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)
If the first shock doesn’t work and the client remains in V-Fib, what is the first vasopressor we give?
Epinephrine
What anti-arrhythmic drugs are commonly given to prevent a second episode of V-Fib?
Amiodarone or Lidocaine.
Hypotension is an important side effect of amiodarone so watch BP as it can lead to further arrthymias because of decreased perfusion.
What are the first signs of lidocaine toxicity?
any CNS changes
Treatment for ACS
Oxygen, Aspirin, Nitro and Morphine
Head up position ( decreases workload on the heart and increases effectiveness/CO)
Thrombolytics
Dissolves the clot that is blocking blood flow to the heart muscle –> decreases the size of the infarction
Medications: alteplase, tenecteplasem reteplase and streptokinase
Should be administered within 6 to 8 hours
TIME IS BRAIN ( within three hours for a stroke client)
Major complication: bleeding
Obtain a good health/bleeding histroy
ABSOLUTE CONTRAINDICATIONS:
Intracranial neoplasm, intracranial bleed, suspected aortic dissection or internal bleeding, reent surgery, stroke, pregnant and ulcers
During and after admin, we take bleeding precautions
Follow-up therapy: Anti platelets are another important factor of thrombolytic therapy
Bleeding precautions
For anticoagulants, antithrombotics and Tylenol overdose / liver disease or damage
Watch for bleeding gums, hematuria and black stools. use electric razor, soft toothbrush, no IM’s. Draw blood when starting IV’s, decrease the number of puncture sites. NO ABG’s
PCI (Percutaneous Coronary Intervention)
Includes all interventions such as angioplasty and stents
Major complication of an angioplasty is an MI. The patient may bleed from the cath site or they could reocclude; If there is chest pain after the procedure, They must go to the cath lab to fix this as they are reoccluding.
Antiplatelets are on BOARD : ASA, Clopidogrel, Abciximab and Eptifibatide ( last two given to clients who have been stented to keep artery open and those waiting to go to the cath lab)
Coronary Artery Bypass Graft ( CABG)
Can be scheduled or emergency procedure
Used with multiple vessel disease or left main coronary artery occlusion
The LEFT main coronary artery supplies the entire left ventricle. Occlusion = death.
CARDIAC REHAB
Smoking cessation
Stepped care plan
Diet changes : less fat, sugar and cholesterol
No isometric exercises- increases the workload of the heart
No Valsalva Maneouver
No straining, suppositorys or docusate ( Use Stool softener)
Sex can be resumed when client is able to walk up a flight of stairs - 1 week to 10 days. Safest time is the morning, when the client is well rested
The best excercise is walking.
S/s of heart failure (Weight gain, Ankle Edema, SOB and Confusion) - pt is at increased risk after MI
Heart Failure Causes + Types
HF is a complication that can result from problems such as cardiomyopathy, valvular heart disease, endo-carditis, acute MI and HTN
Types: Left Sided: blood going back in towards the lungs Pulmonary congestion Dyspnea Cough Blood tinged frothy sputum Restlessness Tachycardia S-3 Orthopnea Nocturnal dyspnea
Right Sided Failure: Blood going backward into body systems. Can be caused by pulmonary embolism - hypoxia and pulmonary HTN increase the workload on the right side of the heart leading the R HF. COPD in the end stages is always hypoxic because the right side if failing from pulmonary edema/HTN
Distended Neck veins Edema Enlarged Organs Weight gain Ascites FVE
Heart Failure Diagnosis
B-type natriuretic peptide
Secreted by ventricular tissues in the heart when ventricular volume and pressures in the heart are increased
Sensitive indicator
Can be positive for heart failure when the CXR does not indicate a problem
If pt is on nesiritide, turn it off 2 hours prior to drawing a BNP
CXR
Enlarged heart, pulmonary infiltrates (fluid) at lung bases
Echocardiogram: Looks at the pumping action or ejection fraction of the heart. An ECG can also give you info on backflow and valve disease
Treatment of HF - ACE, ARBS and Digoxin + Nursing considerations
ACE inhibitors
DOC for HF
results in arterial dilation and increased stroke volume
Monitor for hyperkalemia because it blocks aldosterone, which usually excretes potassium
ARBS
Decrease arterial resistance and cause decreased BP
Monitor for hyperkalemia because it blocks aldosterone, which usually excretes potassium
Both these drugs decreases the workload on the heart by prevent vasoconstriction (decreasing the afterload)
This will increase the cardiac output and keep blood moving forward out of the heart.
Digoxin
Monitor for toxicity, especially in the elderly.
Used when client is in sinus rhythm or a.fib and has accompanying chronic HF
Often given in combination with ACE inhibitor, ARBS, Beta blockers or diuretics
Contractions are stronger, HR decreases
Increasing Cardiac Output and Kidney perfusion
Nursing considerations
Normal dig level = 0.5 - 2 ng/ml
You know dig is working because CO goes up
Before giving, take apical pulse for one minute
monitor electrolytes - Hypokalemia + digoxin = toxicity
Digoxin Toxicity
Early signs: Anorexia, nausea, vomiting
Late: weird arrhythmias and vision changes
Any electrolyte imbalance can promote toxicity
Treatment of HF - Diuretics
Diuresis is a GOOD thing for this client because they can’t handle the fluid.
Diuretics will decrease the preload
Give in the morning, because client will be peeing all day. At night, this will increase their risk for falls.
Treatment of HF - non-pharmacological interventions
Low sodium diet
Decreases fluid retention and helps decrease the preload
Watch salt substitutes as they can contain excessive potassium
Elevate head of the bed
Weigh Daily and report gain of 4.4 lb ( 1-2 kg)
Fluid retention - think heart problems 1st
Report signs and symptoms of recurring failure
Pacemakers
Your natural pacemaker is the SA node - it sends out impulses that make the heart beat
If your heart rate drops to 60 or below, cardiac output can decrease, thus decreasing perfusion to organs such as brain and showing decreased CO symptoms
Pace makers are used for symptomatic bradycardia
They can be temporary ( invasive or non-invasive) or permanent. Most are on demand but you can also see fixed.
Always worry if it drops below set rate
Any pace maker will maintain a certain minimal heart tate depending on the set rate
A demand pacemaker kicks in only when the client needs it
OK for rate to increase, but never decrease
Post procedure care for permanent pace -makers
Monitor the incision
Most common complication is electrode displacement
Monitor ECG for changes
Immobilize arm - avoid extension
Assisted passive range of motion to prevent frozen shoulder
Keep client from raising the arm higher than shoulder height
pt teaching : Check pulse daily - ID card or bracelet - avoid electromagnetic fields and MRI’s
Signs and symptoms of Malfunction
Loss of Capture - no contraction following stimuli ( can affect CO)
Failure to sense - pacemaker fires at inappropriate times
LOOK FOR DECREASED CO S/S
Pulmonary Edema: Risks, Patho and S/S
Who is at risk? Any one receiving IV fluids very quickly, The very young and very old and any person who has a history of heart or kidney disease
Fluid is backed up into the lungs, the heart is unable to move the volume forward. Usually occurs at night when the client goes to bed.
Signs/Symptoms Sudden Onset Breathless Restless/anxious Productive cough ( pink frothy sputum)
Pulmonary Edema Treatment
Priority nursing action is to administer high flow oxygen. Monitor SPO2 and titrate to keep above 90%
Meds:
Furosemide : causes diuresis and vasodilation which traps more blood out in the arms and legs and reduces preload
40mg IVP over 1-2 minutes to prevent otoxicity
Bumetanide: can be given IV push or as a continuous IV infusion to provide rapid fluid removal
1-2mg IVP over 1-2 minutes
Nitro: Vasodilation to decrease afterload = increased CO because the heart is pumping against less pressure and more blood can move forward
Morphine: 2mg IV push for vasodilation to decrease preload and afterload
Nesiritide: IV infusion - short term therapy, not for more than 48 hours, vasodilates veins and arteries and has a diuretic effect
Upright Position; Legs down. Improves CO because gravity helps pumping. promotes pooling of blood in lower extremities
Cardiac Tamponade: Patho and Signs and Symptoms
Blood, Fluids or exudates hae leaked intp the pericardial sac resulting in compression of the heart. This can occur in an MVA, Right ventricular biopsy, an MI, pericarditis or hemorrhage post CABG
Decreased CO Increased CVP because of the pressure BP dropping because CO bottoming out Heart sounds will be muffled or distant Neck veins will be distended Pressures in all four chambers are the same Narrowed pulse pressure Shock Paradoxical pulses Dypsnea Increased pulse
Cardiac Tamponade : Treatment
Pericadiocentesis to remove fluid from around the heart
Surgery
Arterial disorders
If you have atherosclerosis in one place, you have it everywhere
It is a medical emergency if you have an acute arterial occlusion
Client will report numbness and pain. Extremity will be cold. No palpable pulses, More symptomatic in lower extremities
Intermittent claudication - hallmark sign for arterial problems
coldness numbness, decreased peripheral pulses, atrophy, bruit, thick and brittle nails and ulcerations
Pain at rest means SEVER obstruction
Treatment:
Since arterial blood is having problems getting to the tissue, if you elevate the extremity, the pain would increase. WE DANGLE ARTERIES. Usually treated with angioplasty or endarterectomy
Infective endocarditis
S/s - Fever, malaise, murmur, weight loss, splinter hemorrhage and Oslar nodes
Splinter hemorrhages are tiny clots that run vertically under the finger nails.
Oslers Nodes are painful subQ lesions thaat occur in the palms, soles and pads.
Risk factos include: Mechanical heart valve replacement, IV drug use, dental procedures, rheumatic fever and immunosuppression
Paradoxal Pulse
Pulse stops when client takes a deep breath
Thromboangittis obliterans
Characterized by inflammation and thrombosis of the vessels of the hands and feet. It is strongly associated with smoking.
Usually treated with vasodilators and sometimes bypass surgery.
Ulceration is a common complication.
Corrigan’s Pulse
A pulse that is forceful and then suddenly collapses. It is usually found in patients with aortic regurgitation, a condition caused by a leaky aortic valve. The left ventricle of the heart ejects blood under high pressure into the aorta.
Risk Factors for Primary HTN
High salt and fat intake, obesity, stress, alcohol consumption, inactivity, caffeine and vitamin D deficiency
Primary HTN does not have any identifiable causes
Mitral stenosis
is a narrowing of the mitral valve opening that blocks (obstructs) blood flow from the left atrium to the left ventricle. Mitral stenosis usually results from rheumatic fever, but infants can be born with the condition. Mitral stenosis does not cause symptoms unless it is severe. Does not cause syncope
Aortic stenosis
Narrowing of the aortic valve. This causes reduced cardiac output and increased left ventricle pressure.
Syncope is the hallmark
Aortic Regurgitation
also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. Does not cause syncope. Symptoms: chest pain or tightness that increases with exercise and subsides when you're at rest. fatigue. heart palpitations. shortness of breath. difficulty breathing when lying down. weakness. fainting. swollen ankles and feet.
Anticoagulants - Heparin sodium, warfarin (Coumadin), Enoxaparin (Lovenox), dabigatran etexilate (Pradaxa)
DVT Pulmonary embolisms Thromboembolic complications Prevention of clot formation Dialysis Open heart surgery DIC Atrial fibrillation with embolization
Contraindicated if bleeding
SUBQ/IV
Interactions:
Increase heparin action with oral anticoagulants, salicylates, NSAIDS, penicillin, SSRIs.
Decrease heparin action with digoxin, tetracyclines,
antihistamines, cardiac glycosides, nicotine, nitroglycerin.
Increase bleeding risk with garlic, ginger,
ginkgo, green tea.
MoA: Prevents conversion of fibrinogen to fibrin and prothrombin to thrombin by enhancing inhibitory effects of antithrombin III.
Disadvantages: Does not dissolve clots that are already present
Side Effects: Injection site reactions Fever Chills Headache Rash
Adverse Effects: Hemorrhage Hypotension Thrombocytopenia Anaphylaxis
Interventions:
Monitor aPTT (Activated Partial Thromboplastin Time)
Heparin dosage is adjusted to keep the aPTT between 1.5 and 2.5 times
the normal control level.
Have antidote Protamine Sulfate readily available.
Monitor for bleeding.
Do not massage SubQ injection.
Client Eduction: Purpose of medication. Avoid OTC preparations. Bleeding precautions. Carry ID identifying product
A typical aPTT value is 30 to 40 seconds. If you get the test because you’re taking heparin, you’d want your PTT results to be more like 120 to 140 seconds, and your aPTT to be 60 to 80 seconds.
Antiplatelets: Acetylsalicylic acid (Aspirin), Clopidogrel (Plavix), Abciximab (ReoPro IV), Dipyridamole (Persantine), Eptifibatide (Integrilin), Ticlopidine (Ticlid), Tirofiban (Aggrastat), Anagrelide HCL (Agrylin)
Common Uses: Decrease platelet aggregation Arterial thrombi Thrombotic stroke TIA’s Post-MI thrombi Prevents re-occlusion post stent
PO/IV
Interactions:
Increased bleeding when taken with Dong quai, feverfew, garlic, and ginkgo biloba.
Advantages:
Long-term, low-dose ASA therapy has been
found to be both an effective and inexpensive
treatment for suppressing platelet aggregation.
Side Effects:
GI complaints
Tinnitus
Dizziness
Adverse Effects:
Serious Bleeding episodes
Thrombocytopenia
Agranulocytosis
Interventions:
Monitor for bleeding
Safety precautions
Bleeding precautions
Education:
Teach bleeding precautions.
Notify health care provider if surgery is scheduled while
on antiplatelet medication. It should be discontinued at
least 7 days prior to surgery
Hematopoietic Agent : Erythropoietin Stimulating
Agents (ESAs): Epoetin alfa (Procrit),
Darbepoetin alfa
(Aranesp)
Anemia associated with: Chronic renal failure, HIV, and Chemotherapy Reduce need for blood transfusions in surgical clients.
Contrainducations: Uncontrolled hypertension Hypersensitivity to human albumin
SubQ/IV Interactions: Anticoagulants: need for an increase in heparin during hemodialysis Mechanism
MoA: Erythropoietin is one factor controlling the rate of red blood cell production.
Side Effects:
Hypertension Flushing
Headache Seizures
Fever Bone pain
Adverse Effects: Seizures Hypertensive encephalopathy CHF DVT
Interventions:
Monitor hemoglobin. Target hemoglobin should never exceed 12g/dL
Monitor Blood Pressure.
Only use one dose per vial
Do not shake solution, it can cause the glycoprotein to denature. 2g/dl.
Monitor for seizures
Client Education:
Teach patient or family how to take blood pressure.
Teach patient to avoid hazardous activity during
treatment.
Teach patients with renal disease to include high iron and
low potassium foods in their diet: meat, dark green leafy
vegetables, eggs and enriched breads.
Hematopoietic Agent : Folic Acid, Vitamin B9
(Folate) Folacin
Megaloblastic anemia
Pregnancy
Contraindications: Hypersensitivity
Other types of
Anemias
PO/SubQ Interactions: Estrogens, glucocorticoids, Hydantoin increase the need for folic acid.
MoA: Folic acid is needed for erythropoiesis to increase RBCs, WBCs and platelet formation needed in megablastic anemia and is
necessary for DNA and RNA synthesis
Side Effects: Allergic bronchospasm Pruritus Rash General malaise Erythema
Adverse Effects: Confusion Depression Excitability, irritability Anaphylaxis
Interventions:
Monitor Hgb, Hct and reticulocyte count; and
folate levels: 6 – 15mcg/mL baseline, throughout treatment
Identify products taking that cause increase folic acid use: alcohol,
oral contraceptives, estrogens, glucocorticoids.
Education: Teach foods high in folic acid: bran, yeast, dried beans, nuts, fruit, fresh vegetables, asparagus. Take as prescribed, do not double up Advise that urine may become dark
Hematopoietic Agent: Vitamin B12
(Cyanocobalamin)
Anacobin, Nascobal,
Cobex
Vitamin B12 Deficiency, pernicious Anemia, Vitamin B12 malabsorption
Contraindications: Optic nerve atrophy (Leber’s disease) Pregnancy and breastfeeding Cobalt Allergy
IM/SubQ/Nasal/Sublingual/PO
Interactions: Cimetidine, colchicine, chloramphenicol, aminoglycosides, anticonvulsants and potassium products cause a decreased absorption
Side Effects: Fever Diarrhea Pruritus Flushing/itching Pain at injection site
Adverse Effects: Cardiac failure Thrombosis Optic nerve atrophy Pulmonary edema Hypokalemia
Interventions
Monitor potassium levels.
Monitor CBC for increase in RBC, Hemoglobin.
Monitor for CHF or pulmonary edema in cardiac patients
Education:
Life-long treatment is required for pernicious anemia.
Teach foods high in B12 such as: egg yolks, fish, organ meats, dairy products, clams, and oysters.
Immunotherapy : Interleukin-2 (IL-2),
Interferon-alfa
Leukemia Melanoma Non-Hodgkin’s lymphoma AIDS related Kaposi sarcoma
SubQ/IM
MoA: Has antiviral, antiproliferative, and immune-modulatory effects, which means that these drugs inhibit intracellular replication of DNA, interferes with tumor cell growth, and enhances natural killer cell activity.
Advantages: Can improve resistance to invading microorganisms and reduce cell
proliferation.
Side Effects: Flulike syndrome Nausea/Vomiting Diarrhea Anorexia Xerostomia Taste alterations Poor concentration
Adverse Effects: Seizures Transient aphasia Psychoses Suicidal ideation Cyanosis Orthostatic hypotension Thrombocytopenia
Interventions:
Keep prefilled syringes in the refrigerator.
Do not freeze or shake. Protect from light.
Obtain baseline CBC and liver function tests.
Education:
Keep prefilled syringes in the refrigerator.
Do not freeze or shake. Protect from light.
Notify prescriber of adverse effects.
Plasminogen Inactivators/Anti-fibrolytic Agents : Aminocaproic acid (Amicar)
Excessive
bleeding from
hyperfibrinolysis
Contraindications:
Disseminated
intravascular
coagulation (DIC)
IV/PO/1 hour Interactions: Factor IX complex: increased risk of thrombosis
MoA: Promotes clot formation by inhibiting plasminogen activators.
Advantages:
Antidote for thrombolytic therapy with excessive bleeding
Side Effects: Edema Headache Malaise Nausea/Vomiting Diarrhea Abdominal pain
Adverse Effects: Uncommon and generally mild. Rare: Thrombophlebitis Orthostatic hypotension.
Interventions:
Monitor bleeding episode.
Continuous cardiac monitoring – Looking for signs of re-occlusion
Monitor for signs of M
Thrombolytics : Tenecteplase (TNKase), Reteplase (Retavase), Alteplase (tPA), Streptokinase, Urokinase
Acute MI
Thrombolic stroke
Pulmonary embolism
DVT
Contraindications: Intracranial neoplasm Intracranial bleed Suspected aortic dissection Internal bleeding
IV/5-10 mins Interactions: Increased bleeding when taken with oral anticoagulants, NSAIDs, ginkgo, garlic, ginger, green tea. Decreased effects when taken with nitroglycerin.
MoA: Promotes the fibrinolytic mechanism (converting plasminogen to plasmin, which destroys the fibrin in the blood clot). The
thrombus disintegrates when a thrombolytic drug is administered within 4 hours after an acute MI. Necrosis is prevented or minimized.
Advantages: Dissolves clot within 4 hours after an acute MI.
Disadvantages; Risk for Hemorrhage
Side Effects: Bleeding Nausea Vomiting Fever
Adverse Effects: Hemorrhage Anemia Bronchospasms Anaphylaxis Reperfusion anemias MI Stoke
Interventions:
Check baseline vital signs and baseline CBC, PT, INR.
Obtain medical and drug history. Bleeding history.
Have Amicar readily available – Antidote.
Continuous cardiac monitoring.
Continuously monitor for hemorrhage for 24 hours.
Initiate bleeding precautions
Avoid venipuncture/arterial sticks
Education: Explain thrombolytic treatment.
Advise to report lightheadedness, dizziness, palpitations,
nausea, pruritus, or urticaria.
Avoid use of aspirin or NSAIDS for pain or discomfort.
Normal PT and therapeutic PT
11 - 12 seconds
Should be 1.5 to 2.5 the normal when on Coumadin. (15.5 - 35 seconds)
INR and therapeutic INR
0.9 - 1.2
Should be 2 .0 - 3.0 when on Coumadin for Afib and 2.5 -3.5 for a valve
Normal aPTT
30 to 40 seconds
When on Heparin, should be 45 to 100 seconds
Non-pharmacological ways to decrease preload
Increase HOB
Dangle legs
Low Salt diet
Locations of Heart Sounds
Aortic: 2nd intercostal space to right of sternal border
Pulmonic: 2nd ICS to left of sternal border
Erbs: 3rd ICS to the left of sternal border
Tricuspid : 5th ICS to the lower left sternal border
Mitral : Apex, PMI and 5th ICS at MCL
Sickle cell crisis
A sickle cell crisis is pain that can begin suddenly and last several hours to several days. It happens when sickled red blood cells block small blood vessels that carry blood to your bones. You might have pain in your back, knees, legs, arms, chest or stomach. The pain can be throbbing, sharp, dull or stabbing
Stroke. A stroke can occur if sickle cells block blood flow to an area of your brain Acute chest syndrome Pulmonary hypertension Organ damage Blindness Leg ulcers Gallstones Priapism
Third Degree Heart Block
This client is experiencing third-degree atrioventricular (AV) block, or complete heart block, which involves complete inhibition of impulse conduction from the atria to the ventricles, usually at the AV node or bundle of His. The atrial and ventricular rhythms are regular but unrelated to each other. A complete heart block results in bradycardia, decreased cardiac output, syncope, and possibly heart failure/shock. The client is typically symptomatic and requires immediate treatment with transcutaneous pacing until a permanent pacemaker can be inserted. Atropine, dopamine, and epinephrine can be used to increase heart rate and blood pressure until temporary pacing is available.
Milrinone
Milrinone (Primacor) is a phosphodiesterase-3 inhibitor given via IV infusion to increase contractility and promote vasodilation. Milrinone, an inotropic agent, is often prescribed to clients with heart failure unresponsive to other pharmacologic therapies. The medication is usually infused over 48-72 hours in a hospital setting; however, home infusion through a central line is becoming more common as a palliative measure for end-stage heart failure. Milrinone infusion requires central venous access (eg, peripherally inserted central catheter) as the medication is a vesicant and can cause extravasation if infused through a peripheral IV line.
The home health nurse should perform the following:
Ensure that an infusion pump is used to control the rate, and instruct the family on basic troubleshooting (Option 4).
Evaluate medication effectiveness and possible side effects.
Monitor the central line insertion site for infection.
Change the central line dressing as prescribed (Option 3).
Monitor daily weight (Option 1).
Monitor blood pressure for possible hypotension (Option 2).
Implement safety precautions as hypotension increases the client’s risk of falling.
A client may receive a milrinone infusion in the home for palliative treatment of end-stage heart failure. The infusion is set up via an infusion pump and infused through a central line. The client and family should be instructed on basic pump troubleshooting as well as the importance of measuring daily weight and blood pressure.
BNP normal Value
<100 pg/ml
Trop normal Value
<0.01
CK normal Value
20-215 U/L
C-reactive protein normal Value
<8mg/L
