Hypovolemic Shock Dr. Pratik Kanani.pptx

hypovolemic shock emergency medicine

1. HYPOVOLEMIC SHOCK By Dr.pratik kanani (JR1) GUIDE DR. VARSHA S. SHINDE PROFESSOR AND HOD EMERGENCY MEDICINE

2. SHOCK OVERVIEW Shock is an abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation
Shock is the collapse of the cardiovascular system, characterized by circulatory deficiency and the depression of vital functions.

3. TYPES OF SHOCK Types of Shock Subtypes Distributive Shock Septic, anaphylactic, neurogenic Cardiogenic Shock Myocardial infarction, cardiac arrhythmias, valvular pathology, heart failure Hypovolemic Shock Hemorrhagic , burns, gastrointestinal losses Obstructive Shock Pulmonary embolism, cardiac tamponade , tension pneumothorax

4. Approch To Hypovolemic Shock DEFINITION :- Hypovolemic shock occurs when decreased intravascular fluid or decreased blood volume causes decreased preload, stroke volume, and cardiac output (CO). Severe blood loss ( hemorrhage ) can cause decreased myocardial oxygenation, which decreases contractility and CO. This action may lead to an autonomic increase in the systemic vascular resistance (SVR). Hypovolemic shock can also occur due to volume loss from other etiologies . FORMS :- 1.Hemorrhageic Shock 2.Non-Hemorrhagic Hypovolemic Shock

5. HYPOVOLEMIC SHOCK CAUSES : Hemorrhagic : External blood loss (wounds)
Exteriorization JO internal bleeding (hematemesis, melena. Epistaxis,Hymoptysis,etc )
A Internal bleeding ( hemothorax , hemoperitoneum .,etc.)
Traumatic Shock

6. NON HEMORRHAGIC HYPOVOLEMIC SHOCK Non- hemorrhagic hypovolemic shock can be due to one of the following etiologies : Gastrointestinal Losses :- A GI source of hypovolemic shock is the leading source. The gastrointestinal tract usually secretes between 3 to 6 liters of fluid daily. However, most of this fluid gets reabsorbed, and only 100 to 200 mI is lost in the stool. Volume depletion occurs when the GI secretion exceeds the reabsorbed. This fluid loss occurs in the presence of intractable vomiting, diarrhea , bowel obstruction, or external drainage via stoma or fistulas.

7. 2. Renal Losses:- Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually excrete sodium and water in a manner that matches intake. Diuretic therapy and osmotic diuresis from hyperglycemia can lead to excessive renal sodium and volume loss. In addition, several tubular and interstitial diseases beyond the scope of this article cause severe salt-wasting nephropathy.

8. 3. Skin losses:- Excessive fluid loss can also occur from the skin. In a hot and dry climate, skin fluid losses can be as high as 1 to 2 liters /hour. Patients with a skin barrier interrupted by burns or other skin lesions also can experience significant fluid losses that lead to hypovolemic shock.

9. 4. Third space Sequestration:- Sequestration of fluid occurs when intravascular fluid leaves the interstitial compartment leading to effective intravascular volume depletion and hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, burn, post-operatively, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response.

10. PATHOPHYSIOLOGY

11. Factors Affecting Cardiac Output Cardiac output = Heart Rate(HR) × Stroke Volume(SV) SV is dependent on Preload, Afterload and Contractility. The Mean arterial Pressure(MAP) is dependent on CO and SVR. This is important because there is MAP threshold below which oxygen delivery is decreased. CO is dependent on the interplay of cardiac Inotropy (speed and shortening capacity of myocardium), chronotropy (heart contraction rate), and lusitropy (ability of heart muscle to relax and heart chambers to fill). Determinants of inotropy include autonomic input from sympathetic activation, parasympathetic inhibition, circulating catecholamines , and short-lived responses to an increase in afterload ( Anrep effect ) or heart rate ( Bowditch effect ).

12. Increases in the inotropic state help to maintain stroke volume at high heart rates.
During shock states, higher levels of epinephrine will be produced and reinforce adrenergic tone. Epinephrine levels are significantly elevated during induced hemorrhagic shock, but these levels subsequently reduce to almost normal levels after adequate blood pressure is restored.
An acidotic milieu, which is common in shock, further compromises ventricular contractile force and blood pressure. Chronotropy and lusitropy are both influenced by sympathetic input. Norepinephrine interacts with cardiac β1-receptors, resulting in increased cyclic adenosine monophosphate. This leads to a process of intracellular signaling with an increased chronotropy and sequestration of calcium, leading to myocardial relaxation.

13. Shock provokes a myriad of autonomic responses to maintain perfusion pressure to vital organs. Stimulation of the carotid baroreceptor stretch reflex activates the sympathetic nervous system, triggering Arteriolar vasoconstriction, resulting in redistribution of blood flow from the skin, skeletal muscle, kidneys, and splanchnic viscera; An increase in heart rate and contractility that increases CO; constriction of venous capacitance vessels, which augments venous return; Release of the vasoactive hormones epinephrine, norepinephrine, dopamine, and cortisol to increase arteriolar and venous tone; Release of antidiuretic hormone and activation of the renin-angiotensin axis to enhance water and sodium conservation to maintain intravascular volume. These compensatory mechanisms attempt to maintain oxygen delivery to the most critical organs (heart and brain), but blood flow to other organs, such as the kidneys and GI tract, may be compromised.

14. Failure of Compensatory Response Decreased blood flow to the tissues causes cellular hypoxia
Anaerobic metabolism begins lactic acid production
Cell swelling, ion-pump disruption, Influx of Sodium, Efflux of Potassium and reduction in Resting Membrane Potential.
If Low Perfusion States persists: Loss of cellular integrity➡️Breakdown in cellular Homeostasis➡️Irreversible Cell death Cascade of metabolic Features : HYPERKALEMIA HYPERNATREMIA AZOTEMIA HYPER/HYPOGLYCEMIA LACTIC ACIDOSIS.

15. Clinical Features History and physical can often make the diagnosis of hypovolemic shock. For the non- hemorrhagic hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI, renal, openwounds , skin, or third-spacing as a cause of extracellular fluid loss. Symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid-base disorders that accompany hypovolemic shock. Patients With volume depletion can complaint of Intense Thirst Muscle Cramps CLINICAL SIGNS Tachycardia Tachypnea Orthostatic Hypotension Small pulse waves Agitation/Anxiety/ Confusin /Coma. Oliguria Cold extremities. Profused Sweating Collapsed Peripheral Veins. ⬆️Capillary Refilling Time.

16. Initial Daignostic Study to Evaluate a patient in Shock CBC with Differential Counts Electrolytes, BSL,Calcium , Magnesium, Phosphorus BUN, Creatinine Serum Lactate ECG Unine Routine and microbiology analysis Chest Xray PT, INR, aPTT Arterial Blood Gas analysis LFT Blood culuter Cortisol Studies

17. Treatment The ABCDE tenets of shock resuscitation are establishing airway, controlling the work of breathing, optimizing the circulation, ensuring adequate oxygen delivery, and achieving end points of resuscitation. For patients presenting with hypovolemic shock, it is important to differentiate between hemorrhagic versus non- hemorrhagic hypovolemic shock, as this would dictate management. Early resuscitation with prompt bleeding source control is crucial in Hemorrhagic hypovolemic shock to improve survival and reduce blood products transfusion. In terms of hemorrhagic shock resuscitation, using blood products over crystalloid resuscitation resulted in improved outcomes. Balanced transfusion using 1:1:1 or 1:1:2 of plasma to platelets to packed red blood cells results in better hemostasis .

18. For patients in non- hemorrhagic hypovolemic shock, volume resuscitation must be started as soon as possible to restore effective circulatory blood volume. It is sometimes difficult to determine the type of fluid loss. Therefore, it is prudent to start with a warm isotonic crystalloid solution of 30 ml/kg body weight, infused rapidly to restore tissue perfusion quickly. This blouse can be repeated more than once. Effective resuscitation can be monitored by heart rate, blood pressure, urine output, mental status, and peripheral edema . Multiple modalities exist for measuring fluid responsiveness, such as ultrasound to assess IVC compressibility, central venous pressure monitoring, and pulse pressure fluctuation. Vasopressors should not be used for hypovolemic shock because they can worsen tissue perfusion. However, it can be used to catch up with volume resuscitation in the initial resuscitation phase

19. For large fluid volumes, consider using lactated Ringer’s or Plasma- Lyte ® to avoid hyperchloremic metabolic acidosis associated with 0.9% sodium chloride solution. In clinical situations where hypochloremia can be predicted, such as from GI losses due to vomiting or from urinary excretion due to diuretics, there may be an advantage to 0.9% sodium chloride rehydration.

20. Airway control is best obtained through endotracheal intubation.
Sedatives used to facilitate intubation may cause arterial vasodilatation, venodilation , or myocardial suppression and may result in hypotension.
Positive-pressure ventilation reduces preload and CO.
The combination of sedative agents and positive-pressure ventilation will often lead to hemodynamic collapse. To avoid this unwanted situation, initiate volume resuscitation and vasoactive agents before intubation and positive pressure ventilation.

21. Vasopressors Vasopressors are used when there has been an inadequate response to volume resuscitation or if there are contraindications to volume infusion. Vasopressors are most effective when the vascular space is “full” and least effective when the vascular space is depleted. Patients with chronic hypertension may be at greater risk of renal injury at lower blood pressures; however, in others, there appears to be no mortality benefit in raising mean arterial pressure above the 65 to 70 mm Hg range. Although vasopressors improve perfusion pressure in the large vessels, they may decrease capillary blood flow in certain tissue beds, especially the GI tract and peripheral vasculature. In addition to a vasopressor, an inotrope may be needed to directly increase CO by increasing contractility and stroke volume. Careful vasopressor infusion initially through a peripheral IV is unlikely to result in tissue injury and will improve the time to achieve hemodynamic stability

22. Drug Dose Action Cardiac conctility Vasoconstriction Vasodilation Cardiac output Dobutamine 2-20 mcg/kg/min Β 1, some β2 and in large dosages α1 ++++ + ++ Increase Dopamine 0.5-20 mcg/kg/min Αlpha , β,and dopaminergic ++ @ 2.5-5 mcg/kg/min ++ @ 5-20 mcg/kg/min + @ 0.5-2 mcg/kg/min Usually Increase Epinephrine 2-10 mcg/kg/min Alpha and β ++++ @ 0.5-8 mcg/kg/min ++++ @ >8 mcg/kg/min +++ Increase Isoproterenol 0.01-0.1 mcg/kg/min Β 1 and some β2 ++++ ++++ Increase Norepinephrine 0.5-50 mcg/min Primarily α1, some β1 ++ ++++ Slightly Increase Phenylephrine 10-200 mcg/min Pure α ++++ Decreases

23. ENSURING ADEQUATE OXYGEN DELIVERY Control of oxygen consumption is important in restoring the balance of oxygen supply and demand to the tissue (oxygen consumption equation). Hyperadrenergic state results from the compensatory response to shock, physiologic stress, pain, cold treatment rooms, and anxiety. Pain further suppresses myocardial function, impairing oxygen delivery and increasing consumption. Providing analgesia, muscle relaxation, warm covering, anxiolytics, and even paralytic agents, when appropriate, decreases this inappropriate systemic oxygen consumption. Once blood pressure is stabilized through optimization of preload and afterload, oxygen delivery can be assessed and further manipulated.

24. Restore arterial oxygen saturation to ≥91%. If CO can be assessed, it should be increased using volume infusion or inotropic agents in incremental amounts until venous oxygen saturation (mixed venous oxygen saturation [Svo2] or Scvo2) and lactate are normalized.

25. End Point Of Resuscitation The goal of resuscitation is to use hemodynamic and physiologic values to guide therapy in order to maximize survival and minimize morbidity. Hypotension at ED presentation is associated with poor outcomes. Noninvasive parameters, such as blood pressure, heart rate, and urine output, may underestimate the degree of remaining hypoperfusion and oxygen debt, so the use of additional physiologic end points may be informative. If shock or hypotension persists, reassessment at the patient’s bedside is essential while considering the important issues(Table).

26. Disposition Early recognition, treatment, and subsequent transfer of critically ill patients to the intensive care unit improves patient outcomes and improves ED throughput. For prolonged or “boarded” ED stays, constantly reassess the critically ill patient, ensure that care plans are continuing, and consider creating a critical care patient checklist. Often, this will entail ordering tests that are not commonly performed on ED patients or ordering subsequent doses of medicines, particularly antibiotics. Some clinical variables are associated with poor outcome, such as severity of shock, temporal duration, underlying cause, preexisting vital organ dysfunction, and reversibility. Early recognition, intervention, source control, and smooth care transitions optimize outcomes. While associated morbidity and mortality remain high for patients with shock,
integration of protocol-based care pathways with ongoing refinement in response to new information may lead to continued reductions over time. Additional outcome predictions related to physiologic scoring systems, ED-based shock interventions, and the balance between invasive and noninvasive or minimally invasive strategies are still being studied.