Dr. Kristine A.

Baldomero February 1, 2013

Sample Case of CHF CHF

Definition

Pathophysiology
Drugs for CHF Mechanism of Action

Summary

6 week old female chief complaints of lethargy, poor feeding, and respiratory distress. 2 weeks prior to presentation febrile illness with cough, rhinorrhea, and emesis she sweats a lot on her forehead when feeding. noted her to be increasingly lethargic, with tachypnea, and retractions

6 week old female chief complaints of lethargy, poor feeding, and respiratory distress. 2 weeks prior to presentation febrile illness with cough, rhinorrhea, and emesis she sweats a lot on her forehead when feeding. noted her to be increasingly lethargic, with tachypnea, and retractions

G3P2, full term, uncomplicated pregnancy. Delivery was unremarkable Her pediatric follow-up has been poor.

Exam: VS T 36.8, RR 72, HR 160, BP 92/68. Oxygen sat in room air is 99%. mildly cachetic, acyanotic infant who was pale, lethargic, and tachypneic, with mild to moderate subcostal and intercostal retractions. crackles with slightly decreased aeration in the left lower lobe.

The precordium is mildly active. regular rate and rhythm, with a Grade II/VI holosystolic murmur at the mid lower left sternal border with radiation to the cardiac apex abdomen is soft, non-distended, and nontender liver edge is palpable 3 to 4 cm below the right costal margin. There are no palpable masses or splenomegaly.

Bowel sounds are hypoactive. Her extremities are symmetric and cool, with peripheral pulses 1+/4+ in all extremities with no radial-femoral delay. The capillary refill is 4 to 5 seconds (delayed).
CXR moderate cardiomegaly moderate degree of pulmonary edema no pleural effusions.

ECG sinus tachycardia, normal PR and QTc intervals, and a left axis deviation. Voltage evidence of biventricular hypertrophy is present. No significant Q-waves or ST segment changes are noted. An echocardiogram large perimembranous ventricular septal defect with non-restrictive left to right shunting. All cardiac chambers are dilated. Left ventricular contractility is at the lower range of normal. There is no pericardial effusion.

admitted to the hospital and loaded with digoxin, and also started on diuretics and afterload reduction. symptoms improve and she is discharged on 24 calorie/ounce formula due to poor weight gain

FF-up continues to have poor weight gain on higher caloric density formula and continues to have symptoms of heart failure on medical management. She is referred for surgical correction of the ventricular septal defect at 6 months of age.

CHF secondary to VSD Pneumonia

CHF - is a condition in which the heart is unable to pump sufficient blood to meet the needs of the body.

CHF - can be caused by an impaired ability of the cardiac muscle to contract or by an increase workload imposed on the heart. - accompanied by an abnormal increase in blood volume and interstital fluid.

Symptoms Cough Difficulty in breathing Diaphoresis Poor feeding

Signs Cachectic Acyanotic Retraction s murmur Hepatomegaly Cool extremeties Poor CRT

Cardiac failure
Inc venous pressure dec cardiac output
Decreased BP

Increased sympathetic activity

Decreased renal bld flow

Increased renin angiotensin II Increased aldosterone Increased capillary filtration Increased sodium & water retention

EDEMA

 Therapeutic goal
to increase cardiac output

1.
2. 3.

Vasodilators- reduce the load on the myocardium Diuretics- decrease extracellular fluid volume Inotropic agents- increase the strength of contraction of cardiac muscle.

A. Vasodilators: captopril enalapril fosinopril quinapril

hydralazine isosorbide Minoxidil Sodium nitroprusside

B. Diuretics: Bumetanide furosemide

Hydrochlorthiazide Metolazone

C. Inotropic agents:
Digitoxin- cardiac glycosides Digoxin Dobutamine- B adrenergic agonist Amrinone- Phosphodiesterase inhibitor Milrinone

It is useful in reducing the preload and the afterload Dilatation of venous blood vessels
leads to a decrease in cardiac preload by

increasing venous capacitance arterial dilators reduce systemic arteriolar resistance and decrease afterload

Cardiac failure
Inc venous pressure dec cardiac output
Decreased BP

Increased sympathetic activity

Decreased renal bld flow

Increased renin angiotensin II Increased aldosterone Increased capillary filtration Increased sodium & water retention

EDEMA

Cardiac failure
VASODILATOR Inc venous pressure dec cardiac output
Increased sympathetic activity Decreased BP

Decreased renal bld flow

Increased renin angiotensin II Increased aldosterone Increased capillary filtration Increased sodium & water retention

EDEMA

1). Angiotensin converting enzyme (ACE) inhibitors

- are the agents of choice in CHF and are superior to

other vasodilators

1). Angiotensin converting enzyme (ACE) inhibitors

-

blocks the enzyme that cleaves angiotensin I to form the potent vasoconstrictor.
Diminish the rate of bradykinin inactivation decrease the secretion of aldosterone resulting in decreased sodium and water retention

Action on the heart: - decrease vascular resistance, venous tone and blood pressure resulting in an increase cardiac output.

Cardiac failure
Inc venous pressure dec cardiac output
Decreased BP

Increased sympathetic activity

Decreased renal bld flow

Increased renin angiotensin II Increased aldosterone Increased capillary filtration Increased sodium & water retention

EDEMA

Cardiac failure
VASODILATOR Inc venous pressure dec cardiac output
Increased sympathetic activity Decreased BP

Decreased renal bld flow

Increased renin angiotensin II

ACE inhibitor
Increased capillary filtration

Increased aldosterone Increased sodium & water retention

EDEMA

Action on the heart: - blunt the usual angiotensin II mediated increase in epinephrine and aldosterone
Indication: - may be considered for single agent therapy in patients who present with mild dyspnea on exertion and who do not show signs or symptoms of volume overload.

- are useful in decreasing CHF in asymptomatic patients with ejection fraction less than 35% (left ventricular dysfunction)

Early use of ACE inhibitors is indicated in treating patients with all stages of left ventricular failure with and without symptoms.

Captopril Neonate 0.01 to 0.05 mkdose q 8-q12 Infant 0.01-0.5 mkdose bid-tid, max dose 6mg/24hrs Child- 0.3-0.5mkd, max 6mg/kg/day up to 450mg/24hrs Adolescent- 12.5-25 mkd bid-tid,max 450mg/24hrs

3. Adverse effects: - postural hypotension - renal insufficiency - hyperkalemia - persistent dry cough

2. ) Direct smooth muscle relaxant

Examples: Nitrates 1. hydralazine and isosorbide dinitrate 2. amlodipine and felodipine

Relieve pulmonary congestion and peripheral edema. Decrease plasma volume overload and subsequently decrease venous return to the heart

Decrease the cardiac workload and oxygen demand Decrease the afterload by reducing plasma volume Example
thiazide diuretics

loop diuretics

Cardiac failure
Inc venous pressure dec cardiac output
Decreased BP

Increased sympathetic activity

Decreased renal bld flow

Increased renin angiotensin II Increased aldosterone Increased capillary filtration Increased sodium & water retention

EDEMA

Cardiac failure
Inc venous pressure dec cardiac output
Decreased BP

Increased sympathetic activity

Decreased renal bld flow

Increased renin angiotensin II

Diuretic
Increased capillary filtration

Increased aldosterone

Increased sodium & water retention

EDEMA

Furosemide: IM iv neonate: o.5-1mkd oseq8-q24 ,max 2mg/kg/dose Infant and child- 0.5-2mkdose q6-612 PO neonate 1-4mkdose Infant and child 2mkdose qid-bid inc by 1-2 mkd, max dose 6mkdose Continuous iv= 0.05m/k/hr titrate to effect

enhance cardiac contractility and thus increase cardiac output inotropic action is the result of an increased cytoplasmic calcium concentration that enhances the contractility of cardiac muscle.

1.) Digitalis - can increase the contractility of the heart - influence sodium and calcium ion flows in the cardiac muscles thereby increasing contraction of the atrial and ventricular myocardium (positive inotropic effect).
Example: Digoxin

1.

Mode of action:
a. Regulation of cystolic calcium concentration - combine reversibly with the sodiumpotassium ATPase of the cardiac cell membrane resulting in an inhibition of pump activity.

b. increase contractility of the cardiac muscle

- increases the force of cardiac contractility causing the cardiac output to more closely resemble that of a normal heart.

2. Therapeutic use:
A. Digoxin therapy -indicated in patients with severe left ventricular systolic dysfunction after initiation of diuretic and vasodilatation therapy - is not indicated in patients with diastolic or right sided failure

B. Dobutamine therapy

Digoxin TDD Age Premature FT <2yr 2-10yr >10yr and <10kg

po iv/im 20 15 30 20 40-50 30-40 30-40 20-30 10-15 8-12

daily maintenance po iv/im 5 3-4 8-10 6-8 10-12 7.5-9 8-10 6-8 2.5-5 2-3

Dobutamine 12.5mg/ml (20ml) Preload in d5w 1mg/ml (250, 500ml) 2mg/ml(250ml) 4mg/ml(250/ml) Continuous iv infusion= 2.5-15mcg/kg/hr max dose= 40mg/kg/hr

3. Adverse effects: Digitalis toxicity - one of the most commonly encountered adverse drug reaction. - discontinuing the therapy - determine the potassium level

2. Gastrointestinal effects: anorexia, nausea and vomiting 3. CNS efects headache, fatigue, confusion, blurred vision, alteration of color perception, and haloes on dark object.

Factors predisposing to digitalis toxicity: a. electrolyte disturbance- hypokalemia b. drugs: 1.quinidine -by displacing digitalis from plasma protein binding site -by competing with digitalis or renal excretion 2. verapamil 3. Potassium depleting diuretics 4. corticosteroids

Factors predisposing to digitalis toxicity: c. hypothyroidism d. hypoxia e. renal failure f. Myocarditis

B. Beta adrenergic agonist - improves cardiac performance by positive inotropic effects and vasodilatation. - most commonly used inotropic agent other than digitalis Dobutamine- leads to an increase in intracellular cAMP which results in the activation of protein kinase, which leads to increase contraction of myocardial cells.

C. Phosphodiesterase inhibitors: Amrinone and milrinone - are phosphodiesterase inhibitors that increases the intracellular concentration of cAMP

Captopril
PO= 50mg P6

Furosemide
PO= 20mg/tab P2
IV= 20mg/amp= P15

Dopamine (pre-mix)= P420 Dobutamine P280

Thank you

The myocardium like smooth and skeletal muscles respond to stimulation by depolarization of the membrane. This is followed by shortening of the contractile proteins and ends with relaxation and resting state. Unlike skeletal muscle which shows graded contractions depending on the number of muscle cells stimulated, the cardiac muscles are interconnected in groups that respond to stimuli as a unit, contracting together whenever a single cell is stimulated.

Action potential Cardiac contraction 1. Sources of free intracellular calcium 2.Removal of free cystolic calcium a. Sodium-calcium exchange b. Uptake of calcium by the sarcoplasmic reticulum and mitochondria C. Compensatory physiologic response in CHF 1. Increase sympathetic activity 2. Fluid retention 3. Myocardial hypertrophy D. Decompensated heart failure E. Therapeutic strategies in CHF
A. B.