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MECHANISM OF ACTION INDICATION ADVERSE EFFECT

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NAME OF DRUGGENERIC NAME: EPINEPHRINE

BRAND NAME: ADRENALIN

STIMULATES BOTH ALPHA AND BETA-RECEPTORS WITHIN SYMPATHETIC NERVOUS SYSTEM THAT RELAXES BRONCHIAL SMOOTH MUSCLE

TREATMENT AND PROPHYLAXIS OF TRANSITORY ATRIOVENTRICULAR HEART BLOCK, TREATMENT OF HAY FEVER, RELIEF OF BRONCHIAL ASTHMA, TREATMENT OF SYNCOPE CAUSED BY HEART BLOCK OR CAROTID SINUS HYPERSENSITIV

CARDIAC ARRYTHMIAS, EXCESSIVE HYPERTENSION, PALPITATIONS, DYSRHYTMIAS, ANGINAL PAIN IN PREDISPOSED PATIENTS, FLUSHING, NERVOUSNESS, TREMORS, VERTIGO, PAIN, HEADACHE, DIZZINESS, WEAKNESS, STROKE, CEREBRAL HAEMORRHAGE

- OBTAIN PATIENT HISTORY, INCLUDING DRUG HISTORY AND ANY KNOWN ALLERGIES

- MONITOR PULMONARY TEST BEFORE INITIATING THERAPY AND PERIODICALLY THROUGHOUT THE COARSE TO

ITY , DROWSINESS, CONFUSION, HALLUCINATION, AGITATION, ALTERED STATE OF PERCEPTION, AND THOUGHT PSYCHOSIS, NAUSEA, VOMITING, ANOREXIA, BRONCHIAL AND PULMONARY EDEMA, DYSPNEA, URINARY RETENTION, METABOLIC ACIDOSIS, ELEVATED SERUM LACTIC ACID, TRANSIENT ELEVATION OF BLOOD GLUCOSE

DETERMINE EFFECTIVENESS OF MEDICATION

- ASSESS FOR HYPERSENSITIVITY REACTION SUCH AS RASH, URTICARIA, SWELLING OF THE FACE AND LIPS, OR EYELIDS. IF THIS CONDITION OCCURS WITHOLD MEDICATION AND IMMEDIATELY NOTIFY PHYSICIAN.

- MONITOR BP, PULSE, RESPIRATION, AND URINARY OUTPUT AND OBSERVE PATIENT CLOSELY

GENERIC NAME: VASOPRESSIN

BRAND NAME:Pitressin The pressor actions of

vasopressin are complex and incompletely understood. Vasopressin acts via specific renal (V-2) and vascular (V-1) receptors although vascular vasopressin receptors are not as well characterised as are adrenergic receptors.

Vasopressin produces vasoconstriction in non-vital circulations by activation of V-1 receptors. In common with the - adrenergic agonists, V-1 activation leads to increased levels

for prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus.

Tremor

Pounding in the

FOLLOWING IV ADMINISTRATION

- MONITOR FOR PARADOXICAL BRONCHOSPASM OR WHEEZING. IF THIS CONDITION OCCURS WITHOLD MEDICATION AND IMMEDIATELY INFORM PHYSICIAN

- MONITOR BLOOD GLUCOSE AND HBA1c IF PATIENT IS DIABETIC DUE TO LOSS OF GLYCEMIC CONTROL

of the second �messengers inositol phosphate and diacylglycerol, which in turn activate voltage-gated calcium channels. This results in increased intracellular calcium levels, causing vasoconstriction.49

How vasopressin produces vasoconstriction in some vascular beds and vasodilation at others is unclear, but the mechanism is related to endothelial nitric oxide (NO). Vasopressin has been shown to produce vasodilation in the renal,50pulmonary,37mesenteric51,52 and especially in the cerebral vascular beds33-35 by stimulating endothelial NO release.

Although vasopressin has similar pressor actions to the catecholamines, it also has unique actions in reversing some of the

head

Vertigo

Angina

Circumoral pallor

Sweating

Uterine contraction

Abdominal cramps

Bronchial constriction

Nausea

Diarrhea

Allergic reaction

Establish baseline data of BP, weight, I&O pattern and ratio. Monitor BP and weight throughout therapy. (Dose used to stimulate diuresis has little effect on BP.) Report sudden changes in pattern to physician.

Be alert to the fact that even small

pathologic vasodilatory processes that occur in advanced shock (which may be refractory to catecholamine vasopressors). There are two mechanisms by which this has been shown to occur. Firstly, vasopressin inhibits ATP �sensitive potassium channels (KATP) in vascular smooth muscle.53Tissue hypoxia or hypoperfusion due to hypovolaemia and septic shock has been shown to activate KATP channels.54,55Activation of KATP channels produces cellular hyperpolarisation which in turn inhibits voltage�gated calcium channels. Intracellular calcium levels fall, resulting in vasodilation.53

Secondly, vasopressin inhibits the inflammatory cytokine interleukin 1-�.56 Interleukin 1-� is released in response to trauma or infection57,58and produces vasodilation by

doses of vasopressin may precipitate MI or coronary insufficiency, especially in older adult patients. Keep emergency equipment and drugs (antiarrhythmics) readily available.

Check patient’s alertness and orientation frequently during therapy. Lethargy and confusion associated with

stimulating vascular endothelial NO production.56The mechanism by which vasopressin inhibits interleukin-1-� is unknown but it has been shown to be mediated by V-1 receptor activation.

In summary, the pressor actions of exogenously administered vasopressin in shock result not only from the restoration of impaired vasoconstrictor mechanisms (due to correction of relative vasopressin deficiency) but also from the inhibition of pathological vasodilator responses.

headache may signal onset of water intoxication, which, although insidious in rate of development, can lead to convulsions and terminal coma.

Monitor urine output, specific gravity, and serum osmolality while patient is hospitalized.

Withhold vasopressin, restrict fluid intake, and notify

GENERIC NAME: DOBUTAMINE HYDROCHLORIDE

BRAND NAME:DUBUTREX

USED TO INCREASE THE CONTRACTILITY OF THE HEART IN ACUTE HEART FAILURE, AS OCCURS IN CARDOGENIC SHOCK AND

physician if urine-specific gravity is <1.015.

DIRECTLY STIMULATES BETA 1 RECEPTORS TO INCREASE MYOCARDIAL CONTRACTILITY AND STROKE VOLUME. DECREASE PERIPHERAL VASCULAR RESISTANCE, REDUCES VENTRICULAR FILING PRESSURE AND FACILITATE AV NODE CONDUCTION

 

MYOCARDIAL INFARCTION; IT IS ALSO USED IN SEPTIC SHOCK. OTHER CIRCUMSTANCES IN WHICH ITS INOTROPIC ACTIVITY MAY BE USEFUL ARE DURING CARDIAC SURGERY AND POSITIVE AND EXPIRATION PRESSURE VENTILATION (PEEP)

DOSE-RELATED INCREASES IN HEART RATE AND BLOOD PRESSURE, ECTOPIC BEATS, ANGINA OR CHEST PAIN, PALPITAIONS; DOSAGE SHOULD BE REDUCED OR TEMPORARILY STOPPED IF THEY OCCUR. VENTRICULAR TACHYCARDIA MAY OCCUR RARELY. OTHER ADVERSE EFFECTS THAT HAVE OCCURRED OCCASIONALY INCLUDE HYPOTENSION, DYSPNEA, PARAESTHESIAS, HEADACHE,

NAUSEA AND VOMITING, LEG CRAMPS

- ASSESS PATIENTS CONDITION BEFORE TREATMENT, RULE OUT HYPOVOLEMIA, AND CORRECT FLUID VOLUME BEFORE INITIATING DOBUTAMINE TREATMENT. IN PATIENTSWITH ATRIAL

GENERIC NAME: DOPAMINE HYDROCHLORIDE

BRAND NAME: INTROPIN

FIBRILLATION, AVOIDE DOBUTAMINE USE WITHOUT INITIAL DIGITALIZATION

- DURING TREATMENT:

MONITOR:ECG FOR DYSRHYTMIAS AND ISCHEMIA, PCWP, CVP, CO2 AND URINARY OUTPUT (<30 ML/HR) DURING INFUSION, MONITOR A BP DROP OF 30 MMHG

- ASSESS FOR CARDIOMAYPATHY OR CHF: BIBASAL CRACKLES, DYSPNEA, NECK VEIN DISTENTION AND S3

IMMEDIATE PRECURSOR OF

EPINEPHRINE IN THE BODY,

EXOGENOUS

ADMINISTRATION

PRODUCES DIRECT

STIMULATION OF BETA-1

RECEPTORS AND VARIABLE

(DOSE DEPENDENT)

STIMULATION OF ALPHA

RECEPTORS (PERIPHERAL

VASOCONSTRICTION), WILL

CAUSE RELEASE OF

NOREPINEPHRINE FROM

STORAGE SITES. THESE

ACTIONS RESULT IN

INCREASED MYOCARDIAL

CORRECTION OF HEMODYANAMIC IMBALANCES PRESENT IN SHOCK AFTER MYOCARDIAL INFARCTION; TRAUMA, ENDOTOXIC SEPTICEMIA, SURGERY AND RENAL FAILURE OR IMBALANCES IN CONDITIONS OF CHRONIC REFRACTORY CARDIAC DECOMPENSATION (EG, CONGESTIVE HEART FAILURE)

ECTOPIC BEATS; TACHYCARDIA; ANGINA PAIN; PALPITATION; HYPOTENSION; VASOCONSTRICTION; VENTRICULAR ARRHYTHMIAS(AT HIGH DOSES); HYPERTENSION; HEADACHE; ANXIETY. DILATEDPUPILS (AT HIGH DOSES). N/V

GALLOP- ASSESS FOR

OXYGENATION OR PERFUSION DEFICIT: CYANOSIS, CHEST PAIN, DIZZINESS, LOSS OF CONSCIOUSNESS AND DECREASE BP

- ASSESS FOR HYPERSENSITIVITY OR ANAPHYLAXIS, WHICH MAY BE LIFE THREATENING

- MONITOR POSSIBLE DRUG INDUCED ADVERSE REACTIONS: CNS:HEADACHE, CV INCREASED HEART RATE HYPERTENSION, PVCs ,

GENERIC NAME: NOREPINEPHRINE

BRAND NAME: LEVOPHED

CONTRACTION AND

CARDIAC OUTPUT,

SYSTEMIC

VASOCONSTRICTION AS

WELL AS INCREASE RENAL

BLOOD FLOW AND SODIUM

EXCRETION

DECREASED URINE OUTPUT. DYSPNEA; GANGRENE OF EXTREMITIES

ANGINA, NONSPECIFIC CHEST PAIN, PHEBLITIS, HYPOTENSION, GI: N/V MUSCULOSKELETAL: CRAMPS, TINGLING SENSATION RESPIARATORY: SHORTNESS OF BREATH, ASTHMA ATTACKS

- MONITOR ELECTROLYTE LEVELS

- ASSESS PATIENTS AND FAMILY’S KNOWLEDGE OF DRUG THERAPY

POWERFUL PERIPHERAL

VASOCONSTRICTOR

( ALPHA-ADRENERGIC

ACTION) AND AS A POTENT

INOTROPIC STIMULATOR OF

THE HEART AND DILATOR OF

BLOOD PRESSURE CONTROL IN CERTAIN ACUTE HYPOTENSIVE STATES. AS AN ADJUNCT IN THE TREATMENT OF CARDIAC ARREST AND PROFOUND HYPOTENSION

ISCHEMIC INJURY; BRADYCARDIA, ARRHYTHMIAS; ANXIETY, TRANSIENT HEADACHE; RESPIRATORY DIFFICULTY; EXTRAVASATIO

-OBTAIN HISTORY OF PATIENTS UNDERLYING DISEASE CONDITION BEFORE THERAPY

-MONITOR VITAL SIGNS AND ECG DURING INFUSION, WATCH FOR DYSRHYTHMIAS AND ISCHEMIA (SOME PATIENTS MAY NOT NEED CONTINUOUS ECG MONITORING) ALSO MONITOR PCWP, CVP, CO2

GENERIC NAME : PHENYLEPHRINE HYDROCHLORIDE

BRAND NAME NEOSYNEPHRINE

CORONORY ARTERIES (BETA-

ADRENERGIC ACTION)

N NECROSIS AT INJECTION SITE;PLASMA VOLUME DEPLETION ON PROLONGED ADMINISTRATION

AND URINARY OUTPUT( REPORT OUTPUT OF <30 ML/HR). IF BP DROPS 30 MMHG, STOP INFUSIOM AND TO THE PHYSICIAN.

-MONITOR FOR POSSIBLE ADVERSE REACTION: CNS: HEADACHE CV: ARRYTHMIAS, ECTOPIC BEATS, TACHYCARDIA, ANGINAL PAIN, PALPITATIONS, HYPOTENSION, BRADYCARDIA, WIDE QRS COMPLEX, CONDUCTION, DISTURBANCE, VASOCONSTRICTION, HYPERTENSION GI: N/V GU: AZOTEMIA RESPIRATORY: ASTHMA ATACKS, DYSPNEA SKIN: NECROSIS, TISSUE SLOUGHING WITH EXTRAVASATION, PILOERECTION -ASSESS FOR HEART

POWERFUL AND SELECTIVE

ALPHA-ADRENERGIC

RECEPTOR AGONIST IN THE

SYMPATHETIC NERVOUS

SYSTEM THAT CAUSE

CONTRACTION OF BLOOD

VESSELS AND

VASOCONSTRICTOR, DECONGESTANT AND MYDRIATIC IN OPTHALMIC CONDITIONS AND PROCEDURES

CNS: HEADACHE, RESTLESSNESS, LIGHT-HEADEDNESS. WEAKNESS CV:

FAILURE: DYSPNEA, NECK VEIN DISTENTION, BIBASAL CRACKLES AND S3 GALLOP

-ASSESS FOR OIXYGENATION AND PERFUSION DEFICIT: DYSPNEA, CYANOSIS, DECREASED BP, CHEST PAIN, DIZZINESS, LOSS OF CONSCIOUSNESS, REMEMBER THAT ACIDOSIS DECREASES EFFECTIVENESS OF DOPAMINE

-MONITOR BLOOD PRESSURE CLOSELY FOR SUDDEN DROP AFTER DRUG IS STOPPED.

-REGULARLY CHECK FOR EXTRAVASATION, CHANGE SITE EVERY 48HRS

-ASSESS PATIENTS AND FAMILYS KNOWEDGE OF

SODIUM BICARBONATE

VASOCONSTRICTIONPALPATION, BRADYCARDIA, ARRHYTHMIA, HYPERTENSION, ANGINA DECREASED CARDIAC OUTPUT EENT: BLURRED VISION GI: VOMITING RESPIRATORY: ASTHMA ATTACK SKIN: PILOMOTOR RESPONSE, COLD FEELING OTHERS: TACHYPHYLAXIS, DECREASED ORGAN PERFUSION, TISSUE SLOUGHING W/ EXTRAVASATIONS, ANAPHYLAXIS

DRUG THERAPY- OBTAIN

PATIENT HISTORY, INCLUDING DRUG HISTORY AND KNOWN ALLERGIES

- OBTAIN BASELINE VITAL SIGNS,NEUROLOGICAL ASSESSMENT, URINARY OUTPUT, AND ECG

- MONITOR VITAL SIGNS, ECG, INPUT-OUTPUT RATIO, AND NEUROLOGICAL STATUS REGULARLY DURING THERAPY

- MONITOR FOR CYANOSIS(EG BLUISH SKIN COLOR AND COLD

EXTREMITIES)

- ASSESS FOR SIGNS OF EXTRAVASATION (EG BLANCHING AND COOLNESS OF SKIN OVER VEIN) AT INFUSION SITE; IF THIS OCCURS NOTIFY PHYSICIAN IMMEDIATELY AND CHANGE INFUSION SITE AS SOON AS POSSIBLE; HAVE PHENTOLAMINE READILY AVAILABLE FOR LOCAL INFILTRATION IN CASE OF EXTRAVASATION.

INCREASES PLASMA

BICARBONATE, WHICH

EXCESS BUFFERS H ION

CONCENTRATIONS;

TREATMENT OF METABOLIC ACIDOSIS; PROMOTION OF GASTRIC, SYSTEMIC AND URINE ALKALINIZATION IN THE CASE OF INTOXICATION AND WEAK ORGANIC ACIDS EG BABITURATES OR ACETYLSALICYL

- ASSESS PATIENTS CONDITION BEFORE STARTING THERAPY AND REGULARLY THEREAFTER TO

REVERSES METABOLIC

ACIDOSIS; NEUTRALIZES

GASTRIC ACID, WHICH

FORMS WATER, NACL, CO2;

RAISES BLOOD PH

IC ACID; IN ORDER TO IMPROVE THE SOLUBILITY OF DRUG SUBSTANCES THAT ARE POORLY SOLUBLE IN NEUTRAL OR ACID MEDIUM, EG METHTREXATE, SULPHONAMIDES; AND IN CASE OF HEMOLYSIS

HYPERNATREMIA, AND SERUM HYPEROSMOLARITY. PARAVENOUS ADMINISTRATION MAY LEAD TO TISSUE NECROSIS

MONITOR DRUG EFFECTIVENESS

- MONITOR BLOOD PRESSURE FREQUENTLY. MAINTAIN BP SLIGHTLY BELOW PATIENTS NORMAL LEVEL AND AVOID SEVERE INCREASE

- MONITOR ECG (CVP OR PWP IF POSSIBLE) CONTINUOUSLY DURING ADMINISTRATION. MONITOR ALSO BP AND PULSE EVERY 5 MINS AFTER PARENTERAL ROUTE,

- MONITOR FOR

HYPERSENSITIVITY REACTION

- MONITOR INPUT-OUTPUT RATIO AND REPORT OUTPUT <30 ML/HR

- MONITOR FOR POSSIBLE INDUCED ADVERSE EFFECTS: CNS: HEADACHE, RESTLESSNESS, LIGHT-HEADEDNESS. WEAKNESS CV: PALPATION, BRADYCARDIA, ARRHYTHMIA, HYPERTENSION, ANGINA DECREASED CARDIAC OUTPUT

EENT: BLURRED VISION GI: VOMITING RESPIRATORY: ASTHMA ATTACK SKIN: PILOMOTOR RESPONSE, COLD FEELING OTHERS: TACHYPHYLAXIS, DECREASED ORGAN PERFUSION, TISSUE SLOUGHING W/ EXTRAVASATIONS, ANAPHYLAXIS

- NOTE FOR PARESTHESIAS AND COOLNESS OF EXTREMITIES TO ASSESS DECREASED PERIPHERAL

BLOOD FLOW

- ASSESS PATIENTS AND FAMILYS KNOWLEDGE OF DRUG THERAPY

- Obtain patient history including drug history and any hypersensitivity.

- Assess respiratory and pulse rate, rhythm, depth, lung sounds and notify the physician.

- Assess for carbon dioxide in GI tract, may lead to perforation if ulcer is severe.

- Assess the client’s fluid balance

throughout the therapy. This assessment includes intake and output, daily weight, edema and lung sounds.

- Symptoms of fluid overload should be reported such as hypertension, edema, difficulty breathing or dyspnea, rales or crackles and frothy sputum.

- Sigs of acidosis should be assessed

such as disorientation, headache, weakness, dyspnea and hyperventilation.

- Assess for alkalosis by monitoring the client for confusion, irritability, paresthesia, tetany and altered breathing pattern.

- Hypernatremia clinical manifestations should be assessed and monitored which includes: edema, weight gain,

hypertension, tachycardia, fever, flushed skin and mental irritability.

- Hypokalemia should also be assessed by monitoring signs and symptoms such as: weakness, fatigue, U wave on ECG, arrhythmias, polyuria and polydipsia.

- IV sites should be observed closely. Extravasation should be avoided as tissue

irritation or cellulitis may occur when taking sodium bicarbonate.

- If infiltration occurs, the physician should be notified immediately. Confer with the doctor or other health care staff regarding warm compresses and infiltration site with lidocaine or hyaluronidase.

- Monitor the client’s serum calcium,

sodium, potassium, bicarbonate concentrations, serum osmolarity, acid-base balance and renal function before and throughout the therapy.

- Tablets must be taken with a full glass of water.

- For clients taking the medication as a treatment for peptic ulcers it may be administered 1 and 3 hours after meals and

at bedtime.