Some Games on Anaesthetist.com

Some Games on Anaesthetist.com

Asthma Cardiac Arrest

Asthma Cardiac Arrest

In the early 1990’s at  the Alfred Hospital in Melbourne a young man was admitted in extremis with severe asthma. He had had many previous admissions some requiring ICU. He was intubated and ventilated, and given salbutamol and adrenaline.

However he went into asystole and was given all resuscitation measures but a rhythm could not be established. His pupils became dilated and fixed and further resuscitation was considered futile.

He was disconnected from the self-inflating bag and most of the staff left the room. After a few minutes a nurse noted that the patient had developed sinus rhythm. Staff were recalled and ventilation was recommenced.

However shortly afterwards he became pulseless  and again went into asystole. After some time resuscitation was again declared unsuccessful. Following disconnection from the breathing system the patient again developed a rhythm and pulses. Each subsequent time he was ventilated the same thing happened.

The staff realized that IPPV was causing the problem. Gentle ventilation with a slow respiratory rate was continued. The patient subsequently made a full recovery. This cases was written up in the journal “Anaesthesia and Intensive Care” in 1991 Vol 19 pp 118-121. Similar cases have since been published.

The problem here was gas trapping leading to high intrathoracic pressure which prevented venous return to the heart and resulted in cardiac arrest.

It is now appreciated that care must be taken with ventilation in asthma to allow ample time for expiration. A low respiratory rate of perhaps 6 breaths per minute should be combined with a long I:E ratio (say 1:6) to prevent gas trapping. Some level of “permissive” hypoxia and hypercarbia  is now considered to lead to better outcomes in ventilated asthmatic patients in preference to gas trapping.

There is not much point having oxygen in the lungs if there is no cardiac output to deliver it to vital organs.

Take Home Message:

Avoid high intra-thoracic pressures and gas trapping in ventilated patients with asthma.

This also applies to shocked patients where blood is returning to the thorax at very low pressure.

 source: http://www.anaesthesiacases.com.au/cases/asthma_cardiac_arrest

Anaesthesia Points to Remember

Beware of conus injuries from needling the spinal cord during spinal anaesthesia. It can lead to lifelong disability and pain. Once you insert your spinal needle more than one space above a line joining the iliac crests then the risks start to escalate.

Maintain adequate levels of blood pressure during anaesthesia. Hypotension  under anaesthesia  continues to be associated with increased morbidity and mortality. Patient age and co-morbidities should influence the minimum acceptable blood pressure. 

The recommended dose of morphine for an IV PCA  should not be greater than 1 mg with a 5 minute lockout, except in opiate dependent patients.

There is no point giving a test dose of antibiotic IV unless you perform minute dilutions into one litre of crystalloid and run it into the patient slowly.

Blood needs to be carefully checked to ensure the correct patient is receiving the correct blood. Errors continue to occur. Mismatched blood transfusion carries a high mortality rate.

When injecting significant amounts of LA it is recommended to have patients awake and communicative to reduce the likelihood of LA toxicity

Aspiration prior to injection does not rule out being intravascular (the side of the vessel wall can be sucked against the bevel of the needle).

Slow injection of LA is essential while maintaining communication with the patient: “Tell me if you are experiencing anything unusual”.

Longer acting LA’s such as bupivacaine  and ropivacaine have a higher incidence of LA toxicity than shorter acting ones such as lignocaine or prilocaine.

LA toxicity with mortality and major morbidity continues to occur.

Laryngeal tumours can create major airway difficulties for anaesthesia with airway obstruction and bleeding

Patients with laryngeal tumours ideally should have an MRI prior to anaesthesia.

Beware of gas trapping with IPPV in patients with respiratory conditions such as asthma and cystic fibrosis. This can lead to cardiovascular collapse. Such patients require reduced respiratory rates and longer I:E ratios to allow sufficient time for gas to be exhaled.

In patients with gastric outlet obstruction be prepared for regurgitation of large volumes of gastric fluid or blood.

Naloxone can precipitate massive sympathetic response with pulmonary oedema. Giving divided doses may diminish this effect.

Take care not to have malleable stylets protruding out the end of ETTs as they can also cause tracheal damage.

Jet ventilation must be used with considerable caution as surgical emphysema and pneumothoraces have been frequently reported. Care must be taken to ensure the upper airway is not obstructed. Gas needs to be able to get out as well as get in.

TIVA continues to be associated with awareness under anaesthesia.

Gas insufflation at laparoscopy can cause asystole or profound bradycardia. Careful monitoring is required. Treatment may require allowing the gas to escape rapidly.

Negative pressure pulmonary oedema may occur following emergence from anaesthesia in younger patients. CPAP or IPPV will usually be required.

Syringe swap continues to cause problems. Take extra care with muscle relaxants and vasopressors.

If your patient is hypotensive consider anaphylaxis, particularly if you have given muscle relaxants or antibiotics. There are many case reports of patients receiving  significant doses of metaraminol and ephedrine prior to anaesthetists starting definitive treatment of anaphylaxis with adrenaline.

source: http://www.anaesthesiacases.com.au/opinion/topics/anaesthesia_points_to_remember

"Take a pencil and paper," the teacher said, "and write an essay with the title 'If I Were a Millionaire.'"

Everyone but Philip began to write furiously. He just leaned back in his chair and folded his arms.

"What's the matter," the teacher asked. "Why don't you begin?"

"I'm waiting for my secretary," he replied

pulmonary function tests

pulmonary function tests

1. spirometry

spirometry is used to measure how much air can be taken in and out as wellas how fast air can move also in and out.
the spirometry is used for the following 3 tests:

• flow volume loops

flow volume loops provide a graphical illustration of a patient`spirometric efforts. flow is plotted against volume to display a contiuous loop from inspiration to expiration.
the loops show FVC and FEV1.
FEV1/ FVC is normally 80%.

COPD: decrease in expiratory flow rate at any giving lung volume, invrease in residual volume.
restrictive disease; decrease in all lung volumes.
fixed large airway ostruction: plateau in both ispiratory and expiratory cycles.
variable extrathoracic obstruction: plateau in the inpiratory limb.

• The severity of the abnormality might be graded as follows:
• May be a physiologic variant: Predicted FEV₁ ≥100%
• Mild: Predicted FEV₁ <100% and ≥70%
• Moderate: Predicted FEV₁ <70% and ≥60%
• Moderately severe: Predicted FEV₁ <60% and ≥50%
• Severe: Predicted FEV₁ <50% and ≥34%

case discussion

hi, here I post this case for open discussion. let us think together and try to answer these questions. I am waiting for your valuable contributions.


A 56-year-old coal miner requires sigmoid colectomy for carcinoma. He has a home nebuliser. His FEV1 is 0.68 litres, and he has 3% reversibility with salbutamol.

Observations/examination Shortness of breath 50 yards. 
Wheezy chest 
Respiratory rate 30/min 
Non-productive cough 
Chest X-ray: bullous lung disease and prominent pulmonary arteries 
ECG: normal 
Saturations: 93% on air. PO2 12 kPa; PCO2 4.5 kPa 
No FBC 
No electrolytes 

Drugs 
He is currently taking 2.5 mg prednisolone (the dose was recently reduced) 

Questions 1. Summarise the case. 
2. What are the main issues? 
3. How would you optimise this patient preoperatively? 
4. What is the likely cause of his COPD? 
5. Present the chest X-ray. 
6. What are the chest X-ray findings in pulmonary hypertension? 
7. Present the ECG. 
8. What ECG findings might you find? 
9. What are the ECG changes seen in heart strain (left and right)? 
10. What are the criteria for pathological Q waves? 
11. What is respiratory failure? 
- Give blood gas definitions of type 1 and 2 respiratory failure 
12. What are blue bloaters and pink puffers? 
- Which is this patient? 
13. How would you anaesthetise this man? 

ArticleDate:20070524 

Oxygen content of blood

The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct measurement gives a capacity of 1.34 ml O2/g Hb.
1.34 is also known as Hüfner’s constant.

The oxygen content of blood is the volume of oxygen carried in each 100 ml blood.
It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023 x PaO2)

Where:

 SO2 = percentage saturation of Hb with oxygen
 Hb = haemoglobin concentration in grams pre 100 ml blood
 PO2 = partial pressure of oxygen (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg)

For a normal adult male the oxygen content of arterial blood can be calculated:

Given arterial oxygen saturation (SpO2) = 100%, Hb = 15 g/100 ml and arterial partial pressure of oxygen (PaO2) = 13.3 kPa, then the oxygen content of arterial blood (CaO2) is:
CaO2 = 20.1 +0.3 = 20.4 ml/100 ml

Similarly the oxygen content of mixed venous blood can be calculated.  Given normal values of mixed venous oxygen saturation (SvO2) = 75% and venous partial pressure of oxygen (PvO2) = 6 kPa, so:
CvO2 = 15.2 + 0.1 = 15.2 ml/100 ml

Oxygen delivery (DO2) and oxygen uptake (VO2)

Oxygen delivery is the amount of oxygen delivered to the peripheral tissue, and is obtained by multiplying the arterial oxygen content (CaO2) by the cardiac output (Q).  For CaO2 = 20.1 ml/100 ml and Q = 5 l/min:

Oxygen delivery (DO2) = 1005 ml/min

The oxygen returned is given by the product of the mixed venous oxygen content (CvO2) and the cardiac output.  For CvO2 = 15.2 ml/100 ml and Q = 5.0 l/min:

Oxygen return = 760 ml/min

Oxygen uptake is the amount of oxygen taken up by the tissues that can be calculated from the difference between oxygen delivery and the oxygen returned to the lungs in the mixed venous blood.

Thus

Oxygen uptake (VO2)  = (oxygen delivery) – (oxygen return) = 1005 – 760 = 245 ml/min

To Summarise:

The primary goal of the cardio respiratory system is to deliver adequate oxygen to the tissues to meet their metabolic requirements, a balance between VO2 and DO2.
The balance between oxygen uptake by the body tissues and oxygen delivery to them is assessed by:

 The oxygen content of mixed venous blood CvO2, which is normally about 15 ml/100 ml
 The extraction ratio, which is the ratio of VO2 to DO2 expressed as a percentage.  Normally the extraction ratio is about 25% but can double to 50% if tissue demand increases

Both of the above indices are dependant on mixed venous saturation (SvO2), and cardiac output.

The figure shown below illustrates that if the level of haemoglobin is halved, the oxygen content of arterial blood will be halved.

Figure 1: Oxygen dissociation curve (ODC)



Carbon monoxide (CO) interferes with the O2 transport function of blood by combining with Hb to form carboxyhaemoglobin (COHb).  CO has about 240 times the affinity of O2 for Hb.  For this reason, small amounts of CO can tie up a large proportion of the Hb in the blood, thus making it unavailable for O2 carriage.  If this happens, the Hb concentration and PO2 of blood may be normal, but its O2 concentration is grossly reduced.  The presence of COHb also shifts the O2 dissociation curve to the left, thus interfering with the unloading of O2.  This is an additional feature of the toxicity of CO.

The sigmoid shape of the oxygen dissociation curve is a result of the cooperative binding of oxygen to the four polypeptide chains.  Cooperative binding is the characteristic of a haemoglobin to have a greater ability to bind oxygen after a subunit has bound oxygen. Thus, haemoglobin is most attracted to oxygen when three of the four polypeptide chains are bound to oxygen. 

Factors that Influence Oxygen Binding 

 Temperature- Increasing the temperature denatures the bond between oxygen and haemoglobin, which increases the amount of oxygen and haemoglobin and decreases the concentration of oxyhaemoglobin (Schmidt-Nielsen, 1997).  The ODC shifts to the right.

 pH- A decrease in pH by addition of carbon dioxide or other acids causes a Bohr Shift.  A Bohr shift is characterized by causing more oxygen to be given up as oxygen pressure increases. The ODC shifts to the right.

 Organic Phosphates:2,3-diphosphoglycerate (2,3-DPG) is a substance made in the red blood cells. It controls the movement of oxygen from red blood cells to body tissues. Haemoglobin uses 2,3-DPG to control how much oxygen is released once the blood gets out into the tissues. The more 2,3-DPG in the cell, the more oxygen is delivered to body tissues. 2,3 DPG binds to haemoglobin which rearranges the haemoglobin into the T-state, thus decreasing the affinity of oxygen for haemoglobin (T and R State).  The ODC shifts to the right.

Hyperbaric oxygen therapy (HBOT)

This is oxygen therapy at greater than atmospheric pressure, usually 2-3 atmospheres, HBOT increases the amount of dissolved O2 in the blood according to Henry’s law.  In 100 ml blood, 0.3 ml O2 dissolves at PO2 of 13.3 kPa (100mmHg).  Thus for 100% O2 at 3 atmospheres, dissolved O2 = 5.7 ml.  HBOT may be used in the treatment of carbon monoxide poisoning.

source: http://www.frca.co.uk/article.aspx?articleid=100175