new heart failure-2
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Outline
Management of Heart Failure Diuretics
VASODILATOR THERAPY IN HEART FAILURE
Angiotensin Converting EnzymeInhibitors
1. VASODILATION
2.
DIURESIS3. REMODELING REGRESSION
B- blockers
Digoxin
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Diuretics can relieve peripheral & pulmonaryedema within hours or days unlike other
agents (ACEIs/-blockers) that requireweeks to months
DIURETIC MONOTHERAPY
IS NOT ALLOWED as they offer ineffectivemaintenance alone.
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Diuretics are recommended when clinical evidenceexists for volume overload
Patients without peripheral/pulmonary edema canbe treated WITHOUT OR INTERMITTANTdiuretics
As-needed diuretic depends on wt gain
changes, neck vein distention (>0.5-1 kg/day or 2kg/week wt gain/swollen legs)
Otherwise, diuretic-free periods or week ends areapplied
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EFFICAY of diuretics depend on sodium load deliveredto their site of action
In HF, compromised GFR increases Na+ re-absorption,leading to minimal efficacy for thiazide & K+-sparingdiuretics.
Loop diuretics (furosemide, bumetanide & torsemide)are the preferred diuretics in HF
They are effective even at creatinine Clcr is less than 5mL/min
Furosemide has addition vasodilating properties decreasingrenal vascular resistance even before diuresis starts
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Diuretics Adverse Effects
1-Azotemia
Normal BUN/creatinine=10-20
Increased both values: progressive renal damage
Increased BUN/creatinine ratio above 20 denotes prerenalazotemia caused by poor renal perfusion &/or overdiuresis
Proper diuretic therapy would improve HF, renal perfusion &helps lower BUN
Prolonged over-diuresis & dehydration may cause decreased
renal perfusion & renal damage, where creatinine will rise aswell
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Diuretics Adverse Effects
2- Hypokalemia
Definition: less than 3.5 mEq/L, HCTZ (50-100 mg/day),incidence is 15-40%
At lower-dose HCTZ & accepting serum levels of
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Diuretics Adverse Effects
3- Hypomagnesemia
Severe hypomagnesemia can lead to muscle
spasms, decreased seizure threshold &cardiac arrythmias
Concurrent hypokalemia & hypomagnesemia
can be seriously dangerous IV MgSO4 is administered to restore serum
Mg2+
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Diuretics Adverse Effects
4- Hyperuricemia
Usual increments in uric acid levels are1-2 mg/dL
Asymptomatic hyperuricemic patients usually do
not require treatments Persistent hyperuricemia >10 mg/dL, or history of
gout, consider urate-lowering agents
5- Hyperglycemia Hyperglycemia & glucose intolerance are side
effects to thiazide & loop diuretics
Family history & other risk factors are evaluated
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Potassium
Supplementation
Serum K+ must be monitored frequently
Hypokalemia can occur few hrs after first dose, & reaches
max after a week Hypokalemia takes several weeks to go to normal after
diuretic withdrawal
K+ replacement: Only KCl should be used because all
hypokalemic diuretics can cause hypochloremic alkalosis If hypochloremia was not corrected, hypokalemia &
alkalosis persist
K+-sparing diuretic or K+-containing food
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Diuretic Therapy
Monitoring
CHF symptoms
Wt Loss (0.5-1 kg/day) and decreasededema
Signs of volume depletion: hypotension,dizziness, weakness, decreased urine output
& raised BUN
Check serum K+, Mg2+, uric acid & glucose
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Diuretic-Independent
Effects of Spironolactone
Both ANGII & aldosterone have direct CV detrimentaleffects:
o Vascular & myocardial hypertrophy & fibrosis,o direct vascular & endothelial damage,
o increased oxidative stress
o
Inhibition of NE uptake by the myocardium Spironolactone addition to maintenance HF therapy,
significantly reduced mortality in severe HF (stage IV)
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VASODILATOR THERAPY IN
HEART FAILURE
Arterial vasodilation decreases afterload &venodilation lowers preload.
Hydralazine (arterial dilator) & nitrates (venousdilator) combination reduces HF symptoms & havemodest reduction of mortality.
ACEIs reduce both preload & afterload and suppress
cardiac remodelling.
It was recommended the use of ACEIs to all systolicHF patients unless contraindicated or intolerated.
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Angiotensin Converting Enzyme
Inhibitors (ACEIs)
VASODILATION, DIURESIS & REMODELINGREGRESSION are the beneficial triad for ACE
inhibition
Vasodilation: decreased ANG II & NE and increasedbradykinin (BK) & substance P
Bradykinin stimulates B1 receptors leading toincreased PGI2, NO & EDRF
BK increases natriuresis via direct tubular effect
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Angiotensin Converting Enzyme
Inhibitors (ACEIs)
Mild diuresis:
Reduction of aldosterone & vasopressin secretion
Enhanced renal blood flow, via increased CO & locallythrough efferent arteriolar vasodialtion
Cardiac & Vascular Remdelling inhibitionby lowering
ANGII type-1 R - hypertrophic effects
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Angiotensin Converting Enzyme
Inhibitors (ACEIs)
FDA-labeled ACEIs for HF: captopril, enalpril,fosinopril, lisinopril, quinapril, ramipril.
No drug is preferred to another Efficacy: ACEIs are effective in ischemic/non-
ischemic HF & all HF stages (I-IV)
Produce relative reduction of 20-30% HF mortality,superior to hydralazine-nitrate or ARBs
ACEIs showed better cardiac remodeling inhibitoryeffect over ARBs
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Various ACEIs
It was recommended captopril, enalpril, lisinopril &ramipril
Captopril & lisinopril have no active metabolites All other agents are PRODRUGS requiring enzymatic
conversion to active metabolites
Captopril has shorter onset and duration of action,administered frequently/day
Captopril is better for initiating ACEI therapy for 2days followed by longer-acting ones in good
responders
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ACE Inhibitors-Induced
Cough
ALL ACEIs can induce cough in 3-15% of patients
It occurs within few weeks to months of treatment &
persist 1-2 weeks after drug withdrawal Changing an ACEI to another or dose reduction do
not stop cough because of the Pharmacologicmechanism (increased Bradykinin & substance P)
Withdrawal of the ACEI drug is the only way to stopACEI-induced cough
If cough persists, shift to another vasodilator: ARB or
hydralazine-nitrate combination
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Angiotensin II Type-1 (AT1)
Receptor Antagonists (ARBs)
They preferentially block AT-1 receptors
They improve HF symptoms: increased
exercise tolerance & ejection fraction
ARBs were not superior to ACEIs in reductionof all-cause mortality, but cough-free
FDA approved valsartan for HF
Triple combination:
ACEI-ARB--blocker should not be used
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Adverse Effects of ACEIs & ARBs
1- Hyperkalemia
ANG II-induced aldosterone secretion is decreased
by ACEI/ARB leading to K+ retention Significant hyperkalemia occurs in
o Renal compromised patients
o K+ supplementation & K+-sparing diuretics K+-losing (thiazide & loop) diuretics concurrent use
leads to either normokalemia or hypokalemia
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Adverse Effects of ACEIs & ARBs
Angioedema (Angioneurotic edema)
It consists of facial/neck edema with airway obstruction(laryngeal& bronchial edema)
Mechanism is unknown but thought to be related to kinins
accumulation Though kinin-related, case reports exist for angioedema
induced by losartan & valsartan
ARBs are an option whenever ACE-induced angioedema occurs
Hydralazine-nitrate combination is another alternative African Americans & females are more vulnerable
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Effects of ACEIs & ARBs
on Kidney Function
HF Patients Beneficial Effect: ACEI/ARB decrease pre- &
afterload increase CO improve renal blood flow.
Non-beneficial Effect: Initial therapy rapid BP fall slow CO response worsening of renal function
Prediction of which event to occur is impossible
ACEI/ARB therapy initiated with low dose, slowincrease in dose/careful BP & renal function monitor
Diuretic dose is adjusted to avoid volume depletion& hypotension
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ACEIs in Asymptomatic Patients
HF patients in Stage A-B, with LVH ordecreased EF but NO signs benefits from
ACEI therapy.
Possibly ACEI retards cardiac remodelling
-blockers may be added to ACEI forasymptomatic HF patients whenevercompelling indication exists (e.g., MI)
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-Blockers in Systolic Heart
Failure
EVIDENCE: -blockers reduce mortality (30%) &hospitalization (40%)
Metoprolol & carvedilol reduce HF symptoms &mortality
They are added to diuretic-ACEI & often digoxin
They should not be delayed till refractoriness toHF therapy occurs
Addition to low-dose ACEI produces betterimprovement of symptoms & mortality
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-Blockers in Systolic Heart
Failure
Contraindication: Unstable HF hospialized patients,symptomatic bradycardia/heart block, resistant asthma
DOSE: Initial low dose, gradual increase every 1-2 weeksaccording to patient tolerance
Transient bradycardia, heart block, hypotension often areasymptomatic, no treatment, but patients advised to standslowly from lying position
If symptoms (dizziness, blurred vision) occur dosereduction &/or lower dose titration
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Metoprolol, Bisoprolol &
Carvedilol
They are FDA approved for HF
Metporolol & bisoprolol are cardioselective
showing myocardial 2-receptor upregulation Carvedilol is mixed ,-blocker with additional
antioxidant activity
Approved for stages II & III and now IV HF
Carvedilol is possibly associated with morehypotension & dizziness
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DIGOXIN
Digoxin Intervention Group (DIG) trial
HF patients Class II/III on digoxin (2-5 years) moderate
decrease of combined mortality/hospitalization but little effecton survival
Digoxin started early to reduce symptoms of HF patients onACEI or -blocker but not yet with improved symptoms
Digoxin is routinely advised for HF patients with chronic atrialfibrilation
Digoxin is avoided in patients with appreciable sinus/AV block
It is not indicated as 1ry therapy for acute decompensated HF
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Digoxin
Digoxin therapy can be delayed till responseto ACEI or -blocker is evident and given to
the still symptomatic patients Digoxin monotherapy or digoxin-diuretic
therapy is no longer recommended
Usual maintenace dose is 0.125-0.25 mg/day
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