It is important to recognize Acute Decompensated Heart Failure (ADHF) as more than just simply a clinical diagnosis but rather as a condition with a wide range of possible clinical presentations. Patients presenting with ADHF typically fall into 1 of 4 recognized hemodynamic profiles that when appropriately identified, provide a particularly useful framework to guide therapy. The correct profile can be determined based on two clinical parameters: perfusion status and congestion. The assessment of a patient suspected to be in ADHF starts with a good history & exam. Signs of poor perfusion include cool extremities, fatigue, altered mental status and low urine output. Signs of congestion include Crackles/Rales on auscultation, JVD, Orthopnea/PND and Peripheral Edema. Some exam findings may be more specific rather than sensitive making the diagnosis challenging. Imaging and more importantly, bedside ultrasound are excellent at evaluating hemodynamics and cardiac function (“the squeeze”) along with presence of pulmonary edema (“B-lines). ECG is vital while lab markers such as BNP/NT-proBNP and Troponin may be elevated and helpful in establishing a diagnosis. Adequate perfusion without congestion (Warm & Dry) is the treatment goal with emphasis placed on prevention. Most patients, however, are adequately perfused but congested on presentation (“Warm & Wet”). They may benefit from LV afterload reduction (Vasodilators) which augment forward flow to the kidneys where excess volume can then be excreted using diuretics. The poorly perfused and non-congested profile (“Cold & Dry”) usually results from the overdiuresis of a Wet & Warm patient causing hypovolemia needing a little fluid. This is not uncommon and can be prevented by adjusting the dose and/or transitioning to oral therapy when our patients have achieved negative fluid balance and are clinically improved. Poorly perfused and congested (“Cold & Wet”) is essentially Cardiogenic Shock. These patients need inotrope therapy and afterload reduction. Cardiac cath if acute coronary syndrome is the determined cause and perhaps even mechanical support (Balloon pump, Impella, LVAD, ECMO). “Warm & Dry” is the treatment goal with emphasis then placed on prevention. #diagnosis #differential #algorithm #management #cardiology #treatment #table #foamed #heartfailure #chf #criticalcare #icu #clinical #pharmacology

In ARDS, we know that the lungs are so diffusely injured that the remaining total area of relatively spared lung may be reduced to the size of a baby’s lungs, hence the “Baby Lung” concept. Despite this, it is also important to realize that in ARDS, lung injury may be diffuse, but not necessarily uniformly distributed, and we often see heterogenous patterns of lung injury mixed with regions of relative lung sparing. In that sense, both lungs may have multiple “Baby Lungs” with different baseline volumes (FRC) that depend on the area of lung spared in those regions. This is where the concept of Lung Strain and Lung Stress come into play. Lung Strain is Tidal Volume/FRC. Consider a patient in ARDS where 6 ml/kg corresponds to 400 ml tidal volume. If a spared region has an FRC of 400 ml, strain is calculated as 1; however, if a neighboring region has an FRC of only 100 ml, then lung strain is 4! 4 times the amount of strain! Likewise, stress and strain are directly correlated to one another. Therefore, even at low tidal volumes and plateau pressures <30, we may be providing lung protective ventilation to one region of spared lung while causing significant lung strain and lung stress to another. Keep this in mind, and always shoot for the minimum in terms of low tidal volumes. 6 ml/kg is what has been classically taught, but if you can get away with 3-4 ml/kg, the risk of lung strain is even further minimized. Same with lung stress; we are taught to keep plateau pressures < 30; but shooting for the lowest possible plateau pressure is likely the best way to minimize lung stress. Ultimately, the goal is to minimize the risk of Ventilator-Induced Lung Injury (Barotrauma, Volutrauma) and promote Lung rest and recovery. #pathophysiology #diagnosis #management #ards #foamed #criticalcare #treatment #respiratory #clinical

There are similarities and differences between these 3 conditions which all carry treatment implications. Each mimic the “Starved state” where Glucagon easily outweighs Insulin. Glucagon stimulates the breakdown of glycogen stores in the liver along with Gluconeogenesis to maintain blood glucose. It also stimulates Lipolysis, which mobilizes fatty acids for beta-oxidation in the liver to produce Acetoacetic acid, a ketoacid that is also converted to beta hydroxybutyrate (BHB). Therefore, in all 3 conditions, serum BHB has limited utility in differentiation. In Starvation Ketosis (SK), acidosis is very mild if at all present. Ketoacids stimulate the pancreas to release Insulin which is enough to keep Lipolysis in check. In Alcoholic Ketoacidosis (AK) we commonly encounter patients who are severely volume depleted and in withdrawal which drastically elevates the stress level along with circulating stress hormones that work synergistically with Glucagon to overwhelm Insulin. This leads to massive production of Ketoacids like BHB. But we also have Lactic Acidosis as well. Recall, NAD+ is a cofactor used to convert Pyruvate to Acetyl-CoA in the TCA cycle. The metabolism of Alcohol depletes NAD+ yielding NADH instead, a cofactor used to convert Pyruvate to Lactate! Patients with AK may, therefore, present with severe acidosis. NAD+ is also a cofactor for Gluconeogenesis which is why patients may also present with Hypoglycemia. In both SK and AK, feed them or give IV dextrose, give thiamine, and watch out for Refeeding Syndrome. If Hyperglycemic, avoid Insulin drips unless also diabetic as you risk causing Hypoglycemia once the Insulin/Glucagon balance normalizes. In both conditions, low levels of circulating Insulin and Ketoacid-induced Insulin release are typically enough to prevent blood glucose > 250 mg/dl or Glucosuria. DKA is essentially a state of NO Insulin; the actions of Glucagon are completely unmitigated, and this leads to severe ketoacidosis, Hyperglycemia > 250 mg/dl and Glucosuria. Treat with Insulin, provided the starting potassium is appropriate to do so. #diagnosis #differential #algorithm #management #treatment #criticalcare #foamed

Perhaps quite too often, the knee-jerk reaction to an elevated Troponin is to call our friends from Cardiology. This becomes a flawed philosophy when taking into consideration the coronary circulation and its potential alterations in the setting of acute illness. The heart consumes a tremendous amount of O2 at baseline, despite receiving only 5% of the resting cardiac output. To compensate, O2 in the coronary circulation is extracted in the myocardium by a much higher degree than it is in any other tissues. In fact, myocardial oxygen extraction is so high, that in conditions imposing greater workloads on the heart (Sepsis, Shock, Hypoxia), the only way to increase myocardial O2 is by increasing coronary blood flow altogether. To do this, the coronary vessels are typically able to dilate significantly…typically. Consider Sepsis, a condition characterized by PERIPHERAL VASODILATION. How can the coronary vessels dilate further if they are already maximally dilated? In many situations they cannot, coronary ischemia ensues, and the Troponin rises. Cardiology cannot help us with this beyond advising us to treat the primary cause. Now consider Tachycardia, often a physiological response to acute illness. Recall, little coronary blood flow occurs during Systole with the majority occurring in Diastole. Even during the Isovolumetric phase of Systole, the LV generates enough compressive force to effectively block off the coronary circulation. There is a bit more Systolic flow on the right side as the RV generates much less force. The faster the heart rate, the less time there is for Diastole and thus, less time for coronary perfusion. In a healthy heart, this may not be an issue as the vessels can easily dilate and respond. But in our patients with CAD with already dilated vessels, or acutely ill patients with systemic vasodilation, this may not be the case. Once again, other than dealing with the primary disturbance Cardiology may not provide much more insight. There is no “one size fits all” in medicine and there are situations which may be similar where Cardiology may truly be needed. Just keep in mind the coronary circulation, the presenting illness, and predisposing conditions of the patient before making the call. #diagnosis #management #cardiology #clinica l#foamed #algorithm #criticalcare

Perhaps quite too often, the knee-jerk reaction to an elevated Troponin is to call our friends from Cardiology. This becomes a flawed philosophy when taking into consideration the coronary circulation and its potential alterations in the setting of acute illness. The heart consumes a tremendous amount of O2 at baseline, despite receiving only 5% of the resting cardiac output. To compensate, O2 in the coronary circulation is extracted in the myocardium by a much higher degree than it is in any other tissues. In fact, myocardial oxygen extraction is so high, that in conditions imposing greater workloads on the heart (Sepsis, Shock, Hypoxia), the only way to increase myocardial O2 is by increasing coronary blood flow altogether. To do this, the coronary vessels are typically able to dilate significantly…typically. Consider Sepsis, a condition characterized by PERIPHERAL VASODILATION. How can the coronary vessels dilate further if they are already maximally dilated? In many situations they cannot, coronary ischemia ensues, and the Troponin rises. Cardiology cannot help us with this beyond advising us to treat the primary cause. Now consider Tachycardia, often a physiological response to acute illness. Recall, little coronary blood flow occurs during Systole with the majority occurring in Diastole. Even during the Isovolumetric phase of Systole, the LV generates enough compressive force to effectively block off the coronary circulation. There is a bit more Systolic flow on the right side as the RV generates much less force. The faster the heart rate, the less time there is for Diastole and thus, less time for coronary perfusion. In a healthy heart, this may not be an issue as the vessels can easily dilate and respond. But in our patients with CAD with already dilated vessels, or acutely ill patients with systemic vasodilation, this may not be the case. Once again, other than dealing with the primary disturbance Cardiology may not provide much more insight. There is no “one size fits all” in medicine and there are situations which may be similar where Cardiology may truly be needed. Just keep in mind the coronary circulation, the presenting illness, and predisposing conditions of the patient before making the call. #diagnosis #algorithm #cardiology #echocardiogram #management #clinical #criticalcare #foamed #treatment

The crusade against “Ab”Normal Saline continues. This is a non-physiologic fluid that can harm our patients in several ways; however, this post will focus on the harms associated with its Chloride (Cl-) content. Our Extracellular Fluid (ECF) is dominated by Na+ whose positive charges are balanced by Cl- and HCO3-. Our Intracellular Fluid (ICF) is dominated by K+ and Mg2+ whose positive charges are balanced by anions on proteins and organic phosphates. The ECF and ICF both work together to maintain this electroneutrality. When we infuse Normal Saline, we introduce a high amount of Cl- into the ECF making it more negative. The ICF responds by taking up an anion that, in reality, we actually need to remain in our ECF, HCO3-. Progressive loss of HCO3- inevitably leads to Metabolic Acidosis. Metabolic Acidosis (H+) is a problem. It disrupts the activities of essentially all our vital organs leading to derangements in function. As acidemia worsens and (H+) accumulates in the ECF, the ICF tries to help out by taking up H+ to buffer against the drop in pH. However, for the ECF and ICF to remain electrically neutral, the ICF must now lose a positive charge of its own so in exchange for H+, K+ leaves the ICF and enters the ECF to maintain electroneutrality in both compartments. This is concerning as a too much K+ in the ECF causes Hyperkalemia, a complication which can easily be fatal if not immediately addressed. Normal saline has been associated with an increased risk of renal failure possibly requiring dialysis or CRRT. The high CL- content induces renal vasoconstriction of the afferent arteriole which reduces renal blood flow and perfusion. Studies have correlated this even in healthy volunteers showing reduced renal blood flow with saline infusions. Many of the patients we are all treating are far from healthy, I’ll leave it to your imagination then to think of the possible outcomes. Balanced crystalloids like LR are safer, more physiologic, and thus easier to use. The only thing “Normal” about saline is when we take it off a patients MAR. #foamed #criticalcare #management #diagnosis #treatment #pharmacology #physiology #crystalloids