N240 Olol - Test 1 - Shock - Test 1

Front 1

SHOCK hypovolemic, cardiogenic, distributive (circulatory - Overview

Back 1

Shock is a clinical syndrome that differs in types, causes and treatments but has in common impaired tissue perfusion.
Poor tissue perfusion sets up the complex sequela of events leading to cellular death and multiorgan system failure.
The shock condition progresses through various stages and becomes irreversible.
Patients will die if shock is not treated early and completely.
Researchers are just beginning to recognize Systemic Inflammatory Response Syndrome and activation of the coagulation system as progressive stages of shock.

Front 2

Shock - General

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+A clinical state of imbalance with impairment of one of the following functions.
+Adequate circulating blood volume
Hypovolemic
+Adequate pumping mechanism
Cardiogenic
+Adequate vascular tone
Distributive, circulatory

Front 3

Types of Shock

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+Hypovolemic – inadequate circulating blood volume.
+Cardiogenic – inadequate pumping mechanism.
++Distributive
+Neurogenic – loss of sympathetic tone.
Anaphylactic – massive vasodilatation due to the powerful effects of histamine.
+Septic-vasodilatation as a result of endotoxin (when bl. Cells lysed) release from pathogens. The process complicated by fever increasing cellular metabolism and oxygen demand.

Front 4

Hypovolemic Shock

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+Any condition that decreases the amount of circulating blood volume by 15-25%.
Can be classified as actual or relative loss.
+Actual hypovolemia occurs with hemorrhage or excessive fluid loss such as diuresis, diaphoresis, vomiting and diarrhea.
+Relative hypovolemia occurs with fluid shifts from the intravascular space to the interstitial space, or peritoneum. Burn victum -3rd spacing, cirusis pt.
+Most common causes of hypovolemic shock are trauma, GI hemorrhage, and obstetrical bleeding.

Front 5

Pathophysiology of Hypovolemic Shock

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+Decreased circulating blood volume
+Decreased venous return- leads to poor stroke vol.
+Decreased stroke volume
+ Starling’s law-more fill l.ven
Harder it contracts
Decreased cardiac output
+Decreased BP
(systematic, all leads to the last)
+Poor tissue perfusion

Front 6

Cardiogenic Shock

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+Failure of the left ventricle to pump blood adequately.
+Usually the result of MI affecting 40% of the left ventricle.
+Other causes: Cardiomyopathy, arrhythmia, endocarditis, valve dysfunction, cardiac tamponade.

Front 7

Pathophysiology of Cardiogenic shock

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+Decreased ventricular emptying
+Decreased stroke volume (weak l.ven)
+Decreased cardiac output
+Decreased blood pressure (leads to…)
+Poor tissue perfusion
+Pulmonary edema- distended neck vein-bl backed into lungs-crackles-+jvd

Front 8

Neurogenic shock

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+A result of damage to the spinal cord.
+Occurs in the first few weeks after spinal injury.
+Self limiting (only last for 1-3 weeks).
+Impulses of the sympathetic nervous system are blocked and patient only has parasympathetic nervous system responses.-instead of tachycardic they become bradycardiac
+Sympathetic – vasoconstriction, tachycardia
+Parasympathetic – vasodilitation and bradycardia (unopposed parasympathetic stimulation)

Front 9

Anaphylactic Shock

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+Massive release of histamine which has a powerful vasodilating effect on blood vessels especially capillary beds.
+Common causes are PCN allergy.
-Caution: patients with PCN allergy may also react to Ancef (similar protein binding on bacteria).
+Check allergies before administering contrast dyes used in diagnostic studies.
-Caution patients with allergies to iodine or seafood.
+Food allergies seafood and peanuts.
+Latex also

Front 10

Pathophysiology ofDistributive Shock

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+Venous pooling in periphery
+Decreased venous return (leads to…)
+Decreased stroke volume (leads to…)
+Decreased cardiac output (leads to…)
+Decreased blood pressure (leads to…)
+Poor tissue perfusion

Front 11

Initial Stage of Shock

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+Characterized by a decrease in MAP (mean arterial pressure) <10mm below normal.
+Represents a decrease in circulating blood volume of less than 500ml.
+S/S decreased pulse volume , slight decrease in BP.
+MAP= DBP + 1/3 pulse pressure
+Ex: 130/70 = 70+(130-70)= 20 +70=90
so later they are 110/70 = 70+(110-70)= 83.3MAP (sign of shock, hard to pick up) but if 100/70 = 80MAP – so assess pt for shock do not rely on BP readings

Front 12

Compensatory Stage of Shock

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+Characterized by a decrease in MAP 10-15 mmHg below normal or a decrease in circulating blood volume by 25-30% or 1000 ml.
+Epinephrine and norepinephrine are released.
+Alpha and beta receptors in effected organs are stimulated to vasoconstrict or vasodilate.
+Alpha receptors cause vasoconstriction to the skin, abdominal organs, and kidneys.
+Beta receptors cause vasodilation to the heart, skeletal muscle, lungs and brain.
+Body shuts down other organs exp. Heart lungs, brain and skeletal

Front 13

Compensatory Stage of Shock

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+Renin angiotensin system is activated. Aldosterone secretion causes the kidneys to retain Na and H2O, and excrete K.
+Decreased intravascular volume causes hydrostatic pressure changes that cause fluid shifts, 500 ml from intracellular fluid and 500 ml from interstitial fluid. So body shifts it into intravascular –fluid shift
+Decreased MAP stimulates posterior pituitary to release ADH which increases the reabsorption of (water) H2O and encourages vasoconstriction.
+If shock is not reversed the patient enters the progressive stage of shock.

Front 14

Signs and Symptoms Early Stage of Shock

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+Increased heart rate and stroke volume – tachycardia
-Bradycardia in neurogenic (spinal)
+Increased respiratory rate and depth
-Crackles in cardiogenic ( pulmonary edema)
+Respiratory alkalosis
+Restlessness (increased bl flow to skeletal) anxiety, feeling of impending doom b/c of increased bl flow to brain
+Skin pale, cool, clammy
-Hot and flushed in septic (warm phase)
+Decreased bowel sounds, decreased urine output (oliguria)
+Increased GLUcose from stress response (hyperglycemic)
+Decreased K, decreased PO2
-Facial edema, stridor in anaphylactic (airway issues) wheezing
-First sign is no urine output or narrow pulse pressure

Front 15

Signs and Symptoms in the Late Stage of Shock

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+Heart rate rapid and thready, decreased BP
+Respiration rapid and shallow, as respiratory system fails respiratory alkalosis becomes respiratory acidosis.
+Skin ashen, mottled, cyanotic -
+Decreased mental status, confusion, comatose , lethargy
+Metabolic acidosis
+Anuric-no output
+Absent BS, GI bleed – ileus -necrosis
+Arrhythmias, hyperkalemia, metabolic acidosis
+Elevated BUN, creatinine
hypoglycemia , hyperkalemia b/c of lysis
Sepsis, DIC
+Cardiac arrest

Front 16

Progressive Stage of Shock

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+Characterized by a decreased MAP 20 mmHG or more below normal.
+Fluid loss of 35-50% of circulating blood volume.
+Decreased blood flow to body organs especially those experiencing vasoconstriction switch to anaerobic metabolism resulting in the production of lactic acid and metabolic acidosis – switches to anarobic route-produces lactic acid so leads to m.a.
+Acidosis increases capillary permeability allowing more fluid to leave the intravascular space for the interstitial space creating edema. -

Front 17

Progressive Stage of Shock 2

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+Failure of the Na-K pump allows water to enter the cell causing cellular rupture. K exits the cell. Hyperkalemia due to cell lysis
+Myocardial depressant factor increases the threshold for action potentials in cardiac cells decreasing contractility. Contributes to MI
+Vasoconstriction of splanchnic vessels causes ischemia of abdominal organs and pancreas.
+GI ulceration and hemorrhage result. Necrosis of the GI mucosa creates a potential portal of entry for bacteria to enter systemic circulation.
+Liver no longer able to detoxify substances
+Toxins and bacteria enter systemic circulation

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Progressive Stage of Shock 3

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+Stress response occurs with circulating catecholamine stimulating the release of glucagon and inhibition of insulin. Initially hyperglycemia from the stress response is followed by hypoglycemia as glucose stores are exhausted.
+Clotting cascade activated by endotoxins of septic shock resulting in DIC.
+At some point the cycle cannot be interrupted and the patient will die.

Front 19

Shock Response in Special Populations

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Pediatrics – Children have smaller blood volumes to begin with so in cases of hemorrhage, children can loose a larger percentage of their total blood volume. Kidneys are not mature and do not compensate as well as the adult kidney

Front 20

Shock Response inSpecial Populations

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+Elderly – Preexisting chronic medical conditions like CAD, and atherosclerosis make the compensatory vascular changes less effective. Hardening of the arteries
+Decrease in beta adrenergic receptors and decreased efficiency of the SA node prevent compensatory tachycardia. Medications like beta blockers, calcium channel blockers also blunt the response.

Front 21

Assessment of the Patient in Shock

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+Vital Signs – pulse will be rapid and thready. Cardiac arrhythmias may be present. BP may be difficult to obtain, may require doppler. In septic shock temperature will be elevated.
+Urine output – Monitor every hour. Report a urine output less than 30 ml/ hour for two consecutive hours.
+Neuro status – Brain is the most sensitive organ in the body to oxygen and glucose changes. Note changes in mental status like confusion, decreased level of consciousness.

Front 22

Assessment for Shock

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+Respiratory status – Monitor rate, depth, effort. Monitor skin color, nail beds for cyanosis, monitor SAO2 continuously and ABG as needed. Auscultate Breathe Sounds for development of ARDS.
+Monitor hemodynamics such as CVP, PAP, PCWP, CO for cardiovascular response and fluid status.
Electrolytes – Monitor K, glucose, and cardiac enzymes.
+H&H surgical dressing for amount and consistency of drainage. Mark the dressing to monitor drainage

Front 23

Diagnosis of Shock

Back 23

Determine the underlying cause of the shock.
Treatment varies with type of shock (see handout)

Front 24

Treatment of Shock - 1

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+Shock is poor tissue perfusion. Goals of treatment are to increase oxygen delivery to tissues and preserve vital functions.
+Maintain patent airway. ABC’s intubating if hypoxic – if unconcious
+Oxygen is always appropriate in shock to improve the imbalance between oxygen demand and supply. Maintain SAO2 at 90%, or PO2 80-100 on ABG.

Front 25

Treatment of Shock - 2

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+Circulation – provide fluids to support cardiovascular function. Crystalloids (NS or RL) for rapid fluid replacement in the initial period. Just fills up the space does not cause fluid shift (lot more used)
+Colloids added after 24 hours to improve intravascular volume. – fluid shifts, attracts fluids into intravascular space– may not need as much
+Consider the need for blood replacement. Remember to protect the patient from hypothermia if large quantities of blood are needed. Consider the need to replace clotting factors. – fresh frozen or clotting factors?? However do the replacement of fluids first – this is 3rd step
+If fluid replacement and blood replacement aren’t successful in reversing shock, consider a vasoactive medication such as dopamine.

+So Crystalloids for 1st 24 hrs then collids may be good

Front 26

Blood Products for treatment of Shock

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Whole blood provides RBC, clotting factors, and volume (no longer available).
PRC restore oxygen carrying capacity of blood volume.
Fresh frozen plasma rich in clotting factors
Platelets improve hemostasis
Cryoprecipitate -Factor VIII and fibrinogen
For volume expansion use ringers

Front 27

Med. treatment for Shock
Dopamine - 1

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+Provides vasoconstriction when fluids and blood replacement are not successful in restoring hemodynamic equilibrium. (BP)
+Use with caution always monitor BP continuously, infuse with IV regulator.
+Avoid infiltration –causes tissue necrosis
+So use injections of regitine for anti-dopamine

Front 28

Med. treatment for Shock
Dopamine - 2

Back 28

+Can be given in low, moderate and high dose infusions
+2-5mcg/kg/min dilates renal, cerebral, and coronary vessels
+5-10mcg/kg/min increases myocardial contractility.
+>10mcg/kg/min constricts arteries and veins

Front 29

Med. treatment for Shock -
Norepinephrine

Back 29

+Levophed (leave them dead)
0.05-20mcg/kg/min
+More potent vasoconstrictor than dopamine.
+Bad reputation because used as a last effort.
+In studies increased MAP without compromising renal or splanchnic vessels.
+Improved survival and normalized hemodynamics over high dose dopamine

Front 30

Med. treatment for Shock -
Phenylephrine

Back 30

+Neo Synephrine
2-10mcg/kg/min
+Only alpha effects
+Effective vasoconstriction
+Doesn’t have the tachycardia seen in high dose dopamine. So good for cardiac pts.

Front 31

Septic Shock

Back 31

+Septic shock is viewed as one condition in a continuum of systemic inflammatory response, sepsis, severe sepsis, septic shock, and multiorgan systems failure.
+Inherent in the process is the initiation of the inflammatory system, hemodynamic instability, and coagulopathy

Front 32

Definition of Septic Shock

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+Distributive shock with imbalance between oxygen supply and demand.
+Cardiac output is normal or increased due to fever.
+Impaired vascular tone caused by the inflammatory response.
+Poor tissue perfusion leads to organ systems failure and death.

Front 33

Causes of Septic Shock

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+Gram negative bacteria producing endotoxins Ex: Eschereshia Coli, Klebsiella, and Pseudomonas.
+Gram positive bacteria Staph Aureus, Toxic Shock Syndrome, Streptococcus pneumoniae.
+Fungal infections and viruses can also cause sepsis.

Front 34

Causes of Septic Shock 2

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+Gram negative bacteria accounts for 1/2 of the total cases of sepsis and is responsible for more deaths than gram positive bacteria.
+Gram positive septic shock is increasing with increased use of intravascular devices

Front 35

Incidence of Septic shock

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+750,000 new cases of sepsis per year.
+Most common cause of death in ICU patients.
+Mortality rate from septic shock has increased 82.6% from 1979-1997.
+Dramatic increase in cases related to increases in immunosupressed patients, greater number of elderly Americans, increased number of chronic illnesses, antibiotic resistance.
+Patients with indwelling lines and catheters are at increased risk for sepsis.
+Poorly identified criteria for diagnosis.

Front 36

Criteria for Diagnosis for Sepsis, Septic shock

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+In 1991 The Society of Critical Care Medicine and the American College of Chest Physicians established universal definitions for the terms SIRS, sepsis, septic shock, and multiorgan systems failure.
+Purpose was to promote earlier detection of sepsis and improve treatment and ultimately outcomes in sepsis.

Front 37

Diagnosis of SIRS
Systemic Inflammatory Response Syndrome

Back 37

+Two or more of the following conditions must be present for a diagnosis of SIRS.
+Temp >38C or below 36C (100.4 or 96.8F).
+Tachycardia > 90BPM
+Tachypnea > 20 breaths per min
+PaCO2 < 32 mmHg
+WBC >12,000mm or <4000mm

Front 38

Diagnosis of Sepsis

Back 38

+Diagnosis of sepsis is made with positive criteria for a diagnosis of SIRS with the addition of a documented infection site. SIRS + infection = Sepsis
+Septic shock occurs with the addition of hypotension, poor tissue perfusion. Sepsis + hypotension, ptp = Septic Shock
+Escalation of the disease from sepsis to septic shock increases mortality from 17-46% (JAMA, 1995).
+Multi-organ systems failure is the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

Front 39

Septic Shock

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+ARDS 18% of cases
+DIC 38% of cases
+Renal failure 50%

+People that have septic shock already

Front 40

Signs and Symptoms of Septic Shock

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+Fever
+Chills
+Fatigue
+Malaise
+Anxiety
+Confusion – often the first sign in elderly
+Symptoms of hypotension and poor tissue perfusion

Front 41

Stages in Septic Shock

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+Warm Phase – hyperdynamic period with elevated cardiac output and bounding pulses. Pt is warm to touch and flushed.
+Cold phase – skin is cool, clammy, pale, hypotension, tachycardia, temperature may be elevated or decreased below normal.

Front 42

Pathophysiology of Septic shock 1

Back 42

+Infecting organism releases endotoxins when lysed.
+Endotoxins stimulate the inflammatory process which results in activation of cytokines such as tumor necrosis factor, Interleukins, and tissue factor.
+Cytokines are proteins that account for the signs and symptoms of early sepsis. Vasodilation, hypotension, increased capillary permeability, fever, and decreased myocardial contractility.
++++Don’t have to know all of this and following Patho slides

Front 43

Pathophysiology of Septic shock 2

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+Primary release of cytokines is followed by release of secondary proinflammatory mediators like nitric oxide a powerful vasodilator that leads to hypotension. Others that cause pulmonary vasoconstriction, and some like tissue factor are thrombogenic.
+Increased platelet aggregation follows with the formation of microemboli release vasocontr.
+Normal fibrinolytic process is inhibited by the effects of neutrophils on activated protein C.
+Imbalance between fibrin clot formation and clot lysis results in imbalance in oxygen delivery.

Front 44

Pathophysiology of Septic shock 3

Back 44

Inflammatory response on overdrive

All proinflammatory responses are normal and necessary when infection presents, but when the response becomes systemic it may overwhelm the compensatory mechanisms in place and lead to septic shock.

Front 45

Pathophysiology Summary

Back 45

Septic shock before fluid resuscitation is characterized by intravascular volume depletion, peripheral vasodilitation, myocardial depression, and hypermetabolism, and coagulopathy resulting in imbalance between oxygen supply and demand and global tissue hypoxia (Sharma, 2003).

Front 46

Sepsis Role in Coagulation

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+Stimulation of the clotting cascade and platelet aggregation without adequate fibrinolytic activity leads to coagulopathy.
+Formation of clots in the microvascularture decreases tissue perfusion and uses up clotting factors.
+Result can be DIC

Front 47

Sepsis Coagulation

Back 47

+Endotoxin theory of being mostly responsible for the effects of septic shock is being researched.
+Many inflammatory mediators are responsible for the effects seen in sepsis from interleukin, tumor necrosis factor, leukocytes.
+Damaged cell theory attributes coagulopathy with exposure to ruptured cell membranes. Ascites fluid and amniotic fluid contains many dead cells and when injected into animal caused DIC. Filtering the amniotic fluid before injecting it made it harmless.

Front 48

Treatment for Septic Shock

Back 48

+Antibiotic therapy is the hallmark treatment of septic shock. Therapy should be initiated as soon as possible and therapeutic levels should be achieved rapidly.
+One other treatment that has been shown to be effective in clinical trials is activated protein C. Marketed as Drotrecogin Alfa (Xigris).
+All other treatments are supportive in nature, addressing oxygen imbalance, hemodynamic stability, metabolic disturbances, and nutrition needs.

Front 49

Xigris

Back 49

+FDA approved Xigris for severe sepsis with acute organ dysfunction at high risk of death.
+Xigris has an antithrombotic effect and antiinflammatory properties. Blocks leukocyte adhesion and inhibits release of cytokines from macrophages.

Front 50

Prowess Study 1

Back 50

Patients received 96 hour infusion at 24mcg/kg/hr or placebo within 48 hours of onset of organ dysfunction. +Patients with increased risk of bleeding or not expected to survive 28 days due to preexisting conditions were excluded.
+Study was terminated early due to a significant lower mortality (25%) in the treatment group versus the placebo group (31%).
+Patient with most severe sepsis were the only group that showed this improvement in mortality.
+Patients with the highest risk of death had the lowest mortality on Xigris.

Front 51

Prowess Study - 2

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+Greatest adverse side effect in the study was bleeding.
+Xigris prolongs APTT so not reliable for monitoring patient’s condition.
+PT (INR) is relatively unchanged by Xigris and should be used to monitor patient’s coagulation.
When reconstituting do not shake, rotate vial.

Front 52

Treatment for Septic shock

Back 52

+Immediate stabilization similar to hypovolemic shock.
+Patient needs to be in ICU for hourly vital signs and urine output.
+Goal for hemodynamic stability MAP 65-90mm Hg, CVP 8-12 mm Hg, urine output >0.5ml/kg/hr.
+Airway management with intubation if needed to deliver high level O2 or if decreased mental status.
+Fluid resuscitation with crystalloids to improve preload.

Front 53

Treatment for Septic Shock

Back 53

+Identify the source of infection, culture sites, remove foreign bodies, drain abscesses, debride or amputate gangrenous tissue.
+Broad spectrum antibiotics
+Vasoactive medications such as dopamine, Norepinephrine, Neosynephrine if fluids don’t correct the problem.