The Critically Ill Patient should receive a systematic head to toe front to back clinical examination each day. Before you start, stand at the end of the bed and take in the scenery. An experienced ICU doctor will acquire an enormous amount of information about a patient by eyeballing the monitor, looking at the patient’s habitus, the machines, the other attached devices, infusion pumps etc.
Then INTRODUCE yourself and explain to the patient, irrespective of level of consciousness, that you are going to examine them, if that’s ok.
Does the patient have an endotracheal tube, nasogastric tube (is it on free drainage?), enteral feeding tube (yellow) or orogastric tube).
Follow the pattern of Inspection, Palpation, Percussion and Auscultation.
Start with the head and evaluate its shape and color. Then move on to the eyes, nose, lips, mouth (inside and outside) and then on to the side of the head and ears.
Move on to the neck – observe for masses, scars and lines (what type of line). Palpate the neck paying particular attention to the trachea (you may want to do a tracheostomy down the line). Feel for crepitus in the supraclavicular area.
Move on to the chest – inspect – look for recent surgical wounds and scars, chest or mediastinal drains, pacemaker wires etc. Observe the breathing pattern – is it symmetrical? Palpate the cardiac apex and the left sternal border. Auscultate for cardiac murmurs, carotid bruits and for breath sounds, looking for loss of air entry, crackles or bronchial breathing.
Move on from the chest to the arms – are they symmetrical? Is the patient moving both arms? Any redness? What color are the fingers – any mottling? Are the fingertips necrotic? Palpate the arms and hands and feel the temperature – hot or cold? Feel the brachial and radial pulses.
Move on to the abdomen: is it scaphoid or globular? If globular consider the 5 Fs: fat, fluid, flatus, feces, fetus. Are there any scars, wounds or drains? Palpate, percuss and auscultate the abdomen.
Move on to the legs. Are they moving? Are they equal in size? Are the quadriceps wasted? Is there mottling or ischemic changes? Is the patient wearing compression stockings (TED) and or sequential compression devices (SCD)? Palpate the legs, feel the pulses and then look at the ankles (pitting edema) and heels (pressure sores).
Assess the skin – are there any rashes? Are they localized or generalized? If generalized is the rash macular, maculo-papular, vesicular (one side consider herpes zoster) or – ominously purpuric. A generalized purpuric rash is either meningococcemia or thrombotic thrombocytopenia purpura until otherwise proven (both disorders are immediately life threatening).
Roll the patient on their side and look at the back – in particular look at the pressure areas and at any pain catheters and their sites (epidural). Look for the presence of a rectal tube and bowel management system.
When you have completed examination, look at the devices around the bedside sequentially. Start with the main monitor and evaluate the ECG – rate (paced?), rhythm, shape (ST segment changes?). Then the pulse oximeter, arterial blood pressure – invasive and non invasive (correlating?), then the temperature and end tidal CO2 (and waveform).
Move on to the ventilator – if one is attached and note whether the patient is breathing spontaneously or not (why?), what mode (AC, SIMV, BiLevel, PSV), rate, tidal volume, fiO2, PEEP, PFR, plateau pressure, and dynamic compliance and resistance).
Is the patient receiving continuous kidney replacement therapy – note the mode (CVVHDF or SCUF), anticoagulation strategy (citrate or heparin), and fluid removal.
Look for intravenous and enteral feed and take note of the rate and the contents. Then move on to the infusions – iv fluids and electrolyte replacement, analgesics and sedatives, vasopressors, inotropes, insulin and corticosteroids.
Before leaving the bedside look around – did you miss anything and machines or drains or infusions? Then clean up any mess that you have made, restore the bedspace to the condition it was in and inform the nurse of any changes you made or any new observations.
This tutorial has been broken up into two videos to make them easier to navigate.
Before approaching an critically ill patient’s bedside you should know who the patient is and why they are in the ICU. The purpose of the history is to lay out the known facts about the patient. Usually the patient in the ICU is unable to give a clear and reliable history. You need to comb through the patient’s chart to locate this information. Dig deep! Events that may have happened months ago may have an impact on the patient today. Don’t forget, you are not the only professional that is treating the patient: ask the nurse – they are excellent historians as they give and receive a concise report at the beginning and end of each shift. It is also worth talking to the primary team, physiotherapist, pharmacist and dietician about the patient. Remember, you are one member of a team: the others may have more knowledge of the patient than you. Nevertheless you need to remain a little bit skeptical about the story that you have been given: make sure the facts match the narrative
In this tutorial I will introduce the 4 Ws of clinical history: Who is this patient? Why are they in hospital and ICU. 3. What is going on with the patient (PROBLEM LIST). 4. Where are we going (what are the physiologic goals and organ based plans?).
WHO? Who is this patient? How old are they? Where do they come from and what is their occupation? How long has this patient been in the ICU – is this a recent admission (the patient is acutely critically ill and likely still being resuscitated)? Has the patient been in the ICU for more than 7 days? In that case the patient may be slow to recover or chronically critically ill.
What type of patient are we dealing with? Surgical or Medical? Postoperative or Critically Ill?
There are three types of critically ill patients: 1. Medical patients with an acute medical syndrome that may have occurred in the setting of low physiologic reserve. These may be children or adults. 2. Surgical patients – who have had complex elective surgery (e.g. cardiac or neurosurgery), emergency surgery or trauma. The patient may have originated as a surgical patient but now has medical problems (e.g. hospital acquired pneumonia). 3. Obstetric patients who may be currently pregnant, recently pregnant and be in ICU as a consequence of pregnancy (pre-eclampsia, post partum hemorrhage) or co-incidental with pregnancy (trauma, bowel obstruction etc.).
WHY?
It is absolutely CRITICAL that you understand the dynamics around the patient’s ICU admission. The patient may have come directly from the emergency room or operating room to ICU, or may have been transferred from a ward or other hospital. In the latter case you will need to ensure that you know exactly what went on there. These are the questions that you must ask, up front about the patient.
Why was the patient admitted to hospital? Why was the patient admitted to ICU? What happened in between?
What was the patient’s admission problem (MAJOR ADMISSION PROBLEM)?
This is the patient’s presenting problem (although it may not be the patient’s main current problem). It is the symptoms and diagnosis that led the patient to come into the hospital originally – e.g. chest pain, shortness of breath, confusion. This may be clarified as “pneumonia” “septic shock” etc.
Between the patient arriving in the hospital and being admitted to ICU clinical episodes may have occurred – you need to know these. Was there a delay with the diagnosis? Was a wrong pathway chosen? Did the patient deteriorate or have a cardiac or respiratory arrest on the ward?
What was the patient’s indication for ICU ADMISSION
This is a remarkably limited list because patients are admitted to ICU for life sustaining therapy consequent of single or multi organ failure. Those injuries can be summarized as follows:
Neurological – Low GCS, Seizures
Cardiovascular – Hypotension, Arrhythmias, Blood Loss
Some patients, for example those with septic shock, may have multiple system problems: confusion, hypotension, hypoxemia, oliguria – AKI.
What complications followed?
Prolonged admission to intensive care is characterized by “second and third hits” – organ injuries such as hospital acquired pneumonia, line sepsis, myocardial ischemia, acute kidney injury, bed sores etc. It is important that you are aware of these problems even if they have now resolved, as complete recovery of organ function at this stage is unlikely, and those organs remain vulnerable (for example, it is important that you do not prescribe non steroidal anti inflammatory agents (NSAIDS) to a patient who has recently recovered from acute renal failure).
What is the patient’s age and baseline health status (BACKGROUND)?
What background medical problems does the patient have? We know that patients with major organ dysfunction (such COPD, pulmonary fibrosis, heart failure (EF<40%), chronic kidney disease, cirrhosis or chronic hepatitis, previous myocardial infarction or active ischemia, connective tissue disease, inflammatory bowel disease, cancer, cerebrovascular disease, carotid arterial disease) have diminished physiologic reserve, and have a worse prognosis when admitted to intensive care. The greatest determinant of outcome, however, is the patient’s age: young patients do better in intensive care than older ones. You also need to know what medications the patient was taking pre-admission: antihypertensives, statins, SGL2 inhibitors, GLP-1 receptor agonists etc. If the patient is taking anti-coagulants you need to know why? Pulmonary embolism, stroke, atrial fibrillation, arterial obstruction, heart valve etc. All of this is relevant.
WHAT?
What PROBLEMS are keeping this patient in intensive care (CURRENT PROBLEMS)?
The patient may remain in ICU for a problem wholly unrelated to the original presenting complaint – failure to liberate from mechanical ventilation, failure to emerge from sedation etc). This is the patient’s main current problem, and it needs to be addressed. In addition, it is important to enumerate the other problems, even if they are apparently trivial.
If you don’t have a precise diagnosis don’t invent one – just list the problems, these can be padded out later
So a patient may be admitted with Hypoxic Respiratory Failure That might evolve to Ventilator Dependent Respiratory Failure That Becomes Acute Respiratory Distress Syndrome Clarified as Community Acquired Pneumonia, secondary to culture positive Staphylococcus Aureus
To identify the problems you need to evaluate the patient’s organ systems in an organized, precise and systematic way. The way I go through the systems is as follows:
NEUROSYSTEM
•The patient has a “Low GCS secondary to….” traumatic brain injury (specify), stroke, encephalopathy, encephalitis, meningitis, cause uncertain etc.
•The patient has “Severe Delirium with a RASS score of…..being treated with…..
•The patient is in “Status Epilepticus being treated with…..with a know or no known history of Epilepsy”
•The patient has “Guillain Barre Syndrome, requiring mechanical ventilation being treated with plasma exchange”
RESPIRATORY SYSTEMPROBLEMS
Problems with the respiratory system are usually 1. problems with the lung parenchyma (gas exchange) or 2. problems with the airway (particularly airway obstruction)
Parenchymal Problems
Acute Hypoxic (AHRF) or Hypercarbic Respiratory Failure
Although rhythm disturbances causing hypotension are technically “cardiogenic shock” nobody really uses that term, generally we describe the problem
•Complete Heart Block requiring external pacing
•Fast Atrial Fibrillation requiring an amiodarone infusion
•Runs of Non Sustained Ventricular Tachycardia requiring……
KIDNEY PROBLEMS
•The patient has “Acute Kidney Injury secondary to (sepsis or rhabdomyolysis or prolonged hypotension) requiring Continuous Kidney Replacement Therapy”
•You might also qualify this with “on a background of CKD”
•“Dialysis Dependent AKI – he receives intermittent hemodialysis for 3 hours each day”
•“AKI no longer requiring Kidney Replacement Therapy”
The patient may have been admitted with a hematology issue e.g. thrombotic thrombocytopenia purpura (TTP) or a complication of chemotherapy or bone marrow transplantation Otherwise
•Anemia, Polycytemia, Thrombocytopenia
INFECTIOUS PROBLEMS
The infection may be the primary problem or it may be secondary
•Wound contaminated with VRE or Pseudomonas
•Patient may have acquired MRSA
•Patient may be isolated due to CPE
RESOLVED PROBLEMS
•If the patient was admitted with sepsis – source control may have resolved the problem
•An underlying cardiac problem may have been fixed by a stent
•An obstructed bowel or leaking aneurysm may have been surgically repaired.
•Acute kidney injury may have resolved
•Is anything ever fully resolved?
WHERE?
We can’t determine where we are going if we don’t know where we are now! From the outset, the physiological parameters under your control must be targeted: level of sedation, heart rate, Blood pressure, PaO2, PaCO2, pH, urinary output, enteral feeding, fluid balance, mobilization etc.
What physiologic targets have we set for this patient?
•Neurological – RASS score (or GCS) target with sedation
You don’t need notes to present a quick history, summary, problem list and goals of therapy. This should be drawn from memory as often the history is presented several times a day at handovers, rounds etc. Keep the narrative succinct – don’t stray off track – we are interested in the FACTS the FACTS and nothing but the FACTS.
Follow the system in the image below:
This Mr Eddie Chambers he is a 73 year old retired farmer from Mayo He is a medical patient He has been in the ICU for 4 Days………having originally been admitted with acute hypercarbic respiratory failure secondary to pneumoni He was admitted to ICU for intubation and mechanical ventilation He subsequently developed septic shock and acute kidney injury, requiring pressors and RRT He has a background history of hypertension treated with calcium channel blockers. His current problems are: ventilator dependent respiratory failure, pressor dependent septic shock and dialysis dependent acute kidney injury He is also malnourished, due to gastroparesis, hypoalbuminemic, anemic and has a hyperchloremic metabolic acidosis and stress hyperglycemia He also has an early sacral pressure sore
Our goals are to: Sedate to a RASS score of minus 2 Reduce the ventilator settings Keep the PaO2 above 8kPa (60mmHg) Keep the PaCO2 between 5.3 and 6kPa (40-45mmHg) A MAP of 70mmHg Fluid balance of -1000ml today on Kidney Replacement Therapy We are starting TPN today, and targeting a Blood glucose below 10mmol/L (180mg/dl) Sit him out in a chair today
REVIEW
This Tutorial Looked at Getting a History in the ICU. It is not easy because the patient is usually not able to communicate effectively. Significant detective work may be required.
Who – who the patient is
Why – the patient came to hospital and why they needed to be admitted to ICU
What is currently wrong with the patient (Problems)
Since the 1920s it has been known that administration of chloride rich intravenous fluids, characterized by a reduced Sodium to Chloride strong ion difference (SID), causes a progressive metabolic acidosis. This iatrogenic hyperchloremic acidosis was particularly problematic in the era before lactate and ketone measurement was widely available, prolonging critical care stay and resulting in, often, unnecessary tests and therapies. During the 2000s a body of literature emerged supporting the hypothesis that hyperchloremia, defined as a plasma chloride of greater than 110mmol/l may be harmful. In a series of retrospective analyses, hyperchloremia was associated with increased mortality across a spectrum of disorders, including surgery and critical illness. Hyperchloremia was also associated with increased risk of kidney injury and the requirement for renal replacement therapy. There was also some data that hyperchloremia may be associated with reduced splanchnic blood flow.
A series of papers that looked at isotonic saline solution (ISS – 0.9% NaCl ), often referred to as “normal” saline, versus Plasmalyte 148 (PL) in Diabetic Ketoacidosis (DKA), demonstrated that ISS was associated with prolonged duration of stay in critical care, usually associated with persistent metabolic (hyperchloremic) acidosis. No studies to date have demonstrated superiority of ISS to PL Four major clinical trials – SALT ED, SMART, BaSics and PLUS– were conducted to compare outcomes of acute and critically ill patients randomized to either balanced salt solutions (sodium lactate products – Hartmann’s, Lactated Ringers or PL) or ISS. The first 2 studies demonstrated that ISS was associated with renal dysfunction and worse outcomes with sepsis. The BaSics and PLUS trials, in their initial reporting, showed no outcome differences. However, these trials were “catch” all ICU studies, including perioperative patients, patients pre-resuscitated with ISS, and, overall very little fluid was administered. The studies were grossly underpowered to detect outcome differences. However, subsequent systematic reviews and meta-analyses that included these data, and subgroup analyses of high risk patients, determined that fluid resuscitation with ISS was associated with worse 30 mortality, particularly in sepsis, and worse renal outcomes.
It is my view that, based on decades of research and experience, “normal” Saline (ISS) should not be used as a first line agent for fluid resuscitation in critical illness. I believe that the current international guidelines for the management of DKA are flawed in that they continue to recommend the administration of an agent that may well be toxic to patients, particularly when alternatives are easily available. Watch the video and make up your own mind.
Hyperchloremic Acidosis is a common problem. It is usually an iatrogenic problem. Unfortunately, the majority of doctors who cause a patient to have Hyperchloremic Acidosis (HCA) are either unaware of the problem or ambivalent to it. For the most part, HCA is caused by the intravenous administration of isotonic saline solution (NS – “normal saline – NaCl 0.9%). This problem has been known about for more than 100 years and led Alexis Hartmann, a pediatrician from St Louis, to construct a balanced intravenous fluids, that he called “Lactated Ringers” solution. Ironically, in clinical practice, HCA is induced as part of the local hospital “protocol” for management of Diabetic Ketoacidosis. Inevitably, as the ketones fall, the Chloride rises, and the acidosis persists.
HCA is the only cause of “normal” anion gap metabolic acidosis and is almost always caused, . In the tutorial I explain that HCA is caused by a reduction in the Na-Cl strong ion difference (SID). The acidosis associated with NaCl 0.9% is more complex that merely a rise in plasma Chloride. Other serum electrolytes, Albumin and Hemoglobin are diluted – and this has an alkalinizing effect. Other resuscitation fluids have different impacts on acid base. Hyperchloremia is also a feature of Renal Tubular Acidosis (RTA), various other nephropathies, the administration of acetazolamide and other drugs, and following surgical transplantation of the ureters into the small bowel, If renal function is normal, and the Chloride level is lower than 125mmol/L, then the patient’s kidneys will resolve the problem over 36 to 48 hours. If the Chloride is very high, acidosis will persist, particularly in patients with poor renal function, and Sodium Bicarbonate infusions may be warranted.
This tutorial looks at an emerging problem in medicine – iatrogenically induced eugylcemic ketoacidosis, associated with the use of SGLT2 (sodium glucose cotransporter 2) inhibitor drugs, also known as Flozins.
There is a global pandemic of metabolic disease caused by escalating ingestion of carbohydrate rich ultra processed food. This results in central obesity, hepatic steatosis (fatty liver) and insulin resistance: together these findings are labelled the “Metabolic Syndrome” (MetS). MetS is associated with systemic inflammation and atherogenesis. In many cases it progresses to Type 2 Diabetes (T2D), the majority of treatments for which increase adiposity and escalate insulin resistance. SLGT2 inhibitors are a relatively new class of drug that work by increasing excretion of ingested glucose by blocking the Sodium-Glucose symporter channel in the proximal tubule of the nephron. The result is mild natiuresis and glycosuria. These agents have been proven effective in the management of T2D and are emerging as effective treatments for other diseases such as congestive cardiac failure and nephropathy. As the name of each of these medications involves the suffix -flozin – they are commonly termed “Flozin” drugs.
One of the major problem with the use of Flozins in the community is failure to discontinue the drug when fasting or not consuming calories. Glucose will continue to be wasted, often generated by gluconeogensis, suppressing insulin secretion, resulting in lipolysis and ketosis. As blood glucose is low there is insufficient insulin present to prevent ketoacidosis. This is one of the causes of euglycemic diabetic ketoacidosis (EDKA). EDKA is associated with both ketoacidosis and hyperchloremic acidosis.
The treatment of EDKA is dextrose (to restore the Kreb’s cycle and suppress ketosis) and insulin – to put some control on the metabolic system. The patient may require a couple of liters of resuscitation fluid – preferably sodium lactate solution (Hartmanns or LR). The ketosis resolves rapidly, but the acidosis resolves slowly because it is principally driven by hyperchloremia. Patients who are being treated with SGLT2 inhibitors that are scheduled for surgery should stop taking these drugs 3 days pre-op. If they are continued inadvertently or surgery is emergent, then a dextrose infusion should be considered and ketones checked routinely.
Tutorials 2 and 3 in the Introduction the Critical Care Series.
The first is titled “What is Critical Illness” and it covers the concept of Physiologic Reserve.
The third tutorial looks at the problem that many healthcare providers encounter: how do I identify the critically ill patient. In this tutorial I discuss the type of scenarios in which you might be called to the patients bedside. I principally discuss Early Warning Scores (EWS) and why I think they are helpful. I also mention the SOFA score.
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:
Patients admitted to intensive care for intensive monitoring, in anticipation of possible aggressive interventions: this is the coronary care model.
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.
Patients who require very intense nursing care, which would not be available elsewhere: an example of this is a burns unit.
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.
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).
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:
Compassion
Communication (with patient and family).
Consideration (to patients, relatives and colleagues) and avoidance of Conflict.
Comfort: prevention of suffering
Carefulness (avoidance of injury)
Consistency
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.”
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.
I guarantee you will learn something from each tutorial.
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.
Proportional assist ventilation has been around in various shapes and forms since the late 1990s. The most advanced current iteration – PAV+ – is unique to Puritan Bennett ventilators. It is a closed loop mode of ventilation. That means that the ventilator dynamically changes the level of assistance that the patient receives in response to patient effort. PAV+ is neither volume controlled nor pressure controlled but is patient (and operator) controlled. The operator adjusts the percentage support that the ventilator delivers to the patient. The patient breathes – triggering the ventilator – and the ventilator amplifies the patient’s breath. Consequently the more work that the patient does to generate muscular effort the more work the ventilator performs to match the patient’s workload.
It has been known for some time that the diaphragm becomes both atrophic and dysfunctional in acute critical illness, in particular due to disuse during control of mechanical ventilation. In most assisted modes, all the patient needs to do is trigger the ventilator. Patient workload may be inversely proportional to ventilator workload. Frequently the patient’s diaphragm and ventilator are out of synchrony.
PAV+ is patient triggered and flow cycled so it should be seen as a form of pressure support ventilation. PAV+ contrasts with standard pressure support in that the degree of support changes from breath to breath and indeed within breath depending on patient effort. Pressure support delivers a fixed airway pressure for every single breath irrespective of patient effort. Consequently if we map patient effort to ventilator workload there is only one point where the two will intersect. Conversely in proportional assist ventilation the workload of the ventilator and the workload of the patient increase and decrease linearly.
PAV+ works by utilizing very high quality flow and pressure sensors. The ventilator determines when the patient initiates the breath and when the breath is completed. Having instructed the ventilator what proportion of work of breathing that the ventilator should perform, one observes, using a work of breathing bar, if the patient is doing satisfactory work or whether they need to increase or decrease their workload. The work of breathing (WOB) is determined by the ventilator by measuring compliance, resistance and intrinsic peep dynamically every 9 to 12 breaths. As such a Green Zone between 0.3 and 0.7 joules per litre is indicative of ideal work of breathing for the patient; I call this the “sweet spot.” As long as the patient’s WOB resides within the sweet spot of the toolbar the bedside clinician can be satisfied that the patient is both comfortable and safe.
As the tidal volume relates to the patient’s neural activity that results in diaphragmatic power one should not be unduly concerned about high or low tidal volumes in this mode.
If one wishes to put a patient on proportional assist ventilation it is imperative that one determines if the patient is breathing spontaneously and taking an adequate minute ventilation prior to using this mode. The reason for this is that there is no backup rate in PAV+. Usually one starts with 70% support: that means 70% of the work of breathing is performed by the ventilator on 30% by the patient. After a couple of minutes, once one has observed the work of breathing bar, one can make adjustments either to increase the workload of the ventilator or to reduce it by keeping the patient within that Green Zone sweet spot. Generally failure of the patient to settle on this mode is manifest by a respiratory rate of more than 35. Once the patient has been on 20% support for an hour or more and is awake, obeying commands, protecting their airway, and not being suctioned frequently then the patient can be extubated.
Studies that have looked at PAV+ versus pressure support have indicated that weaning is more rapid with PAV+.
ORtoICU 