30.Cardiac Failure Harris Hasan

8/21/2019 30.Cardiac Failure Harris Hasan

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Dr HARRIS HASAN SpPD,SpJP(K)DEPARTEMEN KARDIOLOGI FK USU MEDAN


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ACUTE LEFT VENTRICULAR

FAILURE

Acute LV failure can either occur de novo

or on a background of chronic cardiacfailure, i.e. acute-on-chronic cardiac

failure. This is important because the

aetiologies, clinical presentation and

management are quite distinct.


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CLASSIFICATION

Most cases of cardiac failure are

associated with reduced systolic function

and sometimes a low-output state.Diastolic dysfunction may also contribute

to cardiac failure in patients with large

infarct zones, cardiomyopathies,pericardial disease or mitral stenosis.


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AETIOLOGY

Acute de novocardiac failure

Acute MIAcute native valve failure (e.g.chordal

rupture, endocarditis) or acute VSD

Acute myocarditisHypertensive crisis

accelerated hypertension with background

essential hypertensionrenovascular disease (e.g.renal arterystenosis)

phaeochromocytoma


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Cardiac tamponade

Profound bradycardia or tachycardia

Myocardial depression due to drug toxicity

tricyclic antidepressants

blockers

calcium channel antagonists


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Acute-on-chronic cardiac failure

Non compliance with or reduction in

cardiac failure drug therapy (e.g.diuretic,

ACE inhibitor) a common precipitant

Myocardial depressant drug or drugs that

promote sodium / water retention(e.g.corticosteroids, NSAIDs)


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Intercurrent non-cardiac illness in a patients with

chronic cardiac failure

Progression of underlying cardiac disease

Myocardial ischaemia/infarction

Arrhythmias, especially atrial fibrillation

Increased metabolic demand : anaemia,pregnancy, thyrotoxicosis


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CLINICAL PRESENTATION

Acute de novoLV failure usually presents with

rapidly worsening fatigue, dyspnoea and

limitation of effort tolerance. Orthopnoea,

paroxysmal nocturnal dyspnoea and acuterespiratory distress may supervene. There may

also be prodormal symptoms which suggest an

underlying aetiology, e.g.chest pain or

palpitation. Physical signs of cardiac failure and

underlying cardiac diseases are described more

comprehensively.


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INVESTIGATION

Laboratory tests

U & Es - renal failure (predisposes to fluid retention)

- High or low K+ predisposes to arrhythmiasABGs - systemic hypoxia

- Acidosis (may be metabolic due to poortissue perfusion, or mixed due toadditional CO2 retention)

Virology - If viral myocarditis suspected(e.g.antecedentHxof flu-like illness), serology may helpidentify the culprit organism

TFTs

FBC - anaemia (exacerbates cardiac failure),

WCC(infection) ECG

acute or previous MI

ischaemic features

arrhythmia, e.g.atrial fibrillation


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CXR

pulmonary oedema

Pleural effusions, fluid in horizontal fissure

Septal (Kerley B) linesPulmonary pathology

Cardiac size

Echo

- LV function

- LVH (suggests hypertension, aortic stenosis

or hypertrophic cardiomyopathy)-associated with

diastolic dysfunction

- valve disease, e.g.mitral regurgitation, aortic stenosis

- pericardial effusion

- endocarditis

Right heart catheterization


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Key points : examination General - usually distressed or agitated

- tachypnoea

- semiconscious or unconscious insevere/protracted cases

- signs of sympathetic activation/lowcardiac output

pallorsweating

Cool peripheries

Peripheral cyanosis

- Cutaneous stigmata of endocarditis- Signs of non-cardiac ilness

clinical anaemia

Fever

Thyroid signs


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Pulse - usually tachycardic. Relativebradycardia can worsen cardiacfailure by limiting cardiac output

- may be irregular; suggests atrialfibrillation

- may be low ( output) or normal pulse

volume

Blood pressure - hypotension heralds poorprognosis

- hypertension may aggravatecardiac failure

- check for pulsus paradoxus


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JVP - often elevated, but notinvariably so

Precordium - apex usually not displaced in denovocardiac failure; may bedyskinetic in anterior MI

- apex often displaced in chronicheart failure

- murmur (may suggest valvepathology or acute VSD)

- gallop rhythm :S3S4-inspiratory crepitations

- pleural effusions in chroniccardiac failure


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Other - peripheral/sacral oedema,pulsatile hepatomegaly,

ascites, right parasternal lift

most often accompanychronic right-sided cardiac

failure, but are uncommon

in de novo cardiac failure


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MANAGEMENT

Acute cardiac failure should be managed in a high-

dependency or coronary care unit. Patients who are

unable to maintain adequate systemic oxygenation or

acid-base balance despite initial therapy need to be

managed in an intensive care unit with ventilationfacilities. ECG, blood pressure and O2 saturation

monitoring are mandatory.

Initial management

IV access

High-low O2(60-100%)


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Nitrates - this is at least as important as diureticRX.

- buccal GTN 2-5 mg OR- IVI GTN 0.6-12 mg min-1 OR

- IVI isosorbide dinitrate 2-10 mg h-1

- IVI sodium nitroprusside 10-200 g

min-1Opiate - IV morphine 5-20 mg

Loop - IV frusemide 50-100 mg bolus OR

diuretic - IVI frusemide 5-20 mg h-1

The acute effect of loop diuretic isvenodilation;intravascular volume reductionoccurs later


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Digoxin - useful for rate control in atrial

fibrillation; role in cardiacfailure in sinus rhythm controversial

- oral dose:0.5 mg, repeated after 6

hours

- IVI:0.5 mg over 20 min, repeated after

6 hours

Treat identifiable triggers, e.g.aspirin andthrombolysis for acute MI.


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An additional agent (e.g. ACE inhibitor) may be

needed if nitrate therapy fails to controlhypertension. Arrhythmias are often poorly

tolerated. Atrial fibrillation can cause

catastrophic haemodynamic collapse because of

the loss of atrial contribution to ventricular filling.

In these cases DC cardioversion IVI

amiodaronevia a central venous catheter (300

mg over 30 min, followed by 900 mg over 24 h)may be needed.


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Management of resistant cardiac failure

Advanced haemodynamic support

Hypotensive patients with cardiac failuremay benefit from inotropes

Dobutamine 5-20 g kg-1min-1

Dopamine 2.5-5 g kg-1min-1

Adrenaline 1-12 g min-1

Noradrenaline 1-12 g min-1

Intra-aortic balloon pumping


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Renal failure

Patients with fluid overload in whom diuresis isnot achieved may require extracorporealhaemofiltration.

Respiratory failure

If, despite medical management, the patientsremains in a state of repiratory compromise,mechanical ventilation should be considered.

Intubation, paralysis and intermittent positive-

pressure ventilationMask continuous positive airway pressure

ventilation


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CHRONIC CARDIAC FAILUREChronic cardiac failure is a major public health problem in the

UK, affecting between 1 and 2% of the general population. It isassociated with acute high morbidity and mortality and is a

major cause of recurrent hospitalization. Chronic cardiac failure

is characterized by diminished cardiac reserve and a complex

series of maladaptive neurohumoral responses, principallyinvolving the sympathetic and renin-angiotensin axes. The

resultant increased peripheral vascular resistance and sodium

and water retention serve to increase cardiac workload and

worsen LV failure. Current drug therapies in chronic cardiacfailure are directed at preventing sodium and water retention

and antagonizing the humoral responses that cause peripheral

vasoconstriction.


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CLASSIFICATION

Cardiac failure is classified in several ways : acute andchronic, left and right, high output and low output andsytolic and diastolic dysfunction. Cardia failuresymptoms are graded using the New York Heart

Association System.

Diagnosis of diastolic heart failure requires :

Symptoms or sign of heart failure

Normal or mildly abnormal LV systolic functionAbnormal LV relaxation, filling or diastolic distensibility

or stiffness


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AETIOLOGY

The main causes of chronic cardiac failure in westerncountries are :

Ischaemic heart disease

Hypertension

Valvular heart disease Toxic : alcohol, adriamycin, cobalt

Viral myocarditis : Coxsackie, HIV

Other cardiomyopathies : hypertrophic, restrictive, dilated

(sometimes familial)

Infiltrative : amyloidosis, sarcoidosis

Metabolic and nutritional : haemochromatosis, thyroid

dysfunction, beri-beri


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CLINICAL PRESENTATION

The most common cause of chronic cardiac failure is

IHD; cardiac failure usually follows presentation with

an acute MI. In some cases myocardial ischaemia or

infarction is silent and the first presentation may bewith cardiac failure itself. Conversely, some patients

with IHD have asymptomatic LV dysfunction.

However, most patients with chronic cardiac failurepresent with exertional fatigue and breathlessness

and/or symptoms of fluid retention (e.g.oedema), or

with an episode of acute LV failure.


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INVESTIGATIONS Laboratory tests

U & Es - may be concomitant renal failure (due to renovasculardisease, low cardiac output, or to diuretics, ACE inhibitor)

- K+ because of diuretics- Na+an ominous sign in advanced cardiac failure

glucose - prognosis for diabetics with cardiac failure very poor

LFTs - may be deranged because of liver congestion

TFTs - hypo- and hyperthyroidism may exacerbate failure

FBC - anaemia may exacerbate failure

cardiomyopathy screen - ferritin (haemochromatosis), Ca2+(sarcoidosis), viral screen (Coxsackie,enterovirus, HIV)

autoantibody screen - probably disease marker rather thancausitive factor; anti-- and -myosinantibodies

blood group and tissue type - if transplantation being considered


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ECG

Rarely normal in cardiac failure. Look for :

evidence of previous MILVH (large voltages seen both with LVH and cardiacdilatation)

conduction defects

atrial fibrillation

CXR

cardiomegaly

cardiac contour (e.g.left or right enlargement) maygive clue to aetiology

upper lobe venous diversion, interstitial oedema,pleural effusions, Kerley B lines may present.


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Echo

Radionuclide ventriculography

Stress testing

Cardiac catheterization


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MANAGEMENT

Drug therapy

Diuretics

Loop diuretics, e.g. frusemide (typically 40-120 mg d-1)orbumetanide(typically 1-4 mg d-1)

Nitrates

Nitrates, e.g.oral isosorbide mononitrate(30-120 mg d-1)

Vasodilators

Oral ACE inhibitors, e.g.captopril12.5-50 mg tid, enalapril10-20 mgbd or lisinopril10-20 mg d-1

Oral AT1 receptor antagonists, e.g.losartan50-100 mg d-1

In patients with renal dysfunction or intolerance of ACE inhibitorsand AT1 receptor antagonists, the combination of hydralazine, and anitrate is a suitable alternative. The regimen used in the VeHEFT-IItrial was hydralazine75 mg qid and isosorbide dinitrate40 mg qid,although different dosing intervals and nitrate preparations can beused to improve compliance.


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Inotropes

BlockersAntiarrhythmics

Anticoagulants

SurgeryRevascularization

Valve replacementCardiac transplantation


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Causes and precipitating factors in AHF

1. Decompensation of pre-existing chronic heartfailure (e.g.cardiomyopathy)

2. Acute coronary syndromes

a) Myocardial infarction/unstable angina with

large extent of ischaemia and ischaemic

dysfunction

b) Mechanical complication of acute myocardialinfarction

c) Right ventricular infarction


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3. Hypertensive crisis

4. Acute arrhythmia (ventricular tachycardia,ventricular fibrillation, atrial fibrillation or flutter,other supraventricular tachycardia)

5. Valvular regurgitation (endocarditis, rupture of

chordae tendinae, worsening of pre-existingvalvular regurgitation)

6. Severe aortic valve stenosis

7. Acute severe myocarditis

8. Cardiac tamponade

9. Aortic dissection


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10. Post partum cardiomyopathy

11. Non-cardiovascular precipitating factorsa. lack of compliance with medical treatment

b. Volume overload

c. Infections, particularly pneumonia or septicaemia

d. Severe brain insulte. After major surgery

f. Reduction in renal function

g. Asthma

h. Drug abusei. Alcohol abuse

j. phaeochromocytoma


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12. High output syndromes

a) Septicaemia

b) Thyrotoxicosis crisisc) Anaemia

d) Shunt syndromes


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Dyregulation of contractiliy

Frank Starling mechanism?

Force-frequency-relationship?

Catecholamine refractoriness

Neuroendocrine activation

Sympathetic nervous system

RAAS

ADH,endothelin,etcHypertrophy

Low cardiac output

Remodeling

Ischaemia

Fibrosis

Myocyte Death

Apoptosis

Necrosis

Acidosis, radical load

Coronary perfusionPeripheral perfusion? Myocardial oxygen consumption?

Reduced renal blood flowTachycardiaHypotension

Filling pressure?

Wall tension?Cardiac output? Blood volume ?

Vascular resistance?

Precipitating condition

Anaemia, thyroid disease,etc.Critical LV-Deterioration

Previous myocardial injury

Remodeling

Chronic heart failure

Afterload-Chronotropy/Inotropy/Lusitropy mismatch

Hypertensive crisis

Arrhythmias,etc.

Acute critical myocardial injury

Acute myocardial infarction


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Suspected Acute Heart Failure Assess Symptoms & Signs

Heart Disease?

ECG/BNP/X-ray?

Evaluate cardiac

function byEchocardiography/otherimaging

HEART FAILURE, assess by

Echocardiography

Characterize type and severity

Consider other diagnosis

Selected tests

(angio, haemodynamically

monitoring, PAC)

Normal

Abnormal

Abnormal

Normal


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Assessment of Ventricular Function Left

Ventricular Ejection Fraction

Reduced LVEF

Systolic LV dysfunction

Preserved LVEF

Error in evaluation, other causesof heart failure, Diagnostic error

(no heart failure

DiastolicDysfunctionTransientSystolic

Dysfunction


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Goals of treatment of the patient with AHF

Clinical

symptoms (dyspnoea and/or fatigue

clinical signsbody weight

diuresis

oxygenation


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Laboratory

Serum electrolyte normalizationBUN and/or creatinine

S-bilirubin

Plasma BNP

Blood glucose normalization

Haemodynamic

pulmonary capillary wedge pressure to


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Outcome

Length of stay in the intensive care unit

Duration of hospitalization

Time to hospital re-admission

Mortality

Tolerability

Low rate of withdrawal from therapeutic measures

Low incidence of adverse effects


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If moribund BLS, ALS

Analgesia or sedation

Immediate Resuscitation

Patient distressed or in painYES

NO

Increase FiO2, consider

CPAP, NIPPV

NO

YES

Arterial oxygen saturation >95%

Pacing, antiarrhythmics etc

YES

YES

YES

NONormal Heart Rate and rhythm

Vasodilators, consider diuresis

if volume overload

NO

Mean BP >70 mmHg

Fluid challengeNOAdequate preload

Consider inotropes or further

afterload manipulation

Reassess frequentlyYES

NOAdequate Cardiac Output:

reversal of metabolic acidosis,

SvO2>65%, clinical signs of

adequate organ perfusion

Invasive monitoring eg

PAC may be require

Definitive Treatment

Diagnosis algorithm

Definitive Diagnosis

Acute Heart Failure


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Acute heart failure with systolic dysfunction

Oxygen/CPAPFurosemide vasodilator

Clinical evaluation (leading to mechanistic theraphy)

SBP < 85 mmHg

Volume Loading? Inotrope

and/or dopamine > 5

g/kg/min and/ornorepinephrine

No response: reconsider

mechanistic therapy

Inotropic agents

SBP 85-100 mmHg

Good response Oral

therapy furosemide,

ACEI

Vasodilator and/or

inotropic (dobutamine,

PDEI or levosimendan)

Vasodilator (NTG,

nitroprusside, BNP)

SBP > 100 mmHg


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Immediate surgical correction

Pericardiocentesis

Fluids

Inotropes

Consider IABP

DIAGNOSIS

Free wall rupture

Echocardiography

Pericardial effusion (especially if>10 mm)

Echodensities in the effusion

Echo signs of tamponade

E h di h


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Coronary Angiography

Urgent surgical

correction


Stable patient

Medical Therapy

Unstable patientConsider :

IABP

Mechanical ventilation

PAC

Echocardiography

DIAGNOSIS VSR

VSR

Site

Size

Qp:Qs

Diagnosis uncertain

PACOximetry

O2step up>5% RA-RV

E h di h


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Urgent Surgical

Therapy


Stable Patient

Medical Therapy

Unstable patient

Consider

IABP

Mechanical Ventilation

PAC

DIAGNOSIS Acute MR

If Diagnosis Uncertain

Consider TEE

If TEE non Diagnostic

Consider PAC

To exclude VSR

Echocardiography

Echo signs of acute severe MR +/-

Visualization of ruptured papillary

muscle


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Echocardiography

akinetic apex

Hyperdinamic basal IVS, SAM

Discontinue

positive inotropes

nitrates

IABP

Consider

-blockers

-agonists


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Medical therapy

Consider

IABP

Mechanical ventilation

PCI or CABG

VAD

Heart transplant

Cardiogenic shock fromm loss

of ventricular muscle mass

Low EF

No signs of mechanical complication

Echocardiography

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30.Cardiac Failure Harris Hasan