This is the first tutorial in the cardiovascular assessment module. In the tutorial I discuss heart rate, how it originates and how it is controlled. This is principally a discussion about sinus bradycardia and sinus tachycardia. I go on to discuss the parasympathetic nervous system and the sympathetic nervous system, how they function physiologically and how they are impacted by drugs that we administer and disease processes. I provide a detailed discussion of adrenoceptor agonists and antagonists.
I feel like I have been working on this tutorial for several years. I actually have. When one encounters a modern chest drain unit in ICU for the first time or the 50th time it can be quite daunting. How much is draining? Is it oscillating? What does “bubbling” imply? When do you use suction? Why do some nurses leave a meniscus of fluid in the tubing but others don’t? What is the little red cap supposed to do?
This tutorial starts with a discussion of the physiology of pneumothorax and hemothorax, and then progressively visits one bottle, two bottle and three bottle systems. I then go on to explain how relatively modern chest drainage systems work, and how they need to be modified to apply suction – wet and dry. Finally I explain how very modern digital chest drainage systems work.
If you have struggled with understanding chest drains, I guarantee you’ll learn something.
The majority of patient who are admitted to ICU require targeted oxygen therapy during the course of their stay. This tutorial looks at how we assess oxygenation.
The easiest method for assessing oxygenation is to use the PaO2/FiO2 ratio (PFR) as a method of aligning the inspired oxygen tension (the therapy) to the PaO2 (the goal and the response). The PF ratio has been a key component of the diagnostic criteria for ARDS for decades. The PaO2 is measured by performing a blood gas. It represents dissolved oxygen in plasma rather than the oxygen content of blood that is determined by the oxyghemoglobin concentration and saturation (SaO2). The SaO2 can be helpfully estimated using non invasive pulse oximetry (SpO2).
Oxygen is taken up from the lungs continuously and carbon dioxide is excreted. Breathing is cyclical. Most gas exchange occurs during expiration, as inspiration only occupies 10 seconds or so per minute. The lungs hang down in the chest and hang out at a resting volume known as Functional Residual Capacity (FRC) at end expiration. Anything that reduces FRC, reduces the surface area for gas exchange and results in stale gas in or atelectasis of the alveoli. The consequence is ventilation perfusion mismatch and hypoxemia.
The initial treatment for hypoxemia is oxygen therapy delivered through nasal cannula. If that fails, or the patient is distressed, then high flow nasal oxygen (HFNO) is delivered. This improves oxygenation and reduces the work of breathing. If high flow fails, CPAP is delivered. CPAP applies positive pressure throughout the respiratory cycle, preventing phasic atelectasis and redistributing gas withing the lung. FRC is restored. If the patient fails HFNO, then they are intubated and ventilated.
Oxygen is assessed using FiO2, oxygen flow rate, PEEP or CPAP and mean airway pressure.
This tutorial looks at hypernatremia and hyperosmolar syndrome. Hypernatremia is usually caused by three things: 1) Profound dehydration, 2) Too much sodium intake – most of the time this is due to over-resuscitation with isotonic fluids, 3) Central or Nephrogenic Diabetes Insipidis. I explain how to calculate water deficit and water replacement and how to evaluate and treat patients with diabetes insipidus. @ccmtutorials
This discussion came about following a discussion with my colleague, Dr Bairbre McNicholas. It focuses principally on the problem of hyponatremia in elderly patients and undernourished alcoholics. I explain why the lack of dietary salt and protein intake massively inhibits water excretion resulting in hypotonic hyponatremia, often with fluid overload. The traditional approach to managing hyponatremia – fluid restriction – frequently fails because it is a problem of solute “underload” rather than water overload. Commencing iv fluids may precipitate a rapid and potentially dangerous diuresis – hence the most effective therapy for these patients is the FEED them.
Patients who present with symptomatic hyponatremia (usually the Na+ is lower than 120mmol/L) should be treated with hypertonic saline (HTS) and then fluid restricted. The goal of HTS therapy is to reverse the symptoms and raise the plasma Na+ by 5mmol per liter. What then? It depends on the circumstance – acute or chronic, high risk or low risk. This tutorial addresses the issue of rate of correction of plasma sodium, explains why you need to modify that rate in high risk patients (very low sodium, alcoholics, the malnourished, those with liver disease and profound hypokalemia). The reason why you need to be careful is because of concerns regarding the development of Central Pontine Myelinolysis – usually known now as Osmotic Demyelination Syndrome.
I wish to acknowledge the help of my colleagues Dr Bairbre McNicholas, Dr Peter Moran, Prof. John Bates, Dr Leo Kevin and Ms Aoife Boyle for clarifying my thoughts on this topic.
Click on this link for the 2014 European Guidelines (and a good review of the topic).
This tutorial is about the Syndrome of Inappropriate Diuresis. SIAD also known as SIADH is a form of hypotonic hyponatremia associated with iso- or hypervolemia, high urinary osmolality and high urinary sodium. Traditionally this is associated with high levels of circulating vasopressin (antidiuretic hormone – ADH), that may be associated with sepsis, acute critical illness, pneumonia or mechanical ventilation. However, SIAD is also associated with a variety of brain injuries, drugs (SSRIs and anticonvulsants) and a variety of cancers.
Treatment of symptomatic SIAD is with hypertonic saline (150ml of 3% over 20 minutes). Chronic or asymptomatic SIAD is treated with fluid restriction (determined by the Furst equation uNa + uK/pNa – if the result is less than1 the patient is suitable for fluid restriction).
Alternative inexpensive therapies include Urea (30 to 60mg per day), salt tablets plus frusemide or demeclocycline.
Vaptan agents, the block the V2 receptors, appear to be effective for long term therapy. Tolvaptan is available commercially but quite expensive for the majority of patients.
Cerebral salt wasting is associated with subarachnoid hemorrhage. It shares the same blood and urinary profile as SIAD(H) but is associated with hypovolemia. The disorder is self limiting and is treated with isotonic fluids.
If you treat patient with hypoxic respiratory failure you really need to understand what is going on in their lungs. These two tutorials look at diseases of the lung parenchyma and how blood flow and gas flow interact. The first tutorial focuses on alveolar oxygen content and how it is impacted by disease. I explain the concept of airway closure (which will will revisit in detail several times during this series), stale alveolar gas, the various causes of atelectasis and the six S approach to figuring out what is going on in the airways (Slimy, Soggy, Sticky, Stiff, Squished, Shunty).
The next part of the course is all about hypoxic respiratory failure. To treat hypoxemia you must understand it. The purpose of this sequence of tutorials is to lead up to discussions on CPAP and PEEP and provide a platform for understanding Pressure Controlled Modes of Ventilation. The first tutorial looks at oxyhemoglobin saturation, why the oxyhemoglobin dissociation curve is essential knowledge for the practicing clinician, how pulse oximeters work and how to quantify hypoxemia (A-aO2 gradient and PaO2/FiO2 ratio).
ORtoICU 