Shock

Metropolitan Community CollegeFall 2013

Jane Miller, RN MSN

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.

Shock• Not a disease

• Decrease in tissue perfusion due 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 Syndromes• Hypovolemic or low-volume– loss of blood/fluid volume

• Distributive or high-space– Factors that affect the blood vessels

• Mechanical or obstructive– Factors that affect the heart

Blood Composition

• Red blood cells– 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

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

Regulation of Blood Pressure

BP = CO x PVR

Or

BP = HR x SV x PVR

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

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

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.

Pathophysiology of Shock

Sodium

H2O

Potassium

This increase of sodium and H20 into the cell causes potassium to exit, cellular swelling, eventual rupture and cell death

A lack of oxygen changes the cell metabolism from aerobic to anaerobic

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

SIRS

• Systemic inflammatory response syndrome

• Often associated with septic shock

• First phase of shock

• Presents much like sepsis– HR - PaCO2

– RR– Temp– WBC

Signs of Shock• Neurological– Altered mental status– Seizures– Coma

• Cardiovascular– Cardiac output declines–HR increases– Dysrhythmias– Absence of peripheral pulses

• Genitourinary– Decreased filtration– Decreased urinary output

• Integumentary– Pale and fragile

• Musculoskeletal– Weakness and wasting

• Lungs– Increased RR– Decreased O2 saturation

– ARDS

Shock Syndromes• Hypovolemic or low-volume– loss of blood/fluid volume

• Distributive or high-space– Factors that affect the blood vessels

• Mechanical or obstructive– Factors that affect the heart

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

Decreased Blood Volume

Decreased Cardiac Output

Decreased Venous Return

Decreased Stroke Volume

Decreased Tissue Perfusion

Medical Management

• Correct the underlying cause– e.g. stop the bleeding, vomiting,

diarrhea

• Restore intravascular volume

• Redistribute fluid volume

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

Decreased Cardiac Function

Decreased Blood Pressure

Decreased Stroke Volume

Decreased Cardiac Output

Decreased Tissue Perfusion

Mechanical Shock

• Two different types– Cardiogenic• When the heart is unable to pump

effectively• MI, ruptured ventricle, cardiomyopathy

– Obstructive• Physical obstruction• Cardiac tumor, massive PE, cardiac

tamponade

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

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

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

Precipitating Event

Vasodilation

Maldistribution of Blood Volume

Decreased Venous Return

Decreased Cardiac Output

Decreased Tissue Perfusion

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

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

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

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

http://www.google.com/url?sa=i&rct=j&q=&esrc=s&frm=1&source=images&cd=&cad=rja&docid=hggjSrOJBRgS0M&tbnid=DO17K4g-6lsUoM:&ved=0CAUQjRw&url=http://thebolus.org/sepsis-an-often-missed-diagnosis/&ei=ElxEUtnBJPHw2gXi1YDYDg&bvm=bv.53217764,d.b2I&psig=AFQjCNFOj5XIFE9aYdF24NB7mlsi1vGx5g&ust=1380297926463424

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

• 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

• Medications– Vasopressors– Inotropes– Antiemetics & antidiarrheals– Antibiotics– Insulin– Corticosteriods– Blood thinners and clot busters– Opiods– Antianxiety– Sedation– rhAPC

This is not a complete list of medications and some listed will not

be appropriate for all clients experiencing shock

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

Pathophysiology

• Primary or early 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

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

Treatment

• Prevention is key• Antibiotics• Intubation• Fluid resuscitation• Vasopressors• Analgesics• Sedation• Enteral feedings• Glucose monitoring

Nursing Management

• Hand hygiene and skin care • Monitoring of VS• Positioning• Decrease oxygen demands– Pain and anxiety meds– Rest

• Emotional support• Frequent patient assessments

Resources

• Osborn, Wraa & Watson chapter 61• YouTube video on shock– http://www.youtube.com/watch?

v=CbM4UihE1TQ

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