- Myasthenia Gravis
- Guillain-Barré syndrome
- Motor neuron disease
ECGs are frequently presented to candidates sitting the OSCE element of the exam, a systematic approach is essential.
- Name, date, calibration (1mv=1cm, 0.2s=1cm [small square 40 msec])
- Rate = 300/number of big squares between Q-Q
- Rhythm AF, tachy (>100), brady (<60), sinus, heart block
- Axis normal = -30° to +110°
P peaked, tall Dright atrial hypertrophy
notched, broad Dleft atrial hypertrophy
P-R >5 small squares
I degree block: prolonged PR interval
II degree block:
Wekeneback: sequential of PR interval
Mobitz typ II: fixed PR, dropped QRS (2:1, 3:1…)
III degree block: disassociation of P and QRS
QRS wide (<2.5 small squares)
MarroW Dright bundle branch block
WilliM Dleft bundle branch block
Q 1mm wide, 2mm/25% of R-wave
D old MI
Normal in lead I, aVL V6
ST raised: 1mm 2xconsangious limb-leads, 2mm chest-leads
Depression: myocardial ischemia
Reverse tick: digoxin effect
Saddle shaped elevation: acute constrictive pericarditis
T peaked hyperkalaemia
Flat, prolonged, hypokalaemia
Normal in III, V1-2 (and V3 in Negroes)
MI: Hyperacute T-waves, ST-elevation T-wave inversion, Q-waves. Inf. (II, III, aVF) Ant. (V1-4), Lat. (I, aVL,V5-6) Post. look at V1-2. New LBBB.
PE: S-I (deep S-waves in I), Q-III (Q-waves in III), T-III (inverted T-waves in III). More generally a sign of R-heart strain.
Hyperkalaemia: tall tented T, wide QRS
Hypokalaemia: flattened T, prominent U, (muscle weakness, cramps, tetany)
ECG Wave-Maven – is a resource with many “barn-door” ECGs, presented in a quiz format; large database, expert explanations.
- Serum sodium concentration <135 mmol/L.
Mild – between 130 and 135 mmol/L
Moderate – between 125 and 129 mmol/L
Profound – less than 125 mmol/L
- Acute – less than 48 h
- Chronic – greater than 48 h
Clinical practice guideline on diagnosis and treatment of hyponatraemia. Intensive Care Med (2014) 40:320–331
Expanded Case Summary by Dr Matthew James Jackson
This case focuses upon the post-operative management of a frail patient who underwent major surgery, then developed multi-organ failure; subsequent liberation from mechanical ventilation took longer than would normally be expected. In this essay I draw upon my previous review of weaning failure . I consider two aspects of management: acid-base and fluid management, both were relevant to this patient.
A 78 year old patient underwent an aortic valve replacement five weeks prior. He presented to hospital following a fall; critical aortic stenosis was subsequently diagnosed. He suffered from hypertension and had a 40 year pack history. He lived alone and was independent with activities of daily living. He had a Body Mass Index of 19 m2 kg-1. Baseline investigations were essentially normal. At a multidisciplinary meeting, primary valve replacement was considered to be the optimal treatment for his condition.
Operative course was uneventful. Intraoperative transoesophageal echocardiography demonstrated a moderately impaired, hypertrophied left ventricle with a good functioning tissue valve. He failed primary extubation due to inappropriate behaviour on cessation of sedation. His first week in critical care included two subsequent attempts of extubation which failed. Following a normal computer tomography scan of his brain, a percutaneous tracheotomy was performed to aid weaning from ventilation.
Into the second week of his admission, oxygen requirements started to increase. He was diagnosed with a ventilator acquired pneumonia on the basis of a raised Clinical Pulmonary Infection Score; antimicrobials were initiated. During the third week ventilation became increasingly difficult: Acute Respiratory Distress Syndrome was diagnosed. During this period he was paralysed on several occasions, proned (to which he responded well) and ventilated with a FiO2 greater than 80% for one week. At the peak of his illness, the patient was haemofiltered for four days.
During the fourth and fifth weeks attempts were made at reducing respiratory support. He was ventilated on Drager Evita 4 using CPAPASB mode with a positive end expiratory pressure (PEEP), pressure support, and fraction of inspired oxygen (FiO2) set at 10 cm H2O, 18 cm H2O and 50%, respectively. Sedative medication, vasopressor and renal support therapy had been ceased. Clinically he was weak and had gross oedema. Regular furosemide had been initiated to off-load interstitial fluid. His arterial blood gas demonstrated a metabolic alkalosis. The patient was hypoalbuminaemic, but other blood parameters were within normal limits. There were no concerns regarding the surgical wound or valve.
We completed a full review of the patient, guided by the ABC approach . We proposed a weaning according to the following plan. To ensure consistency, we gained agreement from the nursing staff, patient and other intensivists on the unit. The plan was:
- Ventilate the patient with volume controlled ventilation overnight (leaving tidal volume, PEEP, and frequency unchanged)
- Use CPAPASB throughout the day, leaving the settings unchanged.
- Initiate breaks in the pressure support – starting with two 20 sessions each day, and increasing session length by 10 minutes each day.
- Use acetazolamide while the patient remained alkalotic.
- Titrate FiO2 to maintain oxygen saturations above 90%
- Stand the patient with the physiotherapy team, and sit in a chair for at least an hour each day.
- Add a small dose of spironolactone to the furosemide already in use
There was good compliance with the plan for the first week; overnight mandatory ventilation was well tolerated. The patient was too weak to stand initially, therefore, he was hoisted into a bucket chair. Five days into the weaning plan, the patient started to diurese 5-7 litres per day. All diuretics were stopped. Towards the end of the week, his FiO2 had fallen to 25%. Overnight mandatory ventilation was then stopped. He spent a further few days receiving decreasing pressures of CPAPASB, mainly overnight, until he was able to spend a whole day on CPAP-only. The tracheostomy cuff was deflated on the tenth day into the weaning plan and he was decannulated on the eleventh.
The patient remained very weak and spent a total of seven weeks in critical care. He was transferred to a care of the elderly ward for 10 days prior to discharge to a rehabilitation ward.
Various terms are used to describe patients who take longer than expected to be liberated from a ventilator [3, 4]. Prolonged weaning, as defined by a pan-European consensus statement, is a combination of failing more than three spontaneous breathing trials (SBT) and requiring more than seven days of mechanical ventilation following the first SBT . This definition fails to account for any deterioration between SBT, underlying causes or appreciated the spectrum of “difficulty” that might be encountered. A more practical concept is that of weaning delay and weaning failure, defined as the need for ventilatory support for more than two weeks in the absence of any non-respiratory factor preventing weaning and the need for ventilatory support for greater than three weeks in the absence of any non-respiratory factor, respectively .
Prolonged weans are common and consume significant resources. A large multi-centre trial of 2,714 patients found that 6% of intensive care admissions had a prolonged admissions due to weaning delay and failure . The only economic analysis published is 25 years old, it concluded that these patients consume 37% of intensive care resources . A robust, systematic approach might therefore be expected to improve the quality and cost of care. Recently, both a practical bed-side approach and an ABC algorithm have been suggested to manage these patients [1, 6]. Two factors through to be contributing to this patients prolong wean, in addition to his poor pre-morbid health, we a metabolic acidosis and gross oedema—both are associated with difficult respiratory weans, however, robust evidence-based treatment options are limited.
Alkalosis is common following a prolonged wean and is often associated with hypochloraemia, hypophosphataemia and hypoalbuminaemia . An over-compensation of respiratory acidosis and diuretic therapy are frequently contributing factors. Acetazolamide, described in one case-series, may be of benefit, although it is not known whether the resulting physiological improvement is associated with long-term benefits  Overnight ventilation is frequently employed by weaning centres to avoid a nocturnal rise in arterial carbon dioxide and “reset” central acid-base regulation .
Positive fluid balance, poor renal function and low serum albumin are each associated with repeatedly failed SBT . Exogenous albumin has been examined in the acute setting, but not in the chronic, difficult-to-wean patient . Albumin may have a capillary sealing effect; however, supplementation to manipulate plasma oncotic pressure appears misguided.
There are few trials in focusing upon difficult to wean patients, therefore practice must be extrapolated from other patient groups. Given the frequency of this problem and the resources consumed, there is an impetus to develop a more robust evidence base to guide practice. Our ability to affect fluid shifts in this patient population has yet to be investigated. It is my belief that the primary problem is protracted capillary dysfunction as a sequelae to multi-organ failure. Therefore, treatments that focus upon reducing total body sodium and water will have little impact unless the capillary function is restored. Whether the metabolic disturbances in these patients is a driving force of the disease state, or merely a marker of illness is yet to be elucidated.
 NHS Modernisation Agency. Critical Care Programme: Weaning and Longterm Ventilation. London; NHS Modernisation Agency: 2002
 Peñuelas O, Frutos-Vivar F, Fernández C et al. Characteristics and outcomes of ventilated patients according to time to liberation from mechanical ventilation. Am J Respir Crit Care Med 2011; 184:430-37
 Wagner DP. Economics of prolonged mechanical ventilation. Am Rev Respir Dis 1989; 140:S14-18
 Webster NR, Kulkarni V. Metabolic alkalosis in the critically ill. Crit Rev Clin Lab Sci 1999; 36:497-510
 Jones PW, Greenstone M. Carbonic anhydrase inhibitors for hypercapnic ventilatory failure in chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2001; (1):CD002881.
 Brignall KA, Davidson AC. Weaning from mechanical ventilation: art or science? Care Crit Ill 2009; 25:22-28.
 Upadya A, Tilluckdharry L, Muralidharan V et al. Fluid balance and weaning outcomes. Intensive Care Med 2005; 31:1643-47.
 27.Martin GS, Mangialardi RJ, Wheeler AP et al. Albumin and furosemide therapy in hypoproteinemic patients with acute lung injury. Crit Care Med 2002; 30:2175-82.