretics can cause hypokalemia and dig toxicity. Ginseng may elevate digoxin levels St John’s wort decreases absorption of digoxin. Decrease dig absorption with antacids.
MoA: Promotes increased force of cardiac contraction, cardiac output, and tissue perfusion. Decreases ventricular rate. So heart
contraction is stronger, heart rate slows down. This allows more blood to be ejected out of the ventricles in a forward
direction
DIGOXIN TOXICITY IS VERY BAD - elderly are prone to same
Side Effects: Headache and Dizziness
Adverse Effects:
Dig toxicity: anorexia, n/v, weird arrhythmias,
vision changes.
Heart block
Interventions:
Monitor Digoxin level (Normal 0.5-2 ng/mL)
Monitor potassium (Low K+ can increase risk for dig toxicity)
Monitor apical pulse. Hold dig for HR < 60 bpm in adults.
Administer IV dose slowly over 5 minutes.
Monitor for signs of dig toxicity: anorexia, nausea/vomiting, weird
arrhythmias, vision changes.
Antidote: Digoxin immune Fab (Digibind)
Education: Teach client how to take pulse, Signs of Dig Toxicity
Norepinephrine
Used in Shock and acute hypotension
Contraindicated in Tachy dsyrhythmias, Pheochromocytoma, Hypovolemia
IV
Interactions: Increase pressor effect with tricyclics, MAOIs.
Decreased norepinephrine action with alpha blockers
MoA: Potent vasoconstrictor action (alpha-adrenergic effect). It is used in shock states, often when drugs such as dopamine and
dobutamine have failed to produce adequate blood pressure. Causes increased contractility and heart rate by acting on beta receptors of the heart.
Disadvantages:
Has potential to impair cardiac performance and decrease organ and tissue perfusion.
Side Effects: Headache Anxiety Dizziness Insomnia Tremor Palpitations Nausea/vomiting
Adverse Effects: Myocardial ischemia/Dysrhythmias Impaired organ perfusion Tissue necrosis with extravasation. Cerebral hemorrhage Anaphylaxis
Interventions:
Correct hypovolemia prior to use.
Continuous cardiac monitoring.
Precise blood pressure monitoring and HR every 2-3 min.
Taper drug slowly as abrupt discontinuation can result in severe hypotension.
Monitor IV site for extravasation frequently. If extravasation occurs,
inject with phentolamine.
I&O
Direct Acting Vasodilators
DECREASE AFTERLOAD
Hydralazine
(Apresoline)
Nitroprusside
(Nipride)
Common Uses: Hypertension Hypertensive crisis Severe heart failure Acute MI with hypertension and persistent chest pain and /or left ventricular failure
Contraindications: Systemic Lupus, Severe Tachycardia with heart failure
PO/IV Interactions: Increase antihypertensive effects: ACE inhibitors, vasodilators, diuretics, alcohol, MAOIs, tricyclic antidepressants, hawthorn.
MoA: Relaxes smooth muscles of the blood vessels, mainly arteries, causing vasodilation. Promotes an increase in blood flow to the
brain and kidneys
Advantages: Nitroprusside is a potent vasodilator that
rapidly decreases BP in hypertensive crisis.
Disadvantages: Adverse effects eliminate use of these drugs as drug of choice
Side Effects: Headache Dizziness Hyperglycemia Sodium and water retention Peripheral edema
Adverse Effects:
Reflex tachycardia
Hypotension
Rebound hypertension
Interventions:
Monitor vital signs, I&O, glucose.
Daily weight
Nitroprusside: Monitor BP frequently with continuous cardiac monitoring.
Education:
Purpose of medication
Safety precautions
Move slowly from lying or sitting to standing position.
Hypertensive Crisis
A hypertensive crisis is a severe increase in blood pressure that can lead to a stroke. Extremely high blood pressure — a top number (systolic pressure) of 180 millimeters of mercury (mm Hg) or higher or a bottom number (diastolic pressure) of 120 mm Hg or higher — can damage blood vessels.
Direct Vasodilators/ Nesiritide
Acute Treatment of heart failure in clients with dyspnea at rest or minimal activity
Contraindications: Valvular Stenosis, Cardiomyopathy, Pericardial tamponade
IV/ 15 mins
MoA: A B-type natriuretic peptide, which is normally produced by the ventricular myocardium. It relaxes and dilates blood vessels,
lowering blood pressure.
Advantages: Useful for clients decompensating from acute heart failure
Disadvantages: For short term IV use only: up to 48 hours. Nephrotoxic.
Side Effects:
Headache
Dizziness
Nausea/Vomiting
Adverse Effects: Hypotension Irregular HR Chest pain Fever Unusual weakness
Interventions: Monitor creatinine level Monitor vital signs, hourly urine output ECG monitoring Daily weight Monitor for allergic reaction (rash, pruritus, laryngeal edema, wheezing)
Oxygen
Common use: Hypoxemia Severe anemia Carbon monoxide poisoning Shock Heart failure
Route: NC Face Mask, Non rebreather, ET, CPAP/biPAP
MoA:
Inadequate oxygenation produces hypoxemia and significant physiologic changes to all body systems, therefor oxygen is a
first-line drug for all emergency situations. Oxygen also acts as a potent pulmonary vasodilator and is beneficial for clients in
heart failure.
Disadvantage: An FiO2 above 50% for a prolonged
period can lead to oxygen toxicity and detrimental effects to the pulmonary
system
Side Effects: Dry or bloody nose Skin irritation Morning headaches Fatigue ET: mucus plugs, tracheal injury, infection, ET misplacement
Adverse Effects: Oxygen Toxicity
Interventions:
Make sure that the client’s airway and breathing are adequate to
promote optimal oxygenation and ventilation.
Monitor pulse oximetry. Optimal oxygen saturation is at or above
94%.
Notify primary healthcare provider for oxygen saturation less than
90%.
Dobutamine
SHOCK
Contraindications: Aortic Stenosis
IV (1 -2 mins)
Interactions: Increased pressor effect and dysrhythmias with tricyclics, MAOIs.
MoA: The beta1 effects enhance the force of myocardial contraction (positive inotropic effect) and increasing heart rate (positive
chronotropic effect). The beta 2 effects produce mild vasodilation
Advantages: BP is elevated only through the increase in cardiac output
Side Effects: Headache Nausea Tremors Anxiety Dizziness Fatigue Palpitations
Adverse Effects: Myocardial ischemia Tachycardia Dysrhythmias Hypotension Hypertension Hypokalemia
Interventions:
Correct hypovolemia prior to use.
Usual IV dose is 2-20 mcg/kg/min. Administer via electronic infusion
pump for precision. Taper gradually to avoid clinical deterioration.
Continuous cardiac and blood pressure monitoring.
I&O
Monitor vital signs
Assess for signs of myocardial ischemia.
Continuous ECG monitoring
Epinephrine
Used for Cardiac arrest, Asystole, V fib, Acute asthmatic attacks , Anaphylaxis
Contraindications: Closed Angle Galucoma
IVP / Rapid Do not use with MAOIs or tricyclics – hypertensive crisis may occur.
MoA: Vasoconstriction effects: epinephrine binds directly to alpha-1 adrenergic receptors of the blood vessels (arteries and veins)
causing direct vasoconstriction, thus, improving perfusion pressure to the brain and heart.
Cardiac Output: epinephrine also binds to beta-1-adrenergic receptors of the heart. This indirectly improves cardiac output by
increasing heart rate, heart muscle contractility, and conductivity through the AV node
Used to simulate the heart muscle
Side Effects:
Tremors Palpitations
Headache Hypertension
Dizziness Nausea/Vomiting
Adverse effects:
Cerebral hemorrhage
bronchospasms
Interventions:
Elevate extremity for 10-20 seconds to facilitate drug delivery to the
central circulation.
Auscultate lungs
Monitor pulse, BP, respirations.
Continuous cardiac monitoring
Do not administer in same IV site as Sodium Bicarbonate
Loop Diuretics
Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)
Heart Failure Renal Failure Hepatic disease Hypertension Hypercalcemia (increases renal excretion of calcium) FVE
Contraindications: Hypovolemia Anuria Severe electrolyte imbalances Hepatic coma
PO/IV Interactions: Increase ototoxicity with aminoglycosides. Increase bleeding with anticoagulants. Increase digoxin toxicity with digoxin and hypokalemia
MoA: Causes diuresis, but also will cause vasodilation to trap blood out in the arms and legs which reduces preload and afterload.
Advantages: Rapidly removes fluid to help clients in acute
heart failure or pulmonary edema.
Disadvantages: Potassium-wasting Should not be used if a thiazide could alleviate body fluid excess
Side Effects: Nausea Diarrhea Vertigo Constipation Weakness Headache Electrolyte imbalances Abdominal cramping Constipation
Adverse Effects: Severe dehydration Gout Marked hypotension Hyperglycemia Hearing loss Renal failure Thrombocytopenia
Interventions:
Assess vital signs, UOP, electrolytes.
Daily weight
Monitor potassium levels. Observe for signs of hypokalemia.
Monitor digoxin levels if taking digoxin.
Administer IV dose over 1-2 minutes to prevent hypotension and ototoxicity
Education:
Advise to take in the morning and not in the evening to
prevent sleep disturbance and nocturia.
Rise slowly from lying or sitting to standing.
Take with food to avoid nausea.
Eat foods high in potassium.
Pathophysiology of decrease Cardiac Output
Lack of proper perfusion.
Brain: Decreased LOC Heart: Increased Pain Lungs: Sound Wet and SOB Skin: Cool and Clammy Kidneys: UO goes DOWN Pulses: Decreased/ Thready
Arrthymias are no big deal until they affect CO
Pulseless V TACH, V FIB and A-systole
Coronary Artery Disease
Most common type of Cardiovascular disease. Includes Chronic stable angina and Acute Coronary Syndrome.
Chronic Stable Angina: Patho and treatment
Intermittent decreased blood flow to heart that leads to ischemia. This ischemia can lead to temporary pain/pressure in the chest because of the low perfusion due to exertion.
Relieved by Rest and nitro
Treatment:
Nitro
Beta blockers ( for prevention of Angina) - Decreases contractility, decreases CO thus decreasing workload of the heart.
Calcium Channel Blockers ( prevention of angina) - decreases the afterload through vasodilation and increases oxygen to the heart muscle
ASA: Antiplatelet.
Chronic Angina: Client Education and Teaching
Rest frequently Avoid Overeating Avoid excess caffeine of any drugs that increase HR Wait 2 hours after eating to excercise Dress warmly in cold weather ( any temperature extreme can precipitate an attack) Take Nitro prophylactically Smoking Cessation Lose Weight Avoid isometric exercise Reduce Stress
DO EVERYTHING YOU CAN TO DECREASE THE WORKLOAD OF THE HEART
Cardiac Catheterization: Pre and Post Procedure
Pre procedure:
Ask if allergic to Iodine/contrast or Shellfish
CHECK THAT KIDNEY FUNCTION because dye is excreted through the kidneys
Acetylcytsteine is given pre- procedure if client has kidney problems. It protects the kidneys .
HOT SHOT
Palpitations are normal
Post Procedure
Monitor Vital Signs
Watch the puncture site for bleeding and Hematoma formation
Assess Pulselessness, Pallor, Pain, Paresthesia and Paralysis, extremely distal from puncture site, as well as circulation and vascular check
Bed rest, Flat, Extremely straight for 4 -6 horus
Major complication is hemorrhage
report Pain ASAP
If the client is on metformin, you must hold this med for 48 hours post procedure. We are worried about blood sugar impacting the kidneys.
Acute Coronary Syndrome ( MI, Unstable Angina) : Patho and Signs and Symptoms
Decreased Blood flow to the myocardium leads to both iscehmia and necrosis
SIgns and Symptoms :
Pain that is crushing, with pressure radiating to left arm and left jaw, N/V or pain between the shoulder blades
Cold/clammy/ drop in BP and pulse
Cardiac Output drops
ECG changes
Vomiting ( stimulates the vagus nerve which lowers the heart rate)
PVC’s because of hypoxia in the heart
In women, they usually present with GI signs and symptoms, epigastric discomfort or pain between shoulders, an aching jaw or choking sensation.
In the elderly and Diabetic, there will be behavioural changes, less or no pain, fainting and SHORTNESS OF BREATH
CPK-MB
Cardiac specific isoenzyme
Increased with damage to cardiac cells
Elevates within 3 - 6 hours and peaks in 12 to 24 hours
Troponin
Cardiac Biomarker with high specificity to myocardial damage
Elevates within 3 to 4 hours and remains high for up to 3 weeks
Myoglobin
Increased within 1 hour and peaks in 12 hours. Negative results are a good thing
Major Arrhythmias
Pulseless V. Tach, V.Fib and Asystole put the client at risk for sudden death
Priority treatment V. Fib is DEFIB
If the first shock doesn’t work and the client remains in V-Fib, what is the first vasopressor we give? Epinephrine
Amiordarone is an anti-arrhythmic and is used when V.Fib and pulseless VT are resistant to treatment and also for fast arrhythmias ( not a vasopressor)
