Acute heart failure, pulmonary embolism Éva Zöllei University of Szeged Department of Anaesthesiology and Intensive Care Medical Intensive Care Unit

Acute heart failure, pulmonary embolism

Éva Zöllei

University of Szeged

Department of Anaesthesiology and Intensive Care

Medical Intensive Care Unit

Heart failure

- cardiac failure is a pathophysiologic state in which the heart is unable to pump blood at a suficient rate to meet the metabolic demand of the tissues or can do so only with elevated filling pressures - can be the result of impaired systolic or diastolic function or an abnormal pressure or volume load

- compensatory mechanisms increase the circulating blood volume and filling pressures, heart rate, and lead to myocardial hypertrophy

- if these these compensatory mechanisms fail the function of the heart progressively deteriorates

Braunwald Heart Disease

Acute heart failure

- can be defined as the rapid or gradual onset of symptoms of heart failure that necessitates urgent medical care

de novo acute heart failure

the decompensation of chronic heart failure

Dar, Crit Care Med, 2008;36:S3-S8.

Leading causes of death in heart failure:

- life-threatening ventricular arrhythmias (VF/VT)

sudden cardiac death

- acute left heart failure with pulmonary oedema

- cardiogenic shock with multiple organ failure

Signs and symptoms of heart failure

- fatigue, weakness - swelling of ankles - abdominal pain and/or distension - arrhythmias, syncope, sudden cardiac death- dyspnoe

exertional dyspnoeaorthopnoea and coughparoxysmal nocturnal dyspnoeadyspnoea at restacute pulmonary oedema

Causes of heart failure

- impaired contractility (systolic dysfunction)

- impaired filling (diastolic dysfunction)

- excessive hemodynamic load

pressure (aortic and mitral stenosis, pulmonary embolism)

volume (aortic and mitral insufficiency, left-right shunt)

Causes of heart failure

Cardiovascular diseasesischaemic heart diseasehypertensiondiseases of the myocardiumvalvular heart disease

Precipitating factorsnon-compliance or change in medicationarrhythmiasmyocardial ischaemiainfection, systemic inflammationnegative inotropic drugs

The different forms of heart failure 1. Systolic dysfunction

LV volume

LV

pre

ssur

e

The different forms of heart failure 1.

Diastolic dysfunction

LV volume

LV

pre

ssur

e

The different forms of heart failure 2. “backward failure”

ESV , EDV , EDP atrial volume and pressure edema generation (peripherial edemas, dyspnoe,

pulmonary odema)

“forward failure”

decreased cardiac output

impaired tissue perfusion (weakness, fatigue, pallor, cyanosis, cold, clammy skin, hypotension, filiform pulse, drowsiness, confusion, oliguria)

Cardiogenic shock

- cardiogenic shock is defined as evidence of tissue hypoperfusion induced by heart failure after correction of preload- it is characterised by

- reduced blood pressure (SBP <90 mmHg) - high filling pressures (Paop >18 mmHg)- low cardiac output ( CI < 2,2 l/min/m2)- signs of systemic hypoperfusion with or without

evidence of organ congestion


- left heart failure

congestion in the pulmonary circulation

later peripheral edemas

- right heart failure

peripheral edemas

Acute right heart failure/acute cor pulmonale

- cardiogenic shock characterised by a disproportionate elevation of the right heart filling pressures with hypotension and a low cardiac output despite preserved LV systolic function


- acute heart failure

- chronic heart failure

remodelling

neuorohumoral adaptation

The pathomechanism of the failing heart

HF

CO

neuro-humoral stimulation (renin-angiotensin sympatho-adrenerg)

circulation heart

vasoconstriction

afterload

myocardialenergy demand

cell death

cytosol Ca

lusiotropia inotropia

myocardialenergy demand

cell death

Practical recommendations for prehospital and early in-hospital

management of patients with acute heart failure syndromes

Crit Care Med 2008;36(suppl):S129-S139.

General recommendation

" all patients with acute heart failure syndrome should have the appropriate, goal-directed treatment started as early as possible"

- treatment is primarily based on signs and symptoms

+ systolic blood pressure

+ acute coronary syndromes

+ right heart failure

Clinical scenarios

Crit Care Med 2008;36(Suppl):S129-139

Clinical scenario 1. dyspnea and/or congestion with elevated SBP (>140mmHg)

- systolic left ventricular function is likely preserved

- is characterized by an acute elevation of filling pressures that parallels the increase in blood pressure

- symptoms typically develop abruptly

- predominant pulmonary oedema

- minimal systemic odema is present

- patients are often euvolemic or hypovolemic


Acute heart failure with preserved LV systolic function

Kumar, Crit Care Med, 2008;36:S52-S56.

Clinical scenario 2.dyspnea and/or congestion with normal SBP (100-140 Hgmm)

- symptoms generally develop gradually, along with a progressive increase of body weight

- the congestion is reflected by pulmonary and systemic edema, but the systemic edema predominates

- typically filling pressure are chronically elevated

- may also exhibit signs of renal and liver dysfunction, anemia, hypalbuminemia


Clinical scenario 3. dyspnea and/or congestion with low SBP

(<100 Hgmm)

- minimal systemic and pulmonary edema

- symptoms may develop abruptly or gradually

- two subgroups

with hypoperfusion/cardiogenic shock

without hypoperfusion/cardiogenic shock

- metabolic acidosis

- many of them have advanced, end-stage heart failure


Clinical scenario 4. dyspnea and/or congestion with signs of acute coronary

syndome

- may have classic evidence of ACS

- with or without ST elevation

these patients need specific therapy for ACS


Clinical scenario 5. isolated right ventricular failure

- symptoms may occur rapidly or gradually

- do not have pulmonary odema

- may have pulmonary hypertension

- tricuspic regurgitation

- signs of congestion in the systemic circulation

- may have low cardiac output due to decreased left ventricular filling


Treatment options

goal: increase systemic oxygen delivery and unload the heart→ give oxygen→ give morphin to reduce anxiety and sympahetic activity→ reduce systemic vascular resistance with vasodilators→ may use positive inotrops to increase the contractility in case of severe hypotension give vasopressor→ use diuretics in case of fluid overload→ consider non-invasive ventilation for pulmonary odema→ consider the use of mechanical assist devices→ surgical correction of mechanical abnormalities

Vasodilators- "are recommended in all patients with acute heart failure without severe hypotension and cardiogenic shock"

Elkayam, Crit Care Med 2008;36(Suppl):S95-S105.

Vasodilatorsnitroglycerin - relieves pulmonary congestion primarily through direct venodilation

- at higher doses induces coronary artery dilation

- can be administered sublingually or in iv continouos infusion

- slow upward titration is recommended with frequent blood pressure measurement

- the blood pressure limit below which nitrates should not be used varies among patients and clinical settings

Elkayam, Crit Care Med 2008;36(Suppl):S95-S105.

Vasodilatorsnesiritide - recombinant human B type natriuretic peptid

- induces dilation in venous and also in arterial system

- VMAC trial (Vasodilators for treatment of decompensated CHF)

→ no significant difference in symptomatic improvement, in rehospitalisations within 30 days and in the 6 month mortality

- concern regarding renal function and mortality

second-line agent

JAMA 2002;287:1531-1540.

Diuretics

- agressive diuretic monotherapy is not necessary in the majority of patients

- diuretics should only be given when there is evidence of systemic volume overload

- may be helpful in addition to vasodilators

- the recommended initial dose is furosemide 20-40 mg iv

- if resistent, higher doses, combinations or continous infusion may be necessary

Wang, Crit Care Med 2008;36(Suppl):S89-S94.

Diuretics

It is a common misconception that the pulmonary oedema in acute heart failure is the result of excessive blood volume. This is not generally the case, in fact many such patients respond favourably to fluid challenges.

"inotropes may be used early in patients with evidence of poor organ perfusion (cold, clammy skin, renal impairment, liver dysfunction or impaired mentation) and

low cardiac output, high filling pressures who are not responding to other therapies"

" if no improvement in perfusion is observed advanced hemodynamic monitoring should be used"


left

ven

tric

ular

pre

ssur

e

left ventricular volume

decreased contractility

positive inotropic effect

Positive inotropes

left

ven

tric

ular

pre

ssur

e

left ventricular volume

decreased contractility

positive inotropic effectIno-constriktorhigh dose dopamine,noradrenaline

Ino-dilatordobutaminePDE-inhibitorslevosimendane

Positive inotropes

Positive inotropes

- dobutamine - increases cAMP level and Ca release from the sarcoplasmatic reticulum through the beta-adrenergic stimulation of adenylate cyclase

- milrinone - is a phosphodiesterase inhibitor, it impairs the degradation of cAMP

they increase contractility

they increase myocardial oxygen demand (can cause ischaemia!)


Positive inotropes

levosimendane - is a calcium-sensitizer

- improves contractility by binding to troponin C and influencing actin-myosin cross-bridging

- has significant vasodilatory properties (arterial and venous) through the ATP-sensitive K channels

- increases coronary flow reserve

- is safe in acute coronary syndromes - RUSSLAN study

- dobutamin vs levosimendan - LIDO, SURVIVE trials


"if blood pressure remains low after optimising preload, then a vasoconstrictor should be considered (SBP<100 mmHg)"

" norepinephrine is the recommended vasoconstrictor in acute heart failure"


"in patients who have not responded to other therapies early mechanical device therapy may be useful during the first 12 hours (severe and persistent hypotension and hypoperfusion)"

"device therapy should only be recommended when there is potential for myocardial recovery with or without intervention"

→ intraaortic ballon pump (IABP)

ventricular assist devices and arteficial heartCrit Care Med 2008;36(Suppl):S129-139

The diastolic counterpulsation

The hemodynamic effects of IABP

DPTI/TTI DPTI: diastolic pressure time index oxygen supply

TTI: tension time index oxygen demand↓

improved coronary perfusion

"in all acute heart failure patients when dyspnea , respiratory distress and/or pulmonary odema is present, non-invasive ventilation should be used as early as possible "

"NIV should never be used when there is a need for emergent intubation"


Non-invasive ventilation

- haemodynamic effects decreases venous return decreases left ventricular afterload increases cardiac output increases FRC decreases work of breathing

- either CPAP or BiPAP devices can be used

- 3 meta-analysesMasip, JAMA 2005;294:3124-3130

Peter, Lancet 2006;367:11551163.

Winck, Crit Care 2006;10:R69

Non-invasive ventilation mortality need for invasive ventilation

Peter, Lancet 2006;367:11551163.

Correction of structural abnormalities

- acute valvular abnormality due to myocardial infarction, infective endocarditis, degenerative disease- ventricular septal defect as a consequence of an acute myocardial infarction - pericardial tamponade due to ventricular free wall rupture in acute myocardial infarction or other aetiologies- aortic dissection Whatever the cause, specialist opinion should be rapidly sought as it is uncommon for the heart failure to resolve without definitive therapy for the structural deficit.

the horses of Arnold Katz

positiveinotropes

negativeinotropes

vasodilators

Katz, A.M.: Cellular mechanisms in Congestive Heart Failure, Am J Cardiol, 1988;62:3A-8A.

Pulmonary embolism

Severe pulmonary embolism

- massive PE - with haemodynamic instability

syncope

hypotension

cardiogenic shock

- submassive PE - with right ventricular dysfunction and Troponin elevation with normal systemic blood pressure

8.1

15.2

24.5

64.8

0

10

20

30

40

50

60

70

RV-dysfunctio

Hypotensio Shock CPR

Mortalitás

Inhospital mortality

Pathophysiology

- pulmonary arterial obstruction

- secretion of vasoconstrictor compaunds

- reflex pulmonary vasoconstriction

pulmonary arterial pressure and pulmonary vascular resistance rise

as its afterload increases, the right ventricle dilates

the interventricular septum shifts to the left

impaired left ventricular filling

cardiac output decline

hypotension

- impaired coronary perfusion, myocardial ischaemia

death

How to diagnose?

clinical evaluation: history and signs and symptoms

tachypnoe, dyspnoe

tachycardia, diaphoresis, hemodynamic instability

pleuritic chest pain, cough, hemophtysis,

Important: The clinical impact of PE is related to the physical size of the embolic occlusion and the background cardiopulmonary reserve of the patient. Most patients with even major PE (obstructing >50% of the pulmonary vasculature) do not present with shock and early death is unlikely.

Wood KE, Chest 2002;121:877-905.

How to diagnose?

ECG changes (non-specific)anterior T wave inversion, non-specific ST changes right axis deviation partial or complete right bundle branch block right ventricular strain (S1Q3T3)atrial fibrillation and various degrees of AV block

Laboratory tests (non-specific)leukocytosis increased erythrocyte sedimentation rate increased serum transaminases increased brain natriuretic peptide and troponin concentrationincreased D dimer

How to diagnose?

CT pulmonary angiography

- the first-line imaging modality

- patients with a low clinical probability of PE but a positive D-dimer assay and

- all patients with a high clinical probability should have a CT-PA

- with high-quality imaging and interpretation, a positive CT-PA confirms the diagnosis of PE while a negative CT-PA excludes a PE

How to diagnose?

Echocardiographic findings in PE with shockRV dilatation/hypokinesis increased RV/LV end-diastolic area ratio RV pressure overload and volume overload paradoxical septal shift PA dilatation loss of inspiratory collapse of inferior vena cava emboli in transit tricuspid regurgitation

- a normal echocardiogram without signs of RV overload effectively rules out PE as a cause of shock

Management

- an urgent approach to the diagnosis and treatment of PE is imperative as in cases of fatal PE, 60% of patients die within one hour of presentation

- the presence of shock in acute PE is associated with three- to sevenfold increase in mortality

- haemodynamically unstable patients with suspected PE should be transferred rapidly to an ICU or similar environment

General support

- intravenous volume therapy in patients with PE should be carefully titrated to avoid further RV dysfunction

- in patients with PE-induced shock, norepinephrine (noradrenaline) is considered the vasopressor of choice to maintain systemic and RV coronary artery perfusion pressure

Treatment

American College of Chest Physicians and the European Society of Cardiology 2008 guidelines

anticoagulation

- unfractionated heparin

target aPTI twice the upper limit of normal

- low molecular weight heparin

weight adjusted dosing

- coumadins

long term therapy

Treatmentthrombolysis

- first-line treatment for massive PE with cardiogenic shock or persistent arterial hyotension

- consider in selected sub-massive PE patients after assessing bleeding risk

- 100 mg human recombinant tissue plasminogen activator over 2 hours

- check contraindications!

improves haemodynamics, no mortality benefit


Treatment

Catheter embolectomy

- consider in high risk patients when thrombolysis is absolutely contraindicated

Surgical embolectomy

- therapeutic option in high risk patients in whom thrombolysis is absolutely contraindicated or has failed


Treatment

Vena caval filter insertion

- anticoagulation contraindicated

- recurrent PE despite adequate anticoagulation

- temporary interruption of chronic anticoagulation in high risk patients with limited ability to tolerate further PE

IVC filters reduce the frequency of early recurrent PE but increased the risk of DVT

no mortality benefit was demonstrated.


Documents

Acute heart failure, pulmonary embolism Éva Zöllei University of Szeged Department of Anaesthesiology and Intensive Care Medical Intensive Care Unit