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-assesment 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

19. 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.

20. 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

21. Diuretic dosing and administration

22. 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

23. 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

24. Indications and dosing of vasodilators in AHF

25. 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

26. 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

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

28. Use of inotropic drugs in AHF

29. 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.

30. 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

31. Mechanical assist devices

32. 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

33. 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

34. 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

35. 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.

36. 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

37. 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

38. Thank you