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POSTGRADUATE DIPLOMA IN CLINICAL ULTRASOUND Subject 3 Applications of Echocardiography in Perioperative and Critical Care Medicine Tutorial 2 Clinical Applications Acute Pulmonary Oedema
Section 1 Author

Author: Dr Ian Seppelt, MB BS BSc (Med) FJFICM FANZCA Staff Specialist in Anaesthesia and Intensive Care, The Nepean Hospital, Penrith Clinical Lecturer, Dept of Medicine, University of Sydney Ian Seppelt is an anaesthetist and intensive care physician with an interest in echocardiography, cardiovascular monitoring, neuroanaesthesia and neurointensive care. He is an active member of the Clinical Trials Group of the Australian and New Zealand Intensive Care Society and coordinates trials in sepsis, cardiovascular support, neurotrauma and fluid resuscitation. This tutorial will provide practical examples of the utility of echocardiography in intensive care, in this case in determining the underlying pathophysiology in a patient with acute pulmonary oedema. Note that in the intensive care environment the important word is echocardiography not TOE, for transoesophageal examinations are necessary, or even indicated, in fewer than 10% of ICU examinations, whereas the other 90% of the time a transthoracic study provides all the information that is required indeed there are situations where a TTE actually provides better information 1

than a TOE, for example assessing aortic valve gradients or evaluating the right ventricle. It is of course imperative that all intensivists be comfortable with TTE, but it is reasonable to expect cardiac anaesthetists to at least have a working knowledge. Most of the images in this tutorial are transthoracic, as they were in each of the real cases. Some chest X-rays are also shown there is a lot of information to be gained correlating the echocardiographic and radiological findings. No new echocardiographic concepts are introduced this tutorial should consolidate principles learnt previously in this course.

Section 2 Overview
Postgraduate Diploma in Clinical Ultrasound ........................................................ 1 Subject 3 Applications of Echocardiography in Perioperative and Critical Care Medicine ................................................................................................... 1 Tutorial 2 Clinical Applications Acute Pulmonary Oedema ......................... 1 Section 1 Author ........................................................................................ 1 Section 2 Overview ..................................................................................... 3 Section 3 Statement of Objectives.............................................................. 4 Section 3 Statement of Objectives.............................................................. 4 Section 4 Effective Learning Content ......................................................... 5 4.1 Introduction ....................................................................................... 5 4.2 Pathophysiology ................................................................................ 5 4.2.1 Classification .................................................................................. 5 4.2.2 Differential diagnosis ...................................................................... 7 4.2.3 Cardiogenic pulmonary oedema................................................... 8 4.2.4 Noncardiogenic pulmonary oedema ............................................. 8 4.2.5 Paediatric pulmonary oedema ....................................................... 8 4.2.6 Treatment....................................................................................... 9 4.2.7 Echocardiographic assessment of cardiac function ....................... 9 4.3 Case Scenario # 1 ........................................................................... 10 4.4 Case Scenario # 2 ........................................................................... 14 4.5 Case Scenario # 3 ........................................................................... 20 4.6 Case Scenario # 4 ........................................................................... 25 4.7 Case Scenario # 5 ........................................................................... 28 4.8 Case Scenario # 6 ........................................................................... 31 Answers to Clinical Scenarios .................................................................. 37 4.3 Case Scenario # 1 ........................................................................... 37 4.4 Case Scenario # 2 ........................................................................... 39 4.5 Case Scenario # 3 ........................................................................... 41 4.6 Case Scenario # 4 ........................................................................... 42 4.7 Case Scenario # 5 ........................................................................... 43 4.8 Case Scenario # 6 ........................................................................... 44 Section 5 Glossary ................................................................................... 45 Section 6 References ............................................................................... 47

Section 3 Statement of Objectives

3.1 Review the underlying pathophysiology of pulmonary oedema 3.2 Review current thinking on the therapy of acute pulmonary oedema 3.3 For each clinical case presented, interpret appropriately the investigations presented, especially the echocardiography, 3.4 For each case, use the results of 3.3 to develop a reasonable differential diagnosis 3.5 For each case, outline a reasonable management plan for the patient

Section 4 Effective Learning Content

4.1 Introduction
Pulmonary oedema as a pathophysiological entity can be extremely difficult to diagnose accurately let alone treat consistently. Echocardiography is invaluable both diagnostically and in determining the efficacy of treatment. This tutorial builds upon specific skills already gained and seeks to integrate them in a clinical context. It is assumed that the student has already studied left ventricular systolic and diastolic function, segmental wall motion abnormalities, left atrial pressure determination and right ventricular function. The goal is now to use these skills while managing a patients problems.

4.2 Pathophysiology 4.2.1 Classification

Pulmonary oedema is best classified according to mechanism. This list from Braunwalds Heart Disease1 summarises the known causes: 1. Imbalance of Starling Forces a. Increased pulmonary capillary pressure i. Increased pulmonary venous pressure without LV failure (eg mitral stenosis) ii. Increased pulmonary venous pressure secondary to left ventricular failure iii. Increased pulmonary capillary pressure secondary to increased pulmonary arterial pressure (so-called overperfusion pulmonary oedema) b. Decreased plasma oncotic pressure due to renal failure, hepatic failure or protein losing enteropathy c. Increased negativity of interstitial pressure i. Rapid correction of pneumothorax with large applied negative pressures (unilateral) ii. Large negative pressures due to acute airway obstruction along with increased end-expiratory volumes (eg asthma, post obstructive pulmonary oedema) 2. Altered alveolar-capillary membrane permeability (acute lung injury / ARDS) a. Pneumonia b. Inhaled toxins (eg phosgene, ozone, chlorine, Teflon fumes, NO2, smoke) c. Circulating foreign substances (eg endotoxin, snake venoms) d. Aspiration of acidic gastric contents e. Endogenous vasoactive substances (eg histamine, kinins) 5

f. Disseminated intravascular coagulation g. Immunological (eg hypersensitivity pneumonitis, drugs esp nitrofurantoin, leucoagglutinins h. Non thoracic trauma (shock lung) i. Massive transfusion j. Pancreatitis 3. Lymphatic insufficiency a. Post lung transplant b. Lymphangitis carcinomatosis c. Fibrosing lymphadenitis (eg silicosis) 4. Unknown or incompletely understood mechanism a. High altitude pulmonary oedema b. Neurogenic pulmonary oedema c. Heroin overdose d. Pulmonary embolism e. Preeclampsia f. Post cardioversion g. Post anaesthesia h. Post cardiopulmonary bypass

frequently seen in intensive care.

This tutorial will look at examples of the types of pulmonary oedema most

4.2.2

Differential diagnosis

Differential diagnosis is most specifically between cardiogenic and non

cardiogenic causes. The traditional approach to differential diagnosis is as follows2: Cardiogenic Pulmonary Oedema Usually Low-flow state (cool peripheries) Present Present Wet Usually absent

History Acute cardiac event

Noncardiogenic Pulmonary Oedema Uncommon (but possible) High-flow state (warm periphery, bounding pulses) Absent Absent Dry Present

Physical examination
Cardiac output state

S3 gallop Jugular venous distension Crackles Underlying noncardiac disease (eg peritonitis)

Laboratory tests

ECG CXR Cardiac enzymes Pulmonary capillary pressure Intrapulmonary shunting Oedema fluid/ serum protein ratio

Ischaemia/infarction Perihilar distribution May be elevated >18 mmHg Small <0.5

Usually normal Peripheral distribution Usually normal <18 mmHg Large >0.7

A lot of this is often grey in reality. It is impossible to distinguish between cardiogenic pulmonary oedema, ARDS and pulmonary haemorrhage just on a CXR. Prompt echocardiography provides the key to the differential diagnosis. Recent work also suggests B-natriuretic peptide is a useful marker of abnormal LV function.

4.2.3

Cardiogenic pulmonary oedema

Three stages are described1. During stage 1 the elevated left atrial pressure leads to distension and recruitment of small pulmonary vessels and may actually improve gas exchange in the lungs. Often the only symptom at this point is exertional dyspnoea, associated with fine crackles on chest examination. In stage 2 interstitial oedema develops in the loose perivascular interstitial space, leading haziness and loss of hilar demarcation on the CXR, with thickening of the interlobular septa (Kerley B lines). Significant V/Q mismatch leads to hypoxaemia and tachypnoea. In stage 3 alveolar flooding leads to severe hypoxaemia and often hypocapnoea and a severe shunt can develop due to ongoing perfusion of the flooded alveoli.

4.2.4

Noncardiogenic pulmonary oedema

Common intensive care scenarios include acute lung injury / ARDS, head trauma, and subarachnoid haemorrhage. Other rarer possibilities include the hyperosmolar hyperglycaemic syndrome (HHS), tocolytic therapy and preeclampsia. Post obstruction pulmonary oedema is caused by the markedly negative thoracic pressure generated during forced inspiration against a closed airway, with transudation of fluid from pulmonary capillaries into the interstitium. Neurogenic pulmonary oedema is poorly understood but is probably due to central sympathetic nervous system overactivity, leading to sudden onset of clinical pulmonary oedema, hypoxaemia, poor lung compliance and bilateral pulmonary infiltrates. Treatment is with adequate sedation and PEEP. blockade is occasionally necessary.

4.2.5

Paediatric pulmonary oedema

Pulmonary oedema in the neonatal period mandates an echocardiogram to exclude coarctation of the aorta, patent ductus arteriosus, critical aortic stenosis and total anomalous pulmonary venous return. Other possibilities include erythroblastosis foetalis, the placental transfusion syndrome, fluid therapy and myocarditis.

4.2.6

Treatment

Treatment has traditionally has been according to the mnemonic LMNOP, ie L Lasix (frusemide or other loop diuretic) M Morphine, which reduces anxiety and the sensation of breathlessness and may cause some vasodilation N Nitrates, either topical or intravenous glyceryl trinitrate (GTN) for vasodilation O Oxygen P Pressure, in the form of facemask CPAP. CPAP reverses hypoxaemia, recruits alveoli, reduces intrapulmonary shunt, and LV afterload. 10 cm H20 CPAP should be standard therapy in moderate and severe cardiogenic pulmonary oedema4,5. There is no evidence that BiPAP or PSV improves outcomes over CPAP and it is possible there is a higher rate of myocardial infarction with BiPAP6. The use of diuretics is becoming controversial7. Patients with true acute LV failure are not fluid overloaded, and filling pressures are raised by the intense vasoconstriction. Particularly as the patient starts to vasodilate he or she may be significantly hypovolaemic and actually need to be given fluid to maintain cardiac output. Injudicious use of diuretics can make a tenuous situation much worse8,9! Subsequent treatment may include inotropes if required for a low cardiac output state. ACE inhibition and blockade is commenced as soon as it is safe to do so. The patient may well then need investigation of the coronary vasculature and possible revascularisation.

4.2.7

Echocardiographic assessment of cardiac function

A full examination is required, including assessment of LV systolic and diastolic function, cardiac output, RAP and LAP, and valvular function Echocardiographic findings in pulmonary oedema can include: 1. Impaired LV systolic and diastolic function (isolated LV diastolic dysfunction is not uncommon) 2. Valvular dysfunction (MR, MS, AR, AS) 3. Intracardiac shunt 4. Normal (suggesting noncardiogenic cause)

4.3 Case Scenario # 1

4.3.1 Clinical Scenario

A 72 year old man presents to the emergency department in respiratory distress, after waking up unable to breathe. He is an ex smoker with chronic obstructive pulmonary disease and has coronary artery disease with a history of myocardial infarction 5 years ago. He has type 2 diabetes controlled with metformin. Other medications include aspirin, digoxin, atenolol and lisinopril. His usual exercise tolerance is poor, limited by the osteoarthritis in his knees and hips. The ambulance had given him nebulised salbutamol for his respiratory distress. At triage he had a heart rate of 84/min, a blood pressure of 88/45, a respiratory rate of 32/min and an SpO2 of 84%. He was coughing pink sputum and was moved promptly to a resuscitation area. He improves after initial treatment including facemask CPAP, but remained CPAP dependent and hypotensive with a blood pressure of 85/40. An intensive care assessment is requested. The intensivist performed an echocardiogram in the emergency department. 4.3.2 What Is Your Differential Diagnosis? Check your answers

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4.3.3 Look at the Following Echocardiography Images CASE1_1

CASE1_2

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CASE1_3

CASE1_4

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