This is the first tutorial in the cardiovascular assessment module. In the tutorial I discuss heart rate, how it originates and how it is controlled. This is principally a discussion about sinus bradycardia and sinus tachycardia. I go on to discuss the parasympathetic nervous system and the sympathetic nervous system, how they function physiologically and how they are impacted by drugs that we administer and disease processes. I provide a detailed discussion of adrenoceptor agonists and antagonists.
I feel like I have been working on this tutorial for several years. I actually have. When one encounters a modern chest drain unit in ICU for the first time or the 50th time it can be quite daunting. How much is draining? Is it oscillating? What does “bubbling” imply? When do you use suction? Why do some nurses leave a meniscus of fluid in the tubing but others don’t? What is the little red cap supposed to do?
This tutorial starts with a discussion of the physiology of pneumothorax and hemothorax, and then progressively visits one bottle, two bottle and three bottle systems. I then go on to explain how relatively modern chest drainage systems work, and how they need to be modified to apply suction – wet and dry. Finally I explain how very modern digital chest drainage systems work.
If you have struggled with understanding chest drains, I guarantee you’ll learn something.
This is the final tutorial on the basics of Chest Imaging in the ICU. It includes a discussion about the extrapulmonary tissues – pleural and mediastinal and lung diseases (pneumonia, ARDS, PJP etc.).
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.
When patients arrive in the ICU, as soon as they are settled, an AP portable chest x-ray (CXR) is ordered. That x-ray will look different from one done in the radiology department, as the patient is likely semi-recumbent, may be in expiration and the projection is different than from an CXR taken from the back.
The lung has 5 lobes – three on the right and two on the left (the left lung is smaller to accommodate the heart). Each one of these lobes is connected to the trachea by one major airway, that may become plugged off, resulting in atelectasis or collapse of the lobe. As we often need to remove mucus plugs or other material causing these obstructions, it is imperative that you are able to identify the particular lobe that has collapsed. I sequentially go through each lobe of the lungs.
To identify a collapsed lung lobe I suggest that you follow the “Ds” listed in the image below.
In addition, radiologists often report lung units as being “consolidated.” This is a catch all phrase that identifies the presence of liquid or semisolid material in airspaces – infectious exudate, blood, mucus, water-fluid, gastric contents etc. You should be able, with you anatomical knowledge, to identify which lung lobe is affected, in particular if you are planning on performing a broncho-alveolar lavage. @ccmtutorials
One of the most intimidating things about entering the ICU for the first time is the “life support machine” – the mechanical ventilator. Although I have posted an extensive series of tutorials on Mechanical Ventilation, covering most of the modes, oxygen therapy and applied respiratory physiology, I have attempted, in this tutorial, to distill everything to the “least you have to know” in 40 minutes. Keep in mind that modern machines look more like iPhones, and are far easier to use than the devices I grew up with that looked to me, on day 1, like something in the cartoon below.
I start with a discussion about the difference between normal breathing, CPAP and Positive Pressure Ventilation (PPV). PEEP is, effectively, CPAP during PPV. I then go on to discuss pressure limited modes of ventilation; worldwide this are the most widely used modes in ICU. I limit my discussion to Pressure Assist Control, Volume Guaranteed Pressure Control (VG_PC) and Pressure Support Ventilation (PSV). VG-PC is a popular and flexible option as an ICU’s default mode. However, as it is a pressure controlled mode, there is significant variability in tidal volume and airway pressure from minute to minute.
Several important rules are emphasized: the tidal volume should, in general be lower than 6ml/kg of ideal body weight, the plateau pressure lower than 30cmH2O and the driving pressure lower than 15cmH2O. I introduce the Spontaneous Breathing Index (SBI = RR/TV in L). The magic number is 100. We use the SBI to determine the success of weaning on PSV.
Volume Controlled Ventilation is the predominant mode use in the Operating Rooms (Theatres), and Volume Assist Control is a popular mode in North America. In ICU you must set a peak inspiratory flow and be aware that this may be insufficient during assisted breaths and lead to dys-synchrony. Volume Control is often used in ARDS to “lock in” the Tidal Volume (TV) but the operator must be aware that the TV that matters is not what is dialed up on the ventilator, but what the patient exhales.
I go on to discuss how to assess the patient on invasive mechanical ventilation, by looking at whether they are breathing spontaneously, in which case we determine whether they are suitable for a Pressure Support wean or not, or whether or not there is a problem with oxygenation (increase FiO2, PEEP, Mean Airway Pressure and seriously consider Prone Positioning) or Ventilation (increase Respiratory Rate, Tidal Volume or both, reduce PEEP).
The final part of the tutorial looks at Non Invasive Ventilation (NIV), and I explain how, in general we only use 2 modes on standalone devices – CPAP and Spontaneous Timed (S/T). The latter is similar to PSV with a backup rate, but I point out that instead of PEEP+PS the breath is EPAP + IPAP and IPAP is not built upon IPAP, as is the case with PSV. If one is delivering NIV on an ICU ventilator, then “leak” adjustment or “leak sync” should be used.
This tutorial looks at the assessment of PaCO2 on the blood gas and how it interfaces with the pH and the Bicarbonate (HCO3-). The control of PaCO2 is a major physiological mechanism for maintaining homeostasis. CO2 production by the body must be balanced by CO2 elimination. PaCO2 rises when there is hypoventilation, this results in a fall in pH and an rise in HCO3 and this is called “Acute Respiratory Acidosis.” If the patient hyperventilates, the PaCO2 and the HCO3 fall and the pH rises: this is “Acute Respiratory Alkalosis.” When there is chronic CO2 retention, the body adapts by wasting Chloride in the urine, the pH normalizes and the HCO3 rises substantially.
Any patient who is intubated, or who has a laryngeal mask in situ, must undergo end tidal (end of exhalation) CO2 monitoring. The capnography waveform is worth evaluating, particularly if airway obstruction or increased resistance is suspected.
Included in this tutorial are various rules of thumb that you can use to determine the Respiratory Acid Base Status of the Patient – including the “Rule of 40.”
I am now going to move on, in the Introduction to Critical Care course, to a systems based assessment of the patient where you are expected to compile measurements and observations from the clinical information system, radiologic system and monitors to construct an overview of the patient’s status. This is the crux of intensive care medicine and it is not easy. I am going to visit each system sequentially, and some systems will have multiple tutorials. By the end of this process, you will have compiled all of the data, assessed and processed it, and be ready for the big presentation.
The first tutorial in this part is an overview of patient assessment. It is relatively short but essential.
The Second tutorial in this sequence is on at neurological assessment in the ICU. It contains a discussion about the Glasgow Coma Scale, The Richmond Agitation Sedation Scale and CAM-ICU. I also cover the assessment of suffering (PAID) in critical care.
You will need to assess the patients neurologic status, whether or not they appear to be suffering and what interventions, both environmental and pharmacological, that you are administering to help them.
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.
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.
ORtoICU 