What is Critical Care?

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

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

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”

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

The kPa Rules – Part 1: Oxygen

In the early 1970s much of the world adopted the System International (SI) approach to scientific measurement. Unfortunately, the remainder of the world ignored it. This means that, today, we have different units presented in the scientific literature depending on the location of the source of the publication.

The USA is the most notable non SI country and this presents a problem in that the majority of English language textbooks and journals in medicine as well as a lot of the international guidelines and clinical pathways are derived in the US. In critical care this is important – as blood gasses are reported in mmHg in the USA (and most of the literature) and in kPa elsewhere – notably in Europe.

In many of my tutorials I have reported clinical “rules” such as the PaO2/FiO2 ratio, the Alveolar Gas Equation and the majority of the calculations in acid base – in mmHg. This series of two tutorials serve to right the balance. However there is a twist.

In this first tutorial I am not just rehashing the approach to oxygenation by swapping out mmHg for kPa. In fact, the use of kPa to measure and monitor oxygenation provides us with a significant helping hand. Effectively, as atmospheric gas is effectively 100kPa and Oxygen exerts 21% of that – Dalton’s law – then it is clear that the partial pressure of inspired oxygen (PiO2) is 21kPa. Oxygen is poorly soluble in blood and water – the solubility co-efficient is 0.225 – meaning that the quantity of oxygen dissolved in blood is the PaO2 x 0.225 kPa. Oxygen follows Henry’s law – meaning that solubility is related to temperature (37 degrees C) and pressure – the PiO2. In the best case scenario the PaO2 – the partial pressure of oxygen in arterial blood is 13kPa. That means that the gradient between PiO2 and PaO2 is, at a minimal, 8kPa. The greater the stretch between the two the larger the lung injury or ventilation perfusion mismatch.

The oxygen content of blood is 1.34 x Hb x SaO2/100 + (PaO2 x 0.225). I explore the impact of different FiO2s and ambient pressure on the blood oxygen content. Although dissolved oxygen is very low breathing air – the use of supplemental oxygen may dramatically increase it – particularly in hyperbaric conditions.

Finally I address the issue of PaO2/FiO2 as a way of quantifying oxygenation. The PF ratio, as we call it, is a significant component of the ARDS definition. A PF ratio of 200 in mmHg is equivalent to 25 in kPa and a ratio of 100 in mmHg is equivalent to 12.5 in kPa. An easier way to look at this, though, is to divide the PiO2 by the PaO2 – the numbers look similar but you now have a proportion in kPa. That PF ratio of 25 in kPa resolves to 0.25 meaning that only 25% of inspired oxygen is reaching the pulmonary veins (PaO2). Likewise a PF ratio of 12.5 in kPa (100 in mmHg) resolves to 0.125 – which means that only 1/8th of the inspired oxygen is delivered to arterial blood. I think that this is a really good way of assessing oxygenation – and a way of clarifying hypoxemia in your brain.