Hypovolemic Shock: Treatment & Management PDF

Hypovolemic shock Hypovolemic shock When circulatory shock is caused by a severe loss of blood volume or body water, it is called hypovolemic shock. The severity of hypovolemic shock depends on the amount and rate of intravascular volume loss and each person’s capacity for compensation...

Hypovolemic shock Hypovolemic shock When circulatory shock is caused by a severe loss of blood volume or body water, it is called hypovolemic shock. The severity of hypovolemic shock depends on the amount and rate of intravascular volume loss and each person’s capacity for compensation Hypovolemic shock By definition, hypovolemic shock occurs as a consequence of inadequate intravascular volume to meet the oxygen and metabolic needs of the body. Rapid and effective restoration of circulatory homeostasis using fluids, pharmacologic agents, and/or blood products is vital to prevent complications of untreated shock and ultimately death. Classification of hypovolemic shock and precipitating events Hemodynamic relationships among key CV parameters Hypovolemic shock pathophysiology Compensatory mechanisms such as increases in HR, myocardial contractility, and SVR are sufficiently effective for a moderate loss in volume such that measurable falls in SBP are not detected. Losses in excess of 80% generally overwhelm compensatory mechanisms, and the patient’s condition can deteriorate to overt shock with hypotension and signs of hypoperfusion Hypovolemic shock pathophysiology The most distinctive clinical manifestations of hypovolemic shock are arterial hypotension, clinical signs of hypoperfusion, and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic metabolism. Hypovolemic shock pathophysiology If the decrease in MAP is severe and protracted, such hypotension will certainly lead to severe hypoperfusion and organ dysfunction. Regional ischemia develop as blood flow is naturally shunted from organs such as the GI tract or the kidneys to more immediately vital organs such as the heart and brain. Hypovolemic shock pathophysiology Neurohumoral response to hypovolemia Hypovolemic shock symptoms begin to occur with decreases in intravascular volume in excess of 750 to 1500 mL in adult patients. The body attempts to maximize its fluid status by decreasing water and sodium excretion through release of antidiuretic hormone (ADH), aldosterone, and cortisol. Hypovolemic shock pathophysiology Neurohumoral response to hypovolemia MAP is maintained by peripheral vasoconstriction mediated by catecholamine release and the renin- angiotensin system. CO is augmented by catecholamine release and fluid retention. Hypovolemic shock pathophysiology Prolonged tissue hypoxia can lead to organ dysfunction and eventual failure if untreated. Failure of more than one organ is referred to as the multiple organ dysfunction syndrome (MODS). Involvement of the heart is particularly devastating. Preexisting organ dysfunction and buildup of inflammatory mediators can also exacerbate the effects of hypovolemic shock to the point of irreversibility. Hypovolemic shock pathophysiology For example, acute or chronic heart failure can lead to pulmonary edema, further aggravating gas exchange in the lungs and ultimately tissue hypoxia. Only about one-third of early-onset MODS is quickly reversible (within 48 hours) with proper fluid resuscitation. Thus, it is imperative that hypovolemic shock be treated quickly to avoid MODS. Clinical Presentation and Diagnosis Clinical Presentation and Diagnosis Clinical Presentation and Diagnosis Treatment Desired Outcomes The major goals in treating hypovolemic shock are to restore effective circulating blood volume, as well as manage its underlying cause. Delivery of adequate oxygen and metabolic substrates such as glucose and electrolytes to the tissues throughout the body that will optimally bring about a restoration of organ function and return to homeostasis. Treatment Desired Outcomes Concurrent supportive therapies are also warranted to avoid exacerbation of organ dysfunction associated with the hypovolemic shock event. Identifying the bleeding site and achievement of hemostasis are critical in the successful resuscitation of the patient. This frequently involves surgical treatment of hemorrhages. Treatment General Approach to Therapy: “VIP Rule” 1. Ventilate 2. Infuse 3. Pump (mechanical ventilation, IV access (peripheral or central venous lines), an arterial catheter(MAP, ABG) and bladder catheter(monitoring of urine output)) Treatment General Approach to Therapy: “VIP Rule” 1. Ventilate 2. Infuse 3. Pump (mechanical ventilation, IV access (peripheral or central venous lines), an arterial catheter(MAP, ABG) and bladder catheter(monitoring of urine output)) Treatment Upon stabilization, placement of a PA catheter may be indicated based on the need for more extensive cardiovascular monitoring than is available from noninvasive measurements such as vital signs, cardiac rhythm, and urine output. An alternative to the PA catheter is placement of a central venous catheter that typically resides in the superior vena cava to monitor central venous pressure (CVP) comparable survival and fewer complications than PA catheters. Treatment Fluid Therapy: the cornerstone of managing hypovolemic shock ✓ crystalloids (electrolyte-based solutions) ✓ colloids (large molecular weight solutions) ✓ blood products (in case of hemorrhage or severe preexisting anemia) ✓ adjunctive vasopressor support ✓ Warming of all fluids to 37°C (98.6°F) prior to administration is an important consideration to prevent hypothermia, arrhythmias, and coagulopathy because these complications will have a negative impact on the success of the resuscitation effort Treatment Conventional crystalloid solutions are fluids with either: electrolyte composition that approximates plasma known as balanced solutions (e.g., lactated Ringer’s solution [LR] or Plasma-Lyte) or a total calculated osmolality similar to that of plasma such as 0.9% sodium chloride (also known as normal saline [NS] or 0.9% NaCl) ❖Data are lacking demonstrating superiority of hypertonic crystalloid solutions compared with isotonic solutions. Composition of Common Resuscitation Fluids Treatment Crystalloid Solutions, advantages available low cost equivalent outcomes compared with colloids Treatment Crystalloids side effects: fluid overload electrolyte disturbances (sodium, potassium, and chloride) dilutional coagulopathy Treatment Balanced solutions versus NS Balanced solutions NS contains potassium and has a lower can cause hypernatremia, sodium content hypokalemia, metabolic acidosis, can cause hyponatremia and/or and hyperchloremia hyperkalemia hyperchloremia is a potential risk factor for acute kidney injury in critically ill patients However, improvements in outcome have not been consistently documented with balanced crystalloid solutions nor a clear association of NS that contains a higher chloride content with acute kidney injury Therefore, currently there is no consensus in selecting a balanced crystalloid solution over NS. Treatment A reasonable initial volume of an isotonic crystalloid (0.9% NaCl, LR, or Plasma-Lyte) in adult patients is 1000 to 2000 mL administered over the first hour of therapy Ongoing external or internal bleeding requires more aggressive fluid resuscitation  Treatment In the absence of ongoing blood loss, administration of 2000 to 4000 mL of isotonic crystalloid normally reestablishes baseline vital signs in adult hypovolemic shock patients. Selected populations, such as burn patients, may require more aggressive fluid resuscitation. Individualization of therapy is critical with well-defined endpoints to avoid excessive administration of crystalloids. Treatment Treatment Treatment Colloids include packed red blood cells, pooled human plasma (5% albumin, 25% albumin, and 5% plasma protein fraction), semisynthetic glucose polymers (dextran), and semisynthetic hydroxyethyl starch (hetastarch). Colloids are too large to cross the capillary membrane; therefore, they remain primarily in the intravascular space (although a small portion “leaks” into the interstitial space). Colloids can draw fluid from the IS by increasing the plasma colloid osmotic pressure Treatment Administering 500 mL of colloid results in a 500-mL intravascular volume expansion, except for 25% albumin. Because 25% albumin has an oncotic pressure about 5- fold that of normal plasma, it causes a fluid shift from the IS space into the intravascular space. For this reason, 100 mL of 25% albumin results in around 500 mL of intravascular volume expansion. Treatment This - 25% albumin - hyperoncotic solution should generally be avoided in patients requiring fluid resuscitation, because although the intravascular space expands, fluid shifts out of the IS space, potentially causing dehydration. It may be useful in patients who do not require fluid resuscitation but who could benefit from a redistribution of fluid (e.g., ascites, pleural effusions). Treatment Colloids adverse effects: Generally, the major adverse effects associated with colloids are fluid overload, dilutional coagulopathy, and anaphylactoid/ anaphylactic reactions. Hydroxyethyl starch and dextran products have been associated with coagulopathy and kidney impairment. Because of direct effects on the coagulation system with the hydroxyethyl starch and dextran products, they should be avoided in hemorrhagic shock patients. Treatment Colloids adverse effects: In addition to acute kidney injury, hydroxyethyl starch is associated with increased mortality in critically ill patients. As such, hydroxyethyl starch products are no longer recommended. Treatment A “colloid versus crystalloid debate” exists within the critical care literature. Most clinicians today prefer using crystalloids based on their availability and inexpensive cost compared with colloids. These factors are in addition to the previously mentioned colloids adverse events. Despite these general limitations, there is a paradigm shift in a subset of hypovolemic shock patients, i.e., traumatic hemorrhagic shock to minimize crystalloids, increase the use of blood products and plasma. Treatment Blood products: Blood products are indicated in hypovolemic shock patients who have sustained blood losses from hemorrhage exceeding 1500 mL (freshly obtained whole blood is administered). In case of ongoing resuscitation of hemorrhagic shock, packed red blood cells (PRBCs) can be transfused to increase oxygen-carrying capacity in concert with crystalloid solutions to increase blood volume Treatment Blood products: In patients with documented coagulopathies, fresh-frozen plasma (FFP) for global replacement of lost or diluted clotting factors, or platelets for patients with severe thrombocytopenia (< 20–50 × 103/mm3 [20–50 × 109/L]) should be administered. Type O negative blood or “universal donor blood” is given in emergent cases of hemorrhagic shock. Thereafter, blood that has been typed and cross-matched with the recipient’s blood is given. Treatment Blood products: The traditional threshold for PRBC transfusion in hypovolemic shock has been a serum hemoglobin of less than 10 g/dL and hematocrit (Hct) less than 30% (0.30). However, for critically ill patients who have received appropriate fluid resuscitation and have no signs of ongoing bleeding, a more restrictive transfusion threshold of 7 g/dL appears to be safe. Treatment Blood products: Traditional risks from allogeneic blood product administration transfusion reactions and transmission of blood-borne infections in contaminated blood. Recent large studies have also shown that transfusions are associated with increased infection and higher mortality, possibly because of adverse immune and inflammatory effects. Treatment Blood products: Increased thromboembolic events and mortality have been documented for patients receiving PRBCs stored longer than 28 days. Thus, administration of blood products should be restricted whenever possible and used as early as possible following donation. Treatment Vasopressors: Vasopressor is any pharmacologic agent that can induce arterial vasoconstriction through stimulation of the α1- adrenergic receptors or V1 receptor. Vasopressors are typically used concurrently with fluid administration after the latter has not resulted in adequate restoration of MAP and/or tissue perfusion. Treatment Treatment Vasopressors: Vasopressor therapy may improve the hemodynamic profile in shock patients, but data are lacking that they improve mortality. A study found that early use of vasopressors (i.e., phenylephrine, norepinephrine, dopamine, vasopressin) in the resuscitation of patients with hemorrhagic shock may be associated with increased mortality Treatment Vasopressors: If vasopressors are used, norepinephrine is preferable to dopamine secondary to increased incidence of arrhythmias associated with dopamine in the treatment of shock patients. Thus, norepinephrine should be considered the first-line vasopressor therapy for shock patients. Treatment Vasopressors: Epinephrine should be considered as a second-line vasopressor in patients with shock because of its association with tachyarrhythmias, impaired abdominal organ (splanchnic) circulation, and hypoglycemia. In cases involving concurrent heart failure, an inotropic agent such as dobutamine may be needed, in addition to the use of a vasopressor. Treatment Vasopressors: Vasopressors are almost exclusively administered as continuous infusions because of their very short duration of action and the need for close titration of their dose- related effects. Starting doses should be at the lower end of the dosing range followed by rapid titration upward if needed to maintain adequate MAP. Monitoring of end-organ function such as adequate urine output should also be used to monitor therapy. Treatment Vasopressors: Once MAP is restored, vasopressors should be weaned and discontinued as soon as possible to avoid any untoward events. The most significant systemic adverse events associated with vasopressors are excessive vasoconstriction resulting in decreased organ perfusion and potential to induce arrhythmias. Central venous catheters should be used to minimize the risk of local tissue necrosis that can occur with extravasation of peripheral IV catheters. Treatment Hemostatic Agents: A recent study of tranexamic acid in trauma patients with or at risk of significant bleeding demonstrated a decrease in mortality compared with placebo. As such, a recent European guideline recommends the use of tranexamic acid within 3 hours of injury (1 gram IV over 10 minutes then 1 gram over 8 hours) as an adjunctive agent in the management of bleeding trauma patients. Treatment Supportive Care Measures: Lactic acidosis, which typically accompanies hypovolemic shock as a consequence of tissue hypoxia, is best treated by reversal of the underlying cause. Although based on limited retrospective data, administration of alkalizing agents such as sodium bicarbonate has not been demonstrated to have any beneficial effects and may worsen intracellular acidosis. Treatment Supportive Care Measures: Because GI ischemia is a common complication of hypovolemic shock, prevention of stress-related mucosal disease should be instituted as soon as the patient is stabilized. The most common agents used for stress ulcer prophylaxis are the histamine2-receptor antagonists and proton pump inhibitors. Treatment Supportive Care Measures: Prevention of thromboembolic events is another secondary consideration in hypovolemic shock patients. This can be accomplished with the use of external devices such as sequential compression devices and/or antithrombotic therapy such as the low-molecular-weight heparin products or unfractionated heparin. Sequential compression devices are preferred in any hypovolemic shock patient at risk of ongoing bleeding. Treatment OUTCOME EVALUATION Successful treatment of hypovolemic shock is measured by the restoration of MAP to baseline values and reversal of associated organ dysfunction. Therapy goals include: 1. Arterial SBP greater than 90 mm Hg (MAP > 60–75 mm Hg) within 1 hour. 2. Organ dysfunction reversal evident by increased urine output to greater than 0.5 mL/kg/hour (1.0 mL/kg/hour in pediatrics), return of mental status to baseline, and normalization of skin color and temperature over the first 24 hours. Treatment OUTCOME EVALUATION Therapy goals include: 3. HR should begin to decrease reciprocally to increases in the intravascular volume within minutes to hours. 4. Normalization of laboratory measurements expected within hours to days following fluid resuscitation. Specifically, normalization of base deficit and serum lactate is recommended within 24 hours and may be associated with decreased mortality. 5. Achievement of PAOP to a goal pressure of 14 to 18 mm Hg occurs (alternatively, CVP 8–12 mm Hg). Cardiogenic shock ↓ Cardiac output (CO) Due to systolic or diastolic dysfunction ↑ CVP, ↑ PAWP, ↓ CO, ↑ SVR Causes: Myocardial infarction Cardiomyopathy Myocardial depression from metabolic problems Management: Standard management for underlying disorder (e.g., Aspirin, oxygen, morphine for acute MI) Diuretics to decrease preload or fluid if hypovolemic Inotropes to improve contractility and increase CO (dobutamine, dopamine) Obstructive shock ↓ Cardiac output due to extra cardiac obstruction to blood flow Impaired diastolic filling: Cardiac temponade, tension pneumothorax, constrictive pericarditis Impaired delivery of blood to the heart ↑ CVP, ↑ PAWP, ↓ CO, ↑ SVR Managed mechanically (fluid and vasopressor are of limit utility) Impaired systolic contraction: Pulmonary embolism, severe pulmonary hypertension ↑ CVP, ↓ PAWP, ↓ CO, ↑ SVR Management: ✓ Disease specific therapy ✓ Inotropes and vasopressors ✓ Fluids or diuretics based on fluid status Distributive shock Include septic, anaphylactic, and neurogenic shock (e.g., spinal injury) All types of shocks are associated with tachycardia, whereas neurogenic shock is associated with bradycardia. Generalized vasodilation with enhanced vascular permeability resulting in decreased preload. Management: Fluids Crystalloids are preferred Vasopressors Norepinephrine preferred in septic and neurogenic Epinephrine for anaphylactic shock Adjuvant agents Steroids THANK YOU