Category Archives: ccmtutorials

What is Critical Care?

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What is Critical Care Medicine?

  • Critical care medicine is the multidisciplinary healthcare specialty that cares for patients with acute, life-threatening illness or injury (SCCM definition).

Critical Care Medicine is a term used in the North America to describe the practice of medicine in intensive care units (ICU). Elsewhere it is known as Intensive Care Medicine (ICM); in Great Britain, ICUs are often referred to Intensive Therapy Units (ITU). A specialist who practices intensive care medicine is known as an intensivist, and has usually been trained and board certified in anesthesiology, surgery, internal medicine or pediatrics.

Critical Care Medicine is a relatively modern specialty; the first intensive care units opened in Europe in the late 1950s and rapidly spread to North America. Certification of training in this field did not occur in the United States until 1986. By the late 1990s, there were approximately 5000 intensive care units in the USA. For many years intensive care was something of a “free for all” struggle between various interest groups, with the patient often caught in the middle. This arose from the mistaken view of many physicians that intensive care patients were merely sicker versions of the patients that they already looked after on the wards. An open ICU model evolved, with the primary physician making the decisions and a support team of specialists acting as consultants. It has since been shown that the presence of a properly trained intensive care physician in the unit significantly reduces morbidity, mortality and cost. Modern critical care units tend to be “semi closed” with a multidisciplinary team, led by an intensivist, managing most aspects of the patient’s care. Limited external consultations take place, aside from microbiology/infectious diseases, radiology, or where specific specialist input may advance patient care (hematology, cardiology etc).

Three factors differentiate intensive care from other wards in hospitals: 1) a very high nurse to patient ratio, 2) the availability of invasive monitoring, 3) the use of mechanical and pharmacological life sustaining therapies (mechanical ventilation, vasopressors, continuous dialysis).

LEVELS OF CARE

As critical care units are specialized hospital wards, it is worthwhile to elaborate on how we label units. There are many ways to do this but the “level of care” paradigm is the most useful.

Level 0 = a standard ward with a nurse to patient ratio (NPR) of 1:6 or higher

Level 1 = advanced ward based care with a NPR of 1:3 or 1:4 – e.g. an extended recovery unit (PACU)

Level 2 = High Dependency Care – the patient usually has single organ failure or requires intensive monitoring, electrolyte replacement or extensive postoperative care (e.g. HDU). NP ratio is 1:2 or 1:3

Level 3 = Intensive Care. The patient may have multi organ failure, requires invasive ventilation and or continuous kidney replacement therapy, or is comatose or requiring aggressive resuscitation. The patient requires 1:1 NPR (UK Ire) – 1:2 USA.

There are several critical care units in any hospital, but they are not always labelled as such:

•Operating rooms and Recovery

•ED Resuscitation areas

•Labour Ward

•Coronary Care

•PACU (extended postoperative recovery)

•High Dependency (HDU)

•Intensive Care (ICU)

The Critical Illness Paradigm

  • Critical illness is a very specific series of disease syndromes that arise from an enormous spectrum of diseases
  • A wide variety of disease processes are treated with a limited number of interventions, in an intensive nursing environment.

Many doctors and nurses have a very poor understanding of what constitutes an intensive care patient: they are not merely standard medical or surgical patients, sicker than normal, perhaps plugged into ventilators. All intensive care patients fit into one of the following categories:

  1. Patients admitted to intensive care for intensive monitoring, in anticipation of possible aggressive interventions: this is the coronary care model.
  2. Patients admitted to units which act as extensions of the post-operative recovery room, allowing abnormal perioperative physiology to reverse, with or without modulation of the normal stress response. Post operative cardiac care is an example of this model.
  3. Patients who require very intense nursing care, which would not be available elsewhere: an example of this is a burns unit.
  4. Patients who do not necessarily require life sustaining treatments, but whose physiology is taken under control in order to prevent organ injury: neurosurgical critical care.
  5. Patients who have minimal physiologic reserve, and who undergo acute potentially reversible injury, requiring life support until the abnormalities have been reversed and reserve restored: this is the archetypical medical intensive care patient (COPD with pneumonia requiring mechanical ventilation).
  6. Patients who undergo a massive disruption to their physiology, due to an overwhelming stress response to injury, or inadequate compensation to the response: this is the patient frequently seen in surgical intensive care units – major trauma or sepsis such as pancreatitis.

It is important that you are able to differentiate between the types of patients that you look after in ICU: for routine post operative surgical patients fluid balance, analgesia and heart rate control may be the over-riding priorities, rather than feeding, for example. It is also important to realize that patients admitted under one category may enter another: a patient following coronary bypass surgery may develop severe sepsis.

  • It is important to differentiate patients who are in critical care units from those with “critical illness,” which is characterized by acute loss of physiologic reserve.

The patients in groups 5 and 6 have “critical illness”: their admission to ICU has followed an injury which has depleted endogenous reserves, and death is inevitable without life supporting interventions. These patients do not follow predictable courses of illness, such as “the ebb and flow paradigm”, originally described by Cuthbertson. In many cases the course of illness is prolonged, and the underlying causes difficult to discern. Indeed there appears to be great interpatient variability – two patients with the exact same injury may follow different paths: one may follow the standard stress response – acute compensation, followed by hypermetabolism and catabolism and, after 4 to 7 days, resolution with fluid mobilization and anabolism. The second patient may rapidly develop multi organ failure and remain in intensive care for a prolonged period of time. We do not know why this occurs, but suspect a hereditary element. To look at this another way, the standard stress response has evolved as the body’s mechanism to save itself and deal with major injury: the greater the injury, the greater the response. Conversely, an overwhelming response, which will lead to death without life support, cannot be considered normal.

Medical versus Surgical Intensive Care Units

  • Critical illness should not be compartmentalized into medical and surgical, the problems experienced by critically ill patients and the treatments given are essentially the same, although the causes may differ.

Critical illness is a very specific series of disease syndromes that arise from an enormous spectrum of causes. There is no such thing as a medical intensive care patient or a surgical critically ill patient; the syndromes are the same regardless of the origin, although the approach taken may differ amongst patient populations depending on age and chronic health issues. A good intensivist can seamlessly move from medical to surgical units, divisions set up for convenience. In many institutions, internationally, there is only one (mixed) unit, with no distinction between medical and surgical patients. Critical illness is a paradigm where patients are afflicted by syndromes such as ARDS, sepsis, kidneydysfunction, hemodynamic insufficiency, neuroendocrine insufficiency and exhaustion.

A wide variety of disease processes are treated with a limited number of interventions, in an intensive nursing environment.

The Multidisciplinary Team

The intensive care unit is not merely a room or series of room filled with patients attached to interventional technology, it is the home of an organization: the intensive care team. This team – doctors, nurses, therapists, chaplains and other support staff, builds an environment for healing, under the umbrellas of medicine, care and compassion and unit management.

A high quality Critical Care Team will contain the following members:

Critical Care Consultant (Intensivist) – ICU Clinical Nurse Manager
Critical Care Medical Team
Critical Care Nurses
ICU Pharmacists
ICU Physiotherapy Team
IICU Occupational Therapists
ICU Dieticians
ICU Speech and Language Therapists
Healthcare Assistants
Administrative Assistants
Chaplain
Psychologist

Medicine, Care, Compassion and Organization

  • Critical Care is about medicine, care, compassion and organization.
  • The best intensive care units are the ones with the most effective management structures.

Patients are admitted to intensive care, for the most part, with one or more of the following problems: hemodynamic insufficiency, respiratory failure, abnormalities of fluid and electrolytes, sepsis and coma.

I frequently refer to the seven Cs of critical care:

  1. Compassion
  2. Communication (with patient and family).
  3. Consideration (to patients, relatives and colleagues) and avoidance of Conflict.
  4. Comfort: prevention of suffering
  5. Carefulness (avoidance of injury)
  6. Consistency
  7. Closure (ethics and withdrawal of care).

It is not possible to build an effective critical care practice without high quality management which addresses the following issues:

1. Environment (patients, staff and visitors). 2. Organization Structure (multidisciplinary). 3. Teamwork. 4. Gatekeeping (appropriate bed usage). 5. Evidence based practice and cost effectiveness. 6. Continuous Education. 7. Audit with transparency.

Every good intensive care unit will have one or more medical and nursing directors, perhaps a business manager and very strong pharmacy and radiology, infectious disease/microbiology backup.

Critical care is characterized by a very high doctor and nurse to patient ratio. In critical care nurses are present at the bedside 24 hours per day. Not all of that time is spend “doing stuff” – hence, I prefer the moniker “Intensive Care” to “Intensive Therapy.”

Modified from ccmtutorials P Neligan 2000-2001

Announcing a New Series – AN INTRODUCTION TO CRITICAL CARE

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I am going to start release videos from this week onwards that are part of a series known as “An Introduction to Critical Care” – these are based on the original tutorials that composed ccmtutorials.com (alas I lost control over the URL about 10 years ago). The purpose of the series is to provide a sound knowledge foundation for doctors, nurses, medical and nursing students and allied healthcare professionals during their first encounters in critical care.

While I will do my best to keep the tutorials under the 20 minute window, and keep the content as straightforward as possible, I will absolutely not surrender to dogma: every point, every concept, every idea has evolved and been road tested by me over 30 years. I will endeavor to provide you with an Evidence Based Practice of Critical Care, without having to justify each comment and suggestion with reams of data and references. You’ll just have to trust me.

I will also continue the other tutorials series that I have been working through: fluids, respiratory failure/mechanical ventilation and acid base balance. Tutorials from these series will be published intermittently, as time allows – as each tutorial is newly constructed and requires enormous amounts of time. I will also publish intermittent “Hi Impact” Critical Care pieces that cover advanced areas of practice and are targeted at consultants (attending physicians), senior residents and fellows.

Pat Neligan

I guarantee you will learn something from each tutorial.

Pat Neligan, March 2024

Alcoholic and Starvation KETOACIDOSIS

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This tutorial looks at the twin problems of Alcohol related and Starvation Ketoacidosis. These diagnoses are frequently missed by clinicians because 1. they attribute the metabolic acidosis to another cause e.g. lactate or acute kidney injury or 2. they do not routinely measure blood ketones. It is my view that, in any patient presenting with a plasma bicarbonate below 20mmol or mEq/L or a base deficit of -5 or greater, it is mandatory to measure blood ketones (beta-hydroxybutyrate).

I present two cases, the first is a patient who is admitted with abdominal pain and a likely upper GI bleed, with a history of an eating disorder, who has metabolic acidosis. The second patient is an alcoholicwho recently stopped both eating and consuming alcohol. She also has a metabolic acidosis. I discuss the biochemistry of alcohol metabolism and explain why alcoholics are at risk for ketoacidosis. I also explain why this is part of a paradigm of metabolic failure that, without significant attention to detail, may result in therapy that precipitates a variety of withdrawal syndromes: these include acute Wernicke’s Encephalopathy, Alcohol Withdrawal Syndrome, and acute aquaresis and Osmotic Demyelination. Alcoholic ketoacidosis almost always follows cessation of alcohol intake – and one is unlikely to make this diagnosis in a patient who, for example, presents drunk to the ED (this results in a host of other metabolic anomalies, for example hypoglycemia despite high plasma lactate).

Starvation ketoacidosis is seen in patients who are chronically malnourished or fasted for prolonged periods for surgery, in whom the pancreatic Islet cells have either atrophied or are hibernating. Careful attention must be applied to feeding and refeeding: it is imperative that the patient does not lose further lean body mass. On the other hand refeeding syndrome may result in rhabdomyolysis and death. I guarantee you’ll learn something.

kPa “RULES” – Part 2: The “Rules of Acid Base”

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Traditionally rules of thumb regarding the changes in PaCO2 and Bicarbonate in acid base balance have utilized mmHg. Unfortunately, in large tracts of the world, particularly in Europe, blood gases are reported in the SI unit kPa. This tutorial is for those people. I cover various acid base abnormalities – pH vs PaCO2, acute and chronic respiratory acidosis, respiratory alkalosis, metabolic acidosis and alkalosis and go through the various acid base rules of thumb using kPa, with examples. I guarantee you’ll learn something.

Rules:

Rule 1 H+ vs pH: a 1nmol/L increase in [H+} results in a 0.01 fall in pH

Rule 2 PaCO2 in Apnea: In apnea the PaCO2 rises by 1.5kPa in the first minute and by 0.5kPa per minute thereafter (this reduces progressively over time to 0.2-3kPa)

Rule 3 PaCO2 vs pH: For every 1kPa increase in the PaCO2 the pH falls by 0.06

Rule 4 PaCO2 vs HCO3 in Acute Respiratory Failure: For every 1kPa increase in the PaCO2, the HCO3 rises by 1mmol/L

Rule 5 PaCO2 vs HCO3 in Chronic Respiratory Failure: For every 1kPa increase in the PaCO2, the HCO3 rises by 3mmol/L and the Chloride falls by an equal value.

Rule 6 PaCO2 vs HCO3 in Acute Respiratory Alkalosis: For every 1kPa increase in the PaCO2, the HCO3 falls by 2mmol/L

Rule 7 PaCO2 versus Base Deficit in Acute Metabolic Acidosis: For every 1mmol/L increase in the Base Deficit (-BE e.g. from -1 to -2), the PaCO2 falls by 0.13kPa e.g. if the BD is -10 the PaCO2 will fall by 1.3kPa from 5.3 to 4

Rule 8 PaCO2 vs HCO3 in Chronic Metabolic Alkalosis (in ICU): For every 1mmol/L increase in the Base Excess (or HCO3) the PaCO2 increase by 0.13kPa e.g. if the BE is +10 then the PaCO2 will increase from 5.3 to 6.6

@ccmtutorials http://www.ccmtutorials.org

Ketoacidosis

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This tutorial looks at the problem of ketoacidosis and, in particular, focuses on diabetic ketoacidosis. Ketones are produced from free fatty acids in the liver, converted to acetyl coenzyme A and oxidatively metabolized for energy production or packaged in the form of acetoacetate or beta hydroxybutyrate and exported to the tissues. This occurs continuously in the body. Control over metabolism is provided by insulin. When insulin levels are high glucose is utilized primarily for energy production and fatty acid metabolism is curtailed. When insulin levels are low fatty acids become the primary source of energy. In situations of very low carbohydrate intake ketones may be measurable in the blood and we call this ketosis. When plasma ketones exceed 3 millimoles per liter this results in a strong ion effect and ketoacidosis. This is generally only seen in states of metabolic failure such as type 1 diabetes starvation and alcoholism.

The ketones acetoacetate and beta hydroxybutyrate are strong anions and cause metabolic acidosis when they accumulate. This manifests as a fall in the bicarbonate and an increase in the base deficit. Classically there is a widened anion gap metabolic acidosis with full respiratory compensation. Nevertheless the extent of the acidosis is rarely explained by ketones alone. Lactic acidosis is frequently present as is acidosis caused by the accumulation of metabolic junk products. Iatrogenic metabolic acidosis may ensue caused by the administration of hyperchloremic (0.9% NaCl + KCl) saline solutions.

Diabetic ketoacidosis is characterized by loss of control of blood glucose, loss of control of blood lipids and hypercatabolism of proteins. Failure to suppress gluconeogenesis within the liver depletes the tricarboxylic acid cycle reserves and results in uncontrolled ketone production. Patients become hyperglycemic glycosuric, keto acidotic, initially hyponatremic, later hypernatremic, and hyperkalemic. The treatment is to fluid resuscitate the patient, administer insulin by intravenous infusion, replenish glycogen stores and provide glucose for intracellular substrate and prevent further ketone production. Extra care must be taken to avoid hypoglycemia and hypokalemia. @ccmtutorials

Further Thoughts about LACTATE

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This is an opinion piece – a rant if you like about the perceptions and understanding of most healthcare professionals regarding the status of Lactate and Lactic Acidosis. It seems to me that everyone has an opinion on Lactic Acidosis, in my own opinion – they are often misinformed. The bottom line is that the body manufactures and processes vast quantities of Lactate each day and that accumulation of Lactate in the blood – Lactic Acidosis – is a sign of acute illness and multifactorial in origin. The Lactate is not the problem. The Lactate will eventually be processed by the liver and kidneys. You need to identify the underlying problem and control the source. Moreover, as Lactate is a signalling molecule and part of a multi-system process for energy transmission (the “Lactate Shuttle”), particularly when there is a lot of white blood cell activity, a raised lactate late in critical illness is frequently a sign of tissue healing, rather than acute inflammation. The biggest problem that I encounter, on a daily basis is the binary belief that hyperlactatemia means global oxygen debt. Certainly it is associated with hypovolemia (which can be identified by capillary refill time and mixed venous oxygen saturation) but more often it is associated with increased catecholamines associated with the stress response. If you are playing lactate-fluid “whack a mole” – each blood sample leads to a fluid bolus, your patient will become fluid overloaded very quickly. The latter is strongly associated with worse outcomes in critical illness.

I make the following points in this tutorial.

Most clinicians overestimate their knowledge of lactate and consider it a waste product of aerobic metabolism. Lactate is likely the end product of glycolysis and a major fuel source for the body. Lactate is always an Arrhenius acid in the body. Lactate is not a good endpoint of resuscitation (“clearance”). Using Lactate “clearance” as an endpoint usually results in excessive fluid resuscitation. High Lactate and Low Glucose is an Ominous Sign. Nobody can be really sure what is in a bag of Hartmann’s Solution (Ringers Lactate). D-Lactate is likely more harmful than you think. There is no specific treatment for Lactic Acidosis.

Lactic Acidosis

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  1. Lactic acidosis is one of the best biomarkers of acute critical illness, its presence should alert the clinician to a major stress response, where medical and surgical and iatrogenic sources should be considered.
  2. The magnitude and duration of hyperlactatemia (in the acute phase) is predictive of patient prognosis in critical illness. A sustained high lactate reflects a prolonged stress response. The lactate is not the cause or the problem. It is merely a biomarker.

If I were to pick one topic over which I have sweated tear during the past 2 decades, it is lactic acidosis. The problem is that every time I try to explain lactic acidosis, many of those around me become hostile, as if I was committing some atrocity against their religion. And that is because, for the past 100 years, every high school, science, nursing and medical student has been taught that lactate is a waste product that is only made in anerobic conditions. This is 100% ABSOLUTELY completely verifiably WRONG. Lactate, or lactic acid is produced all the time, continuously, in all tissues and is likely the major endpoint of glycolysis. Once produced, it is then either used for oxidative phosphorylation, shuttled to other tissues as a partially metabolized energy source (e.g. the heart and the brain – they love lactate) or metabolized in the liver, principally (the “Cori Cylcle”) – where gluconeogenesis takes place leading to subsequent glycogen storage, fat production or oxidative phosphorylation. As such, glucose is a universal substrate and lactate is a universal fuel.

Lactic acidosis occurs when the production of lactate exceeds the capacity of the liver to clear it. As we produce at least 1250mmol of lactate per day and it is barely measurable in the blood, hepatic clearance capacity is vast. Hyperadrenergic states promote the production of lactate, increase blood glucose and reduce hepatosplanchnic blood flow. The consequence is sometimes called “stress hyperlactatemia” or “aerobic glycolysis.” This is the form of hyperlactatemic seen in sepsis, for example. As such it is an acute phase reactant biomarker – lactate concentration mirrors adrenaline/epinephrine, and should be seen in the same light as CRP, IL-6 and Procalcitonin.

Hyperlactatemia results in metabolic acidosis as a consequence of water dissociation. The strong ion difference (SID) falls. The surplus “hydrogen ions” are mopped up by bicarbonate resulting in a modest fall in pH, but a mEq/L for mEq/L fall in bicarbonate and base excess. Lacate, like Chloride and Ketones, always functions as an acid surrogate and chronic hyperlactatemia is compensated for, usually, by increasing urinary Chloride loss, manifest as hypochloremia.

The terms “Type A” and “Type B” lactic acidosis were introduced by Huckabee in 1961. I believe that these monikers are still useful today. “Type A” represents lactic acidosis associated with blood loss and hypovolemia, intense systemic and splanchnic vasoconstriction, high ejection fraction, low stroke volume and cardiac output and low mixed venous oxygen saturation. Production of lactate increases (and this is multifactorial – not just anerobic), and production falls – due to hepatic hypoperfusion. The treatment is resuscitation, preferably with blood products.

For lactic acidosis, what is not Type A must be Type B – and this represents medley causes (toxic – alcohols), metabolic (end stage liver disease), inflammatory (sepsis), drug induced (metformin and particularly intravenous or inhaled catecholamines).

The term “Clearance” has been used to describe the removal of lactate from the circulation. It is a pharmacological rather than biochemical term, and that has led to some abuse in clinical practice: the belief that “Clearance” can be hurried along with aggressive fluid resuscitation. However, like any particle that is metabolized by the liver, clearance of lactate is determined by the quantity delivered, hepatic blood flow and hepatic clearance capacity. If there is a sustained surge in lactate production, then it may take a while for the liver to clear the surplus from the system while simultaneously dealing with the continued production of lactate by the tissues. In critical illness, we like to see the plasma lactate level falling, but 10-20% is sufficient to be reassuring. A rising lactate is ominous and may indicated inadequate source control or a secondary problem, such as bowel ischemia.

Lactic acidosis may or may not be a marker of tissue perfusion. It is a poor endpoint of resuscitation – and if used as such (the “drive by saline assault”), the result is fluid overload, mutiiorgan dysfunction and prolonged ICU stay.

Sodium Lactate Solutions do not cause lactic acidosis, as they are fully balanced. Most formulations contain a racemic mixture of L-Lactate (which is what the body produces) and D-Lactate (produced by fermentation by bacteria). Blood gas machines do not measure D-Lactate.

I guarantee you’ll learn something.

Ions & The pKa – Local Anesthetics, Opioids and Midazolam

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You may think that this whole ionization and pKa stuff is of little relevance to you as a clinician working in ED, Anesthesiology or ICU, but you are mistaken. The pH of blood (whether or not the [H+] exceeds the [OH-] has major impact on the pharmacokinetics of certain drugs. Moreover, some drugs rely on a differential between extracellular and intracellular pH to be effective.

This tutorial looks at the pharmacology of three types of drugs impacted by pH. These drugs are local anesthetics, opioids and the benzodiazepine – midazolam. All of these agents are weak bases whose degree of ionization varies with pH.

  1. Speed of onset is related to the pKa – the lower the pKa of weak bases the more rapid the onset of action
  2. Duration of action is related to protein binding – particularly albumin (there are other proteins). Albumin depletion is common in critical illness, leading to higher bioavailability and shorter duration of action.
  3. Potency is related to lipid solubility. Fentanyl is highly potent because of this.

This tutorial is supplementary to the acid base course. The material is ESSENTIAL for trainees and practitioners in Anesthesiology and Dentistry. @ccmtutorials http://www.ccmtutorials.org

The Ripple of Ions – Ionization and the pKa

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To truly understand acid base chemistry, it is imperative that you have a grasp of ionization theory. Although this might appear a little nerdy, it is quite straightforward and will also provide you with a basis for understanding the basic pharmacology of local anesthetics and opioids. Particles that disintegrate into component parts that carry charge are known as ions. If that charge is positive they are cations and if it is negative they are anions. Measurement of charge is known as valency, Most electrolytes in the body are univalent – Na, Cl, K, HCO3 – and their valency is quantifiably identical to their molarity (i.e. 140 mmol/L of Na+ = 1mEq/L). Some, however, are divalent – Calcium and Magnesium and Phosphorous. Ionized particles are a major component of acid base chemistry. They may be derived from mineral salts – Na, Cl, K, PO4, Mg, Ca or organic molecules – Lactate, Ketones, Metabolic Junk Products – manufactured in the body. Weak anionic acids are also manufactured – Bicarbonate and Albumin.

The relative quantities of different particles is governed by MASS CONSERVATION. Regardless of the source and quantity of anions and cations ELECTRICAL NEUTRALITY must always hold. Where there is imbalance between anions and cations the electrochemical void is filled by hydrogen or hydroxyl (derived from water dissociation) and acid base abnormalities ensue.

What makes ionized particles “strong” or “weak” acids or bases is determined by the pKa – the Ion Dissociation constant. This is the pH at which the particle is 50% dissociated or associated. As all electrochemical activity in the body occurs withing the physiological range of pH – 6.8 to about 7.65 – whether a ionic particle’s pKa is below or above, essentially 7.4, determines whether it is an acid or a base. For example – Lactic Acid has a pKa of 3.1 – at that point is is 50% associated (LA-H) and 50% dissociated (La-). At the environmental pH falls, for example towards 1, for example in the stomach, the chemical associates more (Lactic Acid). As the pH rises towards 7.4 it dissociates more (Lactate). At all physiologic ranges of pH Lactate is fully dissociated. Likewise, chemicals that have a pKa above the physiologic range pH (i.e greater than 7.6) are bases – and they become more associated at higher pH ranges. Sodium Hydroxide has a pKa of greater than12, which means that at pH 12 it is 50% associated, at pH 15 it is close to 100% associated. At physiologic range pH it is fully dissociated. Particles that are fully dissociated at all physiologic ranges of pH – cations such as Na+, K+, Mg2+ and Ca2+ and anions such as Cl-, Lactate- and Beta-Hydroxybutyrate, are known as STRONG IONS – they never bind to other ions (to create salts), hydroxyl or hydrogen in the body. Particles that are partially dissociated, whose pKa is closer to 7.4 – Bicarbonate, Albumin, Phosphate, Hemoglobin, are WEAK ACIDS and as they pick up more hydrogen ions at lower pH levels, they act as buffers.

Metabolic acid base balance is governed by the relative charge distribution (mEq/L) of STRONG IONS – known as the STRONG ION DIFFERENCE (SID) and the availability of weak acid buffers (ATOT). If the SID reduces, there is excess anion and metabolic acidosis. If the SID increases, there is excess cation or deficient anion and metabolic alkalosis.

I guarantee you’ll learn something. @ccmtutorials http://www.ccmtutorials.org

Weaning From Mechanical Ventilation (the basics)

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This tutorial is about weaning from mechanical ventilation. This is not an easy topic because every professional in the ICU has their own weaning method and their own opinions regarding how best to wean and liberate patients. The literature is unhelpful. Some patients, for example those who have been intubated for a brief period of time, can be awoken and the tube removed after a couple of spontaneous breaths. Other patients require careful multidisciplinary activity over weeks to months to liberate. This tutorial focuses on the in-between group patient who have been intubated for a week or so, who require both clinical and mechanical assessment of their ability to wean and liberate from the ventilator.

Generally the first intervention in weaning is to change the patient over to a spontaneous breathing mode – pressure support or volume support and ensure that alveolar ventilation is adequate to maintain CO2 clearance.

Then a number of clinical and mechanical assessments can be made: is the patient awake, do they have a cough, are they triggering adequately, what is their rapid shallow breathing index (RSBI)? One can estimate muscle strength by performing an occlusion test – either a partial occlusion (P0.1) or a longer occlusion (NIF). Once the patient is assessed as being a candidate for weaning, then one can perform a spontaneous breathing trial (SBT) that is either supported (PS, VS, ATC) or unsupported (T-piece, C-circuit, Trach mask, Swedish Nose).

If the SBT is successful after 90 minutes – extubate the patient. SBTs may fail due to worsening hypoxemia, hypercarbia or hypocarbia, respiratory distress (increase RSBI or use of accessory muscles) or cardiovascular instability (hypotension, hypertension, tachycardia, bradycardia, arrhythmias) or falling levels of consciousness, agitation or acute delirium.