P4 - CHF DUGS

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60 Terms

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HEART FAILURE

cardiac disorder that impairs the ability of the ventricle to deliver adequate quantities of blood to the metabolizing tissues during normal activity or at rest

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  • CLASS I


CLASSES OF HEART FAILURE

  • degree of effort necessary to elicit HF symptoms equals to those that would limit normal individuals


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  • CLASS II


CLASSES OF HEART FAILURE

  • symptoms occurs with ordinary exertion


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CLASS III

CLASSES OF HEART FAILURE

  • symptoms occurs with less- than-ordinary exertion.


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CLASS IV

CLASSES OF HEART FAILURE

  • Symptoms occurs while at rest


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LOW OUTPUT

Metabolic demands are NORMAL but heart is unable to meet them

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HIGH OUTPUT

Metabolic demands are INCREASED (hyperthyroidism anemia)and the heart is unable to meet them

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DIASTOLIC DYSFUNCTION

  • Result of hypertrophy and stiffening of myocardium, reduced filling

  • Reduced CO, normal ejection fraction

  • Does not respond to inotropic drugs


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SYSTOLIC DYSFUNCTION

• Reduced mechanical pumping action

  • Reduced CO and reduced ejection fraction (< 45%)

  • Results from MI

  • respond to inotropic drugs


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PERIPHERAL EDEMA

RIGHT-SIDED FAILURE =

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PULMONARY EDEMA

LEFT-SIDED FAILURE =

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  • Tachycardia

  • Decreased exercise tolerance

  • Shortness of breath

  • Cardiomegaly


Signs and symptoms of all types of HF

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CONCENTRIC CARDIAC HYPERTROPHY

do to protect heart it CHANGE THE SIZE AND SHAPE

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FRANK-STARLING MECHANISM

– increased fiber dilation heightens the contractile force, which then increases the energy released.

  • IT LOOSEN


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AFTERLOAD

– tension in ventricular muscles during contraction.

In the left ventricle,

  • this tension is determined by the amount of force needed to overcome pressure in the pulmonary artery.


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PRELOAD

– force exerted on the ventricular muscle at the end of diastole that determines the degree of muscle fiber stretch.

  • Also known as ventricular end diastolic pressure; also a key factor in contractility


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  • Antibiotics


Digoxin

  • can affect the concentration of digoxin


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  • KIDNEY

  • BILE


  • Digoxin

  • Digitoxin

    • EXERTED


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Cardiac glycosides (DIGOXIN, DIGITOXIN)

  • sodium pump.


MECHANISM OF ACTION

  • inhibit Na+/K+ ATPase, the membrane-bound transporter often called the


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  • disorientation

  • hallucinations


Central nervous system effects

  • IN ERDERLY


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Gynecomastia

is a rare effect

  • it is not certain whether this effect represents a peripheral estrogenic action of these steroid drugs or a manifestation of hypothalamic stimulation.


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POSITIVE INOTROPIC EFFECTS

DEACTIVATION OF renin-angiotensin-aldosterone compensation

THERAPEUTIC EFFECTS of DIGOXIN

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DIGOXIN

With narrow therapeutic index

  • available in tablet, injection, elixir and capsule forms.


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0.5–1.5 ng/mL

DOSAGE AND ADMINISTRATION of Digoxin

  • Therapeutic plasma concentration


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> 2 ng/mL

DOSAGE AND ADMINISTRATION of Digoxin

  • Toxic plasma concentration


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0.25 (0.125–0.5) mg

DOSAGE AND ADMINISTRATION of Digoxin

  • Daily dose (slow loading or maintenance)


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0.5–0.75 mg every 8 hours for three doses

DOSAGE AND ADMINISTRATION of Digoxin

  • Rapid digitalizing dose (rarely used)


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QUINIDINE

RISK OF TOXICITY •increases with coadminstration of

  • DECREASE RENAL CLEARANCE OF DIGOXIN


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  • potassium supplements


C. TREATMENT OF TOXICITY

  • If the patient is hypokalemic: Administer


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  • lidocaine or phenytoin


C. TREATMENT OF TOXICITY

  • Arrhythmias


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  • Cholestyramine


C. TREATMENT OF TOXICITY

  • binds to digitalis glycosides to prevent absorption of digitalis in the bile


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  • purified digoxin Fab fragment antibodies.

    • DIGIbind


C. TREATMENT OF TOXICITY

  • Patients with very high serum digoxin levels


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Diuretics

MOA: to reduce venous pressure and ventricular preload

GOAL: to reduce and eventually eliminate signs and

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THIAZIDE diuretics

lose their effectiveness in HF patients with moderately impaired renal function

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LOOP diuretics

increase sodium excretion to 20-25% of the filtered load

  • reverse pulmonary edema


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POTASSIUM SPARING

Given to patients already on Digoxin or ACE inhibitors

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Vasodilators

reduce pulmonary congestion effective in acute heart failure because they provide a reduction in preload (through venodilation), or reduction in afterload (through arteriolar dilation), or both

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NITRO PRUSSIDE

Vasodilators
- provide potent dilation of both arteries and veins

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HYDRA LAZNE

Vasodilators

  • decreases afterload and increases cardiac output.


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PRA ZOSIN

Vasodilators

  • arteriovenous dilator


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NITRATES

Vasodilators

— decreases preload

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HYDRALAZINE + nitrosovasodilators

Combination of Vasodilators: reduce damaging remodeling of the heart

  • Reduce both preload and afterload


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with ISOSORBIDE DINITRATE

Combination of Vasodilators: reduce damaging remodeling of the heart

  • reduce afterload


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with NITROGLYCERIN

Combination of Vasodilators: reduce damaging remodeling of the heart

  • reduce preload


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ACE INHIBITORS

first line agents in the treatment of HF beneficial effect on cardiac remodeling.

↓PVR ↓afterload ↓salt and water retention ↓ preload

  • added to a diuretic

  • Also indicated for patients with left ventricular dysfunction without symptoms of HF. for long-term management of chronic HF

  • Combine with a β-blocker, diuretic & digoxin Dose must be carefully titrated to the maximum allowable or tolerable dose


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Oma patrilat

inhibits both ACE and neutral endopeptidase increase exercise tolerance

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β-adrenergic blockers (bisoprolol, carvedilol, and metoprolol)

Used in stable severe heart failure used in conjunction with diuretics, ACE inhibitors and usually digoxin

  • should not be taken without diuretics in patients with a current or recent history of fluid retention

  • MONITOR bradycardia and the potential for heart block


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INOTROPIC AGENTS

used in the emergency treatment of patients with HF and in patients refractory to or unable to take digitalis

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. DOPAMINE (IV)

used in acute heart failure , ↑ TPR

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DOBUTAMINE (IV)

↑ CO , ↓ in ventricular filling pressure

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BIPYRIDINES

MOA: Inhibits phosphodiesterases , ↑ cAMP

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INAMRINONE (IV)

INOTROPIC AGENTS
- Unstable in dextrose sol’n has both a positive inotropic effect and a vasodilating effect

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MILRINONE (IV)

INOTROPIC AGENTS

  • ADR: hypotension, thrombocytopenia


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NESIRITIDE (Natrecor®)

A synthetic brain natriuretic peptide (BNP) •approved for the IV treatment of patients with acutely decompensated HF associated with shortness of breath at rest or with minimal activity.

  • MOA: it binds to natriuretic peptide receptors in blood vessels, resulting in increased production in guanosine 3’5’ cGMP in target tissues, which mediates vasodilation


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Natrecor®

NESIRITIDE

  • BN


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ADR: Excessive hypotension

NESIRITIDE (Natrecor®)

  • ADR


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Bosentan

competitive inhibition of endothelin

  • use in pulmonary HPN .

  • teratogenic and hepatotoxic


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Levosimendan

sensitizes the troponin system to calcium inhibit PDE

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Alis kiren

renin inhibition

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  • Carperitide

  • ularitide


NATRIURETIC PEPTIDES

  • atrial natriuretic peptide (ANP)

  • urodilatin