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109 Cards in this Set

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What is the pharmacological action of Dopamine (Intropin)?
Acts directly and by the release of norepinephrine from sympathetic nerve terminals; mediates dilation of vessels in the renal and splanchnic beds to maintain renal perfusion while stimulating the sympathetic response

- Activation of receptors in the kidney cause the renal blood vessels to dilate
- Renal blood vessel dilation
- Increased HR
- Increased Myocardial Contractility
- Increased rate of conduction through AV node
- Vasoconstriction
What is Dopamine(inotropin) used for (indications)?
Correction of hemodynamic imbalances present in shock

- Sympathomimetic of choice for treatment of shock. Stimulates heart and blood pressure; causes a renal and sphlanchnic arteriole dilation that increases blood flow to the kidney, thus preventing the diminished renal blood supply and possible renal shutdown that can occur with epinephrine or norepinephrine. Another therapeutic use in heart failure
What class is prototype Dopamine(inotropin) under?
(Alpha and Beta adrenergic Agonists)
These drugs are generally sympathomimetic
What are the adverse effects of Dopamine (inotropin)?
Tachycardia, ectopic beats, angina pain, hypotension, dyspnea, nausea, vomiting, HA

- Adverse effects of Alpha and beta adrenergic agonists may be associated with drugs effects on SNS:
o Arrhythmias, hypertension, palpitations, angina, dyspnea related to the effects on the heart and cardiovascular system; Nausea and vomiting, related to depressant effects on GI tract; HA, sweating, and piloerection related to sympathetic stimulation
What are some nursing considerations for Dopamine (inotropin)?
- Assessment: Screen for cautions or contraindications: Allergies to these drugs, pheochromocytoma, tachyarrhythmias or ventricular fibrillation, or hypovolemia, general anesthesia with halogenated hydrocarbon anesthetics; and presence of vascular disease. Include screening for baseline status before beginning therapy and for any potential adverse effects: skin color and temp, pulse, blood pressure, and ECG; respirations, adventitious breath sounds; urine output and electrolytes.

- Nursing diagnoses (if any):
o Acute pain related to CV and systemic effects
o Decreased CO related to CV effects
o Ineffective Tissue perfusion related to CV effects
o Deficient knowledge regarding drug therapy

- Implementation:
o Take caution in preparing drugs because even small errors can have serious effects.
o Dilute drug before use to prevent tissue irritation upon injection.
o Monitor Pt response (BP, ECG, Urine output, CO), adjust dose to ensure most beneficial
o Maintain phentolamine on stand by in case extravasation occurs; infiltration of the site with 10mL saline containing 5 to 10 mg phentolamine is effective in saving the area
o Provide thorough patient teaching, include measures to avoid adverse effects, warning signs of problems, and need for monitoring and evaluation, to enhance patient knowledge about drug therapy and promote compliance

- Evaluation:
o Monitor pt response to drug (improvement in BP, ocular pressure, bronchial airflow)
o Monitor adverse effects (CV changes, decreased urine output, HA, GI upset)
o Evaluate effectiveness of teaching plan (pt can name drug, dosage, adverse effects to watch, Specific measures to avoid adverse effect)
o Monitor effectiveness of comfort measures and compliance with regimen
o May be evidenced by:
 Improved perfusion as evidenced by urine output of greater than 30mL/hr (with normal renal function),
 Improved mental status, systolic BP maintained at greater than 90mm hg.
What is Phenylephrine used for (indications)?
) tx of vascular failure in shock or drug-induced hypotension; to overcome paroxysmal supraventricular tachycardia; to prolong spinal anesthesia; as a vasoconstrictor in regional anesthesia; topically for symptomatic relief of nasal congestion and as adjunctive therapy in middle ear infections; ophthalmically to dilate pupils and as a decongestant to provide temporary relief of eye irritation.
What class of drug does Phenylephrine belong to?
Alpha Specific Adrenergic Agonists; vasopressors
What is the mech. of action(s) of Phenylephrine?
powerful postsynaptic alpha-adrenergic receptor stimulant causing vasoconstriction and raising systolic and diastolic blood pressure with little effect on beta-receptors in the heart.
What are the most common adverse effects of Phenylephrine?
fear, anxiety, restlessness, HA, nausea, decreased urine formation, pallor
What are some nursing considerations in drug admin of Phenyephrine?
- Assessment: Screen for known allergies, presence of any cardiovascular disease, thyrotoxicosis, or diabetes which would require cautious use; pregnancy or lactation; chrnonic renal failure which can be exacerbated by drug use.
- Screen for baseline status before beginning therapy and for any potential adverse effects: orientation, affect, reflexes, and vision to monitor for any CNS changes related to drug therapy; blood pressure, pulse, ECG, peripheral perfusion, and cardiac output to establish a baseline and to monitor drug effects and adverse cardiovascular effects; and urinary output and renal function tests to monitor drug effects on renal system.
- Nursing diagnoses (if any):
o Disturbed sensory perception r/t CNS effects
o Risk for injury r/t CNS or CV effects of drug
o Decreased CO r/t BP changes, arrhythmias, or vasoconstriction
o Deficient knowledge regarding drug therapy
- Implementation:
o Do not DC drug abruptly because sudden withdrawal can result in rebound hypertension, arrhythmias, flushing, and even hypertensive encephalopathy and death, taper drug over 2 to 4 days.
o Do not DC drug before surgery; mark pts chart and monitor BP carefully during surgery. Sympathetic stimulation may alter normal response to anesthesia, as well as recovery from anesthesia.
o Monitor BP, pulse, rhythm, and CO regularly, even with ophthalmic preparations in order to DC drug or adjust dosage if CV effects are severe
o When giving Phenylephrine IV, maintain an alpha blocking agent on stand by in case severe reaction occurs; infiltrate any area of extravasation with phentolamine within 12 hours after extravasation to preserve tissue.
o Arrange for supportive care and comfort measures, including rest and environmental control to decrease CNS irritation, HA med to relieve discomfort, safety measures if CNS effects occur to protect the patient from injury; and protective measures if CNS effects are severe.
o Provide thorough pt teaching including dosage, potential adverse effects, safety measures, warning signs of problems, and proper administration for each route used, to enhance patient knowledge about drug therapy and to promote compliance.
- Evaluation:
o Monitor pt response to the drug
o Monitor for adverse effects
o Evaluate effectiveness of the teaching plan
o Monitor the effectiveness of comfort measures and compliance with the regimen
What class of drug is Propranolol (Inderal)?
Class II antiarrhythmic; Beta adrenergic receptor blocker
What is Propranolol used for (indications)?
tx of cardiac arrrhythmias, especially supraventricular tachycardia; treatment of ventricular tachycardia induced by digitalis or catecholamines. Also used as an antihypertensive, antianginal, and antimigraine headache drug.
What are the most common adverse effects of Propranolol use?
bradycardia, CHF, cardiac arrhythmias, heart blocks, CVA, pulmonary edema, gastric pain, flatulence, nausea, vomiting, diarrhea, impotence, decreased exercise tolerance, antinuclear antibody (ANA) development
What are some nursing considerations of Propranolol use?
-assess for contraindications, perform a physical assessment to establish baseline, assess pt’s neuro status to ID possible CNS effects of drug regimen, assess cardiac status closely, including pulse, BP, HR, and rhythm, auscultate heart sounds noting any evidence of abnormal sounds for early detection of heart failure. Monitor RR and depth, inspect abdomen for evidence of distention, ausculate bowel sounds to evaluate GI motility. Evaluate skin for color, lesions, and temperature to detect adverse reactions and to assess cardiac output.

-Nursing diagnoses include: decreased cardiac output, disturbed sensory perception, risk for injury, deficient knowledge
-Implementation- titrate dose to smallest amt needed to decrease risk of adverse effect, continually monitor cardiac rhythm when initiating or changing dose, ensure emergency life support equipment is readily available, administer parenteral forms as ordered only if oral form is not feasible and expect to switch to the oral form as soon as possible, consult with dr to reduce dose in pts with hepatic/renal dysfunction, establish safety precautions, arrange for periodic monitoring of cardiac rhythm when pt receiving long term therapy, provide comfort measures including small frequent meals, access to bathroom, temperature regulation, light control and decreased noise, provide thorough patient teaching

Evaluation- monitor pt response to drug, monitor for adverse effects, evaluate effectiveness of teaching plan, monitor the effectiveness of comfort measures and compliance with regimen.
What class of drug is Labetalol (Normodyne or Trandate)?
Non-selective adrenergic blocker
What is Labetalol (Transdate) used for (indications)?
these agents competitively block the effects of norepinephrine at alpha and beta receptors throughout the SNS, leading to lower BP, slower pulse rate, and increased renal perfusion with increased renin levels. Labetalol is used IV and orally to tx hypertension (hypertensive crisis!) , can also be used to treat hypertension associated with diuretics and has been used to treat hypertension associated with pheochromocytoma (tumor of the chromaffin cells of the adrenal medulla, which periodically releases large amts of norepinephrine and epinephrine in to the system) and clonidine withdrawal.

-hypertension, alone or in combination with other drugs; of label uses include control of BP in pheochromocytoma, clonidine-withdrawal hypertension.
What is the mech of action for Labetalol (Transdate)?
competitively blocks alpha and beta receptor sites in the SNS, leading to lower BP without reflex tachycardia and decreased renin levels.
What are the most common adverse effects Labetalol (Transdate) use?
dizziness, vertigo, fatigue, gastric pain, flatulence, impotence, bronchospasm, dyspnea, cough, decreased exercise tolerance.
What are some nursing considerations w/ Labetalol (Transdate) admin.?
Assess for contraindications or cautions- allergies, presence of bradycardia or heart block which could be worsened, asthma or bronchospasm which could be exacerbated by loss of bronchodilation effect of norepinephrine, shock or HF which could be worsened by blocking of SNS, diabetes which could be aggravated by blocking of SNS and the masking of usual signs and symptoms of hypoglycemia and hyperglycemia, and pregnancy/lactation. Perform physical assmt to establish baseline, monitor vitals and assess cardio status and obtain ECG, monitor result of labs such as renal and liver function studies and electrolyte levels, monitor blood glucose levels.

Nursing diagnoses-decreased cardiac output, ineffective airway clearance, risk for injury, diarrhea r/t increased PNS activity, deficient knowledge
Implementation- do not discontinue abruptly after chronic therapy because hypersensitivity to catecholamines may develop and the pt could have a severe reaction, taper drug slowly over 2 weeks while monitoring the pt. Consult with dr about withdrawing drug before surgery because withdrawal is controversial; effects of SNS after surgery can cause problems. Encourage pt to adopt lifestyle change, including diet, exercise, smoking cessation, and stress reduction, to aid in lowering BP. Assess HR for changes that might suggest arrhythmias, obtain BP in various positions to assess for orthostatic hypotension. Institue safety precautions. Monitor GI function. Monitor for any s/s of liver failure to arrange for discontinuation of med if this occurs. Provide thorough patient teaching.

Evaluation- monitor pt response to drug (improvement of blood pressure and HF). Monitor for adverse effects. Evaluate effectiveness of teaching plan. Monitor effectiveness of comfort measures and compliance with regimen.
What class of drug does Atropine belong to?
Anticholinergic; antimuscarinics
(antiarrhythmics)
What is Atropine used for (indications)?
• Decrease secretions before surgery, tx of parkinsonism, restoration of cardiac rate and arterial pressure following vagal stimulation, relief of bradycardia and syncope due to hyperactive carotid sinus reflex, relief of pylorospasm, relaxation of the spasm of biliary and ureteral colic and bronchospasm, control of crying and laughing episodes associated with brain lesions, relaxation of uterine hypertonicity, management of peptic ulcer, control of uterine hypertonicity, management of peptic ulcer, control of rhinorrhea associated with hay fever, antidote for cholinergic overdose and poisoning from various mushrooms.

• Used to depress salivation and bronchial secretions and to dilate the bronchi, but it can thicken respiratory secretions (causing obstruction of airways).
• Used to inhibit vagal responses in the heart.
What are most common adverse effects of Atropine?
blurred vision, mydriasis, cycloplegia, photophobia, palpitations, bradycardia, dry mouth, altered taste perception, urinary hesitancy and retention, decreased sweating, and predisposition to heat prostration.
What is the mech of action of Atropine?
Competitively blocks ACh muscarinic receptor sites, blocking the effects of the PNS.
What are nursing considerations for Atropine admin.?
-Monitor for adverse rxns, such as HA, tachycardia, restlessness, dizziness, blurred vision, dry mouth, urinary hesitancy, & constipation
-Monitor vital signs, cardiac rhythm, urine output, & vision for signs of impending toxicity
-Provide stool softeners or bulk laxatives as ordered for constipation.
- Assessment: assess for allergy, kidney or liver failure
o Possible adverse effects of PSNS blockade:
 Glaucoma, stenosing peptic ulcer, intestinal atony, paralytic ileus, GI obstruction, severe ulcerative colitis, toxic megacolon, BPH, bladder obstruction, cardiac arrhythmia, tachycardia, myocardial ischemia
o Possible adverse effects of further blocking of cholinergic receptors:
 Myasthenia gravis, muscle spasticity, brain damage
o Pregnancy: potential adverse effects
o HTN: possible additive hypertensive effects
- Implementation: Basically administer safely, relieve adverse effects such as dry mouth (with lozenges, etc), lighting control for photophobia, small and frequent meals to minimize GI upset, high fiber diet to alleviate constipation, encouraging fluids and monitoring heat exposure bc sweating ability is reduced
What class of drug does Nitroprusside (Nitropress, Nipride) belong to?
Vasodilators
What is Nitroprusside (Nitropress, Nipride) used for (indications)?
hypertensive crisis (high BP), maintenance of controlled hypotension during anesthesia, acute CHF; increased preload & afterload
What is the mech of action of Nitroprusside (Nitropress, Nipride)?
Acts directly on vascular smooth muscle to cause vasodilation & drop BP; does not inhibit cardiovascular reflexes & tachycardia; renin release will occur
What are the most common adverse effects of Nitroprusside (Nitropress, Nipride)?
Apprehension, HA, retrosternal pressure, palpitations, cyanide toxicity, diaphoresis, N/V, abdominal pain, irritation at the injection site
What are nursing considerations for pt. receiving Nitroprusside (Nitropress, Nipride)?
-Monitor thiocyanate levels every 72 hours; excessive doses or rapid infusion (> 15 mcg/kg/min) can cause cyanide toxicity.
-Monitor for AE & signs of cyanide toxicity, including profound hypotension, metabolic acidosis, dyspnea, HA, loss of consciousness, imperceptible pulse, absent reflexes, dilated pupils, pink color, distant heart sounds, shallow breathing, ataxia, & vomiting)
-Monitor BP q5mins at the start of infusion & q15 mins thereafter.
-An IV infusion must be wrapped in foil b/c it's sensitive to light.
- Assessment: assess for allergy, kidney or liver failure
o Pregnant or lactating?
o CV dysfxn? (could be exacerbated by drug)
o Assess baseline status (temp, wt, skin color, lesions, BP, EKG, RR, lung sounds, bowel sounds, BG, liver and kidney fxn
- Nursing diagnoses (if any): p687: Ineffective tissue perfusion r/t changes in CO; Impaired skin integrity r/t dermatological effects; Acute pain r/t GI distress, skin effects or headache; Deficient knowledge regarding drug therapy
- Implementation: p687… encourage lifestyle changes (stop smoking, lower salt intake, alcohol intake, increase exercise; monitor BP closely; monitor BG and electrolytes; educate pt
What is the mech of action for lidocaine (class I antirhythmic)
class I: blocks the sodium channels in the cell membrane during an action potential.

Action: Decreases depolarization, decreasing automaticity of the ventricular cells; increase ventricular fibrillation threshold
What are the adverse effects r/t CV & pulmonary for lidocaine (class I antirhythmic)?
CV - arrhythmias
Pulmonary -respiratory depression
What are the contraindications for lidocaine (class I antirhythmic)?
Allergy, bradycardia or heart block, CHF, hypotension or shock, and electrolyte disturbances. Caution in pts with renal or hepatic dysfunction and pregnancy.
What is the mech of action for propranolol (class II antirhythmic)?
class II: blocks beta receptors, causing a depression of phase 4 of the action potential.

Action- competitively blocks the beta receptor sites in the heart and kidneys. Decreases heart rate, cardiac excitability, and cardiac output. Slows conduction through the AV node.
What are the adverse effects r/t CV & pulmonary for propranolol (class II antirhythmic)?
hypotension, bradycardia, AV block, and arrhythmias, and alterations in peripheral perfusion, pulmonary-bronchospasm and dyspnea, decreased exercise tolerance
What are the contraindications for propranolol (class II antirhythmic)?
-sinus bradycardia, AV block, cardiogenic shock, CHF, asthma, respiratory depression, pregnancy, and lactation, caution with use in diabetes and thyroid, renal, or hepatic dysfunction
What is the mech of action for amiodarone (class III antirhythmic)?
Class III antiarrhythmic: blocks potassium channels prolonging phase 3 of the action potential.

Action- blocks potassium channels and slows the outward movement of potassium during phase 3 of the action potential. This action prolongs the action potential.
What is the adverse effects r/t CV & pulmonary for amiodarone (class III antirhythmic)?
CV-arrhythmias,

Pulmonary-none really (others s/e include- nausea, vomiting, weakness, dizziness)

Severe pulmonary toxicity in 15% of pt --> can be fatal
What are the contraindications for amiodarone (class III antirhythmic)?
when used for life threatening arrhythmias, there is no contraindication. Caution-when used in shock, hypotension, respiratory depression, prolonged QT interval, and renal or hepatic disease.
What is the mech of action for diltiazem (class IV)?
Class IV- blocks calcium channels in the cell membrane

Action:Blocks movement of calcium ions across the cell membrane. Depresses the generation of the action potential. Delays phase 1 and 2 of repolarization, slows conduction through the AV node.
What is the adverse effects r/t CV & pumonary for diltiazem (class IV)?
CV-hypotension, CHF, shock,

Pulmomary-none (others s/e include dizziness, weakness, fatigue, depression, GI upset)
What class of drug does Midazolam belong to?
non-barbiturate anesthetics (IV drugs); benzodiazepines
What is Midazolam used for (indications)?
Sedation, anxiolysis, and amnesia before diagnostic, therapeutic, or endoscopic procedures; induction of anesthesia; continuous sedation of intubated patients
What is the mech of action for Midazolam?
Acts mainly at the limbicsystem and RAS; potentiates the effects of GABA; has little effect on cortical function; exact mechanism of action is not understood
What are the adverse effects of Midazolam?
More likely to cause N/V than other anesthetics. Potent amnesiac.

Transient drowsiness, sedation, drowsiness, lethargy, apathy, fatigue, disorientation, restlessness, constipation, diarrhea, incontinence, bradycardia, tachycardia, phlebitis at injection site

Can cause: CNS & respiratory depression, hypotension, and cardiac arrest
What are nursing considerations for Midazolam administration?
• Assess for contraindications or cautions such as allergies; impaired liver or kidney function; myasthenia gravis; personal or family hx of malignant hyperthermia; & caridac or respiratory disease.
• Perform physical assessment – weight to insure proper dosing and GI motility
• Assess neurological status to monitor CNS depression
• Monitor vitals to note adverse effects
• Assess skin
• Monitor labs for possible toxicity

Nursing Dx:
- Impaired Gas Exchange r/t respiratory depression
- Impaired Skin Integrity r/t immobility
- Disturbed Thought Processes & Disturbed Sensory Perception r/t CNS depression
-Deficient Knowledge regarding drug therapy
What class of drug does Fentanyl belong to?
Narcotic agonist
What is Fentanyl used for (indications)?
For analgesia before, during, and after surgery; transdermal patch for management of chronic pain; control of breakthrough pain
What is the mech of action for Fentanyl?
react with the opioid receptors throughout the body to cause analgesia
What are adverse effects of Fentanyl?
Respiratory: Laryngospasm, bronchoconstriction, respiratory depression or arrest. CNS: Sedation, euphoria, dizziness, diaphoresis, delirium, convulsions with high doses. CV: Hypotension, bradycardia, circulatory depression, cardiac arrest.

Can cause: CNS respiratory depression, hypoventilation, arrhythmias
What are nursing considerations for Fentanyl?
• Assess for contraindications or cautions: exercise extreme caution w/ increased intracranial pressure or altered consciousness
• Perform pain assessment
• Perform physical assessment for baseline status before therapy
• Assess CNS effects; evaluate respiratory effects
• Monitor cardiac effects
• Monitor GI and GU effects
• Lab results for toxic effects and possible dose adjustment
What class does vecuronium (Norcuron) belong to?
Nondepolarizing neuromuscular junction blocker
What is vercuronium (Norcuron) used for (indications)?
Short surgical procedures; intubation; mechanical ventilation
What is the mech of action for vercuronium (Norcuron)?
acts as antagonists to ACh at the NMJ and prevent depolarization of muscle cells
What are the adverse effects for vercuronium (Norcuron)?
Body as a Whole: Skeletal muscle weakness, malignant hyperthermia. Respiratory: Respiratory depression, bronchospasm, apnea. CV: hypotension, cardiac arrhythmias GI: constipation, vomiting, regurgitation, and aspiration OTHER: hyperkalemia
What are nursing considerations for vercuronium (Norcuron)?
-Assess respiratory status continuously throughout therapy w/ NMblocking agents. Use only to facilitate intubation or in pt already intubated
-Monitor neuromuscular response w/ a peripheral nerve stimulator intraop.
-Monitor ECG, HR, & BP throughout admin.
-Observe pt for residual distress during the recovery period
-Monitor infusion site frequently
-Admin. anticholinesterase agents (neostigmine, pyridostigmine) if OD/toxicity/reversal
-Keep emergency resp. support equipment ready: eg. ET, vent., O2, Atropine
Nursing Dx:
- Impaired Gas Exchange r/t depressed respirations
- Impaired Skin Integrity r/t immobility
- Impaired Verbal Communication
-Fear r/t paralysis
-Deficient Knowledge regarding drug therapy

Implementation:
- Teach about NMBlocking drugs: drug causes complete paralysis; expect unable to breathe (assistance will be provided); expect to be aware of what's going on (drug doesn't affect LOC).

Evaluation:
-Pt's condition improves.
-Pt maintains adequate ventilation w/ mechanical assistance.
-Pt & his family state an understanding of drug therapy.
Intro to ECG:

What are the major ions involved in an action potential?
Sodium, Potassium, Calcium
Intro to ECG:

How do shifts in these ions across cell membrane effect depolarization?
A stimulus delivered to excitable tissues evokes an AP that is characterized by a sudden change in voltage resulting from transient depolarization & subsequent repolarization.

The point at which the sodium gates open = depolarization threshold. When the cell has reached this threashold, a rapid influx of sodium ions to the interior of the membrane causes the membrane potential to shift from a resting membrane potential of approx. -90mV to +20 mV
Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane. These channels are shut when the membrane potential is near the resting potential of the cell, but they rapidly begin to open if the membrane potential increases to a precisely defined threshold value. When the channels open, they allow an inward flow of sodium ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential. This then causes more channels to open, producing a greater electric current, and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and they are actively transported out of the plasma membrane. Potassium channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism which prevents an action potential traveling back the way it just came.
Name the five common causes of cardiac arrhythmias:
1. Electrolyte disturbances that alter the action potential
2. Decrease in oxygen delivered to the cells
3. Structural damage changing the conduction pathway through the heart
4. Acidosis or accumulation of waste products, altering the action potential
5. Drugs that alter the action potential or cardiac conduction
What are the types of cardiac arrhythmias seen?
-Tachycardia (faster-than-normal heart rate)
-Bradycardia (slower-than-normal heart rate)
-Premature atrial contractions (PACs) or premature ventricular contractions (PVCs)
-Atrial flutter
-Atrial fibrillation or ventricular fibrillation
-Alterations in conduction through the muscle (heart blocks and bundle branch blocks)
What is the absolute refractory period for the myocardium?
Begins in phase 0 thru phase 3. During this period, the cell cannot respond to another stimulus regardless of the strength of the stimulus. “resistant to stimuli”. The second contraction cannot be stimulated until the first is over. The longer length of the abs. refractory period of cardiac muscle is important in maintaining the alternating contraction & relaxation that is essential to the pumping action of the heart and for the prevention of fatal arrhythmias (Porth p. 332).
What is the relative refractory period for the myocardium
Begins at midpoint of phase 3 thru beginning of phase 4. A stronger than normal stimulus can produce depolarization when repolarization has returned the membrane potential to below the threshold potential, but not to the resting membrane potential (Porth p. 332).
What is the suprarnormal (excitatory) period for the myocardium?
(phase 4): weaker than normal stimulus can produce depolarization “sensitive to stimulus”. This short period occurs after relative refractory period and is when many cardiac arrhythmias develop (Porth p. 332).
What is a common example of a stimulus producing depolarization during the supranormal & relative refractory period?
PAC or PVC (premature beats)
Describe what happens during phase 0 depolarization:
Depolarization- cardiac muscle contraction & Na enters the cell through fast channels
Describe what happens during phase 1:
repolarization-Na levels equalize (fast channels close) & K move out of the cell
Describe what happens during phase 2:
Plateau- Ca channels open through slow channels
Describe what happens during phase 3:
Repolarization- cell returns to negative charge (original states); K moves back into cell
Describe what happens during phase 4:
Resting membrane potential- repolarization is complete & ready for another depolarization
Vasoactive drug therapy for cardiac dysfunct:

What type of drug(s) do you give to INCREASE PRELOAD?
volume expanders
Vasoactive drug therapy for cardiac dysfunct:

What type of drug(s) do you give to INCREASE AFTERLOAD?
Vasopressors
Vasoactive drug therapy for cardiac dysfunct:

What type of drug(s) do you give to INCREASE CONTRACTILITY?
Positive inotropes
Vasoactive drug therapy for cardiac dysfunct:

What type of drug(s) do you give to DECREASE PRELOAD?
Diuretics & vasodilators
Vasoactive drug therapy for cardiac dysfunct:

What type of drugs(s) do you give to DECREASE AFTERLOAD?
Vasodilators
Vasoactive drug therapy for cardiac dysfunct:

WHat type of drug(s) do you give to DECREASE CONTRACTILITY?
Negative inotropes
Vasoactive drug therapy for cardiac dysfunct:

Given a pt w/ LOW PRELOAD what are examples of drugs you would use to tx?
To increase: volume expanders such as:
colloids/crystalloids & blood
Vasoactive drug therapy for cardiac dysfunct:

Given a pt w/ HIGH PRELOAD what are examples of drugs you would use to tx?
To decrease:
1. Dilators: ACE inhibitors, NTG, Nitroprusside, Milrinone

2. Diuretics: Furosemide, Thiazides, CAI, K-sparing
Vasoactive drug therapy for cardiac dysfunct:

Given a pt w/ LOW AFTERLOAD what are examples of drugs you would use to tx?
To increase: vasopressors such as:
Phenylephrine
Epinephrine
Norepinephrine
Dopamine
Vasoactive drug therapy for cardiac dysfunct:
Given a pt w/ HIGH AFTERLOAD what are examples of drugs you would use to tx?
To decrease: vasodilators such as:
ACE inhibitors, NTG, Nitroprusside, Milrinone*, Ca Blockers, PDEI
Vasoactive drug therapy for cardiac dysfunct:

Given a pt w/ LOW CONTRACTILITY, what are examples of drugs you would use to tx?
To increase: (+) inotropes such as:
Digitalis (digoxin)
Dobutamine
Dopamine
Milrinone*
Vasoactive drug therapy for cardiac dysfunct:

Given a pt w/ HIGH CONTRACTILITY, what are examples of drugs you would use to tx?
To decrease: (-) inotropes such as beta blockers:
Metoprolol, Labetalol, Esmolol, Ca blockers
What are some common drugs used to control arrhythmias?
Lidocaine, Procainamide, Verapmil, Digoxin, Inderal (propranolol), Atropine
What is preload?
pressure in the ventricle at end diastole: think
volume & compliance

Preload - If the muscle walls of the heart are stretched prior to a stroke then they will squeeze harder on the stroke. To get a greater stretch more blood must be in the heart. This observation is called the ‘Frank-Starling law of the heart’.
Preload is what comes to the heart before contraction. The heart muscle is much like a rubber band. The more you stretch it, the better it will contract. This stretch is accomplished in the heart through filling of the ventricles with blood. Therefore, preload is related to the amount of blood in the ventricle before contraction. If a person is overhydrated, preload will increase. If a person is dehydrated, preload will decrease.
What are two ways to measure the preload of the heart?
in left side of heart: pulmonary capillary wedge pressure (PCWP) use to measure pressure & fluid status

in the Rt side of the heart: RA(CVP)
What are normal values for left side-preload?
in the left heart measured by PCWP:
4-12 mm/Hg
What are normal values for right side-preload?
in the right heart measured by RA (CVP):
2-6 mm/Hg
What is afterload?
Amount of tension developed by the ventricle in order to eject its blood volume

In order to get blood out the heart the back- pressure in the blood vessels must be overcome. The harder it is to get blood out, the less blood will actually leave the heart. You can imagine if the blood vessels are clogged or narrow that this will make things harder.
Afterload is what comes after ventricular contraction or the resistance against which the heart must pump blood. Afterload is determined by two conditions; the blood volume ejected from the ventricle and the compliance of the vascular space into which the blood is ejected. Think of afterload as a hose nozzle. If the hose nozzle is wide open, afterload is decreased due to decreased compliance. If the hose nozzle is almost closed, afterload will increase because the water has so much resistance to push against. Now, if you increase or decrease the amount of water that comes from the nozzle, there will be a further effect on the afterload. Think of afterload as blood pressure. Increased blood pressure is increased afterload, while decreased blood pressure is decreased afterload.
what is the range for normal range for mean arterial pressure (MAP)?
60-90 mmHg
What is the mech of action for class I antiarrhythmics?
Decrease depolarization, Decreasing automaticity of the ventricular cells; increase ventricular fibrillation threshold

• Drugs that block the sodium channels in the cell membrane during an action potential.
• Stabilize the cell membrane by binding to sodium channels, depressing phase 0 of the action potential and changing the duration of the action potential
• These drugs are further broken down into 3 subclasses, reflecting the manner in which their blockage of sodium channels affects the action potential.
What are examples of class Ia antiarrhythmic drugs?
Class Ia Antiarrhythmics:

disopyramide (Norpace), procainamide (Pronestyl), and quindine (generic).
What are examples of class Ib antiarrhythmic drugs?
Class Ib Antiarrhythmics:

lidocaine (Xylocaine) and mexiletine (Mexitil).
What are examples of class Ic antiarrhythmic drugs?
flecainide (Tambocor) and propafenone (Rythmol).
What are the adverse effects r/t CV & pulmonary for class I antiarrhythmics?
CV: development of arrhythmias (including heart blocks), hypotension, vasodilation, and potential for cardiac arrest.

Pulmonary: Respiratory depression --> respiratory arrest can occur.
What is the mech of action for class II antiarrhythmics?
-Competitively block beta receptor sites in the heart and kidneys (causing a depression of phase 4 of the action potential)
-Decrease heart rate, cardiac excitability, and cardiac output
-Slow conduction though the AV node
What are the adverse effects r/t CV & pulmonary for class II antiarrhythmics?
CV: hypotension, bradycardia, AV block, arrhythmias, & alterations in peripheral perfusion

Pulmonary: bronchospasms, dyspnea
What are some examples of class II antiarrhythmic drugs?
Acebutolol (Sectral); Esmolol (Brevibloc); Propranolol* (Inderal).
What is the mech of action for class III antiarrhythmics?
Block potassium channels and slow the outward movement of potassium during phase 3 of the action potential
This action prolongs the action potential
What are the adverse effects r/t CV & pulmonary for class III antiarrhythmics?
CV: hypotension, CHF, & arrhythmia are common

Pulmonary: laryngospasm, respiratory distress, PE
What are some examples of class III antiarrhythmic drugs?
Amiodarone* (Cordarone); Dofetilide (Tikosyn); Ibutilide (Corvert); Sotalol (Betapace); (Betapace AF).
What are important adverse effects for amiodarone (class III arrhythmic)?
associated w/ potential fatal liver toxicity, ocular abnormalities, & development of very serious cardiac arrhythmias

pulmonary toxicity w/ amiodarone: observe for symptoms of dyspnea, cough, & chest pain
What is the mech of action for class IV antiarrhythmics?
Block the movement of calcium ions across the cell membrane
Depress the generation of action potential
Delay phases 1 and 2 of repolarization
Slow conduction though the AV node
What are the adverse effects r/t CV & pulmonary for class IV antiarrhythmics?
CV: r/t vasodilation of blood vessels throughout the body: hypotension, CHF, shock, arrhtyhmias, AV block, bradycardia

Pulmonary: PE
What are some examples of class IV antiarrhythmmic drugs?
Diltiazem (Cardizem); Verapamil (Calan)
What is the mech of action of Adenosine (endogenous glucoside - misc. antiarrhythmic)?
Restores normal sinus rhythm by interrupting re-entrant pathways in the AV node; Slows conduction time through the AV node; Also produces coronary artery vasodilation; Restoration of normal sinus rhythm.
What are the adverse effects r/t CV & pulmonary for Adenosine?
CV: Sinus bradycardia (decreased conduction through AV node), flushing of face (vasodilation)

Pulmonary: dyspnea of short duration (bronchoconstriction),
What is the mech of action of Digoxin/digitalis (Lanoxin), a cardiac glycoside - misc. antiarrhythmic?
Positive inotropic effect leading to increased force of myocardial contraction (increases force and efficiency of myocardial contraction which improves the heart’s effectiveness as a pump—improving SV and CO); Negative chronotropic effect leading to decreased heart rate (at therapeutic levels, slows the rate of SA node depolarization and the rate of impulses through the conduction system of the heart; a decreased heart rate gives the ventricles more time to fill with blood coming from the atria, which leads to increased SV and increased CO.
What are the adverse effects r/t CV & pulmonary for Digoxin?
CV: dysrhythmias (caused by interfering with the electrical conduction in the myocardium); cardiotoxicity leading to bradycardia; ECG changes; AV & SA block.

Pulmonary: none.
Example of a negative inotropic drug?
propranolol (Inderal)
Example of a positive inotropic drug?
digoxin (Lanoxin)
Example of a negative dromotropic drug?
adenosine (Adenocard)