management of acute Heart failure

D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Acute HF

Definition

A physiologic state characterized byInadequate tissue perfusion

Clinically manifested byHemodynamic disturbancesOrgan dysfunction

Initial signs of end organ dysfunction

TachycardiaTachypneaMetabolic acidosisOliguriaCool and clammy skin

End Organ DysfunctionProgressive irreversible dysfunction

Oliguria or anuriaProgressive acidosis and decreased CO Agitation, obtundation, and comaPatient death

--In most cases, AHF arises as a result of deterioration in patients with a previous diagnosis of HF (either HF-REF or HF-PEF), and all of aspects of chronic management apply fully to these patients. --AHF may also be the first presentation of HF (‘de novo’ AHF).--ADHF is not just a worsening of chronic heart failure (HF) any more than an acute myocardial infarction (MI) is just a worsening of chronic angina.-BUN has consistently proved to be a stronger predictor of outcomes than creatinine . One potential explanation of this finding is that BUN may integrate both renal function and hemodynamic information. Unlike the situation in many other cardiovascular conditions, higher blood pressure has consistently been associated with lower risk. Hyponatremia appears to be associated with lower output and greater neurohormonal activation, and risk appears to be increased with evenmild forms of hyponatremia.

-higher diuretic use is associated with a higher incidence of adverse events (especially worsening renal function) and mortality. Interpreting this type of data is highly problematic because of the issue of confounding by indication (i.e., patients who need higher diuretic doses are typically sicker, and thus it is impossible to determine if higher doses of diuretics are simply a marker of greater disease severity or whether they directly contribute to worsening outcomes).-Taken as a whole, the results from DOSE appear to generally support an aggressive approach to decongestion of volume overloaded patients with ADHF, although renal function, electrolytes, and volume status need to be carefully monitored.

What is cardiorenal syndrome in ADHF?Worsening renal function during hospitalization for ADHF represents a major clinical challenge. Often termed cardiorenal syndrome (CRS), this clinical syndrome is characterized by persistent volume overload accompanied by worsening of renal function. Development of CRS, as defined by an increase in serum creatinine of 0.3 mg/dL or more from admission, occurs in as many as one-third of patients hospitalized with ADHF. Development of CRS is associated with higher mortality and increased length of stay in patients with ADHF. Although the underlying mechanisms of CRS remain ill defined, data suggest that higher diuretic doses, preexisting renal disease, and diabetes mellitus are associated with an increased risk. The optimal therapeutic strategy for patients with ADHF and CRS remains unknown. A variety of clinical approaches (hemodynamically guided therapy, inotropes, temporarily holding diuretics, etc.) have all been used with varying results, and there are no largeoutcomes studies to guide management of these challenging patients. Ultrafiltration therapy, which results in the removal of both free water and sodium, is currently being studied as an approach to CRS in an NIH-sponsored, randomized clinical trial that has recently completed enrollment.

Nesiritide=a human BNP that acts mainly as a vasodilator

-Dobutamine: b1 > b2 > a. It is mainly an inotropic agent. -Norepinephrine: b1 > a > b2. Norepinephrine is a potent vasoconstrictor.-Epinephrine: b1 = b2 > a. Potent inotrope.-Isoproterenol (pure b-agonist): b1 > b2. This is a potent inotrope and chronotrope.(dopamine, norepenipherine….add dobutamine, if BB milrinone as phosphodiesterase inhibitors)

--Oxygen should not be used routinely in non-hypoxaemic patients as it causes vasoconstriction and a reduction in cardiac output.--Potent combination {loop+thiazide} is usually only needed for a few days and requires careful monitoring to avoid hypokalaemia, renal dysfunction, and hypovolaemia.--Tolvaptan (a vasopressin V2-receptor antagonist) may be used totreat patients with resistant hyponatraemia (thirst and dehydrationare recognized adverse effects).--Restrict sodium intake to <2 g/day and fluid intake to<1.5–2.0L/day--Large RCT showed that neither type of non-invasive ventilationreduced mortality or the rate of endotracheal intubation (with nitrates, opiates).--Contraindications include hypotension, vomiting, possiblepneumothorax, and depressed consciousness

Mechanical circulatory support

1-Intra-aortic balloon pump:--Support the circulation before surgical correction of specific acute mechanical problems (e.g. interventricular septal rupture and acute mitral regurgitation), during severe acute myocarditis and in selected patients with acute myocardial ischaemia or infarction before, during, and after percutaneous or surgical revascularization. --There is no good evidence that an IABP is of benefit in other causes of cardiogenic shock.--More recently, balloon pumps (and other types of short-term, temporary circulatory support) have been used to bridge patients until implantation of a ventricular assist device or heart transplantation.2-Ventricular assist devices:--Ventricular assist devices and other forms of mechanical circulatorysupport (MCS) may be used as a ‘bridge to decision’ or longer term in selected patients.

INTRAAORTIC BALLON PUMP COUNTERPULSATION

30-cm balloon attached on a large bore catheter

Advanced into aorta until tip is in origin of left subclavian artery

Balloon inflated with helium (35-40 mL) at start of diastole when the aortic valve closes

Balloon rapidly deflated at the start of ventricular systole just before the aortic valve opens

Intraaortic balloon pump counterpulsation

INTRAAORTIC BALLOON PUMP COUNTERPULSATION

Mechanics Inflation of balloon increases peak

diastolic pressure and displaces blood toward the periphery MAP and coronary blood flow

Deflation of balloon reduces end-diastolic pressure which reduces impedance to flow when the aortic valve opens at the beginning of systole ventricular afterload and promotes ventricular stroke output

Indication for IABP

Contraindications to IABP

Significant aortic regurgitation or significant arteriovenous shunting Abdominal aortic aneurysm or aortic dissection Uncontrolled sepsis Uncontrolled bleeding disorder Severe bilateral peripheral vascular disease Bilateral femoral popliteal bypass grafts for severe peripheral vascular disease.

Complications of IABP

Cholesterol EmbolizationCVA Sepsis Balloon ruptureThrombocytopeniaHemolysisGroin InfectionPeripheral Neuropathy

Thank you