Management of acute lvf

management of alvf

1. Management of acute LVF Presenter : Dr. Gautam Chakma Moderator : Prof. Lallan Prasad

2. 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.

3. 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

4. Pathophysiology AHF

5. Causes and precipitating factors in AHF

6. SIGN AND SYMPTOMS OF ACUTE LVF

7. AHF with distinct clinical conditions

8. 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) .

9. 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

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

11. ECG- LA enlargement ,arrhythmias , LVH, previous MI Echocardiography- a ssesment of systolic / diastolic function, EF calculation ,any valvular abnormality ,abnormal wall motion

12. 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

13. 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

14. Differential diagnosis MI Tension PTX Aortic dissection PE Asthma or COPD exacerbation Cardiac tamponade Ruptured viscus Valvular abnormalities

15. Goals of treatment in acute heart failure

16. 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

17. Algorithm for management of acute pulmonary oedema /congestion

18. Pharmacological therapy in acute management Oxygen should be given to all hypoxaemic pts maintain SaO2 95–98 % P atent airway should be ensured and FiO2 can be increased In non- hypoxaemic patients it causes vasoconstriction and a reduction in cardiac output.

19. 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

20. Diuretic dosing and administration

21. 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

22. 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

23. Indications and dosing of vasodilators in AHF

24. 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

25. 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

26. Drugs used to treat AHF that are positive inotropes or vasopressors or both

27. Use of inotropic drugs in AHF

28. 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 .

29. 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

30. Mechanical assist devices

31. 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

32. Underlying diseases and co-morbidities in 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

33. Surgical treatment of AHF Treatment options - n ot often used in heart failure unless there is a correctable problem CABG Angioplasty Valve repair/replacement –AS,AR,MR. Defibrillator implantation Heart transplantation

34. 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. A t least 24h of stable fluid status, BP and renal function S table oral diuretic regimen for at least 48 h. Long-term disease-modifying therapy optimized as much as possible A ppropriate 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.

35. 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

36. 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. R isk of death/re-hospitalization within 60 days of admission vary from 30-60%, depending on the population studied

37. Thank you