HYPOVOLEMIC SHOCK and its role in today life.pptx

ahmad1680333 172 views 27 slides Oct 04, 2024
Slide 1
Slide 1 of 27
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27

About This Presentation

Hypovolemic Shock


Slide Content

HYPOVOLEMIC SHOCK BY DR. HAYA EJAZ PGR EMERGENCY MEDICINE MAYO HOSPITAL, LAHORE

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.

TYPES OF SHOCK TYPES OF SHOCK SUBTYPES DISTRIBUTIVE SHOCK SEPTIC, ANAPHYLACTIC, NEUROGENIC CARDIOGENIC SHOCK MYOCARDIAL INFARCTION, CARDIAC ARRYTHMIAS, VALVULAR PATHOLOGY, HEART FAILURE HYPOVOLEMIC SHOCK HEMORRHAGE, BURNS, GI LOSSES, RENAL LOSSES. LOSSES THROUGH SKIN OBSTRUCTIVE SHOCK PULMONARY EMBOLISM, CARDIAC TAMPONADE, TENSION PNEUMOTHORAX

Approach To Hypovolemic Shock DEFINITON: 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.Hemorrhagic Shock 2.Non-Hemorrhagic Hypovolemic Shock

CAUSES HEMORRHAGIC: External blood loss (wounds) Exteriorization of internal bleeding (hematemesis, melena, epistaxis, hymoptysis , etc ) A Internal bleeding (hemothorax,hemoperitoneum., etc .) Traumatic Shock

NON HEMORRHAGIC HYPOVOLEMIC SHOCK 1. 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 ml 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.

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 cause severe salt-wasting nephropathy.

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 can also experience significant fluid losses that lead to hypovolemic shock.

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

PATHOPHYSIOLOGY

CLINICAL FEATURES History and physical examination can often make the diagnosis of hypovolemic shock. For non-hemorrhagic hypovolemic shock due to fluid losses, history and physical examination should attempt to identify possible Gl , renal, open wounds, 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 complain of: 1. Intense Thirst 2. Muscle Cramps

▸ CLINICAL SIGNS Tachycardia Tachypnea Orthostatic Hypotension Oliguria Cold extremities Small pulse waves Profuse Sweating Agitation/Anxiety/Confusion/Coma Collapsed Peripheral veins. Increased Capillary Refilling Time.

Initial Diagnostic Study to Evaluate a Patient in Shock CBC with Differential Counts Electrolytes BSL BUN, Creatinine Serum Lactate ECG Urine routine and microbiology analysis

Chest X-ray PT, INR, APTT Arterial Blood Gas analysis LFT Blood culture

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.

▸ 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 bolus 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 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.

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 before intubation and positive pressure ventilation.

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.

THANK YOU