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Decrease myocardial contractility Used in decreasing cardiac workload for angina. May precipitate or exacerbate heart failure.
Haemodynamic impairment with low cardiac output. Critical conditions caused by abnormal haemodynamics and including of the following: Severe exercise limitation Diuretic resistant fluid overload Shown by Kidney dysfunction abnormal lab Liver dysfunction results
Inotropic therapy is occasionally required on a truly emergent basis for patients with evidence of critical hypoperfusion, such as lactic acidosis. Such patients require immediate institution of inotropic therapy until the cause of shock is determined and definitive therapy implemented.
Intravascular volume decreased 15% (due to burn) Blood Pressure decreased (Blood returning to heart decreased) Ventricular filling decreased Loss of blood volume (haemorrhage) Loss of body fluid (severe vomiting/ diarrhoea/ continuous nasogastric suctioning) Renal looses fluid (diuretics/ endocrine disorders)
Cardiac output compromised Inadequate tissue perfusion Myocardial infarction (most common cause) Progressive depletion of oxygen causes myocardial ischemia
Poor heart contractility may be caused by:1. Cardiac arrest 2. Dysarythmias 3. Cardiomyopathies 4. Cardiac surgery (due to myocardial damage) 5. Drugs affecting muscle contractility (Digoxin) 6. Cardiac temponade
Digoxin
Blocks an enzyme called Sodium Potassium ATPase, which controls the amount of sodium and potassium that enters a cell
Causing an increase in the amount of sodium and potassium that enters a cell
Heart contracts more forcefully with each heartbeat
Nausea and Vomitting Headache Visual Disturbances Blurring Vision Dysrhythmias AV block
MOA is depending on the dose Low doses Stimulates dopaminergic receptors, especially in the kidneys Leading to vasodilatation and an increased blood flow through the kidneys Treating the cardio and hypo shock
High doses Stimulates beta1-adrenegic receptors Heart to beat more forcefully Increasing co Stimulate alpha adrenergic receptors, vasoconstriction and raising blood pressure
Stimulates both alpha- and beta- adrenergic receptors Immediately after injection, BP rises due to stimulation of alpha1 receptors Beta2 receptors in the bronchi opens the airway and relieves SOB CO increases due to stimulation of beta1 receptors
Acts directly on alpha-adrenegic receptors in vascular smooth muscle to immediately raise blood pressure It also stimulates beta1 receptors in the heart Thus producing a positive inotropic response increase CO Primary indications acute shock or cardiac arrest Vasopressor of choice for septic shock
Bradyarrhythmia Hypertension Extravasation injury Nausea and vomitting Confusion Anxiety Cardiac arrest
Assessment Understand the reason the drug has been prescribed Complete health history including cardiovascular (including HTN, MI), neurologic ( including CVA or head injury ), burns, endocrine, hepatic or renal disease Baseline weight and vital signs, level of consciousness, breath sounds, urinary and cardiac output Evaluate appropriate lab findings
Assessment throughout administration Assess for desired therapeutic effects dependent on the reason for the drug ( e.g. BP, pulse, CO) Continue frequent and careful monitoring of vital signs and urinary and cardiac output as appropriate Assess for and promptly report adverse effects : tachycardia Hypotension Dysrhythmias Decreasing LOC Allergic Reactions
Rationale
Pulse, BP, RR should be within normal limits or within parameters set by the health care provider, ABGs and/or pulse oximetry are within acceptable parameters. Urine output has increased.
Provide supportive nursing measure; e.g. moistening lips if patient is intubated, explanations for all procedures and frequent orientations
Decrease patient anxiety and supplement therapeutic drug effects to optimized outcome.
Minimizing A.E.
Monitor signs of fluid volume excess. Continue frequent cardiac monitoring
Rationale
Because of the critical condition of the patient in shock, a delicate balance between fluid volume excess and deficit exists. Frequent assessment must be made to detect and avoid A.E. External and invasive monitoring devices will detect early signs of A.E.
Weigh patient daily and report weight gain Daily weight is an accurate measure of or loss of 1 kg or more in 24 hour period. fluid status and takes into account intake, output and insensible losses. Weight gain or edema may signal excessive fluid volume.
Patient education
Advise patient to avoid activities requiring mental alertness or coordination until drug effects are realized.
Rationale
This drug may cause blurred vision.
Advise patient to take high fiber food and increase water intake
Patient education
Instruct patient to use caution with activities leading to an increased core temperature(dehydration, strenuous exercise)
Rationale
This drug impairs heat regulation.
Instruct patient to inform for difficulty in breathing. Instruct patient on proper instillation and administration techniques for ophthalmic product.
Singhal, M. (2008, September 10). Inotropes. Retrieved from http://www.scribd.com/doc/5706202/INOTROPES Heart Fail Reviews. (2009, October 30). Indications for inotropic therapy. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772951/table/Tab1 / Texas Heart Institute. (n.d.). Retrieved from http://www.texasheartinstitute.org/HIC/Topics/Meds/inotropic.cf m Lakey, S. (n.d.). Retrieved from http://congestive-heartfailure.emedtv.com/digoxin/digoxin-mechanism-of-action.html Stevenson, L. W. (n.d.). Retrieved from http://circ.ahajournals.org/content/108/3/367.full Adams, M. P., Holland, L. N., & Urban , C. Q. (2011).Pharmacology for nurses. (3rd ed.). Pearson Education International
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Ineffective tissue perfusion Deficient knowledge Risk for injury Sleeping disturbances
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True or False
True or False?
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b) c)
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b) c)
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