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Calcium Channel Blockers, Jung Soo, Chapter 25 Mind Map by Ben Ferguson,…
Calcium Channel Blockers
Furosemide
Mechanism of Action
Inhibits the reabsorption of sodium (NA+) and Chloride (Cl-) from the loop of Henle and distal renal tubule.
Results in a mobilization of excess fluid (edema, pleural effusions). Decreases BP
Increases renal excretion of H2O, sodium, chloride, magnesium, potassium, and calcium.
Indications
Edema due to heart failure
Hypertension
Hepatic impairment, renal disease
Pharmacokinetics
Half-life
30-60 minutes, longer with CKD or renal impairment.
Metabolism and Excretion
IM
10-30 minute onset, unknown peak, 4-8 hour duration
IV
5 minute onset, 30 minute peak, 2 hour duration
PO
30-60 minute onset, Peak in 1-2 hours, duration 6-8 hours
Absorption
PO: 60-67% absorbed after first-pass effect. Lowered absorption in those with acute Heart Failure and/or renal failure.
Distribution
Crosses placenta, enters breast milk
Adverse Reactions
Blurred vision, dizziness, headache, vertigo, hearing loss, tinnitus, hypotension, diarrhea.
Contraindications
Hypersensitivity (drug allergy)
Thiazides (some other diuretics) and sulphonamides (antibiotics).
Classification
Loop Diuretic or "Water Pill"
Also known by the brand name Lasix
Interactions
Other antihypertensives, nitrates, alcohol.
Risk for hypokalemia: other diuretics, stimulant laxatives, and corticosteroids.
Work by preventing calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to contract more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open up.
Jung Soo
Nursing Care
Perform holistic assessment including client's LOC and memory.
Client at increased risk for falls as evidenced by diuretic use (orthostatic hypotension). Perform fall assessment and implement fall prevention strategies.
Educate client to change positions slowly to minimize orthostatic hypotension and risk of falls.
Monitor clients weight
Monitor client's input and output
Monitor client's BP, PR, and RR before and after administration of furosemide.
Assess client for tinnitus and hearing loss before (to establish baseline) and after IV furosemide.
Refer client to OT for functional assessment and home assessment.
Client demonstrating a lack of knowledge about medication and/or lack of support to obtain medication as evidenced by sudden discontinuation of HF medication.
Reinforce the importance of continuing to take prescribed medications even if "feeling better."
Assess client's ability to obtain prescription medications. Refer to allied health to ensure client has adequate support.
Monitor PR prior to digoxin administration. Withhold dose if PR is less than 60.
Educate client about reducing sodium in his diet whenever possible to discourage fluid retention.
Social Determinants
82-year-old Male
Recently Widowed
No Children
Jung Soo presents at ED
Focussed Assessment
Client has gained 9kg in a month (78kg -> 87kg).
Client may retaining fluid due to impaired renal function as a result of Heart Failure.
Edema present in legs. +2 bilaterally
Client reports difficulty breathing
Given IV Lasix (Furosemide)
Medical History
Diagnosis of Heart Failure 5 years ago
Heart Failure (HF)
Can affect the left-ventricle, right-ventricle, or both
Left-ventricular heart failure often leads to pulmonary edema (fluid in lungs).
Two types
Diastolic Failure
Left ventricular filling is impaired. Accompanied by elevated filling (diastolic) pressure during diastole.
The ventricle becomes unable to relax and the muscle becomes stiff.
Systolic Failure
decrease in myocardial contractility resulting in insufficient force to push blood into circulation
Reminder:
Left-ventricle pumps blood to systemic circulation
Right-ventricle pumps blood to pulmonary circulation
Right-ventricular heart failure involves venous congestion, pedal edema, jugular venous distension, ascites, and hepatic congestion.
Occurs due to a reduced ratio of
ejection fraction
(the proportion of blood that is ejected during each ventricular contraction compared with the total ventricular filling volume)
Normal value is approximately 65% of the total volume in the ventricle
A condition in which the heart is unable to pump blood in sufficient amounts (cardiac output) to meet the body's needs
As the body struggles to perfuse all tissues adequately, it will prioritize the brain and heart.
As the kidney does not demand as much blood to function, the body will shunt blood away from it to be used in other places.
This results in impaired filtration of fluids, removal of waste, and eventually leads to AKI and/or CKD
Fluid retention as a result of impaired filtration and elimination.
Causes of Heart Failure
Myocardial deficiency (such as MI, valve issues) which leads to inadequate cardiac contractility and/or ventricular filling
Defects outside of the heart, often systemic such as CAD, hypertension, and/or diabetes. Forces heart to work much harder than normal.
Classes of Heart Failure
Class II
Characterized by ordinary activities causing fatigue and dyspnea.
This stage is an exacerbation of issues relating to Heart Failure.
Additionally, people with structural heart defects begin at this stage.
Class III
Characterized by a marked limitation in normal physical activity
Class I
Mildest form - physical activity of client is not impacted by condition.
Think of this stage as the pre-diabetes stage - things need to be turned around or they're going to get a lot worse and quality of life will be impacted.
This stage does not include structural defects of the heart.
Class IV
Most severe - Characterized as symptomatic at rest or with any physical activity at all.
IMPORTANT
Early detection
of LV systolic function is essential to allow for change in lifestyle and effective pharmacotherapy to
delay or reverse LV remodelling
.
Drug Therapy for Heart Failure
Digoxin
Indications
Heart Failure
Atrial fibrillation
Atrial flutter
Paroxysmal atrial tachycardia
Mechanism of Action
Increases the force of myocardial contraction
Prolongs the refractory period of the AV node.
Increases cardiac output (positive inotropic effect) and slows heart rate (negative chronotropic effect)
Contraindications
Drug Hypersensitivity (allergy)
Uncontrolled ventricular arrhythmias, AV block, Idiopathic hypertropic subaortic stenosis.
Pharmacokinetics
Distribution
Crosses placenta and enters breast milk
Metabolism and Excretion
Excreted almost unchanged (in its original form, not a metabolite) by kidneys
Absorption
60-80% absorption from PO administration of tablets, 70-85% absorbed after administration of elixer.
Half-life
36-48 hours, longer with CKD or renal impairment
IM
30 minute onset, 4-6 hour peak, 2-4 days duration.
PO
30-120 minutes onset, 2-8 hour peak, 2-4 day duration.
IV
5-30 minute onset, 1-4 hours peak, 2-4 days duration.
Adverse Reactions
Fatigue, headache, weakness, blurred vision, yellow or green vision, nausea, vomiting, acute digoxin toxicity, electrolyte imbalances.
Interactions
Thiazide and
loop diuretics
corticosteroids
Piperacillin
HIGH ALERT: Digoxin has a narrow therapeutic range. Dose calculations must be double checked by a second practitioner.
HIGH ALERT: Digoxin is a BEERS LIST drug due to decrease in age-related renal clearance. Close monitoring of dosages and clearance is required in older adults.
Inotropic Drugs
Positive inotropic drugs
Increase the force of myocardial contraction
Phosphodiesterase Inhibitors (PDIs)
Negative inotropic drugs
Reduce the force of myocardial contraction
Chronotropic Drugs
Positive Chronotropic Drugs
Increase the rate at which the heart beats
Negative Chronotropic Drugs
Decrease the rate at which the heart beats
Dromotropic Drugs
Positive Dromotropic Drugs
Increase conduction of electrical impulses (SA node, AV node, bundle of His, & Purkinje fibres)
Negative Dromotropic Drugs
Decrease conduction of electrical impulses (SA node, AV node, bundle of His, & Purkinje fibres)
MI 5 years ago
Chapter 25 Mind Map by Ben Ferguson, Hasti Halakoeei, Jenna Machin, and Katie Neal
References
Cardiology_Graphic-Heart-failure-ejection-fraction. (n.d.). Genesis Care. Retrieved February 4, 2022, from
https://www.genesiscare.com/au/heart-failure/
.
Sealock, K., Lilley, L. L., Snyder, J. S., Collins, S. R., Seneviratne, C., & Lilley, L. L. (2021). Chapter 25: Heart Failure Drugs. In Lilley's pharmacology for Canadian Health Care Practice (Fourth, pp. 408–443). essay, Elsevier.
Vallerand, A. H., Sanoski, C. A., & Quiring, C. (2019). Davis's drug guide for Nurses. F. A. Davis Company.
