Study Objectives
Foundations of Shock and Critical Care
• Explain the different types of shock (hypovolemic, cardiogenic, distributive [septic, anaphylactic,
neurogenic]) and their distinct causes and manifestations.
o Hypovolemic: caused by (in order) decreased blood volume, venous return, stroke
volume, cardiac output, tissue perfusion
▪ Manifestations:
▪ Oliguria
▪ Abdominal distension
o Cardiogenic: caused by Acute MI (most common cause), systolic dysfunction, diastolic
dysfunction, arrhythmias, structural problems
o Manifestations:
▪ Arrhythmias
▪ Feeling of doom (“i’m going to die”)
▪ Pulmonary congestion
o Distributive: caused by loss of SNS control of vessel tone; vessels dilate; blood pools in
periphery; less volume return to the heart; hypovolemia and reduced CO
o Septic: MOST COMMON DISTRIBUTIVE SHOCK; caused by widespread infection or sepsis;
o Severe sepsis = sepsis + organ dysfunction
o Manifestations:
▪ Widespread inflammation: systemic inflammatory response syndrome
(SIRS)
▪ ↑ coagulation: d/t increased inflammation and formation of clots
regardless of bleeding or not
▪ Microthrombi = tiny clots that form in the small blood vessels
▪ Obstruction of microvasculature
▪ Abnormal consumption of clotting factors
▪ Hyperdynamic state: CO may increase as body tries to correct decreased
tissue oxygenation.
o Neurogenic: Imbalance between PNS and SNS; caused by loss of sympathetic nervous
system control (e.g., spinal cord injury, anesthesia, drugs). SNS not able to respond to
body stressor.
o Manifestations:
▪ Warm, dry skin
▪ Urinary retention
▪ Paralytic ileus
▪ Loss of cutaneous and tendon reflexes
▪ Bradycardia
▪ Poikilothermic (takes on temperature of environment)
o Anaphylactic: life-threatening hypersensitivity reaction when antibodies are already
produced to an antigen that causes a systemic anitgen-antibody inflammatory reaction
o Manifestations:
, ▪ Sense of impending doom
▪ Incontinence
▪ Angioedema
▪ Wheezing, stridor
▪ Flushing, pruritus and urticaria
▪ Respiratory distress
• Correlate clinical signs (vital signs, perfusion, mental status changes, urine output) with the
stage of shock.
o Initial:
▪ Vital signs: May still be normal (compensatory mechanisms maintain BP & HR).
▪ Perfusion: Slight decrease in tissue perfusion; skin warm or slightly cool.
▪ Mental status: Alert, may feel anxious or restless.
▪ Urine output: Normal or slightly decreased.
o Compensatory:
▪ Vital signs:
▪ Tachycardia (HR ↑)
▪ Blood pressure: May still be normal due to vasoconstriction, or
slightly decreased systolic.
▪ Respiratory rate ↑ (tachypnea).
▪ Perfusion: Cool, pale skin; capillary refill >2 seconds; weak peripheral
pulses.
▪ Mental status: Restless, anxious, may have difficulty concentrating.
▪ Urine output: Decreased (<30 mL/hr but still present).
▪ Mottling, flushing
▪ Decreased bowel sounds
o Progressive:
▪ Vital signs:
▪ HR ↑ (marked tachycardia, >150), arrhythmias, ischemia, CP d/t MI
▪ BP ↓ (systolic <90 mmHg, MAP <65 mmHg)
▪ Narrowing pulse pressure.
▪ Tachypnea (may progress to shallow, labored breathing), crackles,
pulmonary edema.
▪ Perfusion: Mottled, cold, clammy skin; very weak or absent peripheral
pulses. petechiae
▪ Mental status: Confused, agitated, eventually lethargic, loss of
consciousness
▪ Urine output: Oliguria (<20 mL/hr).
▪ Widespread clotting and bleeding simultaneously. Microthrombi can be
formed and cause stroke; also at risk for DIC which can cause hemorrhage
o Refractory/irreversible:
▪ Vital signs:
▪ Severe hypotension
▪ HR irregular,may be very high initially then bradycardia before
cardiac arrest
▪ severe tachypnea or respiratory failure, usually requires ventilation.
, ▪ Perfusion: Profound hypoperfusion, cyanosis, skin cold and mottled,
jaundice.
▪ Mental status: unconscious, unresponsive.
▪ Urine output: Anuria (no urine production)
• Compare and contrast the hemodynamic profiles (CO, SVR, preload, afterload) for each type of
shock.
o Hypovolemic sock:
▪ Cardiac Output (CO): ↓ (not enough volume to pump)
▪ Systemic Vascular Resistance (SVR): ↑ (compensatory vasoconstriction)
▪ Preload (CVP, PCWP): ↓ (low filling pressures due to fluid loss)
▪ Afterload: ↑ (vasoconstriction increases resistance)
o Cardiogenic:
▪ CO: ↓ (primary problem is pump failure)
▪ SVR: ↑ (compensatory vasoconstriction to maintain BP)
▪ Preload: ↑ (blood backs up → ↑ CVP and ↑ PCWP)
▪ Afterload: ↑ (from vasoconstriction, worsens pump failure)
o Septic Shock (late/advanced phase)
▪ CO: Initially ↑ (hyperdynamic state: warm shock), then ↓ (late/severe stage)
▪ SVR: ↓ (massive vasodilation from inflammatory mediators)
▪ Preload: ↓ (relative hypovolemia from vasodilation, capillary leak)
▪ Afterload: ↓ (low SVR reduces resistance)
o Anaphylactic:
▪ CO: Variable (↓ if severe bronchospasm/edema, sometimes ↑ early from
compensatory tachycardia)
▪ SVR: ↓ (vasodilation from histamine release)
▪ Preload: ↓ (capillary leak + vasodilation → low filling pressures
▪ Afterload: ↓ (low SVR)
o Neurogenic:
o CO: ↓ (bradycardia + vasodilation lower forward flow)
o SVR: ↓ (loss of sympathetic tone → vasodilation)
o Preload: ↓ (venous pooling in dilated vessels)
o Afterload: ↓ (low SVR from loss of tone)
• Demonstrate the prioritization of nursing interventions in shock management, including airway,
breathing, circulation, IV fluid administration, and medication use.
o Airway:
▪ Priority: Maintain a patent airway.
▪ Interventions:
Foundations of Shock and Critical Care
• Explain the different types of shock (hypovolemic, cardiogenic, distributive [septic, anaphylactic,
neurogenic]) and their distinct causes and manifestations.
o Hypovolemic: caused by (in order) decreased blood volume, venous return, stroke
volume, cardiac output, tissue perfusion
▪ Manifestations:
▪ Oliguria
▪ Abdominal distension
o Cardiogenic: caused by Acute MI (most common cause), systolic dysfunction, diastolic
dysfunction, arrhythmias, structural problems
o Manifestations:
▪ Arrhythmias
▪ Feeling of doom (“i’m going to die”)
▪ Pulmonary congestion
o Distributive: caused by loss of SNS control of vessel tone; vessels dilate; blood pools in
periphery; less volume return to the heart; hypovolemia and reduced CO
o Septic: MOST COMMON DISTRIBUTIVE SHOCK; caused by widespread infection or sepsis;
o Severe sepsis = sepsis + organ dysfunction
o Manifestations:
▪ Widespread inflammation: systemic inflammatory response syndrome
(SIRS)
▪ ↑ coagulation: d/t increased inflammation and formation of clots
regardless of bleeding or not
▪ Microthrombi = tiny clots that form in the small blood vessels
▪ Obstruction of microvasculature
▪ Abnormal consumption of clotting factors
▪ Hyperdynamic state: CO may increase as body tries to correct decreased
tissue oxygenation.
o Neurogenic: Imbalance between PNS and SNS; caused by loss of sympathetic nervous
system control (e.g., spinal cord injury, anesthesia, drugs). SNS not able to respond to
body stressor.
o Manifestations:
▪ Warm, dry skin
▪ Urinary retention
▪ Paralytic ileus
▪ Loss of cutaneous and tendon reflexes
▪ Bradycardia
▪ Poikilothermic (takes on temperature of environment)
o Anaphylactic: life-threatening hypersensitivity reaction when antibodies are already
produced to an antigen that causes a systemic anitgen-antibody inflammatory reaction
o Manifestations:
, ▪ Sense of impending doom
▪ Incontinence
▪ Angioedema
▪ Wheezing, stridor
▪ Flushing, pruritus and urticaria
▪ Respiratory distress
• Correlate clinical signs (vital signs, perfusion, mental status changes, urine output) with the
stage of shock.
o Initial:
▪ Vital signs: May still be normal (compensatory mechanisms maintain BP & HR).
▪ Perfusion: Slight decrease in tissue perfusion; skin warm or slightly cool.
▪ Mental status: Alert, may feel anxious or restless.
▪ Urine output: Normal or slightly decreased.
o Compensatory:
▪ Vital signs:
▪ Tachycardia (HR ↑)
▪ Blood pressure: May still be normal due to vasoconstriction, or
slightly decreased systolic.
▪ Respiratory rate ↑ (tachypnea).
▪ Perfusion: Cool, pale skin; capillary refill >2 seconds; weak peripheral
pulses.
▪ Mental status: Restless, anxious, may have difficulty concentrating.
▪ Urine output: Decreased (<30 mL/hr but still present).
▪ Mottling, flushing
▪ Decreased bowel sounds
o Progressive:
▪ Vital signs:
▪ HR ↑ (marked tachycardia, >150), arrhythmias, ischemia, CP d/t MI
▪ BP ↓ (systolic <90 mmHg, MAP <65 mmHg)
▪ Narrowing pulse pressure.
▪ Tachypnea (may progress to shallow, labored breathing), crackles,
pulmonary edema.
▪ Perfusion: Mottled, cold, clammy skin; very weak or absent peripheral
pulses. petechiae
▪ Mental status: Confused, agitated, eventually lethargic, loss of
consciousness
▪ Urine output: Oliguria (<20 mL/hr).
▪ Widespread clotting and bleeding simultaneously. Microthrombi can be
formed and cause stroke; also at risk for DIC which can cause hemorrhage
o Refractory/irreversible:
▪ Vital signs:
▪ Severe hypotension
▪ HR irregular,may be very high initially then bradycardia before
cardiac arrest
▪ severe tachypnea or respiratory failure, usually requires ventilation.
, ▪ Perfusion: Profound hypoperfusion, cyanosis, skin cold and mottled,
jaundice.
▪ Mental status: unconscious, unresponsive.
▪ Urine output: Anuria (no urine production)
• Compare and contrast the hemodynamic profiles (CO, SVR, preload, afterload) for each type of
shock.
o Hypovolemic sock:
▪ Cardiac Output (CO): ↓ (not enough volume to pump)
▪ Systemic Vascular Resistance (SVR): ↑ (compensatory vasoconstriction)
▪ Preload (CVP, PCWP): ↓ (low filling pressures due to fluid loss)
▪ Afterload: ↑ (vasoconstriction increases resistance)
o Cardiogenic:
▪ CO: ↓ (primary problem is pump failure)
▪ SVR: ↑ (compensatory vasoconstriction to maintain BP)
▪ Preload: ↑ (blood backs up → ↑ CVP and ↑ PCWP)
▪ Afterload: ↑ (from vasoconstriction, worsens pump failure)
o Septic Shock (late/advanced phase)
▪ CO: Initially ↑ (hyperdynamic state: warm shock), then ↓ (late/severe stage)
▪ SVR: ↓ (massive vasodilation from inflammatory mediators)
▪ Preload: ↓ (relative hypovolemia from vasodilation, capillary leak)
▪ Afterload: ↓ (low SVR reduces resistance)
o Anaphylactic:
▪ CO: Variable (↓ if severe bronchospasm/edema, sometimes ↑ early from
compensatory tachycardia)
▪ SVR: ↓ (vasodilation from histamine release)
▪ Preload: ↓ (capillary leak + vasodilation → low filling pressures
▪ Afterload: ↓ (low SVR)
o Neurogenic:
o CO: ↓ (bradycardia + vasodilation lower forward flow)
o SVR: ↓ (loss of sympathetic tone → vasodilation)
o Preload: ↓ (venous pooling in dilated vessels)
o Afterload: ↓ (low SVR from loss of tone)
• Demonstrate the prioritization of nursing interventions in shock management, including airway,
breathing, circulation, IV fluid administration, and medication use.
o Airway:
▪ Priority: Maintain a patent airway.
▪ Interventions:
