About Shock

What is Shock?
Rather than a disease in of its own right, shock is a sequelae of life-threatening symptoms that manifest from an underlying pathology. In broad
terms, shock may be described as a state in which blood and oxygen delivery are disrupted to the point that the needs for tissue perfusion and basic
metabolic functions are not met. Regardless of the procuring cause, shock is manifested by a severe and sudden drop in blood pressure and other
drastic changes to the body. Without rapid interventions, it can lead to multisystem organ failure and death. Various compensatory mechanisms are
seen in shock, especially decreased urine output. Three out of the four types manifest with a low cardiac index. To compensate, the systemic
vascular resistance (SVR) is elevated. The opposite is seen in distributive shock. In this form, peripheral vasoconstriction results in low systemic
vascular resistance (SVR). To compensate, the cardiac index is normal to elevated.
How Shock is Classified
Shock is classified based upon the etiology of the underlying condition and the resulting physiological response. The four major classifications
include cardiogenic shock, distributive shock (which also encompasses the subclasses of toxic shock syndrome and neurogenic shock), hypovolemic
shock, and obstructive (also known as extracardiac) shock. These can be remembered by the mnemonic DOCH.
DOCH: The Four Primary Classifications of Shock
/ Distributive shock: Includes toxic shock syndrome and neurogenic shock
/ Obstructive (extracardiac) shock
/ Cardiogenic shock
/ Hypovolemic shock
Cardiogenic Shock Overview
/ Features: low cardiac output and peripheral vasoconstriction
/ Mechanisms: low cardiac index, high systemic vascular resistance (SVR)
/ Common causes: condition that causes heart failure, such as myopathy (myocardial damage) post-myocardial infarction, heart valve
disorders, or arrhythmias
Distributive Shock Overview
/ Features: peripheral vasodilation
/ Mechanisms: Normal to elevated cardiac index, low systemic vascular resistance (SVR)
/ Etiologies: Anaphylaxis, sepsis, or autonomic dysreflexia
/ Mnemonic: D for Dilate, and S for Bee Sting
Hypovolemic Shock Overview
/ Features: Depletion of intravascular fluids (hypovolemia), including loss of both blood and/or extracellular fluids
/ Mechanisms: Decreased cardiac preload, low cardiac index, high systemic vascular resistance (SVR)
/ Etiologies: Hemorrhage (from trauma or postoperative complications), or dehydration
Obstructive Shock Overview
/ Features: Extracardiac vascular obstruction, low cardiac index, high systemic vascular resistance (SVR)
/ Etiologies: Pulmonary emboli, tension pneumothorax, or cardiac tamponade
Pharmacology
Pharmacology for Shock
/ Shock is managed through oxygen administration, vasopressors, and inotropes
/ Pharmacologic agents are given to increase the blood pressure through vasoconstriction
/ If the cardiac index needs to be raised, a drug will be administered to increase the cardiac contractility. Inotropes are administered to
increase the cardiac index by promoting contractility of the heart muscle
/ If the blood pressure needs to be increased, vasopressors are administered to cause arteriole vasoconstriction. Examples include
Vasopressin (Pitressin) and its analog terlipressin
Prototype Drugs Used for Shock
/ Epinephrine: Anaphylaxis
/ Vasopressin (Pitressin): Increases blood pressure by casing vasoconstriction
/ Calcium carbonate: Used in cases that involve hyperkalemia, hypocalcemia, and calcium channel blocker toxicity
/ Magnesium sulphate: Used to treat Torsades de pointes
Clinical Manifestations
Three Common Characteristics of Shock
/ Hypotension: Blood pressure drops as a compensatory mechanism to reserve oxygen
/ Tissue hypoxia: Tissues are not adequately profused as blood supply is impaired, either from low volume and/or decreased cardiac output
/ Metabolic acidosis: Blood becomes as acidic (acidemia) from the inability to rid toxins in circulation
 Cardiovascular Manifestations of Shock
/ Change in pulse: Usually begins with tachycardia as a compensatory mechanism and then progresses to bradycardia as cardiac output
diminishes or blood supply decreases (hypovolemia)
/ Reduced cardiac output: Reason depends on the underlying cause of shock
Vasculature Manifestations of Shock
/ Mean arterial pressure (MAP): Drops below 80 mm/Hg (with the exception of certain forms, such as early-phase septic shock, which
causes vasodilation)
/ Pulse strength: Peripheral pulses may be difficult to palpate, a Doppler (ultrasound device) can be necessary to locate them
/ Mean arterial pressure (MAP) is more of a Critical Care Nursing Class concept. For Med-Surg, its usually not required for nursing students
to fully understand at this time. The basic formula for finding the MAP is as follows: take the diastolic pressure and add 1/3 of the pulse pressure
(which is the difference between the systolic and diastolic). The sum of this is the MAP. The MAP will usually be calculated automatically by an
invasive pressure monitoring device, such as an arterial line (A-Line)
Neurological Manifestations of Shock
/ Decreased level of consciousness (LOC): changes in mental status are multi-factorial. It may decline from hypoglycemia, hypoxia,
hypoprefusion, and alteration in sympathetic nervous system. Early manifestations of decreased LOC include confusion, agitation, and restlessness.
Fatigue, loss of consciousness, and eventually coma can ensue
/ Anxiety: if alert, patients will often be anxious and very verbal about their distress. This is considered a normal psychogenic response. As
mentioned above, this is also be an early form of mental status change, and may progress to more ominous states (such as non-responsiveness)
Respiratory Manifestations of Shock
/ Dyspnea: Breathing becomes labored. Other alterations in normal breathing patterns may also be present
/ Tachypnea, or bradypnea: Tachypnea (rapid respiration rate) is the most common and is likely to be associated with compensatory
responses to acidosis and hypoxia. It may also be associated with a psychogenic effect of situation as the experience can be very stressful for the
patient and result in hypoventilation secondary to anxiety
/ Hypoxia: May be subtle in early phases due to tachypnea (as it can serve to counteract hypoxia at least initially)
/ Aspiration: May occur if a risk is present, (such as cases of anaphylactic shock). This often indicates the need for endotracheal intubation
and mechanical ventilation to preserve survival
Integumentary Manifestations of Shock
/ Diaphoresis: Excessive sweating
/ Pallor: Resulting from decreased tissue profusion and vasoconstriction. Again, the notable exception with pallor is seen in early-phase
septic shock. The patient is usually warm and appears to be flushed. This rosy cheeked appearance results from the vasodilator effect. Patients
with anaphylactic shock may also be appear flushed from angioedema caused by the inflammatory response
Renal Manifestations of Shock
/ Oliguria (less than 30 mL/hour of urine output) or anuria (total or near-total absence of urine output). Decreased renal output is caused by
insufficient tissue perfusion secondary to impaired cardiac output. The kidneys do not receive enough pressure to maintain urine output function.
Note that impaired renal output is often one of the first non-cardiovascular indicators of impaired cardiac output. Sustained effects cab cause severe
kidney damage and may require dialysis
/ Renal compensation: Fluid retention occurs from increased levels of anti-diuretic hormone (ADH)
Decreased cardiac output, low urine output, and acidosis:
Low urine output is a common finding in shock. As blood is reserved for the brain and heart (since theyre more vital to immediate survival), the
kidneys do not receive enough pressure to continue filtering waste. This creates a build-up of toxins in the blood, leading to an acidic environment.
Therefore, metabolic acidosis occurs.
Diagnostics
Physical Examination
/ History and patient presentation (myocardial infarction versus an automobile collision)
/ Data collection: capillary refill, pulse, respiration rate, and LOC
Lab Work and Other Diagnostics
/ ABGs for acid/base balance and O2/CO2, this is especially important in advanced stages, as oxygen saturation may not provide enough
accuracy
/ Blood work: CBC, lactic acid, blood chemistry, indicators of renal function
/ Central venous pressure and arterial line pressure measurements
/ EKG: life threatening rhythms may be present
/ CXR
Collaborative Treatment
Airway Management
/ Active airway management: A mechanical ventilator and intubation is required if airway patency is compromised or if the patient is unable
to breath independently
/ Reduce work of breathing and conserve oxygen for organ use
Oxygenation
/ Simple face mask: Up to 40% concentration
/ Non-rebreather face mask: Up to 80% concentration at 10 L/min
/ Arterial blood gasses (ABGs): Preferred over pulse-oximetry for monitoring the oxygen status of critically ill patients
Circulation
/ IVs: 2 or more large-bore lines should be established
/ Large gauge needle: A 16-gauge intravenous catheter is often used in case a blood transfusion is necessary
/ Blood draw: A blood draw is performed for blood chemistry, complete blood count (CBC), comprehensive metabolic panel (CMP), and
arterial blood gases (ABGs)
/ Acidosis monitoring: Blood pH and ABG values, including PaCO2, HCO3, PaO2, are used to determine if the patient has acidosis
/ Glucose monitoring: Glucose values are obtained to determine if diabetic ketoacidosis is the culprit
/ Hemoglobin: Evaluated to provide insight on oxygenation status (along with ABGs and oxygen saturation). Levels below 7-8 mg/dL often
indicate the need for a blood transfusion (facility policies vary on the hemoglobin cut-off)
Fluid Replacement
/ Normal sodium saline 0.9% (isotonic solution) is most commonly used to maintain blood volume. If not contraindicated by fluid overload,
initial bolus may of 1,000-2,000 mL of saline administered within 20 minutes. In cases of cardiogenic shock, less fluid is usually administered
/ Crystalloid isotonic solution is used for cases of cardiogenic shock
/ Blood transfusions are used when hemoglobin reaches critical levels
/ Volume expanders such as albumin may be used
Pharmacological Management
/ Administered medications are dependent upon the underlying condition, patient presentation, and other factors
/ Drugs that cause vasoconstriction, including epinephrine, dopamine, and vasopressor may be used to clamp down the arteries
Nursing Care Planning
Ventilation
/ Preparation for the patient for endotracheal intubation and assist with placement as needed
/ Administer oxygen as ordered by a simple mask or rebreather mask
Fluid Replacement
/ Administer saline or other fluids
/ Administer blood replacement products
Vitals Monitoring
/ Oxygen saturation
/ Intake and output
/ Continuous monitoring of EKG
/ Blood pressure: continuous monitoring of arterial and central venous pressure *
/ Temperature at least once an hour
/ Respirations
*Note: infants and elderly patients will take longer to present with hypotension
Diagnostic Monitoring
/ Blood draw and monitoring of ABGs
/ Glucose checks and monitoring
Emotional Support
/ Provide patient with reassurance as appropriate
/ Keep the family informed on the status
Hypovolemic Shock
What is Hypovolemic Shock?
Hypovolemic shock can rise from various situations; this is the most common type of shock. The primary manifestation of this type of shock is severe
hypotension which occurs secondary to the loss of blood, intravascular fluid (the fluid that surrounds the blood, such as plasma), or extravascular
fluids. It involves a sudden and drastic fluid loss. The most frequent cause is from the reduction of blood and vascular fluids, such as occurs in
hemorrhage. Prolonged vomiting and diarrhea are common causes of extracellular fluid loss. Common clinical manifestations include altered
mentation, rapid and deep respirations, and cool and clammy skin.
Causes of Hypovolemic Shock
/ Blood loss: resulting from a traumatic accident, injury, excessive intracranial pressure, or hemorrhage.
/ Plasma loss: increases in capillary permeability, permitting for a greater loss through diffusion into the vascular tissue. Increased
permeability of the vessels can occur from sepsis, acidosis (referring to a low pH of the blood), burns, and peritonitis (an infection of the peritoneum,
usually caused by a perforation in the abdominal wall)
/ Extracellular fluid loss: from such causes as severe and prolonged vomiting, diarrhea, diuresis, and sunstroke
Clinical Manifestations of Hypovolemic Shock
/ Neurological: dizziness, agitation, confusion, progressing to a altered mentation and decreased level of consciousness (LOC)
/ Cardiac: initially, tachycardia related to the psychogenic response associated with a traumatic condition, similar to the panic seen during an
asthma attack. Bradycardia will eventually develop as volume becomes more depleted. PVCs (premature ventricular contractions) and dysthymia
may occur from the low blood supply and inadequate profusion. Delayed capillary refill will be evident
/ Integumentary: cool and clammy skin, pallor, overall poor appearance; the patient wont be looking well
/ Renal: sympathetic nervous system will signal the kidneys to shut down function down. Filtration ceases as the blood supply is reserved for
the functions most vital to sustaining life. ADH will also stop being processed, halting the aldosterone-renin-angiotensin pathways, which constricts
the vessels when pressure becomes to low. Without this mechanism in place, vasodilation is worsened and he blood pressure drops more.
Technically speaking, the patient is in acute renal failure during shock but dont expect to observe any useful signs of this in your assessment
Assuming that the patient will either recover or be dead shortly, there isnt time for many of the classic symptoms of renal failure to present
Treatment of Hypovolemic Shock
/ Control wound bleeding: pressure is applied to control bleeding; a tourniquet may be used. A surgical closure of gaping wound may be
necessary
/ Fluid volume replacement: saline, blood transfusion and blood products, plasma expanders, such as albumin are often administered.
Drugs that increase blood pressure may be used as they cause the vasculature to clamp down
/ Administer drugs as ordered, such as dopamine and epinephrine
/ IV access: usually 16-20 gauge (must be large enough for blood transfusion)
/ IV central line, usually established through subclavian, groin, or intrajugular access
Cardiogenic Shock
What is Cardiogenic Shock?
Cardiogenic shock is associated with a sudden impairment of cardiac function that results in increased systemic vascular resistance, often greater
than 1,200 dynes second/cm5. Its caused by an obstruction or deficiency associated with an underlying cardiac pathology. Chronotropic (heart rate)
or inotropic (heart rhythm) factors may be implicated. Cardiogenic shock a vicious cycle where the symptoms lead to responses that exacerbate the
condition.
It begins with impaired cardiovascular functioning secondary to alteration of cardiac output. Hypotension occurs as the cardiac output decreases. To
compensate, the pulse elevates and peripheral vasoconstriction occurs. As the heart must work harder to keep up, oxygen demand increases, which
increases its perfusion needs. The heart eventually becomes ischemic, leading to disruption of contractility and rhythm.
Cardiogenic shock can be caused by any condition, acute or chronic, that manifests in heart failure. Myocardial infarction is the most common cause
of cardiogenic shock. Fortunately, this complication is not very common, occurring in less than 7% of patients recovering from acute coronary
infarction. The majority of these cases involve myocardial infraction of the anterior wall. Various forms of chronic heart failure also run the risk of
cardiogenic shock.
Potential Causes of Cardiogenic Shock
/ Myocardial infarction, especially in the anterior wall
/ Congestive heart failure
/ Congenital heart defects
Clinical Manifestations of Cardiogenic Shock
/ Cardiac symptoms: chest pain and shortness of breath, tachycardia and thready pulse, dysthymias; including: ventricular tachycardia,
supraventricular tachycardia, and ventricular fibrillation, hypotension and orthostatic hypotension (fall more than 10 points when changing from
lying to standing position
/ Respiratory symptoms: dyspnea, tachypnea
/ Neurological symptoms: decreased LOC, possible coma, Inability to concentrate, Irritability, restlessness, uraemic seizures
/ Renal symptoms: oliguria (low urine output, defined as less than 30 mL/hour), hypoperfusion
/ Integumentary symptoms: cool, clammy skin, cyanosis, diaphoresis, pallor
Pharmacological Management for Cardiogenic Shock
/ Dobutamine
/ Dopamine
/ Epinephrine
/ Diuretics and inotropes
Nursing Assessment for Cardiogenic Shock
/ Diligent and frequent monitoring of vitals, including oxygenation saturation, temperature, and cardiac status
/ Administration of standing order drugs, based upon assessment findings. Cardiovascular drugs such as diuretics may be used for
maintenance, depending upon the condition
/ Monitoring and recording of urine intake and output
/ Continuous monitoring of EKG
/ Blood pressure, mean arterial pressure (MAP), and other hemodynamic parameters may be monitored continuously through an arterial line
or a central venous pressure line
/ Thermal control, or active warming
Priority Interventions for Cardiogenic Shock
/ Oxygenation (ventilation as needed)
/ Fluid replacement (saline and blood products
/ Medications to wake up the heart
Obstructive Shock
What is Obstructive Shock?
Just as the name sounds, obstructive shock involves some type of active obstruction or pressure that obscures the function of the heart. It occurs
somewhere in the vasculature other than the coronary arteries (especially the lungs), which explains why its also termed as extracardiac shock. (If
the obstructive source is located within the vasculature of the heart, it is known as cardiogenic shock). The major characterizing feature of distributive
shock is systemic vasodilation coupled with impaired circulation. This leads to inadequate tissue perfusion that progressively worsens with time.
Release of inflammatory mediators observed in most forms of distributive shock result in hemodynamic derangements. Widespread alterations in
vasculature impair the contractility function of the heart and may lead to multiple organ failure.
Potential Causes of Obstructive Shock
/ Tension pneumothorax
/ Myocarditis or myocardial rupture
/ Trauma, such as post-operative from heart surgery
/ Pulmonary emboli
/ Pericardial tamponade: pressure that occurs in the heart as a result of increased fluid accumulation in the myocardium and pericardium
Diagnostics for Obstructive Shock
/ Pericardiocentesis is used in suspected cases of cardiac tamponade
/ Needle thoracostomy is used in suspected cases of tension pneumothorax
Distributive Shock
What is Distributive Shock?
Distributive shock is characterized by peripheral vasodilation and poor circulatory support (or blood distribution). This causes a low systemic vascular
resistance (SVR). The heart attempts to compensate by raising the cardiac index (when its physiologically possible for the heart to do so). There are
various types of distributive shock. The most familiar forms include septic shock, neurogenic shock, and anaphylactic shock.
Forms of Distributive Shock
/ Septic shock: caused by bacteremia, or sepsis of the blood. Common causes include acute respiratory distress syndrome (ARDS) and
systemic inflammatory response syndrome (SIRS)
/ Toxic shock syndrome (TSS): a systemic staph infection, often resulting from improper tampon use
/ Anaphylaxis: a type I hypersensitivity reaction that causes inflammatory obstruction of the upper airways
/ Neurogenic shock: a response to a traumatic brain or spinal cord injury that causes a loss of sympathetic vascular tone. Neurogenic shock
can occur secondary to autonomic dysreflexia
/ Hepatic insufficiency: the liver modulates inflammatory processes. When normal function is impaired, the risk of shock increases
/ Addisonian crisis: this occurs when cortisol levels become extremely depleted in individuals with Addisons Disease due to acute adrenal
failure
/ Heavy metal poisoning: from excessive exposure or ingestion of metals such as
/ Transfusion reaction: an allergic response to a blood transfusion (may occur with or without a type crossing error)
/ Other reactions: includes those to drugs or toxins (Ruggiero, 2008)
Septic Shock
Septic shock can be thought of as vasodilatory shock. It presents with two phases: 1) early hyperdynamic phase, also known as warm septic shock,
and 2) late septic shock, which is called cold or hypodynamic shock. Each phase presents differently. Hemodynamic derangement and impairment of
the normal coagulation cascade is affected. As a result, disseminated intravascular coagulation (DIC) occurs in up to half of all cases. For DIC, the
main focus is to treat the underlying cause as treatment options are limited.
Early Hyperdynamic Phase (Warm Septic Shock)
/ Widened pulse pressure from a reduced diastolic flow
/ Flushed and warm extremities
/ Peripheral vasodilation with rapid capillary refill
/ Compensatory mechanisms increase cardiac output
/ Hepatic dysfunction begins within a few hours of the onset of sepsis
Late Hypodynamic Phase (Cold Septic Shock)
/ Onset of peripheral vascular paralysis
/ Progressive reduction in organ perfusion
/ Blood supply is reserved for organs most critical to survival- heart, brain, and liver
/ Prognosis more likely to insidious and ominous

ARDS and SIRS

Acute respiratory distress syndrome (ARDS) and systemic inflammatory response syndrome (SIRS) can both lead to septic shock. SIRS must meet
at least two out of four of the clinical criteria set forth by the ACCP. These include 1) pulse over 100 beats per minute, 2) temperature over 38C or
 under 36C, 3) respiratory rate over 20 breaths per minute, and 4) hemodynamic indicators, including PaCO2 under 32mm Hg, white blood cell
count over 12,000/L or under 4,000/L.
Anaphylactic Shock
Anaphylactic shock is a form of distributive shock characterized by airway inflammation and obstruction. Its classified as a type I hypersensitivity
reaction (the most severe form of allergic reactions) in which mast cells to release a massive quantity of histamine. Anaphylaxis is life-threatening
unless rapid interventions are performed. Its a systemic reaction that involves multiple organs and body systems. The degree of sensitization
concomitant with various inflammatory markers. IgE antibodies are the primary mediators and IgG antibodies also play a role.
Common triggers of anaphylactic shock include vaccines (usually to toxoids, a bacterial toxin that has inactivated or suppressed by a process), latex,
food, (such as shellfish or peanut butter), venomous insect stings (especially from bees), antibiotics (especially penicillin), immune globulins,
antitoxins (an antibody found in various plants and animals that has the ability to neutralize a toxin but may also harm humans in high amounts or if
sensitive), diagnostic solutions (such as the tuberculin skin test), pollen or other allergen. Physical triggers include cold, heat, and ultraviolet (UV)
radiation.
Initial signs of anaphylaxis include tachycardia, wheezing, dysphagia, pruritus, erythema, uticartia (hives), abdominal pain, chest pain, peripheral
tingling, and sneezing. Symptoms can progress in severity very rapidly, leading to angioedema (facial edema and that may contribute to airway
obstruction), severe hypotension, and stridor (heard without auscultation), from a loss of airway patency.
Observation and inspection is the primary means of diagnosing anaphylactic shock, as the symptoms are extremely apparent and there isnt time to
wait for lab results to return before taking action. The patient is treated through oxygen administration, epinephrine, and repositioning (the head of
the bed is elevated to promote airway patency). Intubation and mechanical ventilation is necessary for severe cases. Once stable, the patient will be
referred to an allergist for allergen specific testing if the source of the trigger remains unknown. Other reactions may occur when the patient is initially
exposed to a medication such as morphine or aspirin; this is considered to be an anaphylactoid reaction, and is not true anaphylaxis.
Neurogenic Shock
Neurogenic shock is a form of distributive shock that occurs in individuals with a traumatic brain or spinal cord injury. Its associated with an
autonomic nervous system response in which sympathetic vascular tone is lost. Neurogenic shock can occur secondary to autonomic dysreflexia, a
common complication of urinary stasis in at-risk patient populations.
Toxic Shock Syndrome (TSS)
TSS is a form of distributive shock secondary to sepsis. The most common cause of TSS is from a systemic staph infection associated with improper
tampon use. Some examples of improper tampon use includes using the same tampon for more than the manufacturers recommended maximum
time (usually 6-8 hours), or using a tampon absorbency rate thats too absorbent for the volume of the menstrual flow (super strength when only light
flow is needed).

Priority Interventions for Distributive Shock

/ Oxygen therapy
/ Fluid administration
/ Vasoactive drugs
/ Blood transfusion
Infection control