congestive heart failure a real threat
DESCRIPTION
Congestive Heart Failure A Real Threat. Etiology. Systolic Dysfunction(Decreased contractility): Reduction in muscle mass(due to ishcemia&MI ) Dilated cardiomyopathies ( idiopathic,viral,alcoholic ) Ventricular Hypertrophy: Pressure overload(systemic or pulmonary hypertension, - PowerPoint PPT PresentationTRANSCRIPT
Congestive Heart FailureA Real Threat
EtiologySystolic Dysfunction(Decreased contractility):Reduction in muscle mass(due to ishcemia&MI)Dilated cardiomyopathies(idiopathic,viral,alcoholic)Ventricular Hypertrophy:
Pressure overload(systemic or pulmonary hypertension,
aortic or pulmonic valve stenosis)
Volume overload(valvular regurgitation,high output states)
Etiology Diastolic Dysfunction(restriction in
ventricular filling): Increased ventricular stiffness
Ventricular hypertrophy Infiltrative Myocardial disease
(endomyocardial fibrosis) Myocardial ischemia and infarction
• Mitral or Tricuspid valve stenosis• Pericardial disease(Pericarditis)
Compensatory mechanisms in heart failureCompensatory response
Benefecial effects of compensation
Detrimental effects of compensation
Increased preload(through Na&water retention)
Optimize stroke volume Pulmonary and systemic congestion and edema formationIncreased MVO2
Vasoconstrition Maintain blood pressure in face of reduced COShunt blood from nonessential organs to heart and brain
Increased MVO2
Increased afterload
Tachycardia (due to SNS activation)
Helps maintain cardiac output
Increased MVO2
Shortened diastolic filling time
ß1-receptor downregulation &desensatizationArrhthemiaMyocardial cell death
Ventricular Hypertrophy and remodeling
Helps maintain COReduces myocardial wall stressDecreased MVO2
Diastolic & systolic dysfunctionMyocardial cell death &ischemia &arrhythemia
Classification(NYHA)Functional Class
Description
I Patient w cardiac disease but wout limitation of physical activity.Ordinary activity does not cause undue fatigue, dyspnea or palpitation
II Patient w cardiac disease that results in slight limitation of physical activity.Ordinary activity results in fatigue, dyspnea or palpitation
III Patient w cardiac disease that results in marked limitation of physical activity.although patients are comfortable at rest, less than ordinary activity will lead to symptoms
IV Patient w cardiac disease that results in an inability to carry on physical activity wout discomfort.symptoms are present even at rest with any physical activity, increased discomfort is experienced.
Classification(AHA)Stage Description
A Patient is at high risk for the development of HF but has no apparent structural abnormality of the heart
B Patient has structural abnormality of the heart but wout symptoms
C Patient has structural abnormality f the heart & current or previous symptoms of HF
D Patient has end-stage symptoms of HF that are refractory to standard treatment
Treatment
Treatment (Con,t) Stage A: Treat Risk factors:
Control Glucose level Control BP Dyslipidemia Thyroid disorder Valvular disease Avoid drugs which aggravate heart failure
Class II
Wet Sx
Diuretics (loop) + ACEDry Sx
ACE + B (no diuretics)
improved
Spironolactone
didn’t improve
digoxin
improved didn’t improved
Spironolactone Plan B
Sx resolve Sx don’t resolve
Spironolactone + B
give digoxin
improved didn’t improve
Give BSpironolactone
Plan B
Class III
directly give ACE inh & Loop
Sx still exist Px responded
Digoxin B & Spironolactone
Didn’t respond Didn’t respond
Plan B Plan B
Class IV (see if you hospitalize him or not)
ACE + Loop D + digoxin(don’t start B)
If Px was already on B
Did not respond optimize it
Plan B
Plan B Stage D
worsening Stage C (II, III, IV)
not improved
Plan B Stage D or worsening Stage C Hospitalize your Px.Optimize drug therapy
if not improved
wet dryGive aggressive diuretic therapy IV (thiazide and loop) to cause profound diuresis(give IV due to diuretic resistance® Give iv high dose® give combination
Give positive inotropic agents(he is already on ACE inh, digoxin)
improve
Taper down +inotrop and go back to chronic Tx
- Tissue hypoperfusion- SBP < 80- Worsening renal
function- ↙Na
hypervolemia dilutional hyponatremia cyanosis
Þ Hemodynamic Monitoring
(monitor BP, temp., CO, T0).
Negative inotropic effect cardiotoxic Sodium &water retention
Antiarrhythmic (disopyramide,flecainide)
Calcium channel blocker(verapamil…)
Itraconazole
Terbinafine
Rosiglitazone
Doxorubicine
Daunomycin
Cyclophosphamide
NSAIDs
Cox-2 inhibitor
Glucocorticoids
Androgens
Estrogens
Salicylate(high dose
Na containing Drugs (carbenicillin, ticarcillin)
Treatment (Con,t) Stage B=Class IACE inhibitors OrBeta blocker if recent or previous MI&
reduced ejection fraction due to remodeling
Stage C Є class II,III,&IVACE inhibitors & Beta blockers In all Px If Sx still exist Or EF still low Add
DigoxinWhen symptoms resolves add
aldactone
Role of drugs in CHF
Angiotensin converting enzyme inhibitors
Cardioprotctive effect Preload & Afterload RA system less Na/water
retention bradykinin level vasodilation mortality, hypertrophy, & fibrosis
ACE inhibitor Approved for Use in HF
Generic Name
Brand Name
Usual daily dose(mg)
Dosing frequancy
Target dosing survival benefit
Prodrug Elimination T1/2
Captopril Capoten 18.75-150 tid 50tid No Renal 2
Enalapril Renitec 2.5-40 bid 10bid Yes Renal 10
Lisinopril Zestril 5-40 qd 10qd No Renal 12
Ramipril Tritace 1.25-20 qdorbid 5bid yes Renal 9-18
BETA BLOCKERS
Mortality Vasoconstriction Carvidilol alpha+beta blocker
&antioxidant effect Bisoprolol Metoprolol
DIGOXIN
+ inotropic effect sympathetic output from CNS(NE) Not mortality but improve Sx Therapeutic level: 0.5-1ng/ml for CHF Max: 1-1.5ng/ml for A fib
Clinical Pharmacokinetics of DigoxinOral bioavailability: Tablets 65% Elixir 80% Capsules 95%Onset of action: Oral 4-6hr IV 1.5-4hrTerminal half –life: Normal renal function 36hr Anuric patient 5daysVolume of distribution 7.3L/kgFraction unbound in plasma 75-80%Fraction excreted unchanged in urine 65-70%
Diuretics Sx relief of edema & pulmonary
congestion Direct vasodilation , Preload DOC: Furosamide: Na excretion 20-
25%
Thiazide: Na Excretion 5-8% Dose: 20-40mg bid
Up to 400mg as max dose
If Clcr>30ml/min dose up to 1-3g/d
Loop Diuretics Used in HF
Furosemide Bumetanide
Usual daily dose 20-160mg/day 0.5-4mg/day
Normal renal function
80-160mg 1-2mg
Clcr:20-25ml/min 160mg 2mg
Clcr<20ml/min 400mg 8-10mg
Bioavailability Average50% 80-90%
Affected by food Yes Yes
T1/20.3-3.4hr 0.3-1.5hr
Spironolactone
Aldosterone, preload,ventricular remodeling
Morbidity &mortality(Rales study) Used if Scr<2.5mg/dl & K<5meq/L Aplerenone No gynecomastia Mortality & morbiity in acute MI
ANGIOTENSIN RECEPTOR BLOCKER
Persistent cough &angioedema due to ACE inhibitors
If persistent HTN Add ARB or CaCh blocker (amlodepine)
If concomitant angina: add nitrate or amlodepine
New Drug Investigation
Natriuretic Peptides:
Atrial Natriuretic Peptides (ANP)
Brain Natriuretic Peptides (BNP
C-type Natriuretic Peptides (CNP)
Neseritide:
Recombinant BNP
New Drug Investigation
Omapatrilat:
Vasopeptidase Inhibitor
ACE inhibitor
INH neutral endopeptidas
Bradykinin & NP
SE: Angiodema
Precipitating factors in Heart failure Decompensation
Noncompliance with drugs or diet
Cardiac Ischemia
Inadequate therapy at time of admission
Cardiac arrhythmias
Uncontrolled hypertension
Thank YOU