NAME OF DRUG GENERIC NAME: EPINEPHRINE BRAND NAME: ADRENALIN

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

INDICATION TREATMENT AND PROPHYLAXIS OF TRANSITORY ATRIOVENTRICULA R HEART BLOCK, TREATMENT OF HAY FEVER, RELIEF OF BRONCHIAL ASTHMA, TREATMENT OF SYNCOPE CAUSED BY HEART BLOCK OR CAROTID SINUS HYPERSENSITIVITY

ADVERSE EFFECT CARDIAC ARRYTHMIAS, EXCESSIVE HYPERTENSION, PALPITATIONS, DYSRHYTMIAS, ANGINAL PAIN IN PREDISPOSED PATIENTS, FLUSHING, NERVOUSNESS, TREMORS, VERTIGO, PAIN, HEADACHE, DIZZINESS, WEAKNESS, STROKE, CEREBRAL HAEMORRHAGE, DROWSINESS, CONFUSION, HALLUCINATION, AGITATION, ALTERED STATE OF PERCEPTION, AND THOUGHT PSYCHOSIS, NAUSEA, VOMITING, ANOREXIA, BRONCHIAL AND PULMONARY EDEMA, DYSPNEA, URINARY

NURSING RESPONSIBLITITIES - OBTAIN PATIENT HISTORY, INCLUDING DRUG HISTORY AND ANY KNOWN ALLERGIES - MONITOR PULMONARY TEST BEFORE INITIATING THERAPY AND PERIODICALLY THROUGHOUT THE COARSE TO DETERMINE EFFECTIVENESS OF MEDICATION - ASSESS FOR HYPERSENSITIVI TY REACTION SUCH AS RASH, URTICARIA, SWELLING OF THE FACE AND LIPS, OR EYELIDS. IF THIS CONDITION OCCURS WITHOLD MEDICATION AND

RETENTION, METABOLIC ACIDOSIS, ELEVATED SERUM LACTIC ACID, TRANSIENT ELEVATION OF BLOOD GLUCOSE

GENERIC NAME: VASOPRESSIN

The pressor actions of vasopressin are complex and incompletely

IMMEDIATELY NOTIFY PHYSICIAN. MONITOR BP, PULSE, RESPIRATION, AND URINARY OUTPUT AND OBSERVE PATIENT CLOSELY FOLLOWING IV ADMINISTRATIO N MONITOR FOR PARADOXICAL BRONCHOSPAS M 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

BRAND NAME: P !"#$$ %

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. n common with the adrenergic agonists! V-1 activation leads to increased levels of the second &messengers inositol phosphate and diacylglycerol! which in turn activate voltagegated calcium channels. This results in increased intracellular calcium levels! causing vasoconstriction."# $ow vasopressin produces vasoconstriction in some vascular beds and vasodilation at others is unclear! but the mechanism is related to endothelial nitric oxide (%&). Vasopressin has been shown to produce vasodilation in the renal!'(pulmonary!)*mesenteric'1!'2 and especially in the cerebral vascular beds))-)' by stimulating

'(" )"#*#%! (% +%, !"#+!-#%! (' )($!()#"+! *# +.,(- %+/ , $!#%! (%, % +.,(- %+/ "(#%!0#%(0"+)12 !( , $)#/ %!#"'#" %0 0+$ $1+,(3$, +%, % , +.#!#$ %$ ) ,4$.

CONTROL

T"#-(" P(4%, %0 % !1# 1#+, V#"! 0( A%0 %+ C "c4-("+/ )+//(" S3#+! %0 U!#" %# c(%!"+c! (% A.,(- %+/ c"+-)$ B"(%c1 +/ c(%$!" c! (% N+4$#+ D +""1#+ A//#"0 c "#+c! (%

+stablish baseline data of ,-! weight! .& pattern and ratio. /onitor ,- and weight throughout therapy. (0ose used to stimulate diuresis has little effect on ,-.) 1eport sudden changes in pattern to physician. ,e alert to the fact that even small doses of vasopressin may precipitate / or

endothelial %& release. 2lthough vasopressin has similar pressor actions to the catecholamines! it also has uni3ue actions in reversing some of the pathologic vasodilatory processes that occur in advanced shoc4 (which may be refractory to catecholamine vasopressors). There are two mechanisms by which this has been shown to occur. 5irstly! vasopressin inhibits 2T- &sensitive potassium channels (62T-) in vascular smooth muscle.')Tissue hypoxia or hypoperfusion due to hypovolaemia and septic shoc4 has been shown to activate 62Tchannels.'"!''2ctivation of 62Tchannels produces cellular hyperpolarisation which in turn inhibits voltage&gated calcium channels. ntracellular calcium levels fall! resulting in vasodilation.') 7econdly! vasopressin inhibits the inflammatory cyto4ine interleu4in 1-&.'8 nterleu4in 1-& is released in response to trauma or infection'*!'9and produces vasodilation by stimulating

coronary insufficiency! especially in older adult patients. 6eep emergency e3uipment and drugs (antiarrhythmics) readily available.

:hec4 patient;s alertness and orientation fre3uently during therapy. <ethargy and confusion associated with headache may signal onset of water intoxication! which! although insidious in rate of development! can lead to convulsions and terminal coma. /onitor urine output! specific gravity! and serum osmolality while patient is hospitali=ed.

vascular endothelial %& production.'8The mechanism by which vasopressin inhibits interleu4in-1-& is un4nown but it has been shown to be mediated by V-1 receptor activation. n summary! the pressor actions of exogenously administered vasopressin in shoc4 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.

>ithhold vasopressin! restrict fluid inta4e! and notify physician if urinespecific gravity is ?1.(1'.

GENERIC NAME: DOBUTAMINE HYDROCHLORIDE BRAND NAME: DUBUTREX USED TO INCREASE THE CONTRACTILITY OF THE HEART IN ACUTE HEART FAILURE, AS OCCURS IN

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

CARDOGENIC SHOCK AND MYOCARDIAL INFARCTION5 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 6PEEP7

DOSE-RELATED INCREASES IN HEART RATE AND BLOOD PRESSURE, ECTOPIC BEATS, ANGINA OR CHEST PAIN, PALPITAIONS5 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,

ASSESS PATIENTS CONDITION BEFORE TREATMENT, RULE OUT HYPOVOLEMIA, AND CORRECT FLUID VOLUME BEFORE INITIATING DOBUTAMINE TREATMENT. IN PATIENTSWITH ATRIAL FIBRILLATION, AVOIDE DOBUTAMINE USE WITHOUT INITIAL DIGITALIZATION

HEADACHE, NAUSEA AND VOMITING, LEG CRAMPS

DURING TREATMENT: MONITOR:ECG FOR DYSRHYTMIAS AND ISCHEMIA, PCWP, CVP, CO8 AND URINARY OUTPUT 69:; ML<HR7 DURING INFUSION, MONITOR A BP DROP OF :; MMHG ASSESS FOR CARDIOMAYPAT HY OR CHF: BIBASAL CRACKLES, DYSPNEA, NECK VEIN DISTENTION AND S: GALLOP ASSESS FOR OXYGENATION OR PERFUSION DEFICIT: CYANOSIS, CHEST PAIN, DIZZINESS, LOSS OF CONSCIOUSNES S AND DECREASE BP ASSESS FOR HYPERSENSITIVI TY OR ANAPHYLAXIS,

GENERIC NAME: DOPAMINE HYDROCHLORIDE BRAND NAME: INTROPIN

CORRECTION OF HEMODYANAMIC IMBALANCES PRESENT IN SHOCK AFTER

WHICH MAY BE LIFE THREATENING MONITOR POSSIBLE DRUG INDUCED ADVERSE REACTIONS: CNS:HEADACHE , CV INCREASED HEART RATE HYPERTENSION, PVC$ , ANGINA, NONSPECIFIC CHEST PAIN, PHEBLITIS, HYPOTENSION, GI: N<V MUSCULOSKELE TAL: CRAMPS, TINGLING SENSATION RESPIARATORY: SHORTNESS OF BREATH, ASTHMA ATTACKS MONITOR ELECTROLYTE LEVELS ASSESS PATIENTS AND FAMILY=S KNOWLEDGE OF DRUG THERAPY

MYOCARDIAL INFARCTION5 IMMEDIATE PRECURSOR OF TRAUMA, EPINEPHRINE IN THE BODY, ENDOTOXIC EXOGENOUS ADMINISTRATION SEPTICEMIA, SURGERY AND PRODUCES DIRECT RENAL FAILURE OR IMBALANCES STIMULATION OF BETA-1 IN CONDITIONS OF RECEPTORS AND VARIABLE CHRONIC REFRACTORY 6DOSE DEPENDENT7 CARDIAC STIMULATION OF ALPHA DECOMPENSATION 6EG, CONGESTIVE RECEPTORS 6PERIPHERAL HEART FAILURE7 VASOCONSTRICTION7, WILL CAUSE RELEASE OF NOREPINEPHRINE FROM STORAGE SITES. THESE ACTIONS RESULT IN INCREASED MYOCARDIAL CONTRACTION AND CARDIAC OUTPUT, SYSTEMIC VASOCONSTRICTION AS WELL AS INCREASE RENAL BLOOD FLOW AND SODIUM EXCRETION ECTOPIC BEATS5 TACHYCARDIA5 ANGINA PAIN5 PALPITATION5 HYPOTENSION5 VASOCONSTRICTIO N5 VENTRICULAR ARRHYTHMIAS6AT HIGH DOSES75 HYPERTENSION5 HEADACHE5 ANXIETY. DILATEDPUPILS 6AT HIGH DOSES7. N<V DECREASED URINE OUTPUT. DYSPNEA5 GANGRENE OF

-OBTAIN HISTORY OF PATIENTS UNDERLYING DISEASE CONDITION BEFORE THERAPY -MONITOR VITAL SIGNS AND ECG DURING INFUSION, WATCH FOR DYSRHYTHMIAS AND ISCHEMIA 6SOME PATIENTS MAY NOT

EXTREMITIES

NEED CONTINUOUS ECG MONITORING7 ALSO MONITOR PCWP, CVP, CO8 AND URINARY OUTPUT6 REPORT OUTPUT OF 9:; ML<HR7. IF BP DROPS :; 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 >RS COMPLEX, CONDUCTION, DISTURBANCE, VASOCONSTRICTION, HYPERTENSION GI: N<V GU: AZOTEMIA RESPIRATORY: ASTHMA ATACKS, DYSPNEA SKIN: NECROSIS, TISSUE SLOUGHING WITH EXTRAVASATION, PILOERECTION

GENERIC NAME: NOREPINEPHRINE BRAND NAME: LEVOPHED

BLOOD PRESSURE CONTROL IN CERTAIN ACUTE HYPOTENSIVE STATES. AS AN

AD?UNCT IN THE TREATMENT OF CARDIAC ARREST AND PROFOUND HYPOTENSION

-ASSESS FOR HEART FAILURE: DYSPNEA, NECK VEIN DISTENTION, BIBASAL CRACKLES AND S: GALLOP -ASSESS FOR OIXYGENATION AND PERFUSION DEFICIT: DYSPNEA, CYANOSIS, DECREASED BP, CHEST PAIN, DIZZINESS, LOSS OF CONSCIOUSNESS, REMEMBER THAT ACIDOSIS DECREASES EFFECTIVENESS OF DOPAMINE ISCHEMIC IN?URY5 BRADYCARDIA, ARRHYTHMIAS5 ANXIETY, TRANSIENT HEADACHE5 RESPIRATORY DIFFICULTY5 EXTRAVASATION NECROSIS AT IN?ECTION SITE5PLASMA VOLUME DEPLETION ON PROLONGED ADMINISTRATION -MONITOR BLOOD PRESSURE CLOSELY FOR SUDDEN DROP AFTER DRUG IS STOPPED. -REGULARLY CHECK FOR EXTRAVASATION, CHANGE SITE EVERY @AHRS -ASSESS PATIENTS AND FAMILYS KNOWEDGE OF DRUG THERAPY - OBTAIN

POWERFUL PERIPHERAL VASOCONSTRICTOR 6 ALPHAADRENERGIC ACTION7 AND AS A POTENT INOTROPIC STIMULATOR OF THE HEART AND DILATOR OF CORONORY ARTERIES 6BETAADRENERGIC ACTION7

GENERIC NAME : PHENYLEPHRINE HYDROCHLORIDE BRAND NAME NEOSYNEPHRINE -

VASOCONSTRICTO R, DECONGESTANT AND MYDRIATIC IN OPTHALMIC CONDITIONS AND PROCEDURES

PATIENT HISTORY, INCLUDING DRUG HISTORY AND KNOWN ALLERGIES OBTAIN BASELINE VITAL SIGNS,NEUROL OGICAL ASSESSMENT, URINARY OUTPUT, AND ECG MONITOR VITAL SIGNS, ECG, INPUT-OUTPUT RATIO, AND NEUROLOGICAL STATUS REGULARLY DURING THERAPY MONITOR FOR CYANOSIS6EG BLUISH SKIN COLOR AND COLD EXTREMITIES7 ASSESS FOR SIGNS OF EXTRAVASATIO N 6EG BLANCHING AND COOLNESS OF SKIN OVER

POWERFUL AND SELECTIVE ALPHA-ADRENERGIC RECEPTOR AGONIST IN THE SYMPATHETIC NERVOUS SYSTEM THAT CAUSE CONTRACTION OF BLOOD VESSELS AND VASOCONSTRICTION CNS: HEADACHE, RESTLESSNESS, LIGHTHEADEDNESS. WEAKNESS CV: PALPATION, BRADYCARDIA, ARRHYTHMIA, HYPERTENSION, ANGINA DECREASED CARDIAC OUTPUT EENT: BLURRED VISION GI: VOMITING RESPIRATORY: ASTHMA ATTACK SKIN: PILOMOTOR RESPONSE, COLD

VEIN7 AT INFUSION SITE5 IF THIS OCCURS NOTIFY PHYSICIAN IMMEDIATELY AND CHANGE INFUSION SITE AS SOON AS POSSIBLE5 HAVE PHENTOLAMINE READILY AVAILABLE FOR LOCAL INFILTRATION IN CASE OF EXTRAVASATIO N.

FEELING OTHERS: TACHYPHYLAXIS, DECREASED ORGAN PERFUSION, TISSUE SLOUGHING W< EXTRAVASATIONS, ANAPHYLAXIS ASSESS PATIENTS CONDITION BEFORE STARTING THERAPY AND REGULARLY THEREAFTER TO MONITOR DRUG EFFECTIVENESS MONITOR BLOOD PRESSURE FRE>UENTLY. MAINTAIN BP SLIGHTLY BELOW PATIENTS NORMAL LEVEL AND AVOID SEVERE INCREASE MONITOR ECG 6CVP OR PWP IF POSSIBLE7 CONTINUOUSLY

SODIUM BICARBONATE -

TREATMENT OF METABOLIC ACIDOSIS5 PROMOTION OF GASTRIC, SYSTEMIC AND URINE ALKALINIZATION IN THE CASE OF INTOXICATION AND WEAK ORGANIC ACIDS EG BABITURATES

DURING ADMINISTRATIO N. MONITOR ALSO BP AND PULSE EVERY B MINS AFTER PARENTERAL ROUTE, MONITOR FOR HYPERSENSITIVI TY REACTION MONITOR INPUT-OUTPUT RATIO AND REPORT OUTPUT 9:; ML<HR MONITOR FOR POSSIBLE INDUCED ADVERSE EFFECTS: CNS: HEADACHE, RESTLESSNESS, LIGHTHEADEDNESS. WEAKNESS CV: PALPATION, BRADYCARDIA, ARRHYTHMIA, HYPERTENSION, ANGINA DECREASED CARDIAC OUTPUT EENT: BLURRED

INCREASES PLASMA BICARBONATE, WHICH EXCESS BUFFERS H ION CONCENTRATIONS5 REVERSES METABOLIC ACIDOSIS5 NEUTRALIZES GASTRIC ACID, WHICH FORMS WATER, NACL, CO85 RAISES BLOOD PH

OR ACETYLSALICYLIC ACID5 IN ORDER TO IMPROVE THE SOLUBILITY OF DRUG SUBSTANCES THAT ARE POORLY SOLUBLE IN NEUTRAL OR ACID MEDIUM, EG METHTREXATE, SULPHONAMIDES5 AND IN CASE OF HEMOLYSIS HYPERNATREMIA, AND SERUM HYPEROSMOLARIT Y. PARAVENOUS ADMINISTRATION MAY LEAD TO TISSUE NECROSIS

VISION GI: VOMITING RESPIRATORY: ASTHMA ATTACK SKIN: PILOMOTOR RESPONSE, COLD FEELING OTHERS: TACHYPHYLAXIS , DECREASED ORGAN PERFUSION, TISSUE SLOUGHING W< EXTRAVASATIO NS, ANAPHYLAXIS NOTE FOR PARESTHESIAS AND COOLNESS OF EXTREMITIES TO ASSESS DECREASED PERIPHERAL BLOOD FLOW ASSESS PATIENTS AND FAMILYS KNOWLEDGE OF DRUG THERAPY

O.!+ % )+! #%! 1 $!("2 %c/4, %0 ,"40 1 $!("2 +%, +%2 12)#"$#%$ ! * !2 . A$$#$$ "#$) "+!("2 +%, )4/$# "+!#, "12!1-, ,#)!1, /4%0 $(4%,$

+%, %(! '2 !1# )12$ c +%. A$$#$$ '(" c+".(% , (C ,# % GI !"+c!, -+2 /#+, !( )#"'("+! (% ' 4/c#" $ $#*#"#.

2ssess the client;s fluid balance throughout the therapy. This assessment includes inta4e and output! daily weight! edema and lung sounds. 7ymptoms of fluid overload should be reported such as hypertension! edema! difficulty breathing or dyspnea! rales or crac4les and frothy sputum. 7igs of acidosis

should be assessed such as disorientation! headache! wea4ness! dyspnea and hyperventilation. 2ssess for al4alosis by monitoring the client for confusion! irritability! paresthesia! tetany and altered breathing pattern. $ypernatremia clinical manifestations should be assessed and monitored which includes@ edema! weight gain! hypertension! tachycardia! fever! flushed s4in and mental irritability.

$ypo4alemia should also be assessed by monitoring signs and symptoms such as@ wea4ness! fatigue! A wave on +:B! arrhythmias! polyuria and polydipsia. V sites should be observed closely. +xtravasation should be avoided as tissue irritation or cellulitis may occur when ta4ing sodium bicarbonate. f infiltration occurs! the physician should be notified immediately. :onfer with the doctor or other health care staff

regarding warm compresses and infiltration site with lidocaine or hyaluronidase. /onitor 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 ta4en with a full glass of water. 5or clients ta4ing the medication as a treatment for peptic ulcers it may be administered 1 and ) hours after

meals and at bedtime.