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play_arrowFactors affecting Mixed Venous Oxygen Saturation
Dr Swapnil Pawar Written by Dr Madhuri Anupindi

Mixed venous oxygen saturation is measured from blood in the pulmonary artery, which contains blood mixed in the right ventricle and is, therefore, representative of oxygen extraction for the whole body. Mixed venous oxygen saturation is a surrogate marker for the overall balance between oxygen delivery and oxygen consumption. It is, therefore, dependent on factors affecting oxygen delivery and oxygen consumption.

Factors affecting oxygen delivery: any factor decreasing oxygen delivery will decrease mixed venous oxygen saturation: oxygen delivery = CO x oxygen content (oxygen content = maximal oxygen-carrying capacity of blood (variably quoted between 1.34 and 1.39) x haemoglobin concentration x haemoglobin oxygen saturation) + solubility constant for oxygen at 37 degrees (0.03ml/L/mmHg) x pa02

Cardiac output: heart rate x stroke volume, stroke volume affected by preload, afterload and contractility
Haemoglobin concentration: affected by conditions such as anaemia
Oxygen saturation of haemoglobin: factors shifting the oxygen haemoglobin dissociation curve will affect the oxygen saturation of haemoglobin
- Factors shifting the curve to the right will decrease haemoglobin’s affinity for oxygen and therefore decrease mixed venous oxygen saturation
  - Acidosis, increased carbon dioxide levels, increased 23DPG concentration, increased temperature
- Factors shifting the curve to the left will increase haemoglobin’s affinity for oxygen and therefore increase mixed venous oxygen saturation
Pao2: increased pao2 increases mixed venous oxygen saturation (hyperbaric, hyperoxia), decreased pao2 decreases mixed venous oxygen saturation  can be caused by lung disease, hypoventilation, diminished inspired oxygen content, right to left shunt)

Factors affecting oxygen consumption: oxygen consumption = cardiac output x (the content of oxygen in arterial blood – the content of oxygen in venous blood)  increased oxygen consumption will decrease mixed venous saturation, and decreased oxygen consumption will increase mixed venous saturation

Metabolic demand
- Increased metabolic demand, e.g. sepsis, hyperthyroidism, fever, shivering, pain, exercise, and stress will increase oxygen consumption.
- Decreased metabolic demand, e.g. analgesia, sedation/paralysis, hypothermia, will decrease oxygen consumption.
Oxygen utilisation
- Histiotoxic hypoxia: cyanide poisoning, Beri-beri  tissues unable to use delivered oxygen; therefore oxygen consumption decreased and mixed venous saturation increased.
- Microvascular shunting in sepsis: increased mixed venous saturation

The post Factors affecting Mixed Venous Oxygen Saturation first appeared on Critical Care Education.

play_arrowPharmacology of 4% Albumin
Dr Swapnil Pawar Written by Dr Madhuri Anupindi

Pharmacology of 4% albumin

Presentation: 4% albumin is a clear, slightly viscous liquid that is often yellow in colour. It comes in a single glass bottle with three different sizes available; 2g in 50ml, 10g in 250ml or 20g in 500ml.

Pharmaceutics: Albumin is manufactured from donated human plasma using mainly chromatographic techniques. It is a preservative free, sterile solution which is iso-oncotic with human serum. It contains 40g/L of human albumin and approximately 140mmol/L of sodium, 128mmol/L of chloride, and 6.4mmol/L of octanoate. It has an osmolality of about 260mOsm/kg and a pH of between 6.7-7.3. It contains no antimicrobial preservatives and should be used immediately after opening the bottle.

Indications:

Used for fluid resuscitation  ongoing debate about utility versus crystalloids but often used as part of burns resuscitation, fluid resuscitation if concerns about volume overload or significant volume of crystalloid already given, in fat embolism, cirrhotic patients or hepatorenal syndrome
Volume replacement: plasmapheresis, large volume paracentesis, post-operative cardiothoracic patients

Pharmacokinetics: (extrapolated from human albumin)

Administration: intravenously
Distribution: within the body total albumin is usually 4-5g/Kg of which 40-45% is intravascular and 55-60% is extra-vascular. These percentages can vary depending on capillary permeability with conditions resulting in increased permeability e.g. sepsis potentially resulting in an increased percentage of albumin within the extra-vascular compartments.
Elimination: the circulation half-life is about 16 hours, and the elimination half-life is approximately 19 days. It is mainly eliminated intracellularly through lysosome proteases which degrade it into amino acids.

Pharmacodynamics:

Cardiovascular
- It helps to maintain plasma colloid osmotic pressure, hopefully thus more effectively expanding intra-vascular volume.
- Protects glycocalyx: the glycocalyx contributes to endothelial barrier integrity, regulation of vascular tone and inhibition of leucocyte adhesion
Metabolic
- Transports multiple drugs and hormones: can affect half-life and serum levels of certain drugs, e.g. phenytoin
- Is a weak acid: comprises the majority of total extracellular acid in human plasma
- Negative acute phase reaction protein
Immunomodulatory
- Protects endothelium and reduces endothelial dysfunction:
  - Modulates arachidonic acid release and protects against ischaemia and reperfusion injury
  - Inhibits apoptosis triggered by oxidative stress by scavenging reactive oxygen species

Adverse effects:

Allergic reactions, including anaphylaxis, nausea, urticaria, increased salivation, mild
Hypotension
May worsen mortality in TBI (SAFE study)
Fluid overload
Blood product so the risk of disease transmission (lowered due to infectious screening of plasma donors, viral inactivation/removal procedures used

The post Pharmacology of 4% Albumin first appeared on Critical Care Education.

play_arrowICU Primary Snippet – iNO & Prostacyclins
Dr Swapnil Pawar Notes by Dr Madhuri Anupindi

Nitric oxide:

Mechanism of action:

Rapidly absorbed into pulmonary circulation  Activates guanylate cyclase (soluble enzyme in cytosol version – natural version is membrane found protein)  converts GTP into cGMP  activates protein kinase G  inhibits IP3-mediated release of calcium, phosphorylates voltage gated ca channels (inactivates), phosphorylates phospholamban (regulates ca pump) which increases ca uptake in sarcoplasmic reticulum  smooth muscle relaxation  pulmonary vasodilation in ventilated regions  hopefully increases VQ matching

Potential adverse effects

Methemoglobinemia
- Nitric oxide reacts with oxyhaemoglobin to form metHb and nitrate and with deoxyhaemoglobin to form nitrosyl haemoglobin  this is converted to methaemoglobin on exposure to oxygen.
- Nitric oxide can also combine with oxygen and water to produce nitrogen dioxide, and nitrite, which can interact with oxyhaemoglobin to produce methaemoglobin and nitrate formation of nitrogen dioxide depends on the nitric oxide concentration, fio2 and the amount of time they are exposed to each other
Adverse effects from nitrogen dioxide: worsens ARDS, bronchiolitis, pneumonitis, airway injury
Renal failure (RR 1.6)
Rebound pulmonary hypertension and hypoxia with abrupt withdrawal
Platelet inhibition
Increased blood flow to the left heart  may cause APO if LV dysfunction.

Inhaled prostacyclin:

Mechanism of action:

Derivative of arachidonic acid
activates G protein-coupled receptors on platelets, and vascular endothelial cells,
activates adenylate cyclase,
increases intracellular cAMP
inhibits further platelet activation + activates protein kinase A
phosphorylates and inhibits myosin light chain kinase
smooth muscle relaxation and vasodilatation
cAMP inhibits platelet aggregation (prevents increased intracellular calcium)

Potential adverse effects

System vasodilatation
- Flushing
- Headache
- Hypotension + tachycardia
Bronchospasm
May increase the risk of bleeding (inhibits platelet function)
Glycine (sterile diluent) can block expiratory filter
increases resistance
Decreased gastric emptying
Inhibition of gastric acid secretion

The post ICU Primary Snippet – iNO & Prostacyclins first appeared on Critical Care Education.

play_arrowICU Primary Snippet – Clot formation following vessel injury
Dr Swapnil Pawar Snippet 4 - hemostatic events following vessel injury 2
The post ICU Primary Snippet – Clot formation following vessel injury first appeared on Critical Care Education.

play_arrowICU Primary Snippet 3 – Smooth Muscle cell contraction
Dr Swapnil Pawar Smooth muscle contraction and relaxation
The post ICU Primary Snippet 3 – Smooth Muscle cell contraction first appeared on Critical Care Education.

play_arrowICU Primary Snippet 2 – Serum Creatinine and Creatinine Clearance
Dr Swapnil Pawar Primary Snippet 2
The post ICU Primary Snippet 2 – Serum Creatinine and Creatinine Clearance first appeared on Critical Care Education.

play_arrowICU Primary Snippet 1 – Critical Illness and Pharmacokinetics
Dr Swapnil Pawar Primary snippet 1
The post ICU Primary Snippet 1 – Critical Illness and Pharmacokinetics first appeared on Critical Care Education.

play_arrow ICU Primary Bedside Preparation – IV Albumin, PRBC and Blood grouping Dr Swapnil Pawar Join us in this episode, where we discuss the pharmacology of IV albumin, PRBC, along with the process of blood grouping and cross-matching.

The post ICU Primary Bedside Preparation – IV Albumin, PRBC and Blood grouping first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside preparation – Blood Thinning Agents Dr Swapnil Pawar Join us as we discuss the pharmacology and pharmacokinetics of blood thinning agents commonly used in the Intensive Care setting. Test yourself on our fun fact questions and more.

The post ICU Primary – Bedside preparation – Blood Thinning Agents first appeared on Critical Care Education.

play_arrow ICU Primary: Bedside Preparation – Renal Physiology Dr Swapnil Pawar In this episode we discuss renal physiology, the concept of renal blood flow versus renal plasma flow, and the impact of renal failure on drug clearance.

The post ICU Primary: Bedside Preparation – Renal Physiology first appeared on Critical Care Education.

play_arrow ICU Primary: Bedside Preparation- Liver functions, Hepatic blood flow and Cytochrome system Dr Swapnil Pawar In this podcast, we discuss liver functions, hepatic blood flow and regulation and the role of the Cytochrome system in drug metabolism.

The post ICU Primary: Bedside Preparation- Liver functions, Hepatic blood flow and Cytochrome system first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside Preparation – Neuromuscular Blockade Dr Swapnil Pawar In this episode, we discuss the physiology of neuromuscular junction, the pharmacology and the principles of neuromuscular monitoring.

The post ICU Primary – Bedside Preparation – Neuromuscular Blockade first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside Preparation – Bleeding Trauma Patient Dr Swapnil Pawar

The post ICU Primary – Bedside Preparation – Bleeding Trauma Patient first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside preparation – An Elderly patient Dr Swapnil Pawar In this episode, we discuss the physiology and pharmacology relevant to an elderly patient admitted to the intensive care unit.

The post ICU Primary – Bedside preparation – An Elderly patient first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside Preparation Part 7 – Thermoregulation Dr Swapnil Pawar In this episode, we discuss 1. How does thermoregulation work in Santa? 2. How does a thermometer work? 3. What are the physiological effects when Santa returns to the North Pole?

The post ICU Primary – Bedside Preparation Part 7 – Thermoregulation first appeared on Critical Care Education.

play_arrow ICU Primary Bedside Preparation Part 6 Dr Swapnil Pawar In this episode, we cover 3 key topics – Carbohydrate metabolism Pharmacology of TPN Measurement of BMR

The post ICU Primary Bedside Preparation Part 6 first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside Preparation Part 5 Dr Swapnil Pawar In this episode, we discuss the pharmacology of oxygen, the physics behind oxygen sensors in the ventilator and the mechanism of oxygen delivery.

The post ICU Primary – Bedside Preparation Part 5 first appeared on Critical Care Education.

play_arrow ICU Primary Bedside Preparation Part 4 Dr Swapnil Pawar In this episode, we discuss the bedside preparation for the ICU Primary exam. The key topics discussed in this podcast – Anatomy of brainstem reflexes Pharmacology of mannitol and hypertonic saline Pharmacology of Phenytoin and Levetiracetam.

The post ICU Primary Bedside Preparation Part 4 first appeared on Critical Care Education.

play_arrow ICU Primary Bedside Preparation – Part 3 Dr Swapnil Pawar In this episode, we use the modified Pomodoro technique for bedside Primary exam preparation. We examine the neurointensive care patient to discuss the anatomy of CSF production, Cerebral blood flow regulation and physics of ICP monitoring.

The post ICU Primary Bedside Preparation – Part 3 first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside preparation Part 2 Dr Swapnil Pawar In this episode, we discuss the modified Pomodoro technique to help Primary candidates prepare for their exams during daily bedside ward rounds. 3 questions were discussed in this episode – Pulse oximeter, Comparison between Noradrenaline and vasopressin, and physiological [...]

The post ICU Primary – Bedside preparation Part 2 first appeared on Critical Care Education.

play_arrow ICU Primary – Bedside preparation Part 1 Dr Swapnil Pawar In this episode, Dr Mike Clifford and I discuss how every ICU trainee can prepare for their primary exams on their day to day ward rounds. We suggest using the modified Pomodoro technique i.e – 3 questions at one [...]

The post ICU Primary – Bedside preparation Part 1 first appeared on Critical Care Education.

play_arrow

Primary Viva – Morphine & BMR

Dr Swapnil Pawar

In this episode, Mike Clifford walks us through his thought process in designing this probing viva on Morphine and BMR.

The post Primary Viva – Morphine & BMR first appeared on Critical Care Education.

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Viva 2 – Cerebral Blood Flow and NMDA Receptor

Dr Swapnil Pawar

Viva written by – Dr Mike Cliford In this episode, we talk about the meta-thinking approach of the college examiner in designing vivas and walk through the viva on cerebral blood flow and NMDA receptor.

The post Viva 2 – Cerebral Blood Flow and NMDA Receptor first appeared on Critical Care Education.