Management of acute LVF

Presenter : Dr. Gautam ChakmaModerator : Prof. Lallan Prasad

Introduction

• Acute heart failure (AHF)- rapid onset of symptoms and

signs secondary to abnormal cardiac function.

• Acute left ventricular failure (ALVF) is AHF due to

abnormal left ventricular function.

• It is often life threatening and requires urgent treatment.

• AHF-acute de novo/acute decompensation of CHF.• Acuteness-days/weeks/hrs-minutes.• CAD most common aetiology(60–70%), particularly

in elderly.• Younger subjects-DCM, arrhythmia, congenital and

valvular heart disease, myocarditis

Pathophysiology AHF

Causes and precipitating factors in AHF

SIGN AND SYMPTOMS OF ACUTE LVF

AHF with distinct clinical conditions

Classifications of AHFS after AMI utilized in CCU and ICCU

Killip classification• Stage I—No clinical signs of HF.• Stage II—Heart failure. Rales,S3 gallop and pulmonary

venous hypertension.• Stage III—Severe HF. Frank pulmonary oedema with rales

throughout the lung fields• Stage IV—Cardiogenic shock.Hypotension (SBP <90

mmHg), peripheral vasoconstriction (oliguria, cyanosis diaphoresis) .

Diagnosis• Diagnosis of AHF is based on the symptoms and clinical

findings,• Supported by appropriate investigations such as ECG, chest

X-ray, biomarkers, and Doppler echocardiography

• CXR- Cardiomegaly,Kerley’s A, B lines, pulmonary congestion-bat wings haziness, Cephalization of veins, pleural effusions

• ECG- LA enlargement ,arrhythmias , LVH, previous MI• Echocardiography-assesment of systolic / diastolic

function, EF calculation ,any valvular abnormality ,abnormal wall motion

• Biomarker of HF NP-useful in diagnosis,assessing severity

predicting short & long-term CVS mortality

• No HF- BNP <100pg/dl , PRO-BNP < 300pg/dl

• HF- BNP >500pg/dl , PRO-BNP >1000pg/dl

• 80% Sensitivity for heart failure

Other tests

• CBC, SE, KFT, LFT, RBS, lipid profile, thyroid function test, CKMB, cardiac TnI/TnT,

• MRI-Gold standard for assesing cardiac mass or volume • Nuclear Studies-Exercise or pharmacologic stress nuclear

SPECT imaging with thallium 201 or Tc 99 may detect ischemia or previous MI and also assess LV function.

• Pulmonary artery catheter may be necessary in selected patients to obtain a more accurate and comprehensive hemodynamic profile during hospitalization

Differential diagnosis

• MI• Tension PTX• Aortic dissection• PE• Asthma or COPD exacerbation• Cardiac tamponade• Ruptured viscus• Valvular abnormalities

Goals of treatment in acute heart failure

Management in the emergency dept.• Diagnosis and treatment are usually carried out in parallel,• Close monitoring of the patient’s vital functions is essential during the initial

evaluation and treatment

Algorithm for management of acute pulmonary oedema/congestion

Pharmacological therapy in acute management

• Oxygen should be given to all hypoxaemic pts maintain SaO2 95–98%

• Patent airway should be ensured and FiO2 can be increased

• In non-hypoxaemic patients it causes vasoconstriction and a reduction in cardiac output.

Diuretics use

• Indicated in symptoms secondary to fluid retention.• Most patients with dyspnoea in AHF caused by pulmonary

oedema • Rapid symptomatic relief by immediate venodilator action and

subsequent removal of fluid.• Start with individualized dose depending on clinical condition

Diuretic dosing and administration

Opiates(Morphine)

• Indicated in early stage of severe AHF associated with restlessness and dyspnoea.

• Morphine induces venodilatation and mild arterial dilatation, and reduces heart rate

• Morphine sulfate 2-5 mg iv over 2-3 mins and can be repeated every 10 to 25 mins until effect is seen

• Opiates induce nausea and depress respiratory drive potentially increasing the need for invasive ventilation

Vasodilators• First line therapy in AHF with an adequate BP and signs of

congestion with low diuresis• Nitrates causes venous and arterial balanced

vasodilation,reduce LV pre-load and after-load, without impairing tissue perfusion.

• Sodium nitroprusside used in severe HF with predominantly increased after-load (hypertensive HF or MR)

• Nesiritide-Recombinant human BNP with venous, arterial, and coronary vasodilatory properties reduce preload and after-load, increase CO without direct inotropic effects.

• Calcium antagonists-Not recommended in treatment of AHF

Indications and dosing of vasodilators in AHF

Inotropes

• Reserved for pts with severely reduced cardiac output compromised vital organ perfusion

• Inotropes cause sinus tachycardia and may induce myocardial ischaemia and arrhythmias.

• There is long-standing concern that they may increase mortality

• Levosimendan, milrinone can counteract the effect of a beta-blocker

Vasopressors

• In cardiogenic shock. • When the combination of inotropic agent and fluid challenge

fails to restore adequate arterial pressure and organ perfusion. • Peripheral arterial vasoconstrictor action raise blood pressure

and redistribute cardiac output from the extremities to the vital organs.

• It may increase the after-load of a failing heart and further decrease end-organ blood flow

Drugs used to treat AHF thatare positive inotropes or vasopressors or both

Use of inotropic drugs in AHF

Other pharmacological therapy

• Cardiac glycosides – used in AF induced heart failure with insufficient ventricular rate-control by b-blockers.

• IV Beta Blocker should not be started during the initial phase of AHFS as acutely decrease cardiac contractility.

• However, a short-acting IV agent(esmolol) may be considered when AHF is ppt. by AF or flutter with a rapid ventricular response

• Anticoagulation-in ACS with or without HF, in AF and to prevent thrombo-embolism.

Non-pharmacological therapy

• Restrict Na intake 2g/day and fluid intake 1.5–2.0 l/day• Non-invasive ventilation- CPAP/NIPPV used when increased

FiO2 fail to improve tissue oxygenation.• Endotracheal intubation and invasive ventilation- Reverse

AHF-induced respiratory muscle fatigue, acute respiratory failure not responding to vasodilators/oxygen therapy/CPAP/NIPPV.

• Mechanical circulatory support- IABP,VAD• Venovenous isolated ultrafiltration reserved for diuretics

resistant/unresponsive cases

Mechanical assist devices

After stabilisation• Diuretics often switched from an IV to an oral form. • Drugs Known to Improve Outcomes in HF- ACEI/ARB, beta

blockers, aldosterone blocking agents should be started as soon as possible

• The DIG trial showed that the addition of digoxin to ACE inhibitors and diuretics reduces rehospitalizations and, in retrospect, mortality in patients with serum concentration of the drug <1 ng/mL

Underlying diseases and co-morbiditiesin AHF

• Underlying cause should be treated-CAD ,valvular disease, aortic dissection, hypertension,arrhythmias

• Precipitating factors -thyrotoxicosis crisis ,anaemia,• Co-morbidities -infections,diabetes, catabolic state,

renal failure ,pulmonary diseases etc. should be identified and treated

Surgical treatment of AHF Treatment options - not often used in heart failure unless there is

a correctable problem• CABG• Angioplasty• Valve repair/replacement –AS,AR,MR.• Defibrillator implantation• Heart transplantation

Pre-discharge and long-term management

• Before discharge pts should be free of dyspnea/symptomatic hypotension while at rest, washing, and walking on the ward.

• At least 24h of stable fluid status, BP and renal function • Stable oral diuretic regimen for at least 48 h.• Long-term disease-modifying therapy optimized as much as

possible • Appropriate education provided to the patient and

family/caregivers. • Follow-up - within approximately 1 month after discharge• Closer follow-up within 7-14 days and early telephone f/u

within 3 days.

Potential newer therapies

• Soluble guanylate cyclase inhibitor – cinaciguat• Chimeric natriuretic peptide• Direct renin inhibitor - Aliskiren• Adenosine antagonist - Rolofylline• Ularitide• Endothelin antagonist - Tezosentan• Cardiac myosite activator – Omecamtiv mecarbil• Istaroxime• Stresscopin• Relaxin

Prognosis

• Patients with AHF have a very poor prognosis. • AMI with severe HF, 12 month mortality 30%.• Acute pulmonary oedema-12% in-hospital and 40% 1

yr mortality have been reported.• About 45% of patients hospitalized with AHF will be

re-hospitalized at least once and 15% at least twice within 12 months.

• Risk of death/re-hospitalization within 60 days of admission vary from 30-60%, depending on the population studied

Thank you