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

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 . Early manifestations of decreased LOC include confusion. pulse. The kidneys do not receive enough pressure to maintain urine output function. 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). 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. or bradypnea: Tachypnea (rapid respiration rate) is the most common and is likely to be associated with compensatory responses to acidosis and hypoxia. This is considered a normal psychogenic response. the kidneys do not receive enough pressure to continue filtering waste. the notable exception with pallor is seen in early-phase septic shock. and eventually coma can ensue / Anxiety: if alert. hypoprefusion. As blood is reserved for the brain and heart (since they’re more vital to immediate survival). it’s usually not required for nursing students to fully understand at this time. blood chemistry. As mentioned above. Other alterations in normal breathing patterns may also be present / Tachypnea. The MAP will usually be calculated automatically by an invasive pressure monitoring device. The sum of this is the MAP. metabolic acidosis occurs. Note that impaired renal output is often one of the first non-cardiovascular indicators of impaired cardiac output. This “rosy cheeked” appearance results from the vasodilator effect. 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. respiration rate. and LOC Lab Work and Other Diagnostics / ABGs for acid/base balance and O2/CO2. This creates a build-up of toxins in the blood. Diagnostics Physical Examination / History and patient presentation (myocardial infarction versus an automobile collision) / Data collection: capillary refill. 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. and restlessness. a Doppler (ultrasound device) can be necessary to locate them / Mean arterial pressure (MAP) is more of a Critical Care Nursing Class concept. Fatigue. such as an arterial line (A-Line) Neurological Manifestations of Shock / Decreased level of consciousness (LOC): changes in mental status are multi-factorial. patients will often be anxious and very verbal about their distress. The patient is usually warm and appears to be flushed. such as early-phase septic shock. which causes vasodilation) / Pulse strength: Peripheral pulses may be difficult to palpate. 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). lactic acid. For Med-Surg. this is also be an early form of mental status change. and acidosis: Low urine output is a common finding in shock. Decreased renal output is caused by insufficient tissue perfusion secondary to impaired cardiac output. and may progress to more ominous states (such as non-responsiveness) Respiratory Manifestations of Shock / Dyspnea: Breathing becomes labored. low urine output. (such as cases of anaphylactic shock). as oxygen saturation may not provide enough accuracy / Blood work: CBC. agitation. loss of consciousness. Again. 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. this is especially important in advanced stages. and alteration in sympathetic nervous system. Therefore. leading to an acidic environment. hypoxia. It may decline from hypoglycemia.

Prolonged vomiting and diarrhea are common causes of extracellular fluid loss. intravascular fluid (the fluid that surrounds the blood. PaO2. including epinephrine. It involves a sudden and drastic fluid loss. agitation. diarrhea.000 mL of saline administered within 20 minutes. burns. / Plasma loss: increases in capillary permeability. progressing to a altered mentation and decreased level of consciousness (LOC) . 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). patient presentation. Common clinical manifestations include altered mentation. dopamine. 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. In cases of cardiogenic shock. or hemorrhage. 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. and arterial blood gases (ABGs) / Acidosis monitoring: Blood pH and ABG values. 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. excessive intracranial pressure. If not contraindicated by fluid overload. Causes of Hypovolemic Shock / Blood loss: resulting from a traumatic accident. comprehensive metabolic panel (CMP). this is the most common type of shock. permitting for a greater loss through diffusion into the vascular tissue. The most frequent cause is from the reduction of blood and vascular fluids. and peritonitis (an infection of the peritoneum. injury. usually caused by a perforation in the abdominal wall) / Extracellular fluid loss: from such causes as severe and prolonged vomiting.9% (isotonic solution) is most commonly used to maintain blood volume.000-2. including PaCO2. confusion. complete blood count (CBC). or extravascular fluids. and cool and clammy skin./ 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. acidosis (referring to a low pH of the blood). and other factors / Drugs that cause vasoconstriction. HCO3. Increased permeability of the vessels can occur from sepsis. diuresis. such as plasma). The primary manifestation of this type of shock is severe hypotension which occurs secondary to the loss of blood. and sunstroke Clinical Manifestations of Hypovolemic Shock / Neurological: dizziness. such as occurs in hemorrhage. initial bolus may of 1. rapid and deep respirations.

To compensate. groin. Delayed capillary refill will be evident / Integumentary: cool and clammy skin. and cardiac status / Administration of standing order drugs. A surgical closure of gaping wound may be necessary / Fluid volume replacement: saline. including: ventricular tachycardia. diaphoresis. leading to disruption of contractility and rhythm. pallor Pharmacological Management for Cardiogenic Shock / Dobutamine / Dopamine / Epinephrine / Diuretics and inotropes Nursing Assessment for Cardiogenic Shock / Diligent and frequent monitoring of vitals. temperature. often greater than 1. PVCs (premature ventricular contractions) and dysthymia may occur from the low blood supply and inadequate profusion. cyanosis. usually established through subclavian. supraventricular tachycardia. and ventricular fibrillation. Chronotropic (heart rate) or inotropic (heart rhythm) factors may be implicated. Various forms of chronic heart failure also run the risk of cardiogenic shock. As the heart must work harder to keep up. defined as less than 30 mL/hour). hypotension and orthostatic hypotension (fall more than 10 points when changing from lying to standing position / Respiratory symptoms: dyspnea. including oxygenation saturation. Hypotension occurs as the cardiac output decreases. mean arterial pressure (MAP). halting the aldosterone-renin-angiotensin pathways. the patient is in acute renal failure during shock but don’t expect to observe any useful signs of this in your assessment Assuming that the patient will either recover or be dead shortly. tachycardia related to the psychogenic response associated with a traumatic condition./ Cardiac: initially. Technically speaking. ADH will also stop being processed. depending upon the condition / Monitoring and recording of urine intake and output / Continuous monitoring of EKG / Blood pressure. and other hemodynamic parameters may be monitored continuously through an arterial line or a central venous pressure line / Thermal control. that manifests in heart failure. The heart eventually becomes ischemic. overall poor appearance. Without this mechanism in place. tachycardia and thready pulse. Myocardial infarction is the most common cause of cardiogenic shock. vasodilation is worsened and he blood pressure drops more. clammy skin. dysthymias. hypoperfusion / Integumentary symptoms: cool. similar to the panic seen during an asthma attack. which constricts the vessels when pressure becomes to low. uraemic seizures / Renal symptoms: oliguria (low urine output. It’s caused by an obstruction or deficiency associated with an underlying cardiac pathology. based upon assessment findings. or active warming Priority Interventions for Cardiogenic Shock / Oxygenation (ventilation as needed) / Fluid replacement (saline and blood products . Cardiovascular drugs such as diuretics may be used for maintenance. acute or chronic. The majority of these cases involve myocardial infraction of the anterior wall. pallor. such as albumin are often administered. Irritability. the patient won’t be “looking well” / Renal: sympathetic nervous system will signal the kidneys to shut down function down. Potential Causes of Cardiogenic Shock / Myocardial infarction. It begins with impaired cardiovascular functioning secondary to alteration of cardiac output. there isn’t 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. blood transfusion and blood products. occurring in less than 7% of patients recovering from acute coronary infarction. Filtration ceases as the blood supply is reserved for the functions most vital to sustaining life. Cardiogenic shock can be caused by any condition. 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. Inability to concentrate. Cardiogenic shock a vicious cycle where the symptoms lead to responses that exacerbate the condition. the pulse elevates and peripheral vasoconstriction occurs. which increases its perfusion needs. Bradycardia will eventually develop as volume becomes more depleted. oxygen demand increases. Drugs that increase blood pressure may be used as they cause the vasculature to “clamp down” / Administer drugs as ordered. Fortunately. plasma expanders. such as dopamine and epinephrine / IV access: usually 16-20 gauge (must be large enough for blood transfusion) / IV central line. possible coma. restlessness.200 dynes second/cm5. a tourniquet may be used. tachypnea / Neurological symptoms: decreased LOC. this complication is not very common. especially in the anterior wall / Congestive heart failure / Congenital heart defects Clinical Manifestations of Cardiogenic Shock / Cardiac symptoms: chest pain and shortness of breath.

Hemodynamic derangement and impairment of the normal coagulation cascade is affected. 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). The heart attempts to compensate by raising the cardiac index (when it’s physiologically possible for the heart to do so). As a result. These include 1) pulse over 100 beats per minute. It occurs somewhere in the vasculature other than the coronary arteries (especially the lungs). Neurogenic shock can occur secondary to autonomic dysreflexia / Hepatic insufficiency: the liver modulates inflammatory processes. 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. There are various types of distributive shock. This leads to inadequate tissue perfusion that progressively worsens with time. This causes a low systemic vascular resistance (SVR).heart. It presents with two phases: 1) early hyperdynamic phase. brain. Widespread alterations in vasculature impair the contractility function of the heart and may lead to multiple organ failure. or sepsis of the blood. it is known as cardiogenic shock)./ Medications to wake up the heart Obstructive Shock What is Obstructive Shock? Just as the name sounds. 2) temperature over 38°C or . For DIC. the risk of shock increases / Addisonian crisis: this occurs when cortisol levels become extremely depleted in individuals with Addison’s 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. obstructive shock involves some type of active obstruction or pressure that obscures the function of the heart. The major characterizing feature of distributive shock is systemic vasodilation coupled with impaired circulation. Release of inflammatory mediators observed in most forms of distributive shock result in hemodynamic derangements. 2008) Septic Shock Septic shock can be thought of as vasodilatory shock. which explains why it’s also termed as extracardiac shock. the main focus is to treat the underlying cause as treatment options are limited. (If the obstructive source is located within the vasculature of the heart. Potential Causes of Obstructive Shock / Tension pneumothorax / Myocarditis or myocardial rupture / Trauma. disseminated intravascular coagulation (DIC) occurs in up to half of all cases. Forms of Distributive Shock / Septic shock: caused by bacteremia. 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. and anaphylactic shock. Each phase presents differently. 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. which is called cold or hypodynamic shock. neurogenic shock. Common causes include acute respiratory distress syndrome (ARDS) and systemic inflammatory response syndrome (SIRS) / Toxic shock syndrome (TSS): a systemic staph infection. also known as warm septic shock. and 2) late septic shock. The most familiar forms include septic shock. SIRS must meet at least two out of four of the clinical criteria set forth by the ACCP. When normal function is impaired.

It’s associated with an autonomic nervous system response in which sympathetic vascular tone is lost. abdominal pain. peripheral tingling. antibiotics (especially penicillin). The most common cause of TSS is from a systemic staph infection associated with improper tampon use. Symptoms can progress in severity very rapidly. It’s 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. Common triggers of anaphylactic shock include vaccines (usually to toxoids. or using a tampon absorbency rate that’s too absorbent for the volume of the menstrual flow (super strength when only light flow is needed). uticartia (hives). Initial signs of anaphylaxis include tachycardia. Once stable. wheezing. Observation and inspection is the primary means of diagnosing anaphylactic shock. severe hypotension. diagnostic solutions (such as the tuberculin skin test). and repositioning (the head of the bed is elevated to promote airway patency). IgE antibodies are the primary mediators and IgG antibodies also play a role. under 36°C. 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). chest pain. Other reactions may occur when the patient is initially exposed to a medication such as morphine or aspirin. (such as shellfish or peanut butter). a bacterial toxin that has inactivated or suppressed by a process). dysphagia. immune globulins. venomous insect stings (especially from bees). Neurogenic shock can occur secondary to autonomic dysreflexia. and 4) hemodynamic indicators. Anaphylaxis is life-threatening unless rapid interventions are performed. pollen or other allergen. Anaphylactic Shock Anaphylactic shock is a form of distributive shock characterized by airway inflammation and obstruction. and ultraviolet (UV) radiation. Some examples of improper tampon use includes using the same tampon for more than the manufacturer’s recommended maximum time (usually 6-8 hours).000/µL or under 4. The patient is treated through oxygen administration. from a loss of airway patency. including PaCO2 under 32mm Hg. white blood cell count over 12. pruritus. Neurogenic Shock Neurogenic shock is a form of distributive shock that occurs in individuals with a traumatic brain or spinal cord injury. and stridor (heard without auscultation). erythema. as the symptoms are extremely apparent and there isn’t time to wait for lab results to return before taking action. and is not true anaphylaxis. leading to angioedema (facial edema and that may contribute to airway obstruction). It’s a systemic reaction that involves multiple organs and body systems. The degree of sensitization concomitant with various inflammatory markers. latex. Physical triggers include cold. and sneezing. the patient will be referred to an allergist for allergen specific testing if the source of the trigger remains unknown. heat. this is considered to be an anaphylactoid reaction. a common complication of urinary stasis in at-risk patient populations. epinephrine. 3) respiratory rate over 20 breaths per minute. Priority Interventions for Distributive Shock / Oxygen therapy / Fluid administration / Vasoactive drugs / Blood transfusion Infection control . food.000/µL. Intubation and mechanical ventilation is necessary for severe cases. Toxic Shock Syndrome (TSS) TSS is a form of distributive shock secondary to sepsis.