1. Metropolitan Community College Fall 2013 Jane Miller, RN MSN
Shock
Metropolitan Community College
Fall 2013
Jane Miller, RN MSN

2. Objectives Define pathophysiology of shock, including classifications.
Identify physiologic events during shock if progresses.
Identify etiology of shock including hypovolemic, cardiogenic, distributive, and obstructive shock.
Identify clinical manifestations, treatment modalities, and nursing interventions for each type of shock. Identify the potential for multiple organs dysfunction syndrome.
Define intervention activities for shock prevention.

3. Shock Not a disease Decrease in tissue perfusion due to Can lead to
Alteration in blood or plasma volume
Alteration in peripheral vascular resistance
Alteration in the hearts ability to pump
Can lead to
Multiple organ dysfunction syndrome (MODS)
Death
Shock is not a disease, you can’t “catch” shock. Instead it is the result of some other cause. The book describes shock as “a rude unhinging of the machinery of life”.
Shock is a clinical manifestation of the body’s inability to adequately perfuse the tissue. For some reason the body cannot get blood to all of the tissue. That could be due to an alteration in the blood or plasma volume (i.e. hemorrhage), from an alteration in the peripheral vascular resistance (i.e. conditions that cause vasodilation) or from an alteration in the hearts ability to pump the blood (i.e. MI which damages the heart muscle).

4. Shock Syndromes Hypovolemic or low-volume Distributive or high-space
loss of blood/fluid volume
Distributive or high-space
Factors that affect the blood vessels
Mechanical or obstructive
Factors that affect the heart
Hypovolemic is just as it sounds, it is a major loss of the intravascular volume of blood or body fluid such as plasma.
Distributive (or circulatory) is when an injury or toxin affects the blood vessels and results in a redistribution of blood/fluid. Unlike hypovolemic shock the intravascular volume remains the same. An example would be a person with a peanut allergy. Ingestion of peanuts causes vasodilation and pooling of blood in the periphery.
Obstructive is a condition that slows or obstructs the blood flow into or out of the heart

6. Blood Composition Red blood cells White blood cells Platelets Plasma
Transport oxygen and carbon dioxide to and from cells
White blood cells
Protect against foreign matter
Platelets
Form a plug at the site of injury
Plasma
Liquid that blood cells are suspended in

9. Regulation of Blood Pressure
Stroke Volume (SV)
Amount of blood leaving the left ventricle with each heart contraction
Cardiac Output (CO)
Amount of blood leaving the left ventricle per minute
CO = HR x SV
Peripheral Vascular Resistance (PVR)
Resistance to the flow of blood by vascular musculature and diameter of the blood vessels
Vasoconstriction causes the PVR to increase and vasodilation causes the PVR to decrease.

10. Regulation of Blood Pressure
BP = CO x PVR Or
BP = HR x SV x PVR

11. Regulation of Blood Pressure
When you have a decrease in HR, SV, or PVR what do you get?
A decrease in BP and subsequently tissue perfusion
What is the definition of shock?
Shock is a clinical manifestation of the body’s inability to adequately perfuse the tissue.

12. Pathophysiology of Shock
Results from inadequate tissue perfusion
Inadequate tissue perfusion impairs cellular metabolism
Impaired cellular metabolism results in impaired oxygen and glucose use
If this is not corrected cellular death occurs
Shock results in a decrease of blood pressure
from decreased volume, decreased cardiac pump function, and decreased PVR
This decreased blood supply deprives the cells of oxygen and nutrients which impairs cellular metabolism.

13. Normal Cellular Function
Nutrients are broken down into ATP
ATP is used for cellular functions
ATP can be synthesized aerobically or anaerobically
Aerobic metabolism is more efficient
Anaerobic is not only less efficient it produces lactic acid.
Energy metabolism occurs within the cell where nutrients are chemically broken down and stored as adenosine triphosphate (ATP). Cells use ATP as energy to perform functions such as conduction of electrical impulses, muscle contraction, biochemical synthesis.
ATP can be produced both aerobically (in the presence of oxygen) or anaerobically (absence of oxygen). Aerobic metabolism is a much more efficient and effective from of energy production because it produces a greater amount of ATP per mole of glucose.
Anaerobic metabolism is not only less efficient it has a toxic end product, lactic acid.

14. Pathophysiology of Shock
Sodium
This increase of sodium and H20 into the cell causes potassium to exit, cellular swelling, eventual rupture and cell death
Potassium
As the body responds to an infection, illness, or injury that decreases the availability of oxygen in the blood, sodium moves into the cell which pulls water in. This shift causes potassium to exit the cell. This loss of potassium alters nervous, cardiovascular, and muscular cell function. In addition, cellular metabolism shifts from aerobic to anaerobic function which means less ATP is produced (food for the cell) and toxic lactic acid increases. These fluid and electrolyte shifts cause impaired function of the cell, it will swell, and eventually rupture. The release of cellular enzymes causes further damage to other cells.
A lack of oxygen changes the cell metabolism from aerobic to anaerobic

15. Impaired Glucose Use
Impaired cellular metabolism also produces insulin resistance
As the body responds to the stress it produces more glucose to assist in healing
Because the body doesn’t use the glucose properly blood glucose levels rise
Insulin resistance and glucose toxicity further impair cell metabolism
Insulin resistance is an unresponsiveness to the normal effects of insulin. It is thought to be the result of an increased production of serum cytokines which are released as a part of the stress response.
In response to an illness or injury the body initiates the stress response which triggers gluconeogenesis (the formation of glucose from non carbohydrate sources i.e. glycerol and proteins). It does this to supply enough energy to begin the healing process. The liver and kidneys produce glucose in response to hormones released as a part of the stress response (i.e. epinephrine, norepinephrine, glucagons, and cortisol).

16. SIRS Systemic inflammatory response syndrome
Often associated with septic shock
First phase of shock
Presents much like sepsis
HR - PaCO2 RR
Temp
WBC
SIRS is a systemic response of the immune system that can be triggered by both infectious and noninfectious causes. It was originally only associated with sepsis but research as shown it does not require an infectious agent. Now it is thought to be the first phase of shock.
Immune system response that begins the cascade of events in response to inflammation.

18. Signs of Shock Neurological Cardiovascular Altered mental status
Seizures
Coma
Cardiovascular
Cardiac output declines
HR increases
Dysrhythmias
Absence of peripheral pulses
The brain needs both oxygen and glucose to function. Without these the patient will suffer altered mental status, coma, and eventual death
The cardiac output may initally be elevated but will eventually decline due to alterations in pre and afterload. In addition, toxins released from damaged cardiac cells cause further damage and dysrhythmias

19. Genitourinary Integumentary Musculoskeletal Lungs Decreased filtration
Decreased urinary output
Integumentary
Pale and fragile
Musculoskeletal
Weakness and wasting
Lungs
Increased RR
Decreased O2 saturation
ARDS
The kidneys will have decreased filtration due to decreased blood flow and the urinary output decreases as a result of the shift of sodium and water into cells.
The skin becomes pain and fragile as blood is diverted away from the skin to the vital organs.
Muscle cells begin to breakdown causing weakness and wasting
The pulmonary system suffers acute lung injury which eventually leads to ARDS

20. Shock Syndromes Hypovolemic or low-volume Distributive or high-space
loss of blood/fluid volume
Distributive or high-space
Factors that affect the blood vessels
Mechanical or obstructive
Factors that affect the heart
Hypovolemic is just as it sounds, it is a major loss of the intravascular volume of blood or body fluid such as plasma.
Distributive (or circulatory) is when an injury or toxin affects the blood vessels and results in a redistribution of blood/fluid. Unlike hypovolemic shock the intravascular volume remains the same. An example would be a person with a peanut allergy. Ingestion of peanuts causes vasodilation and pooling of blood in the periphery.
Obstructive is a condition that slows or obstructs the blood flow into or out of the heart

21. Hypovolemic Shock
Can result from a loss of blood, plasma, or body fluids
Hemorrhagic shock is most common
Trauma, GI bleeds, ruptured AAA
Other causes
Diarrhea
Vomiting
Inadequate repletion of fluid loss
Burns, heat stroke, third spacing
Hypovolemic shock is the result of significant fluid loss that alters the amount of circulating volume in the body. This fluid loss includes blood, plasma, or body fluids. Hemorrhage is the most common cause of hypovolemic shock and can be caused by trauma, GI bleeds, ruptured AAA, surgery. Other causes of hypovolemic shock are the result of fluid loss from things like diarrhea, vomiting, inadequate repletion of fluid loss from burns, heat stroke, or third spacing.
Third spacing is the shifting of fluid from the intercellular and intravascular compartment into the interstitial space.

22. Decreased Blood Volume
Decreased Venous Return
Decreased Stroke Volume
The sequence of events in hypovolemic shock begins with a decrease in the intravascular volume. This results in decreased venous return of blood to the heart and subsequent decreased ventricular filling. Decreased ventricular filling results in decreased stroke volume or the amount of blood ejected from the heart, and decreased cardiac output. When cardiac output drops, BP drops and tissues cannot be adequately perfused. When cells are not adequately perfused hypoxia occurs which leads to cellular injury and if not corrected, cellular death.
Decreased Cardiac Output
Decreased Tissue Perfusion

23. Medical Management Correct the underlying cause
e.g. stop the bleeding, vomiting, diarrhea
Restore intravascular volume
Redistribute fluid volume
Correct the underlying cause
Apply pressure, tourniquet, surgery if bleeding
Administer antiemetics if vomiting, antidiarrheals for diarrhea
Restore intravascular volume
Crystalloids: Normal saline, LR
Colloids: Albumin, PRBC

24. Mechanical Shock
A condition that slows or obstructs blood flow in or out of the heart
Ineffective pump
Physical obstruction
A decrease in blood flow through the heart decreases stroke volume and cardiac output
Hypotension
Decreased tissue perfusion
Mechanical shock is a condition that slows or obstructs blood flow in or out of the heart.

25. Decreased Cardiac Function
Decreased Stroke Volume
Decreased Cardiac Output
In addition you will get pulmonary congestion and decreased coronary artery perfusion which leads to further myocardial damage.
Decreased Blood Pressure
Decreased Tissue Perfusion

26. Mechanical Shock Two different types Cardiogenic Obstructive
When the heart is unable to pump effectively
MI, ruptured ventricle, cardiomyopathy
Obstructive
Physical obstruction
Cardiac tumor, massive PE, cardiac tamponade

27. Medical Management
Limit further myocardial damage and preserve healthy myocardium
Remove source of obstruction
Improve cardiac function by increasing cardiac contractility and decrease ventricular afterload
If having an MI you want to stop the MI. Angioplasty
Pericardial window, chest tube
Improved contractility = inotropes
After load: The amount of resistance the left side of the heart has to overcome in order to eject blood.
Combo of dobutamine and nitroglycerin

28. Mechanical Assistive Devices
A mechanical assistive device may be needed if first line treatments fail
Intra-aortic balloon pump
Left or right ventricular assist devices
Last option
Heart transplant
These provide temporary circulatory assistance. They increase stroke volume, improve coronary artery perfusion, decrease preload, decrease cardiac workload, decrease myocardial oxygen demands
preload is stretch. The amount of volume being returned to the right side of the heart from systemic circulation. Afterload is squeeze. The amount of resistance the left side of the heart has to overcome in order to eject blood.

29. Distributive Shock A precipitating event causes massive vasodilation
Blood pools in the periphery
Decreased venous return results in decreased stroke volume and cardiac output
Hypotension
Decreased tissue perfusion
Distributive shock occurs when a precipitating event such as a toxin, injury, or infection causes massive vasodilation. This vasodilation causes the blood volume to be abnormally displaced in the peripheral blood vessels. This is called “pooling” in the periphery.
This pooling results in decreased venous return to the heart. A decreased venous return to the heart results in decreased stroke volume or the amount of blood ejected from the heart, and decreased cardiac output. When cardiac output drops, BP drops and once again tissues cannot be adequately perfused.

30. Maldistribution of Blood Volume
Precipitating Event
Vasodilation
Maldistribution of Blood Volume
Decreased Venous Return
A precipitating event activates the inflammatory response which causes vasodilation and pooling of the blood. This pooling results in a decrease in the volume of blood that returns to the heart. Less blood in the heart means a decrease in the cardiac output, decreased BP, decreased tissue perfusion.
Decreased Cardiac Output
Decreased Tissue Perfusion

31. Distributive Shock Three different types Anaphylactic shock
Insect bites, medication allergies, food allergies
Neurogenic shock
Spinal cord injury, anesthetic agents, severe pain
Septic Shock
Bacterial and viral infections
Distributive or circulatory shock is a global term for the types of shock that cause a redistribution of blood/fluid. There are three different types:
Anaphylactic
Neurogenic
Septic

32. Anaphylactic Shock Results from an antigen-antibody reaction
Symptoms are usually immediate
Blood pooling in the periphery
Pulmonary vasocontriction
Maintenance of an airway is critical

33. Neurogenic Shock
Imbalance between the sympathetic and parasympathetic stimulation of vascular smooth muscle
This causes vasodilation
Caused by injury or medications that affect the spinal cord or medulla
Clinical symptoms may be different
Hypotensive, bradycardic, vasodilation
Sympathetic nervous system is responsible or the elevation of HR and BP along with vasoconstriction during times of stress. Fight or flight

34. Septic Shock
Occurs when an infectious agent causes systemic decompensation
Acute circulatory failure characterized by persistent hypotension unexplained by other causes
3 principle actions occur with sepsis
Inflammation
Coagulation
Fibrinolysis
When sepsis occurs regulatory mechanisms have failed and uncontrolled inflammation overwhelms the body, coagulation produces thrombi that block the microvasculature throughout the body causing cellular death and organ dysfunctions. Fibrinolysis is impaired due to a lack of circulating activated Protein C which is a normal component of anticoagulation

36. Nursing Management Prevention 2 large bore IVs
Place patient in modified trendelenburg position
Monitor for signs of transfusion reaction
Monitor for fluid overload and pulmonary edema
Monitor VS, especially temperature
Monitor patients at high risk for shock closely. Watch VS, LOC, skin color and temp, urinary output, CBC, BMP, ABGs, peripheral pulses for signs of shock
2 large IVs provide the ability to administer fluid, blood, and medication simultaneously and provide for rapid infusion while correcting the underlying issue.
Modified trendelenburg promotes venous return to the heart while not compromising breathing.
Large infusions of cold fluids can cause hypothermia and those in distributive shock are often hyperthermic.

37. Apply oxygen, administer meds, monitor labs
Monitor for skin breakdown, turn q 2 hrs, and provide skin care
Watch for DVT
Monitor ECG
Wound care
I&O
Enteral or parental nutrition
ROM
Emotional support for patient and family

38. Medications Vasopressors Inotropes Antiemetics & antidiarrheals
Antibiotics
Insulin
Corticosteriods
Blood thinners and clot busters
Opiods
Antianxiety
Sedation
rhAPC
Vasopressors: antihypotensives i.e levophed, epinephrine, neo-synephrine, vasopressin
Inotropes: increase contractility i.e. dobutamine, digoxin
rhAPC is recombinant human activated protein C. Part of fibrinolysis that acts as a clot buster. It’s use is controversial. The recommendation is for those who are at high risk of death and have a low bleeding risk.
This is not a complete list of medications and some listed will not be appropriate for all clients experiencing shock

39. MODS Multiple Organ Dysfunction Syndrome End result of severe sepsis
Triggered by a critical injury or disease process that initiates a massive systemic inflammatory response
Multiple injuries, burns, hypovolemic shock, acute pancreatitis, ARDS, acute renal failure
Does not require an infectious trigger
MODS is multiple organ dysfuction syndrome. It is the end result of severe sepsis. It can also be activated by a critical injury or disease process that initiates a massive systemic inflammatory response. It does not require an infectious process. Triggers include things like multiple injuries, burns, hypovolemic shock, acute pancreatitis, ARDS, acute renal failure.
Mortality from MODS ranges from %.

40. Pathophysiology Primary or early MODS Secondary or late MODS
Hypoperfusion that triggers inflammatory and stress responses
Secondary or late MODS
Excessive inflammation following the initial insult
Manifested in organs distant from the original injury
Three primary mechanisms: inflammation, coagulation, and fibrinolysis
Primary or early MODS follows the same pathophysiological track as shock. When further tissue injury occurs the body triggers and even greater response and start progressive organ dysfunction or secondary or late MODS.
Secondary or late MODS follows the same pathophysiological path as sepsis where three primary mechanisms are activated
inflammation
coagulation
fibrinolysis

41. Clinical Manifestations & Diagnosis
Depend on the area or areas affected
Early MODS is difficult to monitor
Late MODS follows a specific pattern
Measured using the SOFA score
Evolves over 14 days to weeks
Diagnostic tests are specific to the organ system(s) that are failing
The clinical manifestations of MODS depends on the area or areas affected. Early MODS is difficult to monitor because it is dependent on the area affected. For example a patient with a thoracic injury may develop ARDS which is the beginning of MODS.
Secodary MODS follows a specific and predictable patter of injury that can be observed and measured with the use of the SOFA (sequential organ failure assessment) score. The SOFA measures specific tests such as glascow coma score, use of inotropes, creatinine level, ect… and produces a score from 1 to 4. The higher the score the more advanced MODS. MODS evolves over 14 days to weeks as each organ system begins to fail.
(SOFA score 61-9, pg. 1979)
S/S include (chart on page 1979)
SOB, ascites, jaundice, hyperglycemia, increased heart rate, encephalopathy, fever, DIC, poly or anuria, increased bilirubin, BUN, and creatinine

42. Treatment Prevention is key Antibiotics Intubation Fluid resuscitation
Vasopressors
Analgesics
Sedation
Enteral feedings
Glucose monitoring

43. Nursing Management Hand hygiene and skin care Monitoring of VS
Positioning
Decrease oxygen demands
Pain and anxiety meds
Rest
Emotional support
Frequent patient assessments

44. Resources Osborn, Wraa & Watson chapter 61 YouTube video on shock