What New in Acute Heart Failure

8/13/2019 What New in Acute Heart Failure

1/64

WH Ts NEW IN CUTE HE RTFAILUREINTENsIVIsTs PERsPECTIVE

Dr Mukesh Kumar Gupta(MD,FNB)

Senior consultant critical care medicine

Medanta The Medicity, Gurgaon


2/64


3/64


4/64

DEFINITIONS OF HE RT F ILUREHeart 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


5/64

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.


6/64

DEFINITION OF ACUTE HEART FAILURE

ACUTE HFis defined as a rapid onset orchange 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


7/64

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 failureforms 95% of HF


8/64

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


9/64

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


10/64

EPIDEMIOLOGY OF HEART FAILURE

Data from Framingham Heart Study per 1000 population

Prevalence

Age Men Women 5059 8 8

8089 66 79

All ages 7.4 7.7

Incidence

Age Men Women

5059 3 2

8089 27 22

All ages 2.3 1.4


11/64

GRADING OF HEART FAILURE

NYHA classification


12/64

GRADING OF HEART FAILURE

ACC/AHAclassification


13/64

TWO CLASSIFICATIONS OF THE SEVERITY OF HEART FAILURE IN THE

CONTEXT OF ACUTE MYOCARDIAL INFRACTION

Killip Classification Forrester Classification

Designed to provide a clinical estimate of the severity ofcirculatory derangement in the treatment of acute

myocardial infarction

Designed to describe clinical and haemodynamicstatus in acute myocardial infarction

Stage I No heart failure

No clinical signs of cardiac decompression

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 Heart failure

Diagnostic criteria include rales. S3 gallop andpulmonary venous hypertension.

Pulmonary congestion with wet rales in the

lower half of the lung fields

Stage III Severe heart failure.

Frank pulmonary oedema with rales throughout

the lung fields

Stage IV Cardiogenic shock

Signs include hypotension (SBP


14/64

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 50-

55%

In LVSD heart failure the EF is


15/64

Normal Systolic Function

Systolic Dysfunction


16/64

DIASTOLIC HEART FAILURE (HF-PEF)

Accounts for 20-40% of patients

Ventricles are normal-sized with normalemptying

But there is an impairment in the ability of theventricles 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


17/64

NORMAL MITRAL INFLOW PATTERN

EA


18/64

DIASTOLIC RELAXATION IMPAIRMENT

E- 57 cm/s

A- 117 cm/s

dtE- 257 ms

E/A 240 msec, IVRT- >90 msec


19/64

IVRT

Normal

RelaxationDefect

Pseudo-

Normalization

Restrictive

pattern

MITRAL INFLOW PATTERNS

A

E

E/A 240 ms,

IVRT- >90 ms

E/A 0.9-1.5,

dtE- 160-240

ms,

IVRT- 2,

dtE-


20/64

MITRAL ANNULAR TISSUE DOPPLER

e- 1.9 cm/s

Mitral inflow E/e= 67/1.9 = 30 s/o LVEDP


21/64

CAUSES AND PRECIPITATING FACTORS OF AHF

Ischemic heart disease

Acute coronary syndromes

Mechanical complications of acute MI

Right ventricular infarction

Valvular

Valve stenosis Valvular regurgitation

Endocarditis

Aortic dissection

Myopathies

Post partum cardiomyopathy

Acute myocarditis

Hypertension / arrhythmia

Hypertension

Acute arrhythmia

Circulatory failure

Septicemia

Thyrotoxicosis

Anaemia

Shunts

Tamponade

Pulmonary embolism

Decompensation of preexisting

chronic HF

Lack of adherence

Volume overload

Infections, especially pneumonia

Cerebrovascular insult

Surgery

Renal dysfunction

Asthma, COPD

Drug abuse

Alcohol abuse


22/64

CHANGING PATTERN OF ETIOLOGY

McMurray J J, Stewart S Heart 2000;83:596-

602


23/64

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


24/64

FRANK-STARLING CURVES


25/64

PATHOPHYSIOLOGY OF HF


26/64


27/64


28/64

Acutelydecompensated

ChronicHF

Cardiogeni

c shock

ACS

and HF

CLINICAL CLASSIFICATION OF ACUTE HEART

FAILURE

Hypertensive

AHF

Pulmonar

y oedema

Right HF


29/64

DIAGNOSIS OF HEART FAILURE


30/64

ALGORITHM FOR THE DIAGNOSIS OF

HEART FAILURE


31/64

InitiaI assessment of patient with suspected acute heart failure


32/64

E.D. EVALUATION OF ACUTE HEART FAILURE


33/64

HYPERTENSIVE ACUTE HEART FAILURE


34/64

HYPOTENSIVE ACUTE HEART FAILURE


35/64

NORMOTENSIVE ACUTE HEART FAILURE


36/64

A CLINICAL ASSESSMENT OF PATIENTS WITH AHF

Dry and warm Wet and warm

Dry and cold Wet and cold

Pulmonary congest ion

Tissueper

fus

ion

Clinical classi f icat ions


37/64

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


38/64

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


39/64

INVASIVE HEMODYNAMIC MONITORING

Invasive hemodynamic monitoring should be consideredin

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.

LindenfieldJ et at. HFSA 2010 Comprehensive Heart FailureGuidelines. J Card Fail 2010:16e1-e 194.

GOALS OF TREATMENT IN ACUTE HEART FAILURE


40/64

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


41/64

INITIAL TREATMENT ALGORITHM IN AHF

Acute heart failure

Immediate symptomatic treatment

Patient distressed or in pain

Arterial oxygen saturation

Analgesia, sedation

Pulmonary congestion

Yes

Normal heart rate and rhythm

Medical therapy

Diuretic vasodilatorYes

Increase FiO2Consider CPAP,

NIPPV, mechanicalventilation

Les

s

Pacing,

Antirrhythmics

electroversionN0


42/64

INDICATIONS AND DOSING OF DIURETICS IN AHF

Fluid retention DiureticDaily dose

(mg)

Comments

Moderate Furosemide or

Bumetanide or

Torasemide

20 40

0.5 1

10 - 20

Oral or i.v. according to clinical symptoms

Titrate dose according to clinical response

Monitor K, Na, creatinine, blood pressure

Severe Furosemide

Furosemide infusion

Bumetanide

Torasemide

40 100

5 40 mg/h

1 4

20 100

i.v. Increase dose.

Better than very high bolus doses

Oral or i.v.

Oral

Refractory or

loop diuretic

Add hydrochlorthiazide

Or metalazone

Or spironolactone

50 100

2.5 10

25 50

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

With alkalosis Acetazolamide 0.5 mg i.v.

Refractory to

loop diuretics

and thaizides

Add dopamine (renal

vasodilation) or

dobutamine

Consider ultrafiltration or haemodialysis if co-

existing renal failure

Hyponatraemia

INTRAVENOUS VASODILATORS USED TO TREAT


43/64

INTRAVENOUS VASODILATORS USED TO TREAT

ACUTE HF


44/64

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


45/64

TREATMENT STRATEGY IN AHF ACCORDING TO LV FILLING


46/64

TREATMENT STRATEGY IN AHF ACCORDING TO LV FILLING

PRESSURE

Pulmonary congestion andSBP > 90 mmHg

Adequate CO

Reversal of acidosis

SvO2 > 65%

Adequate organ perfusion

Vasodilators, diuretics

if volume overload

Adequate filling pressure

Yes

Fluid challengeNo

Increase FiO2Consider CPAP,

NIPPV, mechanical

ventilation

No

Reassess frequentlyYes


47/64

DEVICES IN MANAGING HEART FAILURE


48/64

CIRCULATORY ASSIST DEVICES


49/64

CURRENT AHA RECOMMENDATIONS OF

IABP


50/64

PROS AND CONS OF IABP


51/64

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


52/64

CRITERIA FOR IMPLANTATION OF A VENTRICULAR

ASSIST DEVICE


53/64

PERCUTANEOUS LVAD

Left Ventricular Assist Device


54/64

ADVANTAGES AND DISADVANTAGES OF

LVAD


55/64

IABP VERSUS LVAD

30 Day Mortality was not superior to IABP


56/64

EXTRACORPOREAL MEMBRANE

OXYGENATION


57/64


58/64

DEVICES IN ADHF - SUMMARY


59/64

HEART TRANSPLANTATION

IINDICATIONS



60/64


cCONTRA INDICATIONS

TREATMENT GOALS AND STRATEGIES


61/64

TREATMENT GOALS AND STRATEGIES

DURING THE COURSE OF THE PATIENTS JOURNEY

Phase Diagnostic strategy Action Goals Players

Acute Assess clinical status

Identify cause of

symptoms

Treat and stabilize

Initiate monitoring

Plan required interventions

Stabilze, admit and

triage to

appropriate

department

Paramedics

Primary care/ER

physicians

Intensivists

Nurses

Cardiologists

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

Hospital physicians

Cardiologists

CV nurses

HF management team

Chronic Target symptoms,adherence and

prognosisIdentify decompensation

early

Optimize pharmacological

and device treatment

Support self care behaviourRemote monitoring

Reduce morbidity

and mortality

Primary care

physicians

HF management teamCardiologists

End of life Identify patient concernsand symptoms

Symptomatic treatment

Plan for long term care

Palliation

Provide support

for patients and

family

Palliative care team


62/64

RECOMMENDED COMPONENTSOF HF M N GEMENT PROGR MMES

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 caremanagement

Patient involvement in symptom monitoring and flexible diuretic use

Psychosocial support to patients and family and/or caregiver


63/64

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.


64/64

THANK YOU

Documents

What New in Acute Heart Failure