8shock

Shock

• Shock is defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand.

• The result of shock is global tissue hypoperfusion and is associated with a decreased venous oxygen content and metabolic acidosis (lactic acidosis).

• Clinically, shock may have a predominant cause, but as the shock state persists or progresses to irreversible end organ damage, other pathophysiologic mechanisms become operative

• Shock is classified into four categories by etiology(1) hypovolemic (caused by inadequate circulating

volume)(2) cardiogenic (caused by inadequate cardiac

pump function)(3) distributive (caused by peripheral vasodilatation

and maldistribution of blood flow)(4) obstructive (caused by extra cardiac obstruction

to blood flow).

Pathophysiology • The onset of shock -- autonomic responses, many of which serve to maintain

perfusion pressure to vital organs. • Stimulation of the carotid baroreceptor stretch reflex activates the sympathetic

nervous system leading to:• (1) arteriolar vasoconstriction, resulting in redistribution of blood flow from

the skin, skeletal muscle, kidneys, and splanchnic viscera;• (2) an increase in heart rate and contractility that increases cardiac output;• (3) constriction of venous capacitance vessels, which augments venous return; • (4) release of the vasoactive hormones epinephrine, norepinephrine,

dopamine, and cortisol to increase arteriolar and venous tone; and • (5) 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 DO2 to the most critical

organs—the coronary and cerebral circulation. During this process, blood flow to other organs such as the kidneys and gastrointestinal tract may be compromised.

• In the early phases of septic shock, these physiologic changes produce a clinical syndrome called the systemic inflammatory response syndrome or SIRS, defined as the presence of two or more of the following features:

• (1) temperature greater than 38°C (100.4°F) or less than 36°C (96.8°F);

• (2) heart rate faster than 90 beats/min; • (3) respiratory rate faster than 20 breaths/min; and• (4) white blood cell count greater than 12.0 x 109/L, less than 4.0 x

109/L, or with greater than 10 percent immature forms or bands.• 5) As SIRS progresses, shock ensues, followed by multiorgan

dysfunction syndrome (MODS) manifested by myocardial depression, adult respiratory distress syndrome, disseminated intravascular coagulation, hepatic failure, or renal failure.

• The fulminate progression from SIRS to MODS is determined by the balance of anti-inflammatory and proinflammatory mediators or cytokines that are released from endothelial cell disruption

• The cellular response to decreased DO2 ( oxygen delivery per minute ) is adenosine triphosphate depletion leading to ion-pump dysfunction, influx of sodium, efflux of potassium, and reduction in membrane resting potential. Cellular edema occurs secondary to increased intracellular sodium, while cellular membrane receptors become poorly responsive to the stress hormones insulin, glucagon, cortisol, and catecholamines. As shock progresses, lysosomal enzymes are released into the cells with subsequent hydrolysis of membranes, deoxyribonucleic acid, ribonucleic acid, and phosphate esters. As the cascade of shock continues, the loss of cellular integrity and the breakdown in cellular homeostasis result in cellular death. These pathologic events give rise to the metabolic features of hemoconcentration, hyperkalemia, hyponatremia, prerenal azotemia, hyper- or hypoglycemia, and lactic acidosis.

ABCDE tenets of shock resuscitation

• establishing Airway• controlling the work of Breathing• optimizing the Circulation• assuring adequate oxygen Delivery, and• achieving End points of resuscitation

Establishing Airway

• Airway control is best obtained through endotracheal intubation for airway protection, positive pressure ventilation (oxygenation), and pulmonary toilet. Sedatives, which are frequently used to facilitate intubation, can exacerbate hypotension through arterial vasodilatation, venodilation, and myocardial suppression. Furthermore, positive pressure ventilation reduces preload and cardiac output. The combination of these interventions can lead to hemodynamic collapse. Volume resuscitation or application of vasoactive agents may be required prior to intubation and positive pressure ventilation.

Controlling the Work of Breathing

• Control of breathing is required when tachypnea accompanies shock. Respiratory muscles are significant consumers of oxygen during shock and contribute to lactate production. Mechanical ventilation and sedation decrease the work of breathing and have been shown to improve survival. SaO2 should be restored to greater than 93 percent and ventilation controlled to maintain a PaCO2 35 to 40 mm Hg. Attempts to normalize pH above 7.3 by hyperventilation are not beneficial. Mechanical ventilation not only provides oxygenation and corrects hypercapnia but assists, controls, and synchronizes ventilation, which ultimately decreases the work of breathing. Neuromuscular blocking agents are used as adjuncts to further decrease respiratory muscle, oxygen consumption and preserve DO2 to vital organs

Optimizing the Circulation

• Circulatory or hemodynamic stabilization begins with intravascular access through large-bore peripheral venous lines. Trendelenburg positioning, historically considered necessary for maintaining perfusion in the hypotensive patient, does not improve cardiopulmonary performance compared with the supine position. It may worsen pulmonary gas exchange and predispose to aspiration. If a volume challenge is urgently required, rather than using the Trendelenburg position, an alternative is to raise the patient's legs above the level of the heart with the patient supine.

• Fluid resuscitation begins with isotonic crystalloid; the amount and rate are determined by an estimate of the hemodynamic abnormality. Most patients in shock have either an absolute or relative volume deficit, except the patient in cardiogenic shock with pulmonary edema

• Vasopressor agents are used when there has been an inadequate response to volume resuscitation or when a patient has contraindications to volume infusion

Assuring Adequate Oxygen Delivery

• Once blood pressure is stabilized through optimization of preload and afterload, DO2 can be assessed and further manipulated. Arterial oxygen saturation should be returned to physiologic levels (93 to 95 percent) and hemoglobin maintained above 10 g/dL.13 If cardiac output can be assessed, it should be increased by using volume infusion and inotropic agents in incremental amounts until venous oxygen saturation (SmvO2 or ScvO2) and lactate are normalized.

Achieving End Points of Resuscitation

Hypovolemic shock • 2 types • Hemorrhagic hypovolemia

– Thorax– Pulmonary parenchymal trauma– Pulmonary vascular injury– Intercostal vascular injury – Aortic disruption– Massive hemoptysis– Abdomen/pelvis/retroperitoneum– Solid organ injuries (liver, spleen, kidney)– Vascular (trauma, aneurysmal rupture)– Gastrointestinal hemorrhage

(esophageal varices, ulcers, vascular anomalies, etc.)

– Gynecologic disorders (ruptured ectopic pregnancy, peripartum hemorrhage, abnormal uterine bleeding, ovarian cyst rupture, etc.)

– Major vascular injuries– Large soft tissue injuries

• Non hemorrhagic hypovolemia

• Gastrointestinal disorders: vomiting, diarrhea, ascites

• Burns• Environmental

exposure or neglect• Renal salt wasting

Resuscitation Fluids

• Isotonic crystalloid– Normal saline (NS)– Lactated Ringer's (LR) solution– Ringer's acetate

• Colloids– Albumin: 5% and 25%

concentrations– Fresh-frozen plasma– Hetastarch: 6% hydroxyethyl starch

concentration– Dextran -40 (molecular weight 40

kDa) 10% solution– Dextran -70 (molecular weight 70

kDa) 6% solution– Gelatin

• Hypertonic solutions– Saline: 7.0 to 7.5% NaCl– Saline and dextran: 7.5%

NaCl and 6% Dextran-70

• Oxygen carrying resuscitation fluids– Hemoglobin-based oxygen

carriers– Fluorocarbon-based

oxygen carriers

• Blood– Packed red blood cells

Cardiogenic shock

• Cardiogenic shock is defined as a state of decreased cardiac output (CO) producing inadequate tissue perfusion despite adequate or excessive circulating volume.

• Clinical signs of cardiogenic shock include evidence of poor CO with tissue hypoperfusion (hypotension, mental status changes, cool mottled skin) and evidence of volume overload (dyspnea,

Causes • Acute myocardial infarction• Pump failure

– Mechanical complications– Acute mitral regurgitation

secondary to papillary muscle rupture

– Ventricular septal defect– Free-wall rupture

• Right ventricular infarction• Severe depression of cardiac

contractility– Sepsis– Myocarditis

• Mechanical obstruction to forward blood flow– Aortic stenosis– Hypertrophic

cardiomyopathy– Mitral stenosis

• Regurgitation of left ventricular output– Chordal rupture– Acute aortic

insufficiency

Management

• Intra- aortic balloon pump• Emergency cardiac revascularisation

• Airway ( endotracheal intubation, positive pressure )• Acute myocardial infarction –aspirin, heparin• Hypotension managed by small fluid challenge ( NS 100 to

250 ml ) • Vasoconstrictors ( dopamine , dobutamine)• Phosphodiesterase inhibitor ( amrinone , milrinone )

combined with dopamine or dobutamine •

Septic shock

• Sepsis is a heterogeneous clinical syndrome that can be caused by any class of microorganism. Although gram-negative and gram-positive bacteria account for most sepsis cases, fungi, mycobacteria, rickettsia, viruses, or protozoans can cause similar presentations

• Infection = microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms.

• Bacteremia = the presence of viable bacteria in the blood.

• Systemic inflammatory response syndrome = the systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following conditions: (1) temperature >38°C or <36°C; (2) heart rate >90 beats/min; (3) respiratory rate >20 breaths/min or PaCO2 <32 mm Hg; and (4) white blood cell count >12,000/ L, <4000/ L, or >10% immature (band) forms.

• Sepsis = the systemic response to infection, manifested by two or more of the following conditions as a result of infection: (1) temperature >38°C or <36°C; (2) heart rate >90 beats/min; (3) respiratory rate >20 breaths/min or PaCO2 <32 mm Hg; and (4) white blood cell count >12,000/ L, <4000/ L, or >10% immature (band) forms.

• Severe sepsis = sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to lactic acidosis, oliguria, or an acute alteration in mental status.

• Septic shock = sepsis-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured.

• Sepsis-induced hypotension = a systolic blood pressure <90 mm Hg or a reduction of 40 mm Hg from baseline in the absence of other causes for hypotension.

• Multiple organ dysfunction syndrome = presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

Management

Anaphylactic shock

• Anaphylaxis is a severe systemic hypersensitivity reaction characterized by multisystem involvement, which may include hypotension or airway compromise. Anaphylaxis is a potentially life-threatening cascade caused by the release of mediators from mast cells and basophils in an IgE-dependent fashion

• DRUGS • -Lactam antibiotics• Acetylsalicylic acid (ASA)• Trimethoprim-sulfamethoxazole• Vancomycin• Nonsteroidal anti-inflammatory drugs (NSAIDs)• Virtually any drug• FOODS AND ADDITIVES • Shellfish• Soybeans• Nuts• Wheat• Milk• Eggs• Salicylates• Seeds• Sulfites

• OTHERS • Hymenoptera stings• Insect parts and

molds• Radiographic contrast

material• Latex

Treatment

• Emergency treatment: rapid administration of epinephrine

• First line treatment :– ABC of resuscitation– Epinephrine , intravenous fluids and oxygen

• second line treatment :– Coticosteroids – Anti histamines – Agents for allergic bronchospasm ( magnesium

sulphate )

Neurogenic shock

• Neurogenic shock, characterized by hypotension and bradycardia, occurs after an acute spinal cord injury that disrupts sympathetic outflow, leaving unopposed vagal tone

Management