Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

AHF In Critical Illness


Published on

Critical care Cardiology

Published in: Education, Health & Medicine

AHF In Critical Illness

  2. 2. <ul><li>Acute or decompensated heart failure is responsible for about 1million hospital admissions each year in the united states, and it is the leading cause of hospital admissions for adults over the age of 65 </li></ul><ul><li>AHF is the primary or underlying diagnosis in many patients admitted to the ICU </li></ul><ul><li>It may present with left or right heart failure, or combination of these conditions </li></ul><ul><li>The cardiac dysfunction may be systolic or diastolic (with preserved ejection fraction) and the underlying pathological mechanism may be cardiac or extracardiac and may induce transient or permanent damage </li></ul>AHF
  3. 3. <ul><li>Heart failure occurs when the heart is unable to either receive adequate venous return from, or pump blood into, the arterial system at a sufficient rate to meet the metabolic demands of the body </li></ul><ul><li>Acute heart failure is defined as the rapid onset of symptoms and signs secondary to abnormal cardiac function. It may occur with or without previous cardiac disease. The cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to preload and after load mismatch </li></ul><ul><li>It is often life threatening and requires urgent treatment </li></ul>AHF
  4. 4. <ul><li>Acute heart failure is a common problem encountered by intensive care clinicians and can represent a threat to life </li></ul><ul><li>In its severest form, it is a medical emergency that presents with severe pump failure and symptoms of impaired organ perfusion </li></ul>
  5. 5. Early Recognition And Management Of The Patient With AHF <ul><li>The main goals of acute management of the patient with AHF ARE TO </li></ul><ul><li>Resuscitate the patient to stabilize the condition and prevent further deterioration </li></ul><ul><li>  Assess the severity of the problem so that the patient can be moved to an appropriate setting that can provide optimal monitoring and support </li></ul><ul><li>  Determine the possible etiology of the acute heart failure. This will enable early intervention when an acute reversible problem exists </li></ul>
  6. 6. <ul><li>Immediate assessment and resuscitation </li></ul><ul><li>The first line assessment and treatment are closely inter-related and should occur simultaneously. They include the following tasks: </li></ul><ul><ul><li>  Resuscitation of the patient </li></ul></ul><ul><ul><li>  Institution of basic monitoring </li></ul></ul><ul><ul><li>  Clinical history </li></ul></ul><ul><ul><li>  Physical examination </li></ul></ul><ul><ul><li>  Assessment of severity of AHF </li></ul></ul>Early Recognition And Management Of The Patient With AHF
  7. 7. <ul><li>Breathing The failing myocardium will be further compromised by hypoxaemia and steps to prevent this occurrence are essential. Oxygen should be administered in as high a concentration as possible to maximise tissue oxygenation. The response to oxygen therapy should be assessed by continuous pulse oximetry and regular blood gas analysis </li></ul>Early Recognition And Management Of The Patient With AHF Resuscitation
  8. 8. Resuscitation <ul><li>The immediate priorities when treating a patient with acute heart failure are the same as for any acute illness </li></ul><ul><li>Therefore, attention should be paid to ensuring the ABCs are adequate </li></ul><ul><li>Airway takes only a few seconds. The most likely reason that a patient is unable to maintain an adequate airway is a reduced level of consciousness . Oral or nasopharyngeal airways may be sufficient to prevent airway obstruction but endotracheal intubation is required in some cases. Intubation can sometimes be avoided (preferably) with proper and rapidly acting conservative therapy </li></ul>Early Recognition And Management Of The Patient With AHF
  9. 9. <ul><li>The reasons for initiating ventilatory support are essentially two-fold </li></ul><ul><li>The first reason is to reverse respiratory muscle fatigue that is secondary to hypoperfusion </li></ul><ul><li>The second reason is to reduce the whole body oxygen requirements in a patient who is in a critical condition, by resting the respiratory muscles and therefore reducing the oxygen needs of that significant muscle group </li></ul>Early Recognition And Management Of The Patient With AHF Resuscitation Breathing
  10. 10. <ul><li>Circulation Therapies aimed at improving the circulatory status are dependent on the </li></ul><ul><li>pathophysiological classification of AHF </li></ul><ul><ul><li>Loss of myocardial contractility </li></ul></ul><ul><li>-Partial e.g .: coronary artery disease </li></ul><ul><li>-Generalized e.g. : dilated cardiomyopathy and pericarditis </li></ul><ul><li>Impediment to cardiac filling and emptying </li></ul><ul><li>-Pressure :hypertension </li></ul><ul><li>-Volume : excessive intravascular volume </li></ul><ul><li>-Valvular disease </li></ul><ul><li>-Pericardial disease </li></ul><ul><li>-Restrictive disease </li></ul><ul><li>Abnormal organisation or signaling of cardiac contractility </li></ul><ul><li>tachyarrhythmia </li></ul><ul><li>bradyarrythmia </li></ul>Early Recognition And Management Of The Patient With AHF Resuscitation
  11. 11. Basic monitoring <ul><li>These patients can be extremely ill and their clinical condition can fluctuate very quickly. The initiation of basic monitoring is thus vital to aid in the assessment of the patient’s condition as well as to guide therapy and warn of problems All patients should have the following parameters monitored: </li></ul><ul><ul><li>  Continuous electrocardiogram </li></ul></ul><ul><ul><li>  Blood pressure </li></ul></ul><ul><ul><li>  Respiratory rate </li></ul></ul><ul><ul><li>  Temperature </li></ul></ul><ul><ul><li>  Continuous oxygen saturation with a pulse oximeter </li></ul></ul>Early Recognition And Management Of The Patient With AHF
  12. 12. Clinical history <ul><li>A good clinical history is often difficult to obtain in a patient with severe acute heart failure. It is important to speak with the patient’s family or care givers as they can often provide the necessary details </li></ul><ul><li>Taking the clinical history is important TO : </li></ul><ul><ul><li>  Decide - Does this patient have acute heart failure? </li></ul></ul><ul><ul><li>  Obtain clues to the etiology of the acute heart failure </li></ul></ul><ul><ul><li>  Determine whether the cause of acute heart failure is due to an acute coronary syndrome that may require immediate intervention </li></ul></ul><ul><ul><li>  Avoid potential complications of your acute therapy </li></ul></ul>Early Recognition And Management Of The Patient With AHF
  13. 13. Key questions Early Recognition And Management Of The Patient With AHF Clinical history <ul><li>Is the patient dyspnoeic? </li></ul><ul><li>Breathlessness is the most imp alteration due to left ventricular failure and the main symptom that the patient describes </li></ul><ul><li>De novo or on top of CCF? </li></ul><ul><li>Help to classify causes </li></ul><ul><li>Symptoms of ACS? </li></ul><ul><li>Affects therapeutic implications </li></ul><ul><li>Medications? </li></ul><ul><li>AHF can be ppted by certain medications or affected by medications non compliance </li></ul>
  14. 14. Additional symptoms <ul><ul><li>□ None, indeed the patient could be: ▫Truly asymptomatic </li></ul></ul><ul><ul><li>or  </li></ul></ul><ul><ul><ul><li>▫ Asymptomatic because of sedentary lifestyle </li></ul></ul></ul><ul><ul><li>  Fatigue </li></ul></ul><ul><ul><li>  Weakness </li></ul></ul><ul><ul><li>  Swelling of ankles </li></ul></ul><ul><ul><li>  Abdominal pain and/or distension </li></ul></ul><ul><ul><li>  Palpitations </li></ul></ul><ul><ul><li>  Syncope or pre-syncope </li></ul></ul><ul><ul><li>  Central nervous symptoms such as decreased level of consciousness </li></ul></ul>Early Recognition And Management Of The Patient With AHF Clinical history
  15. 15. <ul><li>Co-morbid conditions </li></ul><ul><li>The main question to be asked at this stage is whether the AHF has arisen de novo or as a decompensation of a chronic condition. This can be assessed by asking the patient about other co-morbidities that are associated with a diagnosis of chronic heart failure such as DM, HTN, IHD, AF </li></ul>Early Recognition And Management Of The Patient With AHF Clinical history Other imp points
  16. 16. <ul><li>Drug-induced AHF </li></ul><ul><li>Non-cardiac medications can cause an exacerbation of heart failure </li></ul><ul><li>□ Medications for diabetes mellitus have been reported to increase plasma volume </li></ul><ul><li>□ Non-steroidal anti-inflammatory drugs can promote sodium and fluid retention, interfere with the pharmacological mechanism of ACE inhibitors and decrease the effectiveness of loop diuretics </li></ul><ul><li>□ Tricyclic antidepressants increase the risk for ventricular arrhythmia </li></ul><ul><li>□ Theophylline and β-agonist bronchodilatators may also exacerbate heart failure by inducing tachyarrhythmias </li></ul>Other imp points Early Recognition And Management Of The Patient With AHF Clinical history
  17. 17. Physical examination <ul><li>The purpose of the physical examination is to confirm the symptoms of AHF and to start to understand the category of AHF that the patient is experiencing </li></ul>Early Recognition And Management Of The Patient With AHF Signs of AHF SIGNS OF CONGESTION SIGNS OF LOW CARDIAC OUTPUT Elevated JVP Cool peripheries Pulsus alternans Decreased level of consciousness Hepatojugular reflux Confusion Parasternal lift hypotension Displaced apical impulse Low volume carotid pulse Gallop rhythm Tachycardia or inappropriate bradycardia Murmur (MR,TR) Peripheral edema Ascitis, hepatomegaly
  18. 18. Assessment of severity of AHF <ul><li>It allows the clinician to make an accurate risk assessment and to communicate his findings with other colleagues </li></ul><ul><li>A rapid assessment should be made to identify patients who should be transferred to the Intensive Care Unit (ICU) and those who can be safely managed on a ward setting </li></ul><ul><li>A greater degree of heart failure is suggested by worsening dyspnoea, obtundation, hypotension and oliguria . These patients will be cyanosed and will have a metabolic acidosis </li></ul>Early Recognition And Management Of The Patient With AHF
  19. 19. Assessment of severity of AHF <ul><li>Which patients with acute heart failure should be transferred to the ICU ? </li></ul><ul><li>Have failure of other organ systems apart from the heart </li></ul><ul><li>Need protection of their airway or mechanical ventilatory assistance </li></ul><ul><li>Are not responding to basic medical treatment </li></ul><ul><li>Three scores to describe severity of illness in chronic heart failure patients are: </li></ul><ul><li>  New York Heart Association functional classification </li></ul><ul><li> ‘ Cold, Warm, Dry, Wet’ system </li></ul><ul><li>  Framingham criteria </li></ul>Early Recognition And Management Of The Patient With AHF
  20. 20. <ul><li>Multiple extra-cardiac pathologies may result in acute heart failure by changing the cardiac loading conditions e.g. high output states due to sepsis in a patient with poor physiological reserve </li></ul>Pressure overload HTN, AS, PE Impaired myocardial filling AR, Output failure Volume overload MS, Tmaponade, Pericardial constriction, restriction Myocardial disease IHD, myocarditis, Metabolic or toxic disease Dysrhythmias Brady or tachyarrhythmias
  21. 21. <ul><li>Acute heart failure often presents with a different clinical picture compared to chronic heart failure due to the rapid onset preventing development of normal compensatory responses </li></ul><ul><li>Heart failure should never be the final diagnosis </li></ul><ul><li>The terminology that is commonly used to describe the pathophysiological and clinical disturbances is not all complete. However it does provide a basis for understanding the patient’s condition and overall status </li></ul>
  22. 22. <ul><li>This terminology describes the side of the heart the predominant problem is on. The clinical picture will vary dramatically depending on whether the patient has a predominantly left or right sided problem </li></ul>Category of AHF Right and/or left heart failure Forward/backward heart failure This terminology describes whether the predominant problem is with forward flow (perfusion) or backward flow (congestion) Systolic and/or diastolic heart failure Diastolic heart failure is often presumed to be present when symptoms and signs of heart failure occur in the presence of preserved left ventricular systolic function
  23. 23. <ul><li>These are the tests that should be performed on the patient to both confirm the physical findings and to provide a clinical diagnosis </li></ul><ul><li>Electrocardiogram </li></ul><ul><li>The negative predictive value of a normal ECG to exclude LV systolic dysfunction exceeds 90% </li></ul><ul><li>Chest radiograph </li></ul><ul><li>A chest X-ray should be performed early for all patients with AHF to evaluate pre-existing chest or cardiac conditions (cardiac size and shape) and also to determine the presence of pulmonary congestion </li></ul><ul><li>A cardiothoracic ratio >0.50, and the presence of pulmonary venous congestion are useful indicators of abnormal cardiac function with a decreased ejection fraction and/or elevated left ventricular filling pressure </li></ul>
  24. 24. Diagnosis <ul><li>Laboratory tests in AHF </li></ul><ul><ul><li>  Urea and electrolytes </li></ul></ul><ul><ul><li>  Arterial blood gases </li></ul></ul><ul><ul><li>  Full blood count </li></ul></ul><ul><ul><li>  Coagulation profile </li></ul></ul><ul><ul><li>  Blood glucose </li></ul></ul><ul><ul><li>  Cardiac troponin </li></ul></ul><ul><ul><li>  B-type natriuretic peptide (BNP, NT-pro BNP) </li></ul></ul><ul><ul><li>  Liver function tests </li></ul></ul>
  25. 25. Laboratory tests in AHF <ul><li>The preferred biomarker for myocardial damage is cardiac troponin (I or T), which has nearly absolute myocardial tissue specificity, as well as high sensitivity, thereby reflecting even microscopic zones of myocardial necrosis </li></ul><ul><li>Apart from the acute coronary syndromes there are other conditions can cause increases in the troponin enzymes like shock, renal failure, sepsis and hypovolaemia </li></ul><ul><li>Care must be exercised in these conditions not to attribute troponin rises to acute myocardial ischaemia unless there is either clinical or electrocardiographic evidence to corroborate this </li></ul><ul><li>If cardiac troponin assays are not available, the best alternative is CK-MB </li></ul>Diagnosis
  26. 26. <ul><li>B-type natriuretic peptide (BNP) </li></ul><ul><li>Plasma concentration of certain natriuretic peptides (ANP, BNP and NT-pro BNP) can be helpful in the diagnostic process </li></ul><ul><li>BNP has been proposed as a tool to distinguish acute heart failure from other causes of acute dyspnoea. These peptides may be most useful clinically as a ‘rule out’ test due to consistent and very high negative predictive values </li></ul><ul><li>Plasma levels of ANP and BNP increase in accordance with the severity of the heart failure </li></ul>Laboratory tests in AHF Diagnosis
  27. 27. <ul><li>Echocardiography </li></ul><ul><li>Echocardiography is an essential tool for the evaluation of the functional and structural changes underlying or associated with AHF, as well as in the assessment of acute coronary syndromes </li></ul><ul><li>Early echocardiographic evaluation is warranted to define global and regional cardiac function and detect any mechanical problem such as severe valvular lesion (progressive mitral regurgitation) or septal or free wall rupture leading to AHF </li></ul>Diagnosis
  28. 28. <ul><li>Echocardiography may show atrial or ventricular dilatation and signs of hypertrophy </li></ul><ul><li>The most important parameter of heart function is the LV ejection fraction for distinguishing patients with cardiac systolic dysfunction and those with preserved systolic function </li></ul><ul><li>One of the most important reasons for the widespread use of echocardiography to determine EF is that a clear association between EF and prognosis has been demonstrated </li></ul>Diagnosis Echocardiography
  29. 29. <ul><li>Principles of management is to preserve an adequate oxygen supply/demand balance for both the myocardium and the body as a whole </li></ul><ul><li>The immediate goals of treatment include </li></ul><ul><ul><li>Improvement of tissue perfusion and oxygenation </li></ul></ul><ul><ul><li>Correction of underlying HD abnormalities </li></ul></ul><ul><ul><li>Correction of underlying cause of cardiac decompensation </li></ul></ul><ul><ul><li>Control of symptoms </li></ul></ul>
  30. 30. Reducing demand <ul><li>This entails reducing the heart rate and the ventricular afterload to reasonable limits by </li></ul><ul><li>Relieving anxiety with reassurance and anxiolytics </li></ul><ul><li>Preventing or treating pain with analgesics </li></ul><ul><li>Tachycardia can be reduced by ensuring there is an adequate preload with cautious fluid challenges to maximize stroke volume </li></ul><ul><li>Afterload can then be reduced with vasodilators and if the patient is volume overloaded, diuretics </li></ul><ul><li>Oxygen demand can be further reduced in the ICU setting by sedating the patient and instituting mechanical ventilation </li></ul>Management
  31. 31. <ul><li>30 to 40% of cardiac output may be required to support the work of breathing in a dyspnoeic patient </li></ul>Reducing demand Management
  32. 32. Increasing supply <ul><li>In some patients, however, the systemic demand for oxygen will still be higher than its delivery. In these patients, oxygen delivery will need to be increased further </li></ul><ul><li>The first step to achieve this aim should always be through the addition of a vasodilator if possible </li></ul><ul><li>Further treatments include the transfusion of blood to increase the oxygen carrying capacity of blood </li></ul><ul><li>And the judicious use of inotropic agents to increase myocardial contractility </li></ul>Management
  33. 33. Non-specific therapy <ul><li>General care </li></ul><ul><li>Such as thromboprophylaxis, adequate nutrition and correction of electrolyte imbalances. Septic complications are common in this patient group and should be identified and treated immediately </li></ul>Management
  34. 34. Ensuring adequate oxygenation <ul><li>All patients should receive oxygen therapy </li></ul><ul><li>If oxygen via a normal face-mask fails to improve the oxygen saturation of hemoglobin, then non-invasive ventilation via either CPAP or biphasic positive airway pressure (BIPAP) can be tried </li></ul><ul><li>Some patients will need to be sedated and receive mechanical ventilation via an endotracheal tube </li></ul>Management
  35. 35. Obtaining adequate heart rate and rhythm <ul><li>Tachycardias It is preferable to ensure the heart rate is less than 100 beats per minute in this patient group </li></ul><ul><li>The first step with these patients is to relieve anxiety, stress and/or pain </li></ul><ul><li>The second step is then to ensure that the circulating volume is appropriate and that the patient is in sinus rhythm </li></ul><ul><li>If conversion to sinus rhythm is not possible, then control of the heart rate can be achieved with agents such as diltiazem or digoxin </li></ul>Management
  36. 36. <ul><li>Bradycardias and heart block lead to a reduced cardiac output. These need to be treated in critically ill patients especially if there is evidence of a global oxygenation deficit. Temporary transcutaneous or transvenous pacing can be a lifesaving procedure in patients presenting with shock and complete heart block </li></ul>Management Obtaining adequate heart rate and rhythm
  37. 37. Optimization of preload <ul><li>The achievement of an adequate circulating volume is a vital part of the management for this group of patients </li></ul><ul><li>Most of these patients will be volume deficient and will therefore respond to a fluid challenge </li></ul><ul><li>Some of the patients, especially those with acute on chronic cardiac failure, may be volume overloaded. These will be better treated with diuresis </li></ul>Management
  38. 38. Increasing cardiac output <ul><li>If all of the measures above fail to restore tissue oxygenation, it may be warranted to increase systemic oxygen delivery </li></ul><ul><li>In practice this means either increasing the contractility state of the heart with a positive inotropic agent or reducing the systemic vascular resistance. Of these two options, when possible, vasodilatation is preferable as this will lead to a reduced work of the heart at the same time as increasing systemic oxygen delivery </li></ul>Management
  39. 39. Correction of structural problems <ul><li>Some patients with acute heart failure will present secondary to a structural problem </li></ul><ul><li>This may be a valvular abnormality or could be a defect in the intraventricular septum as a consequence of an acute myocardial infarction </li></ul><ul><li>Other common issues include pericardial tamponade following cardiac surgery, aortic dissection or free wall rupture. 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 </li></ul>Management
  40. 40. Cardiogenic shock <ul><li>Severe left ventricular failure will result in hypotension with failure of tissue perfusion. This pattern of heart failure has a high mortality. The most severe form of this problem is known as cardiogenic shock </li></ul><ul><li>Cardiogenic shock is defined as evidence of tissue hypoperfusion induced by heart failure after correction of preload. It is characterised by a reduced blood pressure (SBP <90 mmHg or a drop of mean arterial BP >30mmHg) and/or low urine output (below 0.5ml/kg/hour) with a pulse rate >60 /minute with or without evidence of organ congestion </li></ul>
  41. 41. <ul><li>Cardiogenic shock is diagnosed after documentation of myocardial dysfunction and exclusion or correction of factors such as hypovolaemia, haemorrhage, sepsis, pulmonary embolism, tamponade, aortic dissection, pre-existing valvular disease, hypoxia and acidosis </li></ul><ul><li>Treatment of cardiogenic shock comprises supportive therapy following the principles described above as well as correcting or treating the underlying cause </li></ul><ul><li>The most common cause of cardiogenic shock is extensive acute myocardial infarction. Recent estimates of the incidence of cardiogenic shock range from 5% to 10% of patients with myocardial infarction and the mortality rate from 50% to 80%. In patients presenting with cardiogenic shock secondary to acute myocardial infarction, reperfusion of the compromised coronary artery is vital </li></ul>Cardiogenic shock
  42. 42. <ul><li>The intra-aortic balloon pump is inserted percutaneously via the femoral artery into the descending aorta </li></ul><ul><li>The balloon inflates during diastole to improve coronary and cerebral blood flow and deflates immediately prior to systole resulting in a reduction in afterload </li></ul><ul><li>The balloon pump is used most commonly following cardiac surgery in patients with poor ventricular function but also has a role in the management of severe cases of heart failure where the underlying cause may be corrected e.g. by coronary re-vascularisation or valve repair </li></ul>Intra-aortic balloon pump Cardiogenic shock
  43. 44. Ventricular assist devices <ul><li>Ventricular assist devices are small mechanical pumps that are placed in the arterial tree or between the ventricle and the descending aorta. </li></ul><ul><li>Their original role was to support the circulation of patients awaiting transplant but it is now recognized that their use in some patients with acute heart failure facilitates a recovery of the myocardium. </li></ul><ul><li>In many cases the recovery has been so impressive that the device has been removed and the patient has recovered without the need for heart transplant. </li></ul><ul><li>It is therefore recognized now as a bridge to recovery in certain causes of heart failure e.g. myocarditis. </li></ul>Cardiogenic shock
  44. 46. Left heart backward failure <ul><li>Patients often present with extremely high systemic blood pressure resulting in acute pulmonary oedema and AHF </li></ul><ul><li>In such cases a reduction in afterload is the most important aspect of treatment </li></ul><ul><li>The aim should be to reduce systemic blood pressure by 30% rather than to normal values. The sublingual administration of nitroglycerine (0.4 to 0.6 mg, repeated every 5 to 10 minutes four times as needed) is of value </li></ul>
  45. 47. <ul><li>Nitroglycerine is effective in patients with acute cardiogenic pulmonary oedema due to both ischaemic and non-ischaemic causes </li></ul><ul><li>If systemic blood pressure is acceptable nitroglycerine can be administered intravenously (0.3 to 0.5 µg/kg/min) as well </li></ul><ul><li>Frusemide (furosemide, 20 to 80 mg intravenously) should be given shortly after the diagnosis of acute pulmonary oedema is established </li></ul><ul><li>Morphine sulphate (3 to 5 mg intravenously) is effective in ameliorating many of the symptoms of acute pulmonary oedema and can be safely administrated to most patients in this condition </li></ul>Left heart backward failure
  46. 48. Right heart backward failure <ul><li>Right heart failure is characterised by elevation of the right heart pressures transmitted backwards into the portal vein circulation </li></ul><ul><li>Dyspnoea is not prominent because of the initial absence of pulmonary congestion. Clinical signs include ascites with tender, congestive hepatomegaly. The latter may occur rapidly, sometimes with, particularly in the presence of considerable tricuspid regurgitation, systolic pulsation of the liver, anasarca and hepatojugular reflux </li></ul><ul><li>Clinical manifestations include anorexia, bloating, nausea and constipation. In critically ill patients the diagnosis of right heart failure can be difficult to make. Most of the signs described above are non-specific and occur in other sick patients without heart failure. The diagnosis is therefore one of exclusion and requires a high index of suspicion </li></ul>
  47. 49. Conclusion Acute heart failure is a syndrome with a high mortality There are a large number of causes of this syndrome and it can present in a number of differing patterns that depend on the underlying pathophysiology It often presents with a different clinical picture compared to chronic heart failure Treatment is a combination of supportive measures and definitive therapy that depends on the aetiology
  48. 51. AHF 1-American Heart Association. Heart Disease and Stroke Statistics – 2005 Update. Dallas, TX: American Heart Association2005 . 2- Nieminen MS, Harjola V-P. Definition and Aetiology of acute heart failure syndromes. Am J cardiology 2005;96(suppl):5G-10G References