WHATs NEW IN ACUTE HEART FAILURE : INTENsIVIsTs PERsPECTIVE

Dr Mukesh Kumar Gupta(MD,FNB) Senior consultant critical care medicine Medanta The Medicity, Gurgaon

DEFINITIONS OF HEART FAILURE

Heart failure is a clinical syndrome characterized by decreased systemic perfusion, inadequate to meet the body's metabolic demands as a result of impaired cardiac pump function - Cleveland Clinic A pathophysiologic state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with metabolic requirements of the tissues -E Braunwald

DEFINITION OF HF
Physiological:

Inability of the heart to pump sufficient oxygenated blood to the metabolizing tissues despite an adequate filling pressure.
Working Clinical Definition: Clinical syndrome consisting of symptoms such as breathlessness, fatigue, and swelling of ankle caused by cardiac dysfunction.

DEFINITION OF ACUTE HEART FAILURE

ACUTE

HF is defined as a rapid onset or

change in the signs and symptoms of HF, resulting in the need of urgent therapy It may present as new HF or worsening HF in presence of chronic HF It may be associated with worsening symptoms or signs or as a medical emergency such as acute pulmonary edema

TYPES OF HEART FAILURE

Chronic Heart Failure (CHF) Acute Heart Failure (Cardiogenic Shock) Systolic Failure (LVSD): HF-rEF Diastolic Heart Failure (LVDD): HF-PEF Left Heart Failure (LVF) Right Heart Failure (Congestive CCF) Forward Failure and Backward Failure High output failure -Thyrotoxicosis, Paget's, Anemia, Pregnancy, A-V fistula Low output failure forms 95% of HF

HEART FAILURE SOME STATISTICS

Affects 10% of people over 65 years

Affects over 50% of people with 85+ years Approx 10% of patients with HF die each yr. Most common condition for which patients 65 + require admission to hospital It is NOT a single disease A syndrome Results from any cardiac disorder that impairs the ability of the ventricles to fill with or eject blood

EPIDEMIOLOGY OF HEART FAILURE

Clinical criteria Prevalence 1-2 % Males > Females; in 65+ Prevalence 7% 50% of LVSD is asymptomatic NEF HF varies from 15 to 50%

Incidence 0.2 to 0.3 %; es with age

EPIDEMIOLOGY OF HEART FAILURE

Prevalence Age 5059 8 8089 66 All ages Men 8 79 7.4 7.7 Women

Incidence

Age 5059 3 8089 27 All ages

Men 2 22 2.3

Women

1.4

Data from Framingham Heart Study per 1000 population

GRADING OF HEART FAILURE

NYHA classification

GRADING OF HEART FAILURE

ACC/AHA classification

TWO CLASSIFICATIONS OF THE SEVERITY OF HEART FAILURE IN THE CONTEXT OF ACUTE MYOCARDIAL INFRACTION
Killip Classification
Designed to provide a clinical estimate of the severity of circulatory derangement in the treatment of acute myocardial infarction

Forrester Classification
Designed to describe clinical and haemodynamic status in acute myocardial infarction

Stage I

No heart failure No clinical signs of cardiac decompression

Heart failure Diagnostic criteria include rales. S3 gallop and pulmonary venous hypertension. Pulmonary congestion with wet rales in the lower half of the lung fields Severe heart failure. Frank pulmonary oedema with rales throughout the lung fields Cardiogenic shock Signs include hypotension (SBP <90 mmHg), and evidence of peripheral vasoconstriction such as oliguria, cyanosis and sweating

1) Normal perfusion and pulmonary wedge pressure (PCWP estimate of atrial pressure)
2) Poor perfusion and low PCWP (hypovolemic) 3) Near normal perfusion and high PCWP (pulmonary oedema) 4) Poor perfusion and high PCWP (cardiogenic shock)

Stage II

Stage III

Stage IV

Kiliip T, 3rd Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 1967;20: 457-464. Forrester JS Diamond GA, Swan HJ, Correlative classification of clinical and haemodynamic function after acute myocardial infarction. Am J Cardiol 1977:39:137-145

SYSTOLIC HEART FAILURE (HF-REF)

Most common type of Heart Failure; 60-70%

LV is usually dilated & enlarged.

Fails to contract normally due to WMA & Ischemia Cannot pump sufficient blood to meet needs Normal ejection fraction (EF) is at least 5055% In LVSD heart failure the EF is <40 -45% This carries a 10% mortality per annum

Normal Systolic Function

Systolic Dysfunction

DIASTOLIC HEART FAILURE (HF-PEF)

Accounts for 20-40% of patients Ventricles are normal-sized with normal emptying But there is an impairment in the ability of the ventricles to fill with blood during diastole because of stiff myocardium due to hypertrophy The heart fails to relax normally (relaxation poor) Generally affects older women

NORMAL MITRAL INFLOW PATTERN

E A

DIASTOLIC RELAXATION IMPAIRMENT

A- 117 cm/s

E- 57 cm/s

dtE- 257 ms

E/A <0.9, dtE- >240 msec, IVRT- >90 msec

MITRAL INFLOW PATTERNS

E A

IVRT
Normal

Relaxation Defect
E/A <0.9, dtE- >240 ms, IVRT- >90 ms

PseudoNormalization
E/A 0.9-1.5, dtE- 160-240 ms, IVRT- <90 ms

Restrictive pattern

E/A 0.9-1.5, dtE- 160-240 ms, IVRT- 70-90 ms

E/A >2, dtE- <160 ms, IVRT- <70 ms

MITRAL ANNULAR TISSUE DOPPLER

e- 1.9 cm/s

Mitral inflow E/e= 67/1.9 = 30

s/o LVEDP

CAUSES AND PRECIPITATING FACTORS OF AHF

Ischemic heart disease
Acute coronary syndromes

Circulatory failure
Septicemia Thyrotoxicosis Anaemia Shunts Tamponade Pulmonary embolism

Mechanical complications of acute MI

Right ventricular infarction

Valvular
Valve stenosis Valvular regurgitation Endocarditis Aortic dissection

Decompensation of preexisting chronic HF

Lack of adherence Volume overload Infections, especially pneumonia Cerebrovascular insult Surgery Renal dysfunction Asthma, COPD Drug abuse Alcohol abuse

Myopathies
Post partum cardiomyopathy Acute myocarditis

Hypertension / arrhythmia
Hypertension Acute arrhythmia

CHANGING PATTERN OF ETIOLOGY

McMurray J J, Stewart S Heart 2000;83:596602

MECHANISMS OF HEART FAILURE

Restricted Filling: MS, Restrict CM, Constr Pericarditis Pressure Load on Ventricle: HT, AS, PS, Coarctation

Volume load on Ventricle: MR, AR, VSD, TR, PR

Myocardial Contraction: CAD, DCM, Myocarditis Arrhythmia: Severe Brady or Tachycardia, AF, HB

FRANK-STARLING CURVES

PATHOPHYSIOLOGY OF HF

CLINICAL CLASSIFICATION OF ACUTE HEART FAILURE

Hypertensive AHF Acutely decompensated Chronic HF Pulmonar y oedema ACS and HF

Cardiogeni c shock

Right HF

DIAGNOSIS OF HEART FAILURE

ALGORITHM FOR THE DIAGNOSIS OF HEART FAILURE

InitiaI assessment of patient with suspected acute heart failure

E.D. EVALUATION OF ACUTE HEART FAILURE

HYPERTENSIVE ACUTE HEART FAILURE

HYPOTENSIVE ACUTE HEART FAILURE

NORMOTENSIVE ACUTE HEART FAILURE

A CLINICAL ASSESSMENT OF PATIENTS WITH AHF

Clinical classifications Tissue perfusion

Dry and warm

Wet and warm

Dry and cold

Wet and cold

Pulmonary congestion

ASSESSMENT OF LV FUNCTION IN AHF

Tavazzi L, Maggioni AP, Lucci D, et al: Nationwide survey on acute heart failure in cardiology ward services in Italy. Eur Heart J 2006; 27:12071215

ECHOCARDIOGRAPHY. EXTREMELY USEFUL

Determining LV ejection fraction Volume and dimensions Wall motion abnormalities Valvular function Presence or absence of endocarditis

With the tissue Doppler obtain an estimate of the LV end diastolic pressure by determining the E:E ratio. When the diagnosis of ADHF is in doubt a markedly elevated E:E ratio suggests elevated LV enddiastolic pressure

INVASIVE HEMODYNAMIC MONITORING

Invasive hemodynamic monitoring should be considered in a patient:

Who is refractory to initial therapy Whose volume status and cardiac filling pressures are unclear Who has clinically significant hypotension (typically SBP < 80 mm Hg) or worsening renal function during therapy Or who is being considered for cardiac transplant and needs assessment of degree and reversibility of pulmon. hypertension Or in whom documentation of an adequate hemodynamic response to the inotropic agent is necessary because of end organ dysfunction.
Lindenfield J et at. HFSA 2010 Comprehensive Heart Failure Guidelines. J Card Fail 2010:16e1-e 194.

GOALS OF TREATMENT IN ACUTE HEART FAILURE

Immediate (ED/ICU/CCU)
Improve symptoms
Restore oxygenation Improve organ perfusion and haemodynamics Limit cardiac / renal damage Minimize ICU length of stay

Intermediate (in hospital)

Stabilize patient and optimize treatment strategy Initiate appropriate (life saving) pharmacological therapy Consider device therapy in appropriate patients

Minimize hospital length of stay

Long term and pre-discharge management

Plan follow up strategy Educate and initiate appropriate lifestyle adjustments Provide adequate secondary prophylaxis Prevent early readmission Improve quality of life and survival

INITIAL TREATMENT ALGORITHM IN AHF

Acute heart failure
Immediate symptomatic treatment

Patient distressed or in pain

Yes

Analgesia, sedation Medical therapy Diuretic vasodilator Increase FiO2 Consider CPAP, NIPPV, mechanical ventilation Pacing, Antirrhythmics electroversion

Pulmonary congestion

Yes

Arterial oxygen saturation

Les s

Normal heart rate and rhythm

N0

INDICATIONS AND DOSING OF DIURETICS IN AHF

Fluid retention Moderate Diuretic
Furosemide or Bumetanide or Torasemide

Daily dose (mg)

20 40 0.5 1 10 - 20 40 100 5 40 mg/h 14 20 100 50 100 2.5 10 25 50

Comments
Oral or i.v. according to clinical symptoms Titrate dose according to clinical response Monitor K, Na, creatinine, blood pressure i.v. Increase dose. Better than very high bolus doses Oral or i.v. Oral Combination better than very high dose of loop diuretics MTZ more potent if creatinine clr < 30ml/min Spironolactone best choice if no renal failure and normal or low serum potassium

Severe

Furosemide Furosemide infusion Bumetanide Torasemide

Refractory or loop diuretic

Add hydrochlorthiazide Or metalazone Or spironolactone

With alkalosis Refractory to loop diuretics and thaizides

Acetazolamide Add dopamine (renal vasodilation) or dobutamine

0.5 mg

i.v. Consider ultrafiltration or haemodialysis if coexisting renal failure Hyponatraemia

INTRAVENOUS VASODILATORS USED TO TREAT ACUTE HF

DOSING OF POSITIVE INOTROPIC AGENTS IN AHF

* This agent also has vasodilator properties ** In hypotensive patients (SBP < 100 mmHg) initiation of therapy without a bolus is recommended

TREATMENT STRATEGY IN AHF ACCORDING TO SYSTOLIC BLOOD PRESSURE

Oxygen/NIV Loop diuretic =/- vasodilator Clinical evaluation

SBP > 100 mmHg

SBP 90-100 mmHg

SBP < 90 mmHg

Vasodilator (NTG, nitroprusside, nesiritide, levosimendan)

Vasodiltor and /or Inotrope (dobutamine, PDEI, levosimendan)

Consider preload correction with fluids Inotrope (dopamine)

Good response Stablise and initiate diuretic, ACEI/ARB, betablocker

Poor response Inotrope, vasopressor Mechanical support Consider PAC

TREATMENT STRATEGY IN AHF ACCORDING TO LV FILLING PRESSURE

Vasodilators, diuretics if volume overload

Pulmonary congestion and SBP > 90 mmHg

Yes

Adequate filling pressure

No

Fluid challenge

Adequate CO Reversal of acidosis SvO2 > 65% Adequate organ perfusion

No

Increase FiO2 Consider CPAP, NIPPV, mechanical ventilation

Yes

Reassess frequently

DEVICES IN MANAGING HEART FAILURE

CIRCULATORY ASSIST DEVICES

CURRENT AHA RECOMMENDATIONS OF IABP

PROS AND CONS OF IABP

IABP IN HIGH RISK STEMI

IABP did not show any benefit in Mortality but showed an increase in strokes And bleeding.

CRITERIA FOR IMPLANTATION OF A VENTRICULAR ASSIST DEVICE

PERCUTANEOUS LVAD

Left Ventricular Assist Device

ADVANTAGES AND DISADVANTAGES OF LVAD

IABP VERSUS LVAD

30 Day Mortality was not superior to IABP

EXTRACORPOREAL MEMBRANE OXYGENATION

DEVICES IN ADHF - SUMMARY

HEART TRANSPLANTATION
IINDICATIONS

HEART TRANSPLANTATION
cCONTRA INDICATIONS

TREATMENT GOALS AND STRATEGIES DURING THE COURSE OF THE PATIENTS JOURNEY
Phase Acute Diagnostic strategy
Assess clinical status Identify cause of symptoms

Action
Treat and stabilize Initiate monitoring Plan required interventions

Goals
Stabilze, admit and triage to appropriate department

Players
Paramedics Primary care/ER physicians Intensivists Nurses Cardiologists Hospital physicians Cardiologists CV nurses HF management team

Subacute

Assess cardiac function Identify aetiology and co-morbidities

Initiate chronic medical treatment Perform additional diagnostics Perform indicated procedures

Shorten hospitalization Plan post discharge follow up

Chronic

Target symptoms, adherence and prognosis Identify decompensation early

Optimize pharmacological Reduce morbidity and device treatment and mortality Support self care behaviour Remote monitoring Palliation Provide support for patients and family

Primary care physicians HF management team Cardiologists Palliative care team

End of life Identify patient concerns Symptomatic treatment

and symptoms Plan for long term care

RECOMMENDED COMPONENTS OF HF MANAGEMENT PROGRAMMES

Multidisciplinary approach frequently led by HF nurses in collaboration with physicians and other related services First contact during hospitalization, early follow-up after discharge through clinic and home based visits, telephone support and remote monitoring Target high risk symptomatic patients Increased access to health care (telephone, remote monitoring and follow up)

Facilitate access during episodes of decompensation

Optimised medical management Access to advanced treatment options Adequate patient education with special emphasis on adherence and self care management Patient involvement in symptom monitoring and flexible diuretic use Psychosocial support to patients and family and/or caregiver

CONCLUSION

Heart failure remains a major contributor to

hospitalizations, morbidity and mortality in India and

worldwide.

Early recognition, understanding pathophysiology and prompt treatment of AHF would help in management and improve long term outcome.

THANK YOU