This is the first in a new series of “”Bedside Tutorials in Critical Care” that reflects issues that we dynamically come across while doing rounds in the ICU.
Vasopressors are very widely used drugs in critical illness – norepinephrine (noradrenaline) is the most widely prescribed catecholamine, used in most types of shock and considered the standard of care vasopressor in septic shock. Epinephrine, these days may be added as an inotrope or used in neurogenic or anaphylactic shock. Vasopressin is used to restore vascular tone as a form of hormone replacement therapy.
Norepinephrine and Epinephrine concentration and dosing is extremely confusing. Many ICUs dose these agents in micrograms (mcg) per minute. This translates to ml/hour – often the bedside practitioner has not made the conversion. Consequently, when asked “how much norepinephrine the patient is on?” the response may be 5 or 10ml per hour. This is unsatisfactory, as, based on weight, there may be a tremendous variability in the dose received. Moreover the concentration of norepinephrine varies widely. In our hospital we have been required to use a pre-diluted formula of 4mg in 50ml (delivered by syringe driver) resulting in a concentration of 80mcg/ml. Conversely, epinephrine needs to be drawn up, using 1mg ampoules, usually 3mg in 50ml or 60mcg/ml (conveniently this works out as 1mcg/min/ml. Peripherally infused norepinephrine is constructed by placing 4mg in 250ml, leading to a concentration of 16mcg/ml.
Alternatively, norepinephrine may be diluted 16mg in 250ml to yield 64mic/ml. When a patient is transferred from another hospital or another country, it may be really difficult to translate the dilution and concentration used there to match up dosage. And that is important – escalating doses of pressors are suggestive of failure of source control, but 10ml/hour is twice to dose delivered to a 50kg person than a 100kg person. And at what dose do you start vasopressin?
Consequently, I strongly recommend that you use mcg/kg/minute as your dosing strategy for both norepinephrine and epinephrine. The starting dose is 0.01-0.03mcg/kg/min and it is titrated upwards to achieve a mean arterial pressure of 65mmHg. Once the dose has exceeded 0.25mic/kg/min, the patient should receive vaspressin 0.03 international units per minute. If 40iu is diluted in 50ml, to deliver 0.03 iu/min, the infusion should run at 2.3ml/hour.
This tutorial looks at the diagnosis and management of the patient with septic shock. See below for a transcript of this major tutorial.
SEPSIS AND SEPTIC SHOCK
Introduction
Sepsis is defined as life threatening organ dysfunction due to a dysregulated host response to infection. In other words, normally, once we are infected with bacterial, fungi or viruses, our immune system activates, mops up the pathogens, clears away debris and returns to normal afterwards. That does not occur in systemic sepsis – either due to an overwhelming infection (e.g. bowel perforation) or an anomaly within the immune system: there is an initial massive release of inflammatory and cytotoxic material (sometimes called a “cytokine storm”) and then immunoparalysis, due to loss of inflammatory reserve. The patient is a “sitting duck” for further infection.
Septic Shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality. There are anomalies of the cardiovascular system, neurohormonal system and autonomic nervous system. At the bedside, the clinical presentation is of acute organ dysfunction, the most common of which are hypotension, tachypnea and confusion. The most basic definition of septic shock is that it is an infected state characterized by persistent hypotension despite adequate fluid resuscitation and lactate levels ≥ 2 mmol/L. It requires the need for vasopressor therapy to maintain a mean arterial pressure (MAP) ≥ 65 mmHg.
Septic shock is a major cause of morbidity and mortality worldwide, especially in intensive care units. Understanding the pathogenesis of septic shock is critical to improving therapeutic interventions and outcomes.
PATHOGENESIS OF SEPSIS AND SEPTIC SHOCK
The pathogenesis of septic shock involves a series of immune, inflammatory, and metabolic responses. This intricate cascade is initiated by infection, typically from a bacterial pathogen, but can also be caused by fungi, viruses, or parasites. The resultant immune response goes haywire, leading to dysregulation of the inflammatory process, endothelial dysfunction, microcirculatory failure, metabolic derangements, and organ failure.
Initial Infection and Immune Response
Sepsis starts with the encroachment of a pathogen (usually bacteria) into the bloodstream or tissues. The immune system detects these pathogens via pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) present on immune cells like macrophages, dendritic cells, and neutrophils. These receptors recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), which trigger an innate immune response.
Once the infection is recognized, a cascade of signaling events is initiated, leading to the production of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukins (IL-1, IL-6, IL-8), and interferons. This cytokine storm is crucial for recruiting immune cells to the site of infection, increasing vascular permeability, and amplifying the immune response. This happens in all situations when infection occurs and it is self limiting.
However, in septic shock, the initial immune activation becomes dysregulated. Massive release of proinflammatory mediators overwhelms the body’s control mechanisms, causing a systemic inflammatory response (SIRS) that causes intense collateral damage to tissues distant to the site of infection. There is widespread activation of and damage to endothelial cells, resulting in glycocalyx disruption and capillary leak, the coagulation system, resulting in microvascular coagulation, and the complement cascade, resulting in tissue damage.
Once of the major issues to understand in early sepsis is that due to dysregulation, much of the body’s inflammatory reserve and homeostatic mechanisms are used up early. Consequently, it may take some time to restore innate immunity (immunoparalysis), making the patient vulnerable to secondary infections, and neurohormonal reserve – particularly vasopressin and, later, cortisol.
Impact of Sepsis on the Endothelium and Microcirculation
Endothelial cells lining the blood vessels play a central role in maintaining vascular integrity, regulating blood flow, and controlling inflammation. In septic shock, the release of proinflammatory cytokines and mediators causes endothelial activation and dysfunction. This results in:
Increased vascular permeability: capillaries become leaky and protein rich fluid extravascates into the interstitium, expanding and damaging its gelatinous structure (“fracking the interstitium”). This results in reduced circulating volume, tissue edema and organ dysfunction. such as nitric oxide (NO), prostacyclin, and other vasoactive substances.
Vasoplegia – Pathological vasodilatation across the arteriolar and venular network is a characteristic component of septic shock. The causes are multifactorial, but include increased production of vasodilators like nitric oxide, bradykinin, and prostacyclin. This is manifest by low blood pressure, caused by increased unstressed blood volume, reduced venous return, reduced stroke volume and reduced arterial resistance.
Microcirculatory dysfunction: the microcirculation is characteristically disrupted in sepsis. This is characterized by clot deposition in small vessels, platelet aggregation, disruption of the glycocalyx and endothelial swelling. Blood flow is reduced, and this leads to tissue hypoxia and organ dysfunction, particularly in the lungs, kidneys, liver, bowel and heart.
Coagulopathy: Septic shock is associated with coagulopathy likely due to activation of the coagulation cascades following endothelial disruption, resulting in widespread microthrombosis. The platelet count falls dramatically, and then, due to loss of coagulation reserve, bleeding results.
Metabolic Changes in Sepsis (including Lactate)
Although I don’t cover metabolic changes in the video tutorial – it is worth looking at them to develop a holistic understanding of sepsis/multi-organ dysfunction.
There is insulin resistance – resulting in hyperglycemia, and subsequent relative hypoinsulinemia. Increased blood glucose provides fuel for pathogens and exacerbates immune dysfunction.
Mitochondrial function and oxygen utilization become dysfunctional. The impact of this on outcomes is poorly understood, but it may be part of the motor behind multi-organ failure, particularly in the kidneys.
Principle utilization of skeletal and visceral proteins as sources of energy, principally by gluconeogesesis. The body is unable to use fat stores as a source of energy, and “autocannibalism” results. This may be a significant component of “polymyopathy” of critical illness.
Aerobic Glycolysis – although the body produces approximately 1.5 mol of Lactate per day, this is usually rapidly cleared by the Liver (Cori cycle) such that plasma lactate is unmeasurable. I acute critical illness including sepsis, lactate conversion to pyruvate is reduced and lactate production increased due activation of lactate dehydrogenase by epinephrine (adrenaline). Reduced or dysfunctional hepatic blood flow results in reduced lactate metabolism. The consequence is hyperlactatemia and metabolic acidosis. The degree of acidosis strongly correlates with the severity of acute critical illness. A plasma lactate in excess of 2mmol/L is considered clinically relevant.
Organ Dysfunction and Failure (MODS – Multi-Organ Dysfunction Syndrome)
It is imperative that clinicians quantify the degree of organ failure in acute critical illness at an early stage. A useful tool for monitoring MODS is the SOFA score.
The most easily quantified systems for identifying MODS are the respiratory system, the cardiovascular system, the central nervous system, the kidneys, coagulation and the liver.
Respiratory – hypoxic respiratory failure that may progress to Acute Respiratory Distress Syndrome (ARDS)
Cardiovascular – hypotension, hypoperfusion
CNS – confusion, delirium
Kidneys – oliguria, acute kidney injury
GI/Liver – Ileus, hyper or hypolglycemia, hyperbilirubinemia
Blood – coagulopathy, thrombocytopenia
The mechanisms behind each of these injuries are beyond the remit of this article. One should calculate the SOFA score on each critically ill patient each day.
SCREENING THE PATIENT FOR SEPSIS
Every hospital has its own screening tool for sepsis, and, despite 30 years of proposals, there is no universally accepted tool. Below is a summary of the options currently available.
Quick SOFA (qSOFA) Score (2016)
The qSOFA score is based on three clinical criteria:
Respiratory rate ≥ 22 breaths per minute
Altered mentation (Glasgow Coma Scale < 15)
Systolic blood pressure ≤ 100 mmHg
A qSOFA score of 2 or more points indicates a high risk of sepsis and warrants immediate further evaluation and intervention.
Although the qSOFA score is a useful rule of thumb, it is neither sensitive nor specific and not recommended as a standalone screening tool by the Surviving Sepsis Campaign.
Respiratory rate: >20 breaths per minute or PaCO2 < 32 mmHg
White blood cell count: >12,000/mm³, <4,000/mm³, or >10% immature bands
Patients who meet 2 or more criteria are considered to have SIRS, and if the cause is infection, it may progress to sepsis.
Early Warning Scores
Most hospitals use Early Warning Scores (EWS) to identify the deteriorating patient on the ward, but these are now commonly combined with SIRS and other criteria for identifying sepsis. EWS looks at common bedside observations and categorizes the variation from normal. These include heart rate, respiratory rate, need for oxygen, blood pressure, level of awakeness (AVPU) and temperature. The more systems that are abnormal the higher the score and the more likely that an intervention (e.g. consulting the critical care team) will take place. I am a big fan of EWS.
If medical review determines that the patient indeed is likely to have sepsis, a “bundle” of care (such as “sepsis-6”) is activated and the patient follows a sepsis pathway. Although such pathways are used worldwide, I am going to follow a slightly different 10 point therapeutic route that mirrors the Surviving Sepsis Guidelines and is more applicable to critical care.
MANAGING THE PATIENT WITH SEPTIC SHOCK
Step 1 Put in an IV line
TAKE BLOOD IMMEDIATELY FOR:
1. Blood Cultures
2. CRP or Procalcitonin/ FBC (WCC) / Lactate
This will give us an idea of the level of inflammation (WCC, CRP and Lactate) over the next hour or two and, hopefully will help us guide antibiotic therapy
Step 2 Through that IV line
ADMINISTER
Broad Spectrum Antibiotics (e.g. co-amoxyclav) based on your best guess source.
Upto 30ml/kg of intravenous fluid, preferably a balanced solution such as Hartmann’s, Lactated Ringers, or Plasmalyte-148.
Step 3 Vasopressors
If the MAP (or adjusted MAP target) does not reach 65mmHg after fluid resuscitation (do NOT give more than 5L of iv fluid) then the patient requires VASOPRESSORS.
The vasopressor of choice is norepinephrine (noradrenaline -NAD). This is an extremely effective agent: it restores the stressed blood volume, increases diastolic blood pressure – improving coronary blood flow, has inotropic effects – thus maintains stroke volume, and preferentially perfuses the midline structures, rather than the extremities. The major benefit of norepinephrine versus epinephrine in this setting is NAD’s lack of B2 adrenoceptor effect – it does not raise blood glucose or lactate.
Norepinephrine should be administered relatively early, and it does not require a central line: NAD can be safely delivered by a proximal peripheral cannula.
Step 4: Hormone Replacement Therapy
If the dose of norepinephrine is rising (the exact level is unclear – I turn to this drug early) then an ultra low dose infusion of arginine vasopressin is indicated. Vasopressin works via V1 receptors to increase vascular tone, and V2 receptors to maintain vascular volume. The dose is typically 0.03 units per minute – this will have no physiological impact on normal patients – in the setting of sepsis or severe blood loss vasopressin (as hormone replacement therapy) restores vascular tone, improves the effectiveness of norepinephrine and improves renal blood flow and urinary output. There is no downside, and I typically wean norepinephrine off before stopping vasopressin.
If High Dose Vasopressors are Not Working – consider Corticosteroids
Corticosteroids in this setting may have 2 benefits: 1. Damping down the initial hyperinflammatory response (some evidence in community acquired pneumonia), 2. As hormone replacement therapy (glucocorticoids are co-factors for catecholamine function).
Step 5 Identify and Control the Source of the Infection
The source is either medical or surgical. Medical sources are commonly – urinary tract, respiratory, intracranial (meningitis) or catheter related bloodstream infections.
As part of the workup, various cultures should be sent: blood culture, sputum culture, urine culture. A chest x-ray should be performed and tailored imaging to confirm the suspected source of the problem (CT abdomen, pelvis, chest, spine, brain)
Surgical sources are medley – they range from necrotizing soft tissue infections, to retained products of conception, perforated bowel or viscus, pilonidal abscess, intra-abdominal abscess, pancreatitis, spinal abscess, wound infection or wound dehiscence. Your cannot medically manage a surgical problem.
Step 6 Be Careful of the Search Satisficing Error
If the patient is persistently hypotensive despite multiple high dose pressors you need to expand your search for the problem. Is this cardiogenic shock (consider and echocardiogram) or a missed head or spinal injury (neurogenic shock or raised ICP). Does the patient have abdominal compartment syndrome (hypotension, oliguria, high airway pressures and intra-abdominal pressure of >20mmHg) or another compartment syndrome – cardiac tamponade, too much PEEP, tension pneumothorax etc.
If the lactate does not fall, you have a continued problem: there is still splanchnic hypoperfusion (the patient is under-resuscitated), the bowel or splanchnic circulation are ischemic, or the source is not controlled. Be careful of overvaluing hyperlactatemia in patients on epinephrine (adrenaline) infusions – this directly drives up lactate levels.
If there is severe mottling – there is no flow to the microcirculation – and that is what you can see on the skin – you cannot see the lungs, bowel and liver which are also suffering. Two things should be considered – is norepinephrine doing more harm than good (lower your MAP target and reduce the NAD) and is the patient still under-resuscitated. In this setting it is reasonable to “empty the kitchen sink” into the patient – giving plasma, 20% albumin and even 8.4% NaHCO3 to expand the plasma volume and restore blood flow.
Step 7 Prevent Further Complications
Once the patient is in the ICU and relatively stable you need to back off on therapeutic interventions, and take measures to prevent iatrogenic complications. These include:
Stopping further crystalloid resuscitation – NO maintenance fluids – to avoid both fluid and solute overload.
Wake the patient up and avoid over sedation, give the patient a day-night cycle and proper sleep hygiene to ensure that they don’t develop deliriu,
Avoid intubation if at all possible, if not – carefully watch the tidal volumes and airway pressures to avoid ventilator induced lung injury.
Sit the patient up and sterilize the mouth to avoid ventilator associated pneumonia.
Remove central lines when no longer needed.
Give stress ulcer prophylaxis (if indicated).
Watch carefully for bed sores – turn and mobilize the patient.
Address nutrition, bowel hygiene and the microbiome at an early stage.
Step 8 Deresuscitate and Normalize the Patient
After 7 days one should be aiming to return the patient to their baseline weight – and that means deresuscitating the crystalloids from the patients body, either spontaneously, using diuretics or using continuous kidney replacement therapy (CKRT). The fluid balance should be even by day 7. In addition, nutrition should be started by day 3 and the patient should be receiving full nutrition by day 7. Sedation and other “consciousness clouding” drugs should be discontinued. Antibiotics should be de-escalated and stopped.
Step 9: Start Rehab Early
The multidisciplinary team are an essential component of modern critical care – a patient lying sedated in a bed, endlessly, develops medley complications. Sleep hygiene is imperative. Early mobilization and assessment by physiotherapy, occupational therapy, speech therapy etc. is essential. The microbiology team should assess the need for antimicrobials on a daily basis and care taken to avoid hospital acquired infections. Finally, critical illness takes a massive psychological toll – intensive care units should have a staff psychologist to deal with the patients mental health needs, to prevent PTSD.
Step 10: If the Patient is Not Getting Better They Are Getting Worse
If the patient does not recover rapidly within 7 days then they are likely to enter phase of chronic critical illness, where the body’s vital systems seem to go into a state of hibernation. Often they develop severe muscle weakness, resulting in difficulty liberating from mechanical ventilation (a tracheostomy may be required), the autonomic nervous system may become dysfunctional – manifest by rapid swings in blood pressure and heart rate, the neuroendocrine system may be burnt out and the patient may develop immunoparalysis.
There is no magic bullet to restart the body in chronic critical illness. The majority of patients will eventually recover. Unfortunately, many don’t – multiple infectious and iatrogenic hits results in progressive multi-organ failure and ultimately death. Although in hospital sepsis outcomes have improved dramatically since the turn of the century, little progress has been made on chronic critical illness; unfortunately.
This tutorial looks at the problems of Hypotension and Shock. I define the difference between the concepts – not all hypotensive patients are shocked and not all shocked patients are hypotensive. I then go through a system for exploring the hypotensive or shocked patients’ status to determine the underlying problem – illustrated by a series of clinical scenarios.
One of the reasons that we perform portable AP chest x-rays (CXR) in the ICU is to confirm the correct positioning of hardware: endotracheal tubes, central lines, feeding tubes, pulmonary artery catheters, pacemaker wires and chest tubes. This tutorial discusses the correct position of each of these devices and looks at malplacement and complications.
The ideal location of the tip of the endotracheal tube is 3 to 5cm above the carina, below the clavicles and at the level of the T4 spinous process. If tube is too far in, there is a risk of endobronchial intubation and atelectasis of an entire lung (usually the left lung, but not infrequently the right upper lobe also).
The ideal location of a central line, placed in the SVC distribution (internal jugular, subclavian or PICC) is at the junction of the Superior Vena Cava and the Right Atrium. Although inadvertent arterial puncture is less likely, these days, due to ultrasound guided insertion, the tip of a central line can end up can end up in all kinds of places. The tip placement, for prolonged infusions in critical care (for example – pressors or TPN), needs to be confirmed by chest x ray. The major complication of central lines is pneumothorax due to inadvertent pleural puncture during placement.
The pulmonary artery catheter is floated through the right heart and lodged into a peripheral branch of the pulmonary artery, aided by a balloon. The ideal location of the tip is in the lower zone of the lung, and the appearance of the catheter may be a V – the tip is in the left pulmonary artery or a B – the tip is in the right pulmonary artery. It should not be curled up in the RV or, worse, in the inferior vena cava.
Intra-aortic balloon pumps are inserted in cardiology, to manage cardiogenic shock, and following cardiac surgery. The balloon inflates in diastole to increase diastolic pressure, increasing coronary artery perfusion pressure and improving cardiac performance. The tip of the IABP should be distal to the left subclavian artery as it comes off the thoracic aorta. If the tip is too proximal, there is a risk of ischemia to the left arm, if it is not high enough, then it doesn’t function as required and may injure the kidneys.
Chest drains are typically placed to drain air and fluid from the pleural cavity. The tip of the chest tube needs to be where the “stuff” that you wish to drain is located: in the lung apices for air (if the patient is erect or semi erect), in the bases for fluid. There are two “eyes” on each chest tube – both need to be located inside the pleura or air will leak into the subcutaneous tissues.
Finally you need to be able to identify single lead and dual lead pacemakers, implantable defibrillators (ICD) and loop recorders on chest x-ray.
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)
Expiratory dysynchrony is a major unrecognized problem in critical care. Usually it takes one of two forms: a terminal upstroke on the pressure waveform, indicating pressure cycling (breath too long) or a W shaped anomaly in the expiratory flow waveform – indicative of the breath being too short or too long. I call this the “Wibbly Wobbly Waveform”.
This tutorial looks at expiratory dysynchrony – why it happens and how to make adjustments to resolve the problem. I also introduce a relatively new technology: IE Sync.
The introduction of the active expiratory valve was a disruptive technology in critical care mechanical ventilation. This valve flutters when the airway pressure rises above the targeted level – to vent off surplus gas, but maintain airway pressure. It led to the development of newer modes of ventilation (and adjustments to older modes) that allowed the patient to breathe spontaneously independent of the ventilator. As such this was a development of intermittent mandatory ventilation (IMV) – without the risk of breath stacking and expiratory dys-synchrony.
The major mode of ventilation that evolved from the active expiratory valve has several different aliases – BiLevel, BIPAP, BIVENT, DuoPAP etc. but they are all, essentially, pressure controlled intermittent mandatory ventilation modes – that allow the patient to breathe supported or unsupported at a high (Phigh) or low (Plow) airway pressure.
I have chosen the term “Bilevel Pressure Control (BL-PC)” to describe this mode. This tutorial introduces BL-PC, from the perspective of IMV, explains the technology and then discusses the setup and use of the mode. It is a mode of ventilation that is used widely as the “default mode” in many ICUs and can be used in any patient at any time. @ccmtutorials http://www.ccmtutorials.org
This weeks tutorial is on SIMV-Pressure Control. Although this is one of the lesser used modes of ventilation, I sometimes see my colleagues using it in the operating room. And for good reason. Anesthesia ventilators are not set up in the same way as ICU vents. In particular – if you choose “PC” Pressure Control – that is what you get – pressure control; NOT pressure assist control. Hence there is no real provision for patient ventilator interaction. If you choose “SIMV” as pressure control, volume control or volume guaranteed pressure control, then the patient can breath and interact with the ventilator and receive pressure supported breaths. Consequently, conventional SIMV modes, these days, are far more likely to be used in the operating room than in the ICU.
The second reason that I wanted to cover SIMV Pressure Control is to set the groundwork for a different mode “BiLevel Pressure Control” that is built on a similar platform, looks a bit like SIMV, and has significant benefits for those of you who might choose SIMV-PC in ICU.
Most modes of ventilation offer two ways of supporting the spontaneous breath – assist control and SIMV. In SIMV-PC the spontaneous breath can be unsupported, pressure supported or partially supported using Automatic Tube Compensation (ATC). This tutorial covers the type of patient to whom you might deliver SIMV-PC; how to set up the mode; what it looks like on a ventilator screen and the strengths and weaknesses of the mode. @ccmtutorials http://www.ccmtutorials.org
For most of us, the terms CPAP (continuous positive airway pressure) and PEEP (positive end expiratory pressure) have existed for all of our careers. But this was not always the case. Although mechanical ventilation, including the positive pressure variant, was a child of the 1950s – PEEP was not described until the late 1960s and even then was seen as a therapy for postoperative atelectasis in cardiac surgery patients. PEEP subsequently became the mainstay of therapy for hypoxic respiratory failure, but was always used in associated with positive pressure breaths. CPAP was developed in the early 1980s as a therapy for sleep disordered breathing. Over two decades the non invasive CPAP therapy and the invasive ventilation (pressure targeted breaths with PEEP) coalesced such that CPAP became a therapy for hypoxic respiratory failure and congestive heart failure, and pressure support (BiPAP or NIV) became a therapy for sleep apnea.
Strictly speaking PEEP and CPAP are different. It is possible to apply PEEP at end expiration and then commence the next breath from atmospheric pressure (try slapping your hand over your mouth mid expiration – then remove it and take a breath) – spontaneous PEEP. However this is almost never used in clinical practice. In CPAP the patients sinusoidal respiratory pattern persists – but starts and ends at an elevated baseline pressure. In PEEP the positive pressure breath starts and ends at that pressure (i.e. pre inspiration and end expiration). So, these days, in most scenarios PEEP and CPAP are indistinguishable. How they are delivered is, of course, different. Nevertheless they serve the same functions 1. To overcome airway resistance that causes disrupted or obstructed gas flow in expiration; 2. To reduce the work of breathing by reducing the magnitude of negative pleural pressure required to generate a tidal volume; 3. Most importantly – to restore functional residual capacity (FRC); 3. To prevent derecruitment of vulnerable lung units in the posterior dorsal segments of the lungs.
PEEP does not easily re-expand collapsed lung tissue – this is usually achieved by applying a recruitment maneuver (30cmH2O or more for 10 seconds during anesthesia, for 30 seconds in lung injury). The application of PEEP then prevents derecruitment. As such the majority of lung tissue may be re-expanded during anesthesia. This may not be the case in diseased lungs – the principle is to restore a functional residual capacity even if that effectively utilizes the inspiratory reserve volume.
This is likely the most important of the four tutorials on Pressure Support Ventilation. As you may recall, PS is an unusual mode of ventilation because it is flow cycled – that is – the ventilator cycles to expiration as specific, user set, percentage of peak flow. The default expiratory sensitivity is usually around 25%. Expiratory dys-synchrony is frequently missed by bedside clinicians who have not been schooled in waveform analysis. This tutorial covers everything you need to know. @ccmtutorialshttp://www.ccmtutorials.org
Next time I am going to commence a series of tutorials on hypoxia-hypoxemia. This will start with a discussion about how we measure hypoxemia – in particular oxyhemoglobin saturation (Tutorial 12). I will then go on to discuss atelectasis, shunt, ventilation-perfusion mismatch and introduce oxygen therapy (Tutorial 13).
ORtoICU 