Shock

Fluid loss from diuresis, vomiting, blood loss

hypovolemic

Septic, neurogenic, anaphylactic are three forms of this shock

Distributive shock

Blood volume unchanged

Distributive shock: Neurogenic, anaphylactic, septic

SIRS

Generalized inflammation in organs REMOTE from initial insult In Sepsis or massive tissue damage Damage to tissues/vessels and having a release of cytokines and other agents from cells Cardiogenic: damage to heart muscle/tissue- ischemia causes a release of cytokines and inflammatory mediators Subsequent damage to other types of tissue- Liver, lungs, kidneys is SIRS

Patient needs lot of volume/fluids

Hypovolemic, septic

Bradypnea

Neurogenic

tension pneumothorax, pericardial fluid build-up, aortic dissection

Obstructive shock

Management of Anaphylactic shock

Maintain airway Administer EPINEPHRINE oxygen Intubation (Teach: ID and avoid causative agent)

MODS - clinical manifestations

(Most common causes: Sepsis and Septic shock) Tissues shutting down: Tachypnea/hypoxemia Petechiae/bleeding Jaundice (liver) Abdominal distention (GI) Oliguria-->anuria (kidney) Tachycardia (heart compensating for other problem) Hypotension Change in LOC

SIRS triggers

Mechanical tissue trauma: burns, crush injuries, surgery Abscess formation: intra-abdominal, extremities Ischemic or necrotic tissue: PANCREATITIS, vascular disease, myocardial infarction (decreased tissue perfusion) microbial invasion: Bacteria, virus, fungi Endotoxin release: Gram - bacteria Global perfusion deficits: Post cardiac resuscitation, shock states Regional perfusion deficits: Distal perfusion deficits

II: Compensatory

Neural compensation by SNS ↑ Heart rate (except neurogenic) ↑ Heart rate and contractility Narrowed pulse pressure Vasoconstriction Rapid, deep respirations causing respiratory alkalosis Redistribution of blood flow from nonessential to essential organs ThirstCool, moist skin Bronchodilation Oliguria Endocrine compensation (RAAS, ADH, glucocorticoids release) Diminished bowel soundsRestlessness progressing to confusion Renal reabsorption of sodium, chloride, and water Hyperglycemia↑ Urine specific gravity and ↓ creatinine clearance Vasoconstriction Glycogenolysis and gluconeogenesis Chemical compensation

Bounding pulse

Neurogenic and septic shock

Warm and dry extremities

Neurogenic and septic(early)

-Neurogenic shock

Neurogenic shock occurs when a disturbance in the nervous system affects the vasomotor center in the medulla. In neurogenic shock, there is an interruption of impulse transmission or a blockage of sympathetic outflow resulting in vasodilation, inhibition of baroreceptor response, and impaired thermoregulation. Consequently, these reactions create vasodilation with decreased SVR, venous return, preload, and cardiac output and a relative hypovolemia. loss of sympathetic tone causing massive vasodilation; Caused by: trauma, spinal shock, and epidural anesthesia

Nursing process: Oxygenation

PRIORITY Monitor airway and V/S

III: Progressive

Progressive tissue hypoperfusion Dysrhythmias Anaerobic metabolism with lactic acidosis ↓ BP with narrowed pulse pressure Failure of sodium-potassium pump Tachypnea Cellular edema Cold, clammy skin Anuria Absent bowel sounds Lethargy progressing to coma Hyperglycemia ↑ BUN, creatinine, and potassium Respiratory and metabolic acidosis

Nursing process: Fluid Therapy

Provide hemodynamic support through fluids

Nursing process: Drug therapy

Provide hemodynamic support through medications

Patient assessment findings MODS

Pulmonary: -Acute respiratory distress syndrome -Predisposing factor such as shock or sepsis -Unexplained hypoxemia (↓ PaO2, ↓ SaO2) -Dyspnea -Tachypnea -PaO2/FiO2 ratio <300 for acute lung injury and <200 for ARDS -Bilateral pulmonary infiltrates on chest x-ray -PAOP <18 mm Hg Cardiovascular: -Hyperdynamic or hypodynamic -EARLY (HYPERDYNAMIC; LOOKS LIKE INFECTION) -LATE (HYPODYNAMIC; LOOKS LIKE SHOCK) Hematological: -Disseminated intravascular coagulation -Fibrin split products >1:40 or D-dimer >2 mg/L -Thrombocytopenia -Prolonged PT and aPTT -INR >1.5 -Bleeding -Petechiae Renal: -Acute tubular necrosis -Oliguria -↑ Serum creatinine, ↑ BUN -Urinary sodium >20 mEq/L Liver; -Hepatic dysfunction/failure -↑ Serum bilirubin -↑ AST, ALT, LDH -Jaundice -Hepatomegaly -↑ Serum ammonia -↓ Serum albumin Central nervous system: -Cerebral ischemia/infarction -Lethargy -Altered level of consciousness -Fever Metabolic: -Lactic acidosis -↑ Serum lactate level >30 mg/dL

Nursing process: Ventilation

Respiratory Therapist manages the ventilator, adjusts the settings and provides chest physical therapy to improve ventilation and chest expansion

Systemic Inflammatory Response Syndrome (SIRS)

SIRS is widespread inflammation that can occur in patients with diverse disorders such as infection, trauma, shock, pancreatitis, or ischemia. It may result from or lead to MODS. SIRS is most frequently associated with sepsis. Sepsis is defined as infection associated with SIRS. The inflammatory cascade maintains homeostasis through a balance between proinflammatory and antiinflammatory processes. Inflammation is normally a localized process; SIRS is a systemic response associated with the release of mediators. These mediators cause an increase in the permeability of the endothelial wall, shifting fluid from the intravascular space into extravascular spaces, including the interstitial space. Intravascular volume is reduced, resulting in a condition of relative hypovolemia. Other mediators cause microvascular clotting, impaired fibrinolysis, and widespread vasodilation.

ID source of infection

Septic

Coagulation disorders

Septic (DIC)

Hyperthermia

Septic shock

May start with dopamine

Septic shock

Use dopamine for

Septic shock

-Septic Shock

Septic shock is one component of a continuum of progressive clinical insults including SIRS, sepsis, and MODS. Endotoxins and other mediators causing massive vasodilation; most common cause is gram-negative bacteria (Urosepsis- more frequent in older adults, UTI)

Parameters and Care of Septic shock

Septic shock: Sepsis with hypotension despite adequate fluid resuscitation, along with perfusion abnormalities Hypotension Lactic acidosis, oliguria, acute change in mental status Patients receiving inotropic agents or vasopressors may not exhibit hypotension Administer antibiotics Maintain adequate ventilation and oxygenation Maximize oxygen delivery; minimize oxygen demand Replace fluid Administer vasoactive medications Correct acid-base abnormalities Monitor and support organ function Consider hydrocortisone if poor response to fluids and vasoactive medication12

IV: Refractory

Severe tissue hypoxia with ischemia and necrosis Life-threatening dysrhythmias Worsening acidosis Severe hypotension despite vasopressors SIRS Respiratory and metabolic acidosis MODS Acute respiratory failure Acute respiratory distress syndrome Disseminated intravascular coagulation Hepatic dysfunction/failure Acute kidney injury Myocardial ischemia/infarction/failure Cerebral ischemia/infarction

Patient assessment findings SIRS

Tachycardia (HR ≥90 beats/min)Respiratory rate >20 breaths/min or PaCO2 <32 mm Hg Temperature >38° C (hyperthermia) or <36° C (hypothermia) Administer antibioticsRemove source of infection Maintain adequate ventilation and oxygenation Replace fluid

Which causes obstructive form of shock?

Tension pneumothorax

Neurogenic shock

decreased or normal HR

Thready pulse

hypovolemic, cardiogenic, septic shock

Hypovolemic shock treatment

identifying, treating, and eliminating the cause of the hypovolemia and replacing lost fluid. Examples of treating the cause include surgery, antidiarrheal medication for diarrhea, and insulin for hyperglycemia. The type of fluid lost is considered when determining fluid replacement. Isotonic crystalloids such as normal saline are generally used first, although blood and blood products may be administered if the patient is bleeding. The 3-for-1 rule is used which recommends the replacement of 300 mL of isotonic solution for every 100 mL of blood lost. BURN PATIENT IS AT GREATEST RISK Administer a vasopressor (Norephinephrine) if fluid resuscitation is unsuccessful

Multiple Organ Dysfunction Syndrome (MODS)

may develop from severe hypotension and reperfusion of ischemic cells causing further tissue injury -Inadequate tissue perfusion may cause organ failure in the lungs (adult respiratory distress syndrome), kidneys (renal failure), heart (decreased coronary artery perfusion, decreased cardiac contractibility), and the gastrointestinal tract (necrosis). Assess: Organ function, provide ventilatory support, inotropic medications) Take interventions to compensate for dysfunction: admin. of clotting factors, dialysis

Stabilize spine

neurogenic shock

Hypothermia

neurogenic shock, septic shock

Obstructive shock treatment

relieve the source of the compression or obstruction. Cardiac tamponade -pericardiocentesis, or the removal of fluid from the pericardial sac. tension pneumothorax -needle thoracentesis to remove the accumulated intrathoracic pressure. The risk of pulmonary embolism may be reduced by early surgical reduction of long bone fractures, devices to enhance circulation in immobile patients (e.g., sequential compression devices), range-of-motion exercises, and prophylactic anticoagulant therapy.

May need oxygen

All shock

MI, heart failure

Cardiogenic

Neurogenic shock treatment

treating the cause, including reversal of offending drugs or glucose administration for hypoglycemia. Immobilization of spinal injuries with traction devices (halo brace to maintain alignment) or surgical intervention to stabilize the injury assists in preventing severe neurogenic shock. For patients receiving spinal anesthesia, elevating the head of the bed may prevent the progression of the spinal blockade up the cord. IV fluids are infused to treat hypotension; however, they must be given cautiously to prevent fluid overload and cerebral or spinal cord edema. Vasopressors are frequently required to maintain perfusion. Alpha- and beta-adrenergic agents, such as dopamine or norepinephrine, are preferred because pure alpha-adrenergic agents, such as phenylephrine, are associated with persistent bradycardia. Hypothermia is common so the patient is rewarmed slowly, because rapid rewarming may cause vasodilation and worsen the patient's hemodynamic status. Atropine is used for symptomatic bradycardia; however, a temporary or permanent pacemaker may be required.

Flushing of skin

Neurogenic (possibly), anaphylactic

Peripheral edema

cardiogenic shock

I: Initiation

↓ Tissue oxygenation caused by: No observable clinical indications ↓ Intravascular volume (hypovolemic) ↓ CO may be noted with invasive hemodynamic monitoring ↓ Myocardial contractility (cardiogenic) Obstruction of blood flow (obstructive) ↓ Vascular tone (distributive) Septic (mediator release) Anaphylactic (histamine release) Neurogenic (suppression of SNS)

Management of MODS

-Control infection (antibiotics) -Provide adequate tissue oxygenation (88-92% SaO2, Hg above 7-9) -Restore intravascular volume (aggressive fluid resuscitation, isotonic crystalloids) -Support organ function

Physical assessment findings

-Hypoxia, tachypnea progressing to >40/min, hypocarbia) -Pale skin, mottled or dusky color, cool, diaphoretic, warm, flushed with fever (distributive shock), and exhibit a rash (anaphylactic and septic shock) -Angioedema (anaphylactic) -Wheezing -BP within expected range during initial stage, but increase during progressive stage then drop to less than 50-60 mm Hg -Tachycardia progressing to greater than 140/min -Pulse weak and thready or bound with distributive shock -decreased cardiac output -central venous pressure decreased (hypovolemic shock) -CVP increased with increased systemic vascular resistance in cardiogenic shock -Decreased urine output -Seizures

Obstructive Shock

-Mechanical blockage in the heart or great vessels -occurs when there is a physical impairment to adequate circulatory blood flow. -Causes of obstructive shock include impaired diastolic filling (cardiac tamponade, tension pneumothorax, constrictive pericarditis, compression of the great veins), increased right ventricular afterload (pulmonary embolism, severe pulmonary hypertension, increased intrathoracic pressures), and increased left ventricular afterload (aortic dissection, systemic embolization, aortic stenosis). Obstruction of the heart or great vessels either impedes venous return to the right side of the heart or prevents effective pumping action of the heart. This results in decreased cardiac output, hypotension, decreased tissue perfusion, and impaired cellular metabolism -secondary to cardiac tamponade or tension pneumothorax, the central venous pressure is high.

Cardiogenic shock

-Pump failure or heart failure -the central venous pressure is increased because of poor myocardial contractility and high filling pressure in the ventricles -can occur when the heart fails to act as an effective pump. A decrease in myocardial contractility results in decreased cardiac output and impaired tissue perfusion. Cardiogenic shock is one of the most difficult types of shock to treat and carries a hospital mortality of 67%.

Distributive Shock

-Widespread vasodilation and increased capillary permeability Vascular capacitance increases, relative hypovolemia -also known as vasogenic shock, describes several different types of shock that present with widespread vasodilation and decreased SVR (sytemic vascular resistance)-the force opposing the movement of blood. This force is created primarily in small arteries and arterioles. Neurogenic, anaphylactic, and septic shock are forms of distributive shock. Vasodilation increases the vascular capacity; however, the blood volume is unchanged, resulting in a relative hypovolemia. This causes a decrease in venous return to the right side of the heart and a reduction in ventricular filling pressures. Anaphylactic shock and septic shock are also complicated by an increase in capillary permeability, which decreases intravascular volume, further compromising venous return. Eventually, in all forms of distributive shock, stroke volume, cardiac output, and blood pressure decrease, resulting in decreased tissue perfusion and impaired cellular metabolism.

Septic shock treatment

-administration of IV fluids to keep the central venous pressure at 8 mm Hg or greater (but not >15 mm Hg) and the heart rate at less than 110 beats per minute, administration of vasopressors to keep the mean arterial pressure at 65 mm Hg or greater, and administration of dobutamine, packed red blood cells, or both to keep the central venous oxygen saturation (ScvO2) at 70% or greater.

Hypovolemic Shock

-of or relating to a decrease in the volume of circulating blood of 10-15% or more

Anaphylactic shock treatment

-remove the antigen, reverse the effects of the mediators, and promote adequate tissue perfusion. If the anaphylactic reaction results from medications, contrast dye, or blood or blood products, the infusion is immediately stopped. Airway, ventilation, and circulation are supported. Laryngeal edema may be severe enough to require intubation or cricothyrotomy if swelling is so severe that an endotracheal tube cannot be placed. Oxygen is administered to keep the SpO2 greater than 90%. Removal of the offending agent is achieved by removing the stinger, administering antivenom, stopping the drug, performing gastric lavage, or flushing the skin. Epinephrine is the drug of choice for treating anaphylactic shock. Epinephrine is an adrenergic agent that promotes bronchodilation and vasoconstriction. For mild reactions, epinephrine 0.1 to 0.25 mg (1.0 to 2.5 mL of a 1:10,000 solution) is administered intramuscularly or subcutaneously. The dose may be repeated at 20- to 30-minute intervals until anaphylaxis is resolved. To block histamine release, diphenhydramine (Benadryl), an H1-receptor blocker, or ranitidine, an H2-receptor blocker, may decrease some of the cutaneous symptoms of anaphylaxis, but both are considered second-line treatment.31 Corticosteroids such as methylprednisolone (Solu-Medrol) are used to reduce inflammation. Fluid replacement, positive inotropic agents, and vasopressors may be required.

A client has emergency surgery for a ruptured appendix. After assessing that the client is manifesting symptoms of shock, the nurse should: 1) Prepare for a blood transfusion 2) Notify the physician immediately 3) Elevate the HOB 30 degrees 4) Increase the liter flow of the O2 being administered

4) increase the liter flow of the O2 being administered

Lab findings: shock

ABGs: decreased tissue oxygenation (decreased pH (<7.20-7.3), decreased PaO2 (<45-79m Hg), increased PaCO2 (>46-67 mm Hg) Serum lactic acid: increases due to anaerobic metabolism (>24-30 mg/dL) Serum glucose and electrolytes: serum glucose can increase during shock (>200-400 mg/dL) Cardiogenic shock: Cardiac enzymes- creatine phosphokinase (>160 female >204 males), troponin (>0.5 ng/mL) Hypovolemic shock: Hgb and Hct -decreased with hemorrhage (<6-11/ <18-38%), increased with dehydration (>16-18/>50-54%) Septic shock: Cultures - blood, urine, wound ------Coagulation tests - PT (>27 sec), INR (>5), aPTT (>70 sec)

Remove offending agent

Anaphylactic

Stridor

Anaphylactic

Air hunger

Anaphylactic shock

Antigen/antibody reaction

Anaphylactic shock

Epinephrine 1st line agent

Anaphylactic shock

-anaphylactic shock

Antigen-antibody reaction causing massive vasodilation; allergens inhaled, swallowed, contacted, or introduced IV are among the causes A severe allergic reaction Antigens, which are foreign substances to which someone is sensitive, initiate an antigen-antibody response. Once an antigen enters the body, antibodies (immunoglobulin E [IgE]) are produced that attach to mast cells and basophils. The greatest concentrations of mast cells are found in the lungs, around blood vessels, in connective tissue, and in the uterus. Mast cells are also found to a lesser extent in the kidneys, heart, skin, liver, and spleen and in the omentum of the gastrointestinal tract. Basophils circulate in the blood. Both mast cells and basophils contain histamine and histamine-like substances, which are potent vasodilators.

Compensatory physiologic mechanisms of shock- Chemical compensation.

As pulmonary blood flow is reduced, ventilation-perfusion imbalances occur. Initially, alveolar ventilation is adequate, but the perfusion of blood through the alveolar capillary bed is decreased. Chemoreceptors located in the aorta and carotid arteries are stimulated in response to this low oxygen tension in the blood. Consequently, the rate and depth of respirations increase. As the patient hyperventilates, carbon dioxide is excreted and respiratory alkalosis occurs. A reduction in carbon dioxide levels and the alkalotic state cause vasoconstriction of cerebral blood vessels. This vasoconstriction, coupled with the reduced oxygen tension, may lead to cerebral hypoxia and ischemia. The overall effects of chemical compensation result in an attempt to combat shock by increasing oxygen supply; however, cerebral perfusion may decrease.

Treat shock of unknown etiology, first action by nurse

Assess O2 Sat

Compensatory physiologic mechanisms of shock- Neural compensation.

Baroreceptors (which are sensitive to pressure changes) and chemoreceptors (which are sensitive to chemical changes) located in the carotid sinus and aortic arch detect the reduction in arterial blood pressure. Impulses are relayed to the vasomotor center in the medulla oblongata, stimulating the sympathetic branch of the autonomic nervous system to release epinephrine and norepinephrine from the adrenal medulla. In response to this catecholamine release, both heart rate and contractility increase to improve cardiac output. Dilation of the coronary arteries occurs to increase perfusion to the myocardium to meet the increased demands for oxygen. Systemic vasoconstriction and redistribution of blood occurs. Arterial vasoconstriction improves blood pressure, whereas venous vasoconstriction augments venous return to the heart, increasing preload and cardiac output. Blood is shunted from the kidneys, gastrointestinal tract, and skin to the heart and brain. Bronchial smooth muscles relax, and respiratory rate and depth are increased, improving gas exchange and oxygenation. Additional catecholamine effects include increased blood glucose levels as the liver is stimulated to convert glycogen to glucose for energy production; dilation of pupils; and peripheral vasoconstriction and increased sweat gland activity resulting in cool, moist skin.

Jugular Venous Distention (JVD)

Cardiogenic

May need fluids with caution

Cardiogenic

May be caused from an increase in preload

Cardiogenic shock

Pump problem

Cardiogenic shock

Requires early positive inotropic agents (Dobutamine)

Cardiogenic shock

Dyspnea

Cardiogenic, Anaphylactic shock

Crackles

Cardiogenic, Septic shock

Not a fluid problem

Cardiogenic, neurogenic, anaphylactic

Which is the most significant clinical assessment finding for hypovolemic shock

Decreased urine output

Profound vasodilation

Distributive shock: Neurogenic, anaphylactic, septic

Cardiogenic shock treatment

Diuretics (e.g., furosemide) and venous vasodilators (e.g., morphine, nitroglycerin, nitroprusside) reduce preload and venous return to the heart. Nitroglycerin at low doses (<1 mcg/kg/min) causes venous vasodilation to decrease preload. At higher doses (>1 mcg/kg/min) arterial vasodilation decreases afterload Positive inotropic agents (e.g., dobutamine) are given to increase the contractile force of the heart. As contractility increases, ventricular emptying improves, filling pressures decrease (RAP, PAOP), and stroke volume improves. The improved stroke volume increases cardiac output and improves tissue perfusion. However, positive inotropic agents also increase myocardial oxygen demand and must be used cautiously in patients with myocardial ischemia.

Assessment findings of anaphylactic shock

Dyspnea Airway obstruction Systolic BP <90 or <30 from baseline Palpitations (heart is trying to beat and circulate blood) Urticaria, swelling IgE elevated

Caused from hemorrhage or excessive diuresis

Hypovolemic shock

Fluid problem

Hypovolemic shock

Oliguria

Hypovolemic shock, Cardiogenic, Septic

Tachypnea

Hypovolemic, Cardiogenic, Anaphylactic, Septic

Decreased skin perfusion/mottling

Hypovolemic, Septic

Cool, clammy extremities

Hypovolemic, cardiogenic, anaphylactic, septic (late)

Elevated HR

Hypovolemic, cardiogenic, anaphylactic, septic shock

May be caused from a decrease in preload

Hypovolemic, neurogenic, anaphylactic, septic shock

-Neurogenic Shock diagram

Imbalance between sympathetic and parasympathetic stimulation massive vasodilation Decreased vascular tone Decreased SVR Inadequate Cardiac output Decreased tissue perfusion Impaired cellular metabolism

Compensatory physiologic mechanisms of shock- Endocrine compensation

In response to the reduction in blood pressure, messages are also relayed to the hypothalamus, which stimulates the anterior and posterior pituitary gland. The anterior pituitary gland releases adrenocorticotropic hormone (ACTH), which acts on the adrenal cortex to release glucocorticoids and mineralocorticoids (e.g., aldosterone). Glucocorticoids increase the blood glucose level by increasing the conversion of glycogen to glucose (glycogenolysis) and causing the conversion of fat and protein to glucose (gluconeogenesis). Mineralocorticoids act on the renal tubules causing the reabsorption of sodium and water, resulting in increased intravascular volume and blood pressure. The renin-angiotensin-aldosterone system is stimulated by a reduction of pressure in the renal arterioles of the kidneys and/or by a decrease in sodium levels as sensed by the kidney's juxtaglomerular apparatus. In response to decreased renal perfusion, the juxtaglomerular apparatus releases renin. Renin circulates in the blood and reacts with angiotensinogen to produce angiotensin I. Angiotensin I circulates through the lungs, where it forms angiotensin II, a potent arterial and venous vasoconstrictor that increases blood pressure and improves venous return to the heart. Angiotensin II also activates the adrenal cortex to release aldosterone. Antidiuretic hormone (ADH) is released by the posterior pituitary gland in response to the increased osmolality of the blood that occurs in shock. The overall effects of endocrine compensation result in an attempt to combat shock by providing the body with glucose for energy and by increasing the intravascular blood volume.

Signs and symptoms of various stages of shock

Initial stage: no visible changes in client, only changes cellularly Compensatory stage: Measures to increase cardiac output to restore tissue perfusion and oxygenation: Progressive Stage: Compensatory mechanisms begin to fail (increased BP, Refractory: Irreversible shock and total body failure (BP drops to less than 50-60 mm Hg)