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NR566_Week 3 Study Guide_includes Ch.16, Ch.28, Ch.36, Ch.39

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Course
AIT Nursing (NR566)

Institution
Thompson River University (TRU )

Chapter 16: Drugs Affecting the Cardiovascular & Renal Systems Angiotensin converting enzyme inhibitors (ACEI or ACE Inhibitors) o Drugs: benazepril, captopril, enalapril, fosinopril, lisinopril, and moexipril, perindopril, quinapril, ramipril, trandolapril o Pharmacodynamics: o MOA: Slows or i...

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nr566 week 3 study outline
chapter 16 drugs affecting the cardiovascular amp renal systems
angiotensin converting enzyme inhibitors acei or ace inhibitors
o pharmacotherapeutics o contraindicat

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NR566 Week 3 Study Outline
Chapter 16: Drugs Affecting the Cardiovascular & Renal
Systems
Angiotensin converting enzyme inhibitors (ACEI or ACE Inhibitors)
o Drugs: benazepril, captopril, enalapril, fosinopril, lisinopril, and moexipril, perindopril, quinapril, ramipril,
trandolapril
o Pharmacodynamics:
o MOA: Slows or inhibits the angiotensin converting enzyme which then decrease how much
angiotensin II (AT II) is produced thus lowering BP
o Inhibit RAAS activity=decreased production of both angiotensin II and aldosterone
o Act on the RAAS system: decreases peripheral vascular resistance (decreased afterload)
o Indirectly reduce the secretion of aldosterone=decreased sodium and water retention, reducing
extracellular fluid volume and preload
o Lower vascular resistance w/o decreasing cardiac output (CO) or GFR
o Do not affect CO=Do not produce reflex tachycardia
o Strong evidence for CV and cerebrovascular risk reduction, HF, and slowing of renal disease
o Improves oxygenation to heart muscle, decreases inappropriate remodeling of heart muscle after MI
or with HF, and reduces affects of DM on the kidneys
o Also plays a role in the kinin-kallikrein-bradykinin system: ACEs facilitate the breakdown of
bradykinin into inactive fragments thus reducing the actions of bradykinin (pain, extravascular
smooth muscle contraction, increased vascular permeability, and increased leukocyte chemotaxis)
o Reno-protective for individuals with proteinuria but is not as protective in renal patients without
proteinuria
 Improve insulin sensitivity
 Decrease proteinuria in those with CKD and help with BP control
 In earliest signs of diabetic nephropathy (microalbuminuria) lisinopril is recommended
 Lisinopril reduces the progression of this complication independent of BP control
 Adding an ACE inhibitor to patients with known CKD commonly results in increate crt
 The improvement in proteinuria happens despite this effect
 Because of this, it is acceptable to have up to a 30% increase in crt with d/c of ACE
inhibitor
 Although crt increases acutely, GFR improved long term
 d/c should only be considered for patients with progression and/or significant deterioration in
renal function for patients with hyperkalemia

o Pharmacotherapeutics:
o Contraindications: bilateral renal artery stenosis, angioedema, and pregnancy
o Use with caution:
 Impaired renal function especially in older adults, hypovolemic or hyponatremic states,
hepatic impairment
o Contraindicated in hyperkalemia: reduced aldosterone may worsen the imbalance
 Risk increased with patients with HF r/t reduced blood flow to kidneys
o Contraindicated in pregnancy r/t fetal renal abnormalities in the latter half of pregnancy and
cardiac abnormalities in the first trimester

o Adverse drug reactions (ADRs):

, o ADRs are usually transient, mild, and more common in longer acting agents
o ADRs increase with higher doses
o dry hacking cough, usually only last a week but is often cited as the reason for discontinuance
 (bradykinin and substance P after the drug interrupts the RAAS: d/c drug and see if the
patient improves)
 More common in African Americans and Asian population
 Class phenomenon: changing to a new generation ACE has been associated with less cough
o hypotension (dizziness, HA, fatigue, orthostatic hypotension)
o Tachyphylaxis frequently occurs with continued use
o loss of taste
o Angioedema (serious)
 (can be life threating, occurs with the first dose or within the first month of therapy)
 More common in African Americans and Asian population
o Blood dyscrasias
o teratogenicity
o hyperkalemia
o acute renal failure (serious)
o cholestatic jaundice
o pancreatitis
o rash (switch drugs within the class)
o neutropenia that increases with high does (more common in renal impairment and collagen disease)
o Photosensitivity reactions (enalapril, quinapril, and ramipril)

o Drug interactions
o Additive hypotension with other antihypertensives, nitrates, phenothiazines, and ETOH ingestion
o Due to interference with aldosterone secretion:
 Concurrent use of K supplements, K-sparing diuretics, or cyclosporine may result in
hyperkalemia
o Antihypertensive response is reduced by NSAIDs r/t effect
o Lithium: increased lithium levels and symptoms of toxicity
o Digoxin: increase peak and trough concentrations

o Clinical Use and Dosing

HTN
o Primary HTN (no identifiable cause, Tx depends on interfering with normal physiological mechanisms
that regular BP
o Young Caucasian patients, DM, HF, or MI: drug of choice ACEs and ARBs
o Patients with angina: prevents formation of AT II and decreased pulmonary VR by decreasing retention
of sodium and water reducing extracellular fluid and preload
o Diabetic patients: prevents or slows nephropathy
o Not as effective for African Americans however when combined with a diuretic, race no longer an issue
o Doses vary for each drug
o First dose may cause a steep drop in BP, especially in those taking diuretics
 Diuretics should be stopped for 2 to 3 days to allow rehydration before staring an ACE, ARB, or
DRI
o All three drug classes increase in effectiveness when given with a diuretic
 Reintroduce diuretics after monotherapy dose has been stabilized
 Thiazide diuretics are an excellent combination (foster K loss)
 Start low and go slow, increase the dose at 1 to 2 week intervals until BP is controlled

,Hypertensive Protein-uric Diabetes
o Prevent diabetic nephropathy or slow its progression, ACE or ARB (DRI use off-label)

Angina and Ischemic Heart Disease
 An imbalance between myocardial oxygen supply (MOS) and myocardial oxygen demand
(MOD)
 ACE’s affect both the MOS and MOD
o Prevent formation of AT II decreased PVR thereby MOD
o Decreases the thickening of coronary artery wall results in increase MOS
o Decreases the thickening of ventricular wall results in decreased MOD
o Reduce ECF volume and preload
 Recommended for all symptomatic patients with chronic stable angina
o to prevent MI or death and to reduce symptoms
 Also recommended to CAD patients who also have DM or LV dysfunction
 ACCF/AHA recommend that ACEs be considered in CAD patients even without LV dysfunction
 ACEs and ARBs are appropriate Tx options for stable CAD
 DRIs are not mixed with ACEs or ARBS because r/f hyperkalemia

Post-MI
 Survivors of acute MI have a r/f subsequent morbidity and mortality
 Combo of an ACE, a non ISA beta blocker, antiplatelet therapy, and lipid lowering therapy after MI is
appropriate
 ACE: reduced AT II after myocardial injury, prevention of ventricular remodeling in noninfarcted
myocytes, alteration of ventricular mass, and positive hemodynamic effects on BP and fluid and electrolyte
balance
 ARBS: extremely effective here r/t effect on AT II and AT I receptors
 Bradykinin has cardioprotective effects and a combination of an ACE and an ARB provides complete
inhibition of AT II and increased levels of bradykinin
 ACE (with or w/o ARB) should be started early after MI in stable high risk patients (anterior MI, previous
MI, Killip class II)
o Continue indefinitely for all patients with LV dysfunction (EF <40%) or symptoms of HF and use as
needed to manage BP or symptoms in all other patients
 Dosages usual for treating HTN are used unless HF is present
 DRI: do not have post MI indication because they do not contribute to positive outcomes more than standard
care

Heart Failure (HF)
 CAD is the underlying cause in 2/3 of patients with LV dysfunction
o begins with injury to the myocardium and progresses
 Principle mechanism r/t remodeling
o ACEs and ARBs are useful in treating HF r/t CAD, for their role in reducing remodeling
 Another underlying cause for HF is chronic HTN
o ACEs and ARBs are effective in treating this cause
 DRI: do not carry indication for HF
 ACEs: cornerstone therapy for HF and are recommended for patients with Hx of atherosclerotic vascular
disease, DM, or HTN
o Improve symptoms, decrease morbidity, and increase life expectancy
o Only drugs that address all the pathological mechanisms that produce HF, appropriate for all subsets
of patients unless absolute contraindication
 Useful in prevention: patients who have ventricular dysfunction but no overt symptoms
o (prevent development of HF)

,  ACEs are superior to all other drugs and drug combinations used to treat HF
o Start immediately w/o waiting for symptoms to become overt
 For symptomatic HF, the dose is about half that used for HTN
o Start low and go slow
 In CHF and low EF: the vasodilating effect of ACEs provides adequate perfusion even with SBP <90
 For patients who cannot tolerate an ACE, hydralazine in combination with a long acting nitrate has been
shown to be equally effective in reducing morbidity and mortality from HF
o Especially noted in African Americans

 Rational Drug Selection
 Short-Acting versus Long-Acting
o ADRs (angioedema and renal dysfunction) occur within the first few doses
o Begin therapy with captopril (short acting) which allows for rapid assessment of patient response to
the drug
o Captopril requires frequent dosing r/t short half-life (adherence long term is less likely)
o Other ACEs have once daily dosing therefore when patient tolerance is determined, convert to
another agent to improve adherence
o ARBs and DRIs also allow once daily dosing
 Cost
o Brand name ACEs and ARBs are expensive (order generic)
o Combination drug formulations can reduce costs
o DRIs are expensive brand names
 Difficulty in swallowing
o Ramipril (Altace) is a good choice
o Capsule may be opened and sprinkled on applesauce, added to apple juice, or dissolved in 4 oz of
water with no change in the effectiveness
o Captopril may be crushed: sulfurous odor and requires frequent dosing

o Monitoring:
o Baseline BP and pulse before initiating therapy and with each change in dosage
o Attain weight and other indicators of fluid balance and monitor
o During therapy with ACEs, ARBs, and DRIs: monitor renal function
 Crt before starting therapy, after the first week of therapy, monthly during the first 3 months,
and when increasing the dose
 ACE dose should be reduced if serum crt is more than 2.5
o Obtain K at baseline and with other lab suggested
o For patients on ACEs or ARBs that require renal dose adjustment: assess urine protein prior to
initiation, every 2 to 4 weeks for the first 3 months of therapy, and regularly for up to 1 year
 Increased proteinuria indicates suggests reevaluation of therapy
o For patients on ARBs no change is dosage is required based on renal impairment
o Initial ARB doses may be lower for patients with impaired hepatic function
 LFTs prior to therapy
 Dose may be increased as tolerated
o DRIs need renal and K monitoring
o For ACEs: WBC with diff prior to therapy, monthly for the first 3 to 6 months, and periodically for
up to 1 year
 Patients ARF neutropenia: renal impairment, collagen vascular disease, high doses)
 d/c therapy if neutrophil count <1,000
o Patient education:
o Do not double doses if one is missed,

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