CHF

Dilated CM:

• • Disease of the cardiac muscle characterized by dilation of cardiac chambers and reduction of contractile function.

  • Most common form of CM

  • Majority of cases are idiopathic. Any process that affects myocardium leading to dilation of cardiac chambers and varying degrees of hypertrophy. It is a neurohormonal process. TR and MR common due to effect of chamber dilation stretching on the valvular annulus and apparatus.

  • Atrial and ventricular arrhythmia seen in 1/2 of cases, responsible for SCD.

  • Sx: HF - dyspnea, volume overload.

  • Dx: TTE or radionucleide ventriculography.

  • Tx: Preload and afterload reduction using vasodilator therapy. Low sodium and fluid restriction. BB; flu and pneumo vx; anticoagulation in pts with h/o VTE, AF, or LV thrombus (INR 2 - 3). For bx proven myocarditis - immunosuppressives like prednisone, azathioprine, and cyclosporine. ICD to prevent SCD if EF < 35% or NYHA class II - III sx despite maximal medical therapy for 3 months. CRT in selected patients.

    • Surgical: Cardiac transplantation in patients refractory to medical therapy. IABP or VAD as a bridge prior to cardiac transplantation.

    • Mitral valve annuloplasty or replacement used in patients with severe MR.

HOCM:

• • Most common inherited heart defect.

  • Most common cause of SCD in young people including trained atheletes.

  • Idiopathic form has an early onset (10 - 20 years) without associated HTN.

  • Assymetric hypetrophy of ventricular septum; genetic - mutation in the myosin heavy chain gene - autosomal dominant pattern with variable phenotypic expression and penetrance. Classifed according to presence or absence of LVOT obstruction. Family history of SCD is suggestive of familial type.

  • Tx: Relieve symptoms, prevent endocarditis, arrhythmias and SCD. Avoid strenous activity.

    • BB, CCB - verapamil or diltiazem.

    • Diuretics used with caution because decreased preload may cause hypotension. No nitrates or vasodilators like ACEI and hydralazine.

    • ICD to prevent SCD if genetic mutation, sustained VT, h/o syncope, recurrent VT on Holter, hypotensive response to exercise. LVH with wall thickness >30 mm in young patients, and h/o SCD in 1° relative.

    • Septal myotomy-myectomy with or without MVR.

Restrictive CM:

• • Rigid heart with poor ventricular filling. Infiltrative (amyloidosis or sarcoidosis) and noninfiltrative (diabetic or idiopathic) forms exist.

  • Other etiologies: hemochromatosis, Gaucher's and Hurler's CM (inherited glycogen storage diseases), hypereosinophilic syndrome, and carcinoid heart disease.

  • Dxtic: ECG in amyloid heart characterized by low voltage, poor R-wave progression. In sarcoidosis there is a conduction defect.

    • 2-D echo: thickened myocardium, normal or abnormal systolic fx, abnormal diastolic filling patterns, and elevated intracardiac pressure.

    • Cardiac MRI, PET, and CT useful in cardiac sarcoid

    • C.cath: elevated RV and LV filling pressures seen as classic dip-and-plateau pattern in the RV and LV pressure tracing.

    • RV endomyocardial bx may be dxtic.

  • Tx:

    • Treat underlying cause.

    • Cardiac hemochromatosis: reduce total body iron stores via phlebotomy or chelation therapy with deferoxamine.

    • Cardiac sarcoidosis responds to glucocorticoid therapy.

    • ICD for patients with syncope and/or ventricular arrhythmias. High grade conduction deficits need pacemaker placement.

    • Avoid digoxin in patients with cardiac amyloidosis as digoxin toxicity is common.

Peripartum Cardiomyopathy

• • Defined as LV systolic dysfx Dx in last month of pregnancy up to 5 months postpartum.

  • Viral triggers (coxsackievirus, parvovirus B19, adenovirus, and herpes virus) may replicate unchecked due to immunosuppressive state of pregnancy. Fetal microchimerism is also suggested, in which fetal cells escape in maternal circulation and induce an autoimmune myocarditis. Recently, a cleavage product of prolactin has also been implicated in the development of PPCM.

  • Risk factors: advance maternal age, multiparity, multiple pregnancy, preeclampsia, and gestational HTN. AAF are at high risk.

  • Diagnosis requires an echocardiogram with a depressed EF and/or LV dilatation.

  • Tx: preload and afterload reduction. ACEI used on postpartum, hydralazine in pregnant. BB which are B1 selective (metoprolol and atenolol) used because they avoid peripheral vasodilation and uterine relaxation. Digoxin for inotropic and also for rate control, however, monitor dig levels. Diuretics for preload reduction and symptom relief. Heparin for those with thromboembolism, followed by Coumadin after delivery.

  • The extent of ventricular recovery at 6 months post delivery can predict overall recovery, although continued improvement has been seen 2 - 3 years after diagnosis.

  • Subsequent pregnancies is hazardous and must be avoided, since they deteriorate LVEF and can result in death.

CRT or biventricular pacing appears to be beneficial in patients with an EF of 35% or less, NYHA class III - IV HF, and conduction abnormalities (LBBB and AV delay). It has been demonstrated to improve quality of life and reduce the risk of death in carefully selected patients.

ICD for EF <35% or less, for primary prevention of SCD.

• • Patients should receive at least 3 months of optimal medical therapy prior to reassessment of EF and implantation of an ICD.

  • Following MI or revascularization, EF should be assessed following 40 days of optimal therapy prior to ICD implantation.

  • ICD therapy should be deferred in patients with advanced age, life-shortening comorbidities, and end-stage HF patients who are not candidates for transplantation.

ICU MANAGEMENT OF ACUTE LEFT SIDED (SYSTOLIC) HEART FAILURE

3 hemodynamic measurements are important in management:

1. PCWP

2. CO

3. ABP

Decompensated HF is associated with ▲ PCWP, ▼ CO, but the BP can vary. The management strategies are based on the condition of the BP:

1. ▲ PCWP, ▼ CO, ▲ BP.

   • Oxygen therapy

   • Vasodilator therapy with NTG or nitroprusside. If PCWP stays >20 mm Hg, add diuretic therapy with furosemide.

   • NTG sublingual 0.4 mg x 3 q5 min is first-line therapy for acute pulmonary edema.

   • NTG 1 - 50 mcg/min results in venodilation. Start at 20 mcg/min and increase in increments of 20 mcg until patient symptoms resolve or PCWP is >16 mmHg, without reducing SBP <80 mmHg. To get vasodilation higher doses >50 mcg/min is required. Tolerance develops after 16 -24 hrs. Tx headache with APAP.

   • Nitroprusside is more effective vasodilator than NTG but drugs safety is a concern. Start at 10 mcg/min and increase by 10-20 mcg q10-20min as tolerated, with the same hemodynamic repsone as NTG, describe above. Cyanide toxicity, and in patients with MI/IHD it can cause coronary seal syndrome and precipitate further ischemia. Half life of ~2 min. Cyanide is most likely to accumulate in patients with reduced hepatic perfusion, and more likely to develop if the dose exceed >250 mcg/min for over 48 hrs.

   • Morphine 2 - 4 mg IV boluses act as a transient venodilator that reduces preload while relieving dyspnea and anxiety.

   • ACE-I is beneficial in the long term, but not used in acute management of decompensated left heart failure.

   • Duretic therapy with furosemide 0.5 mg/kg - 1 mg/kg is used if the vasodilator therapy does not reduce the PCWP to the desired wedge pressure, which is the highest pressure that will augment CO without producing pulmonary edema. The desired optimal PCWP in left heart failure is 18 - 20 mm Hg.

   • Nesiritide, is the newest vasodilator, a recombinant form of BNP. Given as bolus 2 mcg/kg, followed by a fixed dose infusion 0.01-0.03 mcg/kg/min. It lowers LV filling pressures and improves sx during the treatment of acute HF.

   • Positive-Pressure Ventilation. Continuous bilevel positive pressure ventilation can rest the respiratory muscles, improve oxygenation and cardiac function. Mechanical ventilation with PEEP can have multiple beneficial effects on pulmonary edema:

     • Decrease preload and afterload, thereby improving cardiac function.

     • Redistribution of lung water from the intra-alveolar to the extraalveolar space where the fluid does not interfere as much with gas exchange

     • Increase lung volume to avoid atelectasis.

   • Milrinone 50 mcg/kg, followed by 0.25 - 0.75 mcg/kg/min stimulate cardiac contractility while promoting peripheral and pulmonary vasodilation. Milrinone is PDE III inhibitor increased cAMP by inhibiting its breakdown. Does not increased myocardial O2 consumption. More effective in increasing CO, than dobutamine, especially in the presence of BB. Bolus at 0.5 mcg/kg/min, f/up a infusion @ 0.1-0.75 mcg/kg/min. Produces a greater reduction in LV filling pressures, and with it a greater risk of hypotension.

2. ▲ PCWP, ▼ CO, normal BP.

   • Inodilator therapy with dobutamine or milrinone, or vasodilator therapy with NTG. If PCWP does not <20 mm Hg, add diuretic therapy with furosemide.

   • BP is not affected in the usual doses, but dobutamine can increase BP, and milrinone can cause hypotension.

   • Dobutamine, which is the most commonly used inotropic agent for the treatment of acute HF, exerts by stimulating B1 and B2 rcp, with little effect on alpha1 rcp. It can increase myocardial O2 consumption and may be not be good in CAD. 1-2 mcg/kg/min starting dose. 5 mcg/kg/min needed frequently for severe hypoperfusion. No added effect if >10 mcg/kg/min. Tachyphylaxis after >72h, and requires higher doses.

   • NTG can replace dobutamine when treating Pt. with IHD. Milrinone is also good, especially when the Pt is on BB.

   • If the PCWP stays >20 mm Hg give diuretics.

3. ▲ PCWP, ▼ CO, ▼ BP.

   • Dopamine in vasoconstrictor doses. Mechanical assist devices can be used as a temporary measure in some cases. It is most useful in the treatment of HF Pts with depressed CO and poor tissue perfusion.

   • MAP should be maintained >60 mm Hg.

   • Dopamine 10 mcg/kg/min, vasopressor dose, inotropic

   • Mechanical cardiac support. IABP, LVAD as a bridge to more definitive therapies PCI or CABG.

4. Caution in use of diuretic therapy: Furosemide IV causes ▼ CO in Pts with acute left heart failure. This is because of a ▼ venous return and an ▲ SVR. ▲ SVR occurs due to the ability of furosemide to stimulate renin release and raise circulating levels of angiotensin, a vasoconstrictor. Diuretic therapy with furosemide IV is indicated only when the first line drugs, do not return the venous pressures to acceptable levels (PCWP <20 mm Hg).

   • Indication for furosemide infusion:

• • 1. Furosemide resistance (80 mg IV bolus results in <2 L of UO in 4 hrs)

    2. Dose: Furosemide, 100 mg IV bolus. Immediately followed by furosemide 40 mg/hr. Double the rate q12 hrs if needed to achieve a urine output of a at least 100 mL/h. Dose should not exceed a maximum of 160 mg/hr).

ICU MANAGEMENT OF RIGHT HEART FAILURE

Applies only to right heart failure from MI and not due to COPD.

1. If PCWP is <15 mm Hg, infuse volume until the PCWP or CVP increases by 5 mm Hg or either one reaches 20 mm Hg.

2. If the RVEDV is < 140 mL/min2, infuse volume until the RVEDV reaches 140 mL/m2.

3. If PCWP >15 mm Hg or the RVEDV is 140 mL/m2 or higer, infuse dobutamine, beginning at a rate of 5 mcg/kg/min.

4. AV dissociation or CHB, sequential A-V pacing and avoid ventricular pacing.

5. The response to volume infusion must be carefully monitored in right heart failure because aggressive volume infusion can overdistend the right ventricle and further reduce CO through interventricular interdependence.

6. Dobutamine is an effective agent for use in treatment of right heart failure.

Drugs used to manage acute decompensated heart failure in ICU