cen online review - amazon s3 · 2016-08-03 · cen online review shock table 4: classification of...

CEN Online ReviewShock

CEN Online Review: Shock — Chapter 1 1

Barb Weintraub, MSN, MPH, RN, PNP-AC, CEN, CPEN, FAEN

Objectives:1. Explain concepts related to the assessment of an emergency department patient experiencing a

shock emergency.2. Describe various patient presentations related to shock emergencies.3. List interventions necessary for a patient presenting with a shock emergency.

CHAPTER 1“Shock is a momentary pause in the act of death” — John Collins Warren

DefinitionShock is a state of impaired tissue perfusion resulting from circulatory failure brought on by a variety of causes.

Normal FunctionNormal function of the body is similar to normal function of a car.

Table 1: Comparison

Car Body

Gas Blood and plasma

Fuel pump Heart

Fuel line Arteries and veins

Shock is Classified by the Cause of Inadequate Perfusion � Hypovolemic shock (low on gas)

§ Decreased cellular perfusion secondary to lack of circulating volume, or not enough gas � Cardiogenic shock (bad fuel pump)

§ Decreased cellular perfusion secondary to failure of the central pump, like a bad fuel pump � Distributive shock (trying to fuel 2 cars with 1 gas line)

§ Decreased cellular perfusion secondary to maldistribution of oxygen to the periphery § It’s like adding a much larger engine without increasing the size of the gas tank

� Obstructive shock (blockage in the fuel line) § Decreased cellular perfusion secondary to obstruction of blood into or out of the ventricles (e.g., pulmonary embolism, pericardial tamponade, tension pneumothorax)

§ This is like getting dirt or blockage in the fuel line

Cellular CascadeThe cascade of events and clinical decline are similar for all causes of shock.

� This cascade is initially reversible, but without treatment becomes irreversible � This cascade begins with cellular injury, cellular inflammation, and ultimately cellular death � The lack of oxygenated blood at the cellular level causes anaerobic metabolism, which causes lactic acid production � Prolonged lactic acidosis leads to microvascular thrombosis and disseminated intravascular coagulation (DIC)



Figure 1: Cellular Cascade

Stages of Shock

Figure 2: Shock

Compensated ShockDecreased Blood Flow to Kidneys

� Increased renin production § Renin causes conversion of angiotensinogen → angiotensin I → angiotensin II § Angiotensin II

· Secretion of aldosterone · Vasoconstriction · Stimulation of antidiuretic hormone (ADH) secretion · Release of adrenaline, noradrenaline, and aldosterone in the adrenal gland



§ Aldosterone · Sodium and water reabsorption by the renal system · Increased excretion of potassium · Constriction of small arteries (arterioles)

§ Adrenaline and noradrenaline · Vasoconstriction

Table 2: Compensation for Shock

Physiology Response

� Sympathetic nervous system (SNS) response § Release of epinephrine/norepinephrine § Vasoconstriction

HR é contractility é BP é

� Renin-angiotensin-aldosterone system (RAAS) § Increased serum sodium levels § Water reabsorption

Urine ê BP é CO é

� Antidiuretic hormone (ADH) release § Renal reabsorption of sodium § Renal reabsorption of water

Urine ê BP é CO é

� Intracellular fluid shift § Increased intravascular volume

BP é CO é

Uncompensated ShockShock at the Cellular Level

� Cell membrane integrity is compromised § Intracellular fluid leaks into interstitium, causing third-spacing and edema § Interstitial fluid is not available to maintain blood pressure, and blood pressure drops

� Interstitial edema in the lungs, causes respiratory insufficiency due to V/Q (ventilation/perfusion) mismatch § Respiratory rate increases to compensate § Dyspnea occurs due to the V/Q mismatch

� Cardiac depression occurs with decreased venous return to the heart § Decreased cardiac output § Loss of perfusion to nonvital organs § Heart rate increases § Dysrhythmias


� Hypotension activates the sympathetic nervous system § Vasoconstrictors epinephrine and norepinephrine are released § Vasoconstriction shunts perfusion to the heart and brain, away from nonvital organs such as the kidney, intestines, and skin, leading to ischemia

§ Urine output decreases as renal perfusion is compromised � Anaerobic metabolism causes a rise in serum lactate acidosis � Gut membrane integrity is compromised and intestinal bacteria are released into the bloodstream � Hypotension worsens, perfusion to heart and lungs ↓, and mentation becomes altered � See the Uncompensated Shock table below for a recap

Table 3: Uncompensated Shock

Physiology Response

� Altered capillary permeability § Leakage into the interstitial space

EdemaBP ê Perfusion ê

� Respiratory insufficiency § Pulmonary edema § V/Q mismatch

CracklesDyspnea RR é

� Cardiac depression § Diminished venous return § Ischemia of nonvital organs

BP ê HR é CO ê Peripheral pulses ê Dysrhythmias

� Tissue hypoperfusion § Severe vasoconstriction § Ischemia of nonvital organs

Urine output ê Lactate éBase deficitMixed venous saturation (below 65%) Cool skinPeripheral pulses ê

� Brain hypoperfusion Altered mental status



CHAPTER 2Hypovolemic Shock

� Definition § Blood, plasma, or fluid loss reduces circulating blood volume and cardiac output

· Most commonly encountered type of shock � Common causes

§ Traumatic hemorrhage · Long bone or pelvic fractures · Solid organ rupture · Open wounds

§ Nontraumatic hemorrhage · GI bleed · Ruptured aortic aneurysm · Posterior epistaxis

§ Fluid shifts · Peritonitis · Massive crush injuries · Severe burns

§ Non-blood fluid losses · Severe vomiting and diarrhea · Excessive diaphoresis

§ Urinary fluid losses · Diabetic ketoacidosis · Diabetes insipidus · Diuretic abuse

Hypovolemic Shock: Assessment � Assess ABCs � Determine cause of hypovolemia � Lab analysis � Trend of vital signs � MAP (mean arterial pressure)

§ Maintain the MAP above 60 mm Hg § MAP = (Systolic pressure + 2(Diastolic pressure)/3

� Urine output � Level of consciousness



Table 4: Classification of Hypovolemic Shock

Parameter Class I Class II Class III Class IV

Blood loss Below 15% 15–30% 30–40% Above 40%

Pulse (beats/min) Below 100 100–120 120–140 Above 140

Blood pressure Normal Normal Decreased Decreased

Resp. rate (breaths/min) 14–20 20–30 30–40 Above 35

Urinary output (mL/h) Above 30 20–30 5–20 Negligible

Central nervous system Slightly anxious Mildly anxious Anxious, confused Confused, lethargic

Hypovolemic Shock: Intervention � Airway control � Control bleeding, reduce fluid loss � Restore circulating volume

§ Isotonic crystalloids · 0.9% sodium chloride (normal saline) · Ringer’s lactate (use carefully, can elevate lactate level) · Adults: 1–2 L bolus · Pediatrics: 20 mL/kg

§ Dextrose NEVER used in fluid resuscitation · Does not contribute to expanding intracellular volume because quickly metabolized, causing plasma to become hypotonic

§ Colloids (1:1 replacement) · May be used after initial fluid resuscitation · Albumin (protein based)

� May cause hypocalcemia � Human product (risk of disease) � Risk of fluid overload

· Hetastarch (non-protein based) � Risk of fluid overload � May increase amylase � May cause coagulopathies

· Dextran (non-protein based) � Risk of fluid overload � May increase bleeding time � Risk of anaphylaxis

· Disadvantages � Higher cost � Higher risk profile � Lack of definitive evidence of reduced mortality



§ Blood replacement (1:1 replacement) · Definitive treatment for hemorrhagic shock

� Use of type-specific, cross-matched blood preferred � If no time, O-negative blood

· Packed RBCs � Best product to rapidly elevate oxygen-carrying capacity � Must be ABO compatible � O-negative blood standard for non-type-specific resuscitation � O-positive blood may be given to men and to women beyond childbearing age � Pediatrics 10 mL/kg

· Massive transfusion � Protocol for rapid replacement of blood lost � Since PRBCs lack clotting factors, ratios are often 1 unit plasma and 1 unit platelets per 1–2 units of PRBCs

· Autotransfusion � Considered in cases of thoracic trauma � Contraindicated if potential for contamination with bowel contents

Cardiogenic Shock � Definition

§ Inadequate tissue perfusion as a result of decreased cardiac output despite adequate intravascular volume § Result of myocardial pump failure

· The most common cause is myocardial infarction, particularly of the left ventricular anterior wall

§ Causes · Myocardial infarction, ischemia · Blunt cardiac trauma · Sustained cardiac dysrhythmias · Acute valvular dysfunction · End-stage cardiomyopathy

Cardiogenic Shock: Clinical Manifestations � Reflects heart failure, inadequate tissue perfusion � Often in conjunction with acute myocardial infarction

§ Cardiac chest pain § Tachypnea, crackles, pulmonary edema § Tachycardia, tachydysrhythmias, S3 heart sound § Altered mental status § Pale, cool, clammy skin § Minimal urine output § Hypotension

Cardiogenic Shock: Assessment � Diagnostics to determine cause of cardiac dysfunction, extent of shock, and organ involvement

§ ECG § Chest X-ray § ABG § Echocardiogram § CBC, platelet count, electrolytes, RFTs, LFTs § Lactate level § SvO2 (mixed venous oxygen saturation) less than 65%



Cardiogenic Shock: Interventions � Airway management with postive end-expiratory pressure (PEEP)

§ PEEP will force pulmonary edema fluid out of the lung interstitium � Decrease preload (venous return to the heart)

§ Semi-Fowler or Fowler position § Nitroglycerin § Diuretics § Morphine

� Increase contractility § Positive inotropes (dobutamine) § Intra-aortic balloon pump (IABP)

� Decrease afterload (resistance the heart must pump against) § Continuous nitroglycerin § Nitroprusside § Antihypertensives

� Cardiac catheterization � Angioplasty � Treat dysrhythmias

CHAPTER 3Distributive Shock

� Definition § Abnormal distribution of intravascular volume as result of

· Decreased sympathetic tone · Increased vascular permeability · Pooling of blood in venous, capillary beds

§ Types of distributive shock · Anaphylactic · Septic · Neurogenic

Distributive Shock: Anaphylaxis � Definition

§ Acute, life-threatening allergic reaction in individuals exposed to an antigen to which they have previously become hypersensitive

� Common antigens § Shellfish and fish § Peanuts and tree nuts § Milk and eggs § Wheat and soy § Some food additives § Insects § Medications § Latex § Iodine

CEN Online Review: Shock — Chapter 2 & 3 8


� Unusual causes of anaphylaxis § Exposure to cold § Exercise

� Anaphylaxis is not the same as anaphylactic shock § Anaphylaxis

· Normal circulation with risk of progression to anaphylactic shock § Anaphylactic shock

· Shock state with compromised circulation � Anaphylaxis vs. anaphylactoid reactions

§ Anaphylaxis · Always IgE mediated · Always requires prior exposure to the antigen

Anaphylactic Shock � Pathophysiology

§ Antigen re-exposure § Hypersensitive antibody response § Vasoactive mediator release

· Massive vasodilation, profound hypovolemia · Increased capillary permeability, fluid shift, vascular collapse

Anaphylactic Shock: Assessment � Clinical manifestations

§ Symptoms rapidly progressive § Onset usually begins with cutaneous manifestations § Urticaria (hives), erythema, pruritus § Dyspnea, cough § Throat tightness, stridor § Wheezing, bronchospasm § Syncope § Chest tightness, palpitations § Angioedema § Hypotension, tachycardia § Respiratory and cardiac arrest

Anaphylactic Shock: Interventions � Remove causative agent if possible � IM epinephrine 1:1000, repeat in 15–20 min as needed � Airway management � High-flow oxygen � IV access

§ Fluid resuscitation § Vasopressors for hypotension

� IV epinephrine 0.1–0.5 mL 1:10,000 as needed � Inhaled Beta-2 agonists (albuterol) � Antihistamine therapy (H1 and H2 blockers) � Corticosteroids � Admission � Epinephrine autoinjector teaching with discharge instructions



Distributive Shock: Septic Shock � Systemic inflammatory response syndrome (SIRS)

§ Cluster of symptoms of systemic inflammation § May or may not be the result of infection § Can be seen with acute pancreatitis and major trauma, including burns

� Sepsis § At least 2 SIRS criteria with known or suspected infection

� Severe sepsis § Sepsis with organ dysfunction

· Cardiovascular failure leading to hypotension · Respiratory failure leading to hypoxia · Renal failure leading to oliguria and/or azotemia · Hematologic failure leading to coagulopathy

� Septic shock § Sepsis with hypotension despite adequate fluid resuscitation

� Multiple Organ Dysfunction Syndrome (MODS) § Progressive failure of initially uninvolved distant organs following severe infectious or noninfectious insults

Septic Shock: Assessment

Table 5: Warm and Cold Septic Shock

Clinical Manifestations Hyperdynamic (warm) Sepsis Hypodynamic (cold) Sepsis

Mentation Malaise, tired, restless Decreasing level of consciousness, stupor, coma

Skin Warm, flushed, dry Cold, clammy, pale, mottled

Heart rate Tachycardia, full pulses Tachycardia, weak, thready pulses

Respiratory rate Above 20/minute Tachypneic, shallow

Urine output Decreased Decreased or anuria

Acid-base values Respiratory alkalosis Metabolic and respiratory alkalosis

Body temperature Fever, shaking and chills Hypothermic, mottled

Septic Shock: Interventions � Fluid resuscitation � Positive inotropes, vasopressors if inadequate response � Identify, remove potential infection sources

§ Indwelling urinary catheters § IV catheters § PICC, central lines

� Obtain wound, blood cultures before antibiotic administration � Timely antibiotic administration



Distributive Shock: Neurogenic Shock � Definition

§ Loss of sympathetic stimulation, resulting in pure parasympathetic stimulation · Massive vasodilation · Body unable to compensate for drop in cardiac output

� Causes § Spinal cord injury (cervical or high thoracic) § Spinal anesthesia § Brain injury

Neurogenic Shock: Clinical Manifestations � Loss of the sympathetic nervous system means the “fight or flight” response is lost and the parasympathetic or “rest and digest” system is unopposed

§ Bradycardia rather than tachycardia § Bradypnea rather than tachypnea § Hypotension § Skin warm, dry, and flushed § Full pulses § Priapism

Neurogenic Shock: Interventions � ABCs to prevent secondary cord injury � Fluid resuscitation � Administer vasopressors (phenylephrine) � Administer atropine for bradycardia � Routine administration of high-dose corticosteroids no longer recommended

Obstructive Shock � Definition

§ Cardiac output and tissue perfusion are inadequate because of resistance to ventricular filling � Causes

§ Pericardial tamponade § Tension pneumothorax § Pulmonary embolism

� Interventions § Correct underlying condition § Pericardial tamponade

· Immediate pericardiocentesis and subsequent surgical repair § Tension pneumothorax

· Immediate needle thoracotomy and chest tube placement · Pulmonary embolism · Intravenous anticoagulation and occasionally, thrombolytics



CHAPTER 4Endpoints of Shock Resuscitation

� MAP above 60–70 mm Hg � CVP 8–12 mm Hg � Urine output of 0.5 mL/kg per hour or 30–60 mL per hour � Normal serum lactate levels � SvO2 65–75% � Systolic BP above 90 mm Hg

Pediatric Considerations � Incidence

§ Hypovolemia is most common manifestation in pediatrics · Higher metabolic rate · Higher body surface to volume ratio · Inability to voice symptoms

§ Septic shock also seen, especially in neonates, due to immature immune systems § Cardiogenic shock also seen with toxic ingestions or sustained SVT

� Assessment § Adequate history is essential in determining the cause of shock § Physical exam

· Dry mucous membranes · No tears · Poor skin turgor · Sunken fontanels · Delayed capillary refill

§ Possibility of child abuse always a consideration § IO access for fluid replacement if IV access is difficult or unavailable

Geriatric Considerations � Tachycardia during shock may be masked by medications (beta blockers) � Hypovolemic shock

§ Prone to dehydration · Medications such as diuretics · Decreased thirst response to volume deficit · Limited mobility

§ If unstable, administer NS 500 mL IV fluid bolus, then 200 mL per hour until SBP above 100 mm Hg · Switch to D5 in 0.45 NS with KCl · Use caution to avoid fluid overload

� Septic shock § Sepsis is an important cause of morbidity and mortality § Frequent causes:

· Pneumonia · Urosepsis

§ Manifestations can be subtle · Altered mental state · Respiratory alkalosis · Normothermia or hypothermia



Resources Abramson, D., Scalea, T. M., Hitchcock, R., Trooskin, S. Z., Henry, S. M., & Greenspan, J. (1993). Lactate clearance and survival following injury. The Journal of Trauma, 35(4), 584–588, discussion 588–9 (classic reference).

Sinz, E., Navarro, K., & Soderberg, E. S (Eds.). (2011). Advanced cardiovascular life support: Provider manual. Dallas, TX: American Heart Association.

Chameides, L., Samson, R. A., Schexnayder, S. M., & Hazinski, M. F. (Eds.). (2012). Pediatric advanced life support: Provider manual. Dallas, TX: American Heart Association.

Blalock A. (1940). Principles of surgical care: Shock, and other problems. St Louis, MO: C. V. Mosby Company (classic reference).

Burns, S. M. (Ed.). (2014). AACN essentials of Critical Care Nursing (3rd ed.). New York, NY: McGraw Hill Education.

Dellinger, R. P., Levy, M. M., Rhodes, A., Annane, D., Gerlach, H., Opal, S. M., … Moreno, R. (2013). Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock: 2012. Critical care medicine, 41(2), 580–637. doi:10.1097/CCM.0b013e31827e83af

Hoyt, K. S., & Selfridge-Thomas, J. (Eds.). (2007). Emergency nursing core curriculum (6th ed.). St. Louis, MO: Saunders Elsevier.

Emergency Nurses Association. (2012). Emergency nursing pediatric course (ENPC): Provider manual (4th ed.). Des Plaines, IL: Author.

Emergency Nurses Association. (2014). Trauma nursing core course (TNCC): Provider manual (7th ed.). Des Plaines, IL: Author.

Hammond, B. B., & Zimmermann, P. G. (2012). Sheehy’s manual of emergency care (7th ed.). St. Louis, MO: Mosby Elsevier.

CEN Online Review: Shock — Resources 13

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