Shock

Cardiogenic Shock Management

12-lead Electrocardiogram: conducted first to rule out MI as the cause of shock Chest Radiograph: to rule out other causes of hypotension and shock (tension pneumothorax or cardiac tamponade) --will also confirm presence of pulmonary edema Cardiac enzymes

Anaphylaxis Shock Management

1st immediately remove trigger if possible --bee sting (remove stinger) --IV blood or med infusion (stop immediately) --if trigger is ingested removal is not possible DO NOT MAKE PT. THROW UP NOT RECOMMENDED Do not delay treatment cardiac arrest and death can occur within minutes administer epi. (priority) can be repeated up to 2 or 3 time 2nd priority assessing the airways, 100% nonrebreather mask

Normal Cardiac Index

2.5 to 4 L/min

Normal CO

4 to 6 L/min

Cardiogenic Shock Epidemiology

5% to 10% in pts. with AMI Higher in men than women-increased prevalence of CAD in males Risk factors --Any disorder that results in the acute deterioration of myocardial mechanical contraction (more than 40% is caused by AMI) --End-stage congestive heart failure --Cardiomyopathy --Hypertension --Diabetes --Multiple vessel artery disease --Acute vascular disease

Septic Shock

A life threatening organ dysfunction caused by a deregulated host response to an infection Occurs when circulatory and metabolic abnormalities are profound, greatly increasing mortality In the worse case further complications such as: Disseminated intravascular coagulopathy-hematological disorder associated with enhanced coagulation Multiple organ dysfunction syndrome

Shock

A life-threatening syndrome that occurs when the circulatory system is unable to supply adequate amounts of oxygen to the tissues to meet basic metabolic requirements --creates a state of tissue hypoxia Without immediate treatment to reverse this imbalance, organ system failure and death may occur **WHEN EVALUATING FOR SHOCK INCLUDE CO, OXYGEN DELIVERY, OXYGEN CONSUMPTION, AND OXYGEN DEBT**

Anaphylactic Shock

A severe and life threatening systemic hypersensitivity reaction Caused by allergic reaction leading to the release of antihistamine and resulting in wide spread venous dilation, increased capillary permeability, and smooth muscle contraction Symptoms --airway compromise (throat/tongue) swelling --circulatory collapse-widespread vasodilation and capillary lead, resulting in decreased venous return and decreased cardiac output

Cardiogenic Shock Patho.

A state of hypoperfusion at the tissue level resulting from severe impairment of ventricular contraction in the presence of adequate vascular volume As a result of damage myocardium, there is a marked reduction in contractility, which reduces ejection fraction (the % of blood ejected from the ventricle with each contraction) and CO Increases the left ventricular filling pressures but decrease CO. Venous oxygen saturation decreases with increase oxygen extraction at tissue level because of low CO

Laboratory Analysis

ABG analysis, SvO2 (ScvO2) base defect, and lactate level ABG provides information on oxygenation, ventilation, and the presence of acidosis and alkalosis, which provides insight on adequacy of treatment In later stages of shock, a metabolic acidosis will be present --the presence of hypoxemia, or decreased PaO2 indicated development of respiratory complications such as acute respiratory distress syndrome

Hypovolemic Shock Assessment Lab Test

ABG's Venous oxygen saturation-decreased oxygen is an indicator of inadequate oxygen delivery Hemoglobin and hematocrit-may decrease if the cause is bleeding Metabolic profile-renal/liver failure AEB increased BUN and creatine, decrease in organ perfusion Lactate/base deficit-increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Decreasing lactate level an in endpoint demonstrating adequate resuscitation

Cardiogenic Shock Lab Test

ABG's-may reflect respiratory alkalosis due to tachypnea (later stage of shock metabolic acidosis) Venous oxygen saturation-decreased SvO2/ScvO2 is an indication of inadequate DO2 Metabolic profile-renal/liver failure test (decreased organ perfusion) Lactate base deficit

Hypovolemic Shock Pathophysiology

Acute loss of circulating fluid volume results in decreased venous return to the right heart and decreased stroke volume and CO, resulting in decreased stroke volume and CO Decreased intraventricular volume results in the initiation of several compensatory mechanisms --Increase in HR in an attempt to increase CO --Sympathetic Nervous system also stimulates the release of epinephrine and norepinephrine, improving contractility and inducing systemic vasoconstriction BP and CO increase, blood flow is redirected from nonessential organs to vital organs (heart & brain) RAAS increases sodium and water reabsorption in the renal tubules, effectively increasing venous return to the right heart --also produces potent systemic vasoconstriction that increases BP and venous return

Neurogenic Shock Actions

Administer IV fluids as ordered Administer IV medication- vasoactive drip, atropine Prepare for transcutaneous pacing or transcentous pacing-treat reoccurring bradycardia Raise the head of the pts. bed slowly (orthostatic hypotension) Apply venous thromboembolism prophylaxis, such as sequential compression devices or medication such as heparin

Anaphylaxis Shock Clinical Manifestation

Airway compromise --SOB, tachypnea, wheezing, stridor, cyanosis, and confusion due to hypoxia Untreated lead to respiratory arrest Circulatory Problems --tachycardia, hypotension, cool ,pale, clammy skin, weak pulses, and edema Also common onset of rapid progression of skin or mucossal changes (rash)

Hypovolemic Shock Actions/ Teachings

Apply 100% nonrebreather mask-maximize oxygenation #1 priority Anticipate and prepare for intubation-may be required to improve oxygenation Insert large-bore IV lines for fluid administration-facilitate a rapid infusion of fluid necessary to reverse Administer fluids replacement and prescribed --Normal saline, lactated ringer's solution, blood products Instruct pt. and family on the cause-may help reduce a reoccurrence Allow family members visitation during hospital treatment and provide frequent updates on condition and treatment-help to decrease a pt. and family anxiety

Cardiogenic Shock Action/Teaching

Apply 100% oxygen via nonrebreather mask Prepare of intubation and mechanical ventilation Administer medications as ordered-vasoactive (norepinephrine or dopamine) Inotropic medication-dobutamine(increase contractility and CO) Diuretics (cautiously) Morphine sulfate Administer fluids Restrict activity Instruct pt. and family about the importance of rest periods-increased activity or stress causes increase myocardial VO2 and can worsen the progressive's shock Teach pt. and family about the cause

Obstructive Shock Actions

Apply 100% oxygen via nonrebreather mask Prepare of intubation and mechanical ventilation Administer meds- vasoactive, anticoagulation, thrombolytic therapy Prepare fore definitive treatment --cardiac tamponade (pericardiacentesis) --PE (suction thrombectomy)

Shock Physical Assesment

Asses: perfusion at the tissue level (level of consciousness), urine output, respiratory status, pulse quality, skin color and/or mottling, and temperature are important to monitor

Arterial Line

BP commonly displayed, and it provides easy access to blood for analysis, especially ABG sample

Physical Assessment Cardiovascular System

Blood pressure is a valuable indicator of fluid status and cardiac output. In shock, BP decreases because of inadequate venous return to the heart, vasodilation, or decrease contractility of the heart muscle --return to the baseline BP level does not mean the resolution of the problem, but prolonged hypotension does indicate the continued presence of shock A common finding indicative of the compensatory stage of shock is a narrow pulse pressure, which results from compensatory vasoconstriction causing an increase in diastolic pressure with only a slight increase in systolic pressure If shock is not resolved and is allowed to progress to later stages, HR will slow, skin color, temp., quality of pulses, and capillary refill indicate perfusion in the extremities.

Obstructive Shock

Cause by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload) causing decreased CO Ex: Cardiac Tamponade, and tension Pneumothorax

Obstructive Shock Patho.

Caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload) causing decreased CO

Neurogenic Shock

Caused by disruption of the sympathetic nervous system, typically as a result of spinal cord injury, regional spinal anesthesia, or an injury to the brain First vascular tone is significantly decreased, hampering vasoconstriction and leaving vessels relaxed and dilated Vascular volume increased in the peripheral vessels, but venous return to the right heart is decreased, resulting in decreased CO Causes systemic hypoperfusion Pts. susceptible to orthostatic hypotension

Physical Assessment CNS

Changes in CNS perfusion may be the initial indication of inadequate DO2 to the tissues Low DO2, the respiratory alkalosis that results from tachypnea causes vasoconstrictions of the carotid arteries, resulting in decreased cerebral blood flow --restlessness, irritability, are several beginning indicators of poor cerebral perfusion Without treatment, continued poor perfusion may progress to lethargy and coma

Cardiogenic Shock

Characterized as inadequate pumping ability of the heart muscles Result of a Acute Myocardial Infraction (AMI) Independent of fluid volume status, the inadequate pumping of the heart results in decreased cardiac output and poor perfusion at the tissue level

Compensatory Stage of Shock

Characterized by initiation of compensatory mechanisms in an effort to maintain adequate volume, CO, and blood flow to the tissues Include: neural, endocrine, and chemical compensations

Septic Shock Clinical Manifestation Late Stage

Cool, pale skin Weak and threated pulses Hypothermia Tachycardia persist, but BP remains low Further stage of end-organ hypoperfusion (lethargy, coma) Anuria may be present

Obstructive Shock Clinical Manifestation

Decreased CO impaired peripheral perfusion decreased level of consciousness decreased urine output poor pulses, pale and cool skin temp decreased bowel sounds Chest pain N/V SOB Muffled heart sounds may be associated with cardiac tamponoade

Cardiogenic Shock Emergency Revascularization

Early revascularization through percutaneous coronary intervention has been shown to increase short and long term survival --Involves a balloon angioplasty or the insertion of a cath. through an artery up into the involved coronary artery and inflation of the balloon to break up the plaque causing the obstruction of flow

Physical Assessment Respiratory System

Early stages of shock are characterized by increased respirations done in an effort to increase oxygenation and decrease carbon dioxide levels due to the metabolic acidosis Measured through Pulse oximetry, but poor peripheral circulation may cause inaccurate readings ABG's may be necessary for more accurate assessment

Neurogenic Shock Management

Focus on providing vascular support while attempting to resolve the primary cause of shock- --continuous fluid resuscitation and the use of Vasoactive IV meds (dopamine, epinephrine, norepinephrine, or phenylephrine)

Cardiogenic Shock Clinical Manifestation

Frequently presents with clinical symptoms of AMI (chest pain, diaphoresis, N/V) With decreased CO-hypotension (decreased level of consciousness), decreased urine output, poor pulses, cool skin, decreased in bowel sounds crackles on auscultation, and decreased saturation of arterial blood and oxygen-results from pulmonary edema As shock progresses --profound hypotension, and bradycardia, organs begin to fail Lab analysis: increased in creatine and liver level (failure). Coma, cyanotic, mottled skin, absent bowel sounds, and anuria

Neurogenic Shock Teaching

If the cause is spinal cord injury, teaching related to the anticipated impact on the pt. immediate and future healthcare issues is vital. Psychosocial support from social worker, clergy, or a professional requested by the family is also essential in the care of the pt.

Hypovolemic Shock Epidemiology

Inadequate intravascular volume producing decreased CO that results when there is a severe loss of blood or fluids due to an acute injury or illness --may be from massive GI bleed, or blunt trauma Severe vomiting, diarrhea, excessive urination, or loss of fluid due to burns Most common cause is blood loss

Physical Assessment Gastrointestinal System

Indicates poor perfusion through sluggish, hypoactive bowel sounds that reflect a slowing of intestinal activity N/V may be present Particularly vulnerable to poor perfusion and ischemia Cell damage allows translocation of intestinal bacteria to the systemic circulation, increasing risk of sepsis Hypoperfusion may indicate a systemic inflammatory response, which if not resolved may be the precursor to multiple organ dysfunction syndrome (MODS)

Septic Shock Management

Indicators of infection --fever, increased WBC count, changes in BP, respiratory rate, and HR Lung consoldilation, frequent or painful urination, peritonitis Lab test-radiographs, CT scan, MRI

Stages of Shock

Initial Progressive Compensatory Refractory Without effected treatment shock progresses through the stages. the earlier the identification and treatment the better is the possible outcome

Septic Shock Clinical Manifestation Early Stage

Initial inflammatory response Tachycardia with bounding pulses Warm, flushed skin, and is febrile BP may be normal Initial signs of decreased organ perfusion(confusion) decreased urine output

Hypovolemic Shock Early stage Clinical Manifestation

Initially the pt. may have no outward symptoms BP may remain within normal limits (HR is typically increased) Restlessness/confusion Urine output decreases-reabsorption of sodium and water Skin-pale, cool, and clammy Pulse-weak, with sluggish capillary refill Hyperventilation (respiratory alkalosis) Decreased or hypoactive bowel sounds-shunting of blood to vital organs Hyperglycemia-initiation of flight or flight response

Septic Shock Teaching

Instruct the pt. and family on the cause, and the importance of meticulous hand washing Allow family members visitation during hospital treatment

Pulmonary Artery Catheter

Is a flexible balloon tipped cath. that is guided through the right side of the heart and into the pulmonary artery Monitoring allows the nurse to obtain detailed information about CO and the variables that affect it: preload(filling pressures), afterload, and contractility Has 2 lumens: --Proximal, distal, thermistor, and inflation CO can be directly obtained Continuously measures the ambient blood temp. around it

Hypovolemic Shock Later Stage Clinical Manifestation

Lethargy Hypotension Metabolic/Respiratory acidosis Anuria Cold/cyanotic skin with weak or absent pulses Dysrhythmias Without effective interventions the pt. enters refractory stage of shock --Coma, severe hypertension, ischemic and necrotic cold extremities, renal failure, and hepatic failure

Proximal Port

Located 30cm from the tip of the cath., typically resting just in the right atrium Used to monitor right arterial pressure, a reflection of right heart preload, and right ventricular end diastolic volume Used to inject the solution to obtain a thermodilution CO

Distal Lumen

Located at the tip of the PA cath. and rests within the pulmonary artery Nurse can monitor systolic, diastolic, and mean PA pressure and the pulmonary wedge pressure, also refered to as pulmonary artery occlusive pressure Used for drawing a venous oxygenation saturation sample, specifically a mixed venous oxygenation sample --provides a mixed sample of blood returned from the superior vena cava, thus providing information on oxygen extraction throughout the entire body

Progressive Stage of Shock

Marked by failure of compensatory mechanism adequate blood pressure and circulating blood pressure and circulating blood volume Extensive shunting of blood to vital organs which results in decreased blood flow to the periphery Without effective treatment, profound hypoperfusion occurs, resulting in worsening metabolic acidosis, electrolyte imbalance due to the failure of the sodium-potassium pump, and respiratory acidosis

Initial Stage of Shock

Marked by hypoxia due to decreased DO2 to the cells Clinical Manifestation Subtle/subclinical but cellular damage may be occurring Invasive hemodynamic monitoring would note decreased cardiac output

Refractory Stage

Marked by prolonged inadequate blood supply to the cells, resulting in cell death and multisystem organ failure Loss of aerobic mechanism, and only extremely inefficient anaerobic metabolism is available Shock is irreversible at this stage

Cardiogenic Shock Medications

Meds that support BP through vasconstriction --Dopamine, nonrepinephrine (maintain adequate mean artiral pressure) Dobutamine-increasw myocardial contactility Nitroglycerin-decrease preload and afterload

Septic Shock Actions

Meticulous hand washing and aseptic technique with all procedures Administer oxygen as ordered Anticipate for intubation Obtain lactate levels Obtain 2 blood cultures from two different sites, obtain urine, sputum, and wound culture Administer antibiotics as ordered AFTER culture Administer vasoactive drip such as norepinephrine as ordered Provide mouth care every 4 hrs Supportive care: nutrition, turning, DVT prophylaxis, ROM, mobilize as tolerated

Hemodynamic Monitoring

Monitoring of BP, CO, and the variables that affect CO provides valuable insights into the presence stage, or resolution of shock Is done through the arterial line and a central venous cath. or pulmonary artery cath.

Cardiogenic Shock Assessment

Neurological Status- decreased level of consiousness, and a result of decreased CO and carotid vasoconstriction Vital signs-hypotension and tachycardia (decreased CO), increased respiratory rate, Oxygenation rate my decrease due to pulmonary edema Hemodynamic parameter- both right/left preload are increased Breath sounds-crackles (pulmonary edema) Urine output- due to decreased CO, increases reabsorption of sodium and fluid Skin color temp.-cold and clammy (signs of progressive shock)

Obstructive Shock Assessment

Neurological status Vital signs Hemodynamic parameters urine output Skin color/ temp. Lab test ABG's Venous oxygenation

Septic Shock Assessment

Neurological status Vital signs Hemodynamic readings Urine output skin color/ temp. Bleeding Lab test ABG's Venous oxygen saturation Metabolic profile Lactate/base deficit Clotting studies

Obstructive Shock Management

Provide oxygen through 100% nonrebreather mask intubation and mechanical ventilation may be needed Shock due to cardiac tamponade --fluid must be drained as quickly as possible Shock due to PD --remove clot via thrombolytic therapy

Physical Assessment Renal System

Provides a clear indication of poor perfusion if urine output decreases Oliguria is a common finding in early stages of shock, because of decreased perfusion of the renal tubules, which stimulates the initiation of the RAAS If unresolved, later stages of shock will present with anuria, increased creatine level, and other signs of acute renal failure

Oxygen Consumption (VO2)

Reflects the amount of oxygen extracted from the blood at a tissue level measured through evaluation of a blood sample (Venous oxygen saturation SvO2)- reflects the amount of oxygenated blood returned to the right heart --Normal range 65 to 75%, when below normal tissue are extracting more oxygen than normal. Results in decreased O2

Anaphylaxis Shock Actions

Remove trigger IMMEDIATELY Administer Epi. IM Apply oxygen 100% nonrebreather mask or possible intubation Insert an IV and administer IV fluids as ordered-helps increase and maintain vascular volume Administer adjunctive meds. as ordered --Antihistamines --Corticosteroids --Inhaled bronchodilators

Distributive Shock

Results of disease states such as sepsis, anaphylaxis, or neurogenic shock that causes poor vascular tone and vasodilation, resulting in increase vascular capacity and venous pooling A state of relative hypovolemia exist due to vasodilation with out a concurrent increase in volume Venous pooling results, causing a decreased venous return to the right heart

Hypovolemic Shock Medical Management

Resuscitation priorities include oxygenation, initiating fluid resuscitation, and identifying and treating the underlying cause Maximizing oxygenation is essential in treatment in pts. with shock --Assessing and stabilizing the pt. airway is the IMMEDIATE FIRST PRIORITY! (high flow oxygen 100% nonrebreather mask) --intubation and positive pressure mechanical ventilation if needed. (positive pressure should be used with caution because of the increased intrathoracic pressure decrease CO further Rapid fluid resuscitation is the mainstay treatment --The type of fluid varies depending on the cause --continue resuscitation until the oxygen debt accumulated has been repaid (stable BP, strong peripheral pulses, warm extremities, adequate urine output Identifying underlying cause --if not apparent diagnostic test can be done (ultrasound, CT) --Once identified stabilize the problem

Obstructive Shock Epidemiology

Risk Factors: extracardiac disorders that impair ventricular filling or emptying Ex. increased right afterload is acute pulmonary embolism

Cardiogenic Shock Treatment Priorities

Stabilizing oxygenation and initiating drug therapy to increase BP and CO Considerations of emergency revascularation, an attempt to restore blood flow through percutaneous coronary interventions Intra-aortic balloon pump therapy to increase myocardial oxygen supply and decrease myocardial oxygen demand If these are not successful, a ventricular assist device may be necessary

Obstructive Shock Teaching

Teach the pt. and family about the cause of PE: avoid prolonged periods of inactivity, walk every hour, and drink plenty of fluids Anticoagulation teaching: use electric razor, soft toothbrush, avoid contact sports --if on coumadin: regular follow up lab testing Limit foods high in vitamin K

Anaphylaxis Teaching

Teaching related to the cause-avoid triggers Administration of EPi pen

Oxygen Delivery (DO2)

The amount of oxygen delivered to the tissue Assessed through the evaluation of cardiac output and arterial oxygen content

Oxygen Debt

The difference between normal VO2 and VO2 during low DO2 state

Distributive Shock

The result of disease that cause poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling Sepsis MOST COMMON- widespread of vasodilation and distributive shock Anaphylaxis-caused by the release of histamine, which results in vasodilation, decreased venous return, and hypotension LEAST COMMON Neurogenic Shock-caused by injury to the brain, genera or spinal anesthesia, or spinal cord injury

Central Venous Catheter

Utilizes a long catheter threaded through the superior vena cava with the distal port resting in the superior vena cava immediately above the junction with the right atrium Monitoring of CVP --used as an estimate of volume returning to the right heart or right heart preload, or the right ventricular end-diastolic volume decreased CVP: a low volume tone state, hypovolemic shock or peripheral vasodilation that occurs as a result of distributive shock Elevated CVP: increase volume that may occur with cardiogenic shock draws a central venous oxygen saturation

Hypovolemic Shock Assessment

Vital signs-BP may remain in normal limits initially because of stimulation of compensatory mechanism. Tachycardia, hypotension and bradycardia Neurological status-decreased level of consciousness occurs as a result of decreased CO and carotid vasoconstriction that occurs as the result of hyperventilation Hemodynamic readings Urinary output-results in decreased CO, increases sodium and water intake Skin color/temp.- cold and clammy sign of peripheral perfusion and progressive shock

Neurogenic Shock Assessment

Vital signs-hypotension due to decreased venous return to the right of the heart. Bradycardia may be present Hemodynamic parameters-CO, CVP, and PAOP are low related to decreased venous return Respiratory Rate and SpO2-respiratory rate may be low because of injury

Anaphylaxis Shock Assessment

Vital signs/hemodynamic parameters --hypotension and decreased filling pressures are present because of widespread vasodilation, resulting in decreased venous return and CO. Tachycardia can be a result Respiratory- SOB, wheezing, and decreased oxygenation Skin/peripheral perfusion- urticaria and angioedema are indicators of an allergic reaction. Pale, cool, clammy skin are indicators or peripheral perfusion related to decreased CO

Neurogenic Shock Clinical Manifestation

Warm, dry skin and flushed appearance due to systemic vasodilation Hemodynamic parameter include decrease CO, decreased right and left filling volume Decreased systemic vascular resistance

Hypovolemic Shock

Where there is rapid fluid loss resulting in inadequate circulating volume Secondary to blood loss from: --Penetrating/blunt trauma: gunshot wounds, knife injury, blood loss into the abdomen due to damage to the live (blunt) --Severe GI bleeds Fluid loss can be caused by severe vomiting/diarrhea Burns can also result in this