1. Shock definition – insufficient oxygen to meet the metabolic demands of cells and organs resulting in inadequate tissue perfusion.
a. Tissue perfusion is dependent on cardiac output, hemoglobin, and the oxygen saturation of the hemoglobin.
b. Shock can be associated with a low blood pressure (BP), but shock IS NOT defined by a BP.
2. Classifications of Shock and Hemodynamics
a. Hypovolemic Shock – volume loss in the tank
i. Hemorrhagic shock results from blood loss
ii. Non-hemorrhagic shock results from fluid loss
iii. Hemodynamics
1. High parameters – heart rate (HR) and systemic vascular resistance (SVR)
2. Low parameters - BP, central venous pressure (CVP), pulmonary artery obstructive pressure (PAOP), cardiac output (CO), cardiac index (CI), stroke volume (SV)
b. Cardiogenic Shock – pump failure
i. Hemodynamics
1. High - HR, PAOP, and SVR
2. Low - BP, CVP, CO/CI, SV, SvO2
c. Obstructive Shock – pressure on the heart
i. Hemodynamics
1. High - RAP, PAOP, and SVR
2. Low - BP, CO/CI, SV
d. Distributive Shock– maldistribution of volume in the pipes (vasodilation)
i. Septic Shock
1. Early (hyperdynamic) phase hemodynamics
a. High – CO/CI, SV
b. Low – SVR, RAP, PAOP, BP
2. Late (hypodynamic) phase hemodynamics
a. High - HR and SVR
b. Low - BP, CVP, PAOP, CO/CI, SV
ii. Anaphylactic Shock – bronchospasm and wheezing
iii. Neurogenic – bradycardia or lack of expected tachycardia
3. Stages of Shock
a. Compensatory Phase – compensatory mechanisms keep organs perfused.
i. Anxiety, restlessness
ii. Tachypneic, respiratory alkalosis, normal PaO2
iii. Slightly tachycardic, strong pulse
iv. Narrowing pulse pressure (BP maintained)
1. Systolic BP within normal range with rising diastolic BP from vasoconstriction
v. Skin pale and cool (except in early sepsis)
vi. Decreasing urinary output (oliguria)
vii. Beta-blockers may mask traditional early S/S such as tachycardia and diaphoresis
b. Progressive Phase – vital organs are hypo perfused
i. Tachypnea, dyspnea, crackles
ii. Tachycardia with weak peripheral pulses
iii. Cool, clammy, mottled skin
iv. Confusion and may complain of nausea
v. Decreasing systolic BP, narrowing pulse pressure
c. Refractory/Irreversible Phase – not responsive to interventions, leading to organ death
i. Multiple Organ Dysfunction (MODS) - ARDS, ATN, DIC, liver failure
4. Shock Compensation
a. Baroreceptors in the carotid sinus and along the aortic arch sense a decrease in stretch and stimulate the sympathetic nervous system (SNS).
b. Chemoreceptors detect changes in blood oxygen, CO2, and pH and increase respiratory rate and depth, resulting in respiratory alkalosis.
c. Sympathetic Nervous System (SNS)
i. Release of epinephrine and norepinephrine = vasoconstriction
ii. Increased contractility, HR, and BP
d. Renin-Angiotensin-Aldosterone System (RAAS)
i. Renin – angiotensin produces vasoconstriction
ii. Aldosterone increases serum sodium levels and water reabsorption
iii. Decreases urine output (UO), increased BP and CO
e. Antidiuretic Hormone (ADH) Release
i. Renal absorption of sodium and water
ii. Decreased UO, increased BP and CO
f. Intracellular fluid shift
i. Increased intravascular volume
ii. Increased BP and CO
5. Hypovolemic Shock Treatment
a. “Plug the holes and fill the tank” and prevent the “trauma triad of death” – hypothermia, acidosis, coagulopathy”
i. Manual pressure, tourniquets, pelvic binders, damage-control surgery to “stop the bleed”
ii. Warmed isotonic crystalloids to reduce risk of hypothermia
1. NS may result in hyperchloremic acidosis
2. LR may result in increased lactate
iii. Blood and blood product replacement
1. Packed RBC transfusion leads to hyperkalemia, hypocalcemia, and hypomagnesemia.
2. RBC causes low 2,3, DPG – shifts oxyhemoglobin dissociation curve to left, and hemoglobin holds onto O2.
3. Fresh frozen plasma, platelets, cryoprecipitate, TXA
iv. Massive transfusion protocol - 10 units RBC’s in 24 hours or 5 units within 3 hours
v. Autotransfusion for blunt chest trauma
vi. Damage Control Surgery
vii. Monitor shock index (HR/SBP) normal 0.5-0.7. > 0.9 occult hemorrhage
6. Cardiogenic Shock Treatment
a. Decrease preload with diuretics, Nitroglycerin, and morphine
b. Increase contractility with positive inotropes (Dopamine) and intra-aortic balloon pump (IABP)
c. Decrease afterload with Nitroglycerin, Nitroprusside, and antihypertensives
7. Obstructive Shock Treatment
a. Pericardial tamponade - pericardiocentesis and surgical repair
b. Tension pneumothorax - needle decompression and chest tube placement
c. Pulmonary embolus – fibrinolytics or embolectomy
d. Advanced pregnant patient lying supine – tilt patient 15 degrees on left side
e. Abdominal compartment syndrome – monitor compartment pressure closely after abdominal surgery, release pressure with fasciotomy or surgery as required
8. Distributive Shock Treatment
a. Anaphylactic Shock
· Remove causative agent
· Epinephrine 0.3-0.5 mg of 1:1000 IM, repeat as needed
· Airway management, high-flow O2, inhaled Beta-2 agonists
· Antihistamines (diphenhydramine and H2 blocker), corticosteroids
b. Neurogenic Shock - ABC’s, fluid resuscitation, vasopressors (Norepinephrine), Atropine
c. Septic Shock
· Identify and remove source of infection
· Cultures, antibiotic administration
· Keep glucose stable
· Fluid resuscitation of 30 ml/kg (2.1 L in 70 kg patient)
· Norepinephrine (Levophed) is the first-line vasopressor, Epinephrine if second vasopressor is needed
· Possible Vasopressin infusion to augment vasopressors
· Positive inotropes – Dobutamine or Dopamine
Shock Resources
1. Criddle, Laura. TCRN: Trauma Nursing. TCAR Education Programs, 2015.
2. Emergency Nurses Association. Trauma Nursing Core Curriculum, 8th ed., 2019.
3. Kent, Kendra. Trauma Certified Registered Nurse Examination Review. Springer, 2017.
4. Sheehy, S. Sheehy’s Manual of Emergency Care, 7th ed. Elsevier, 2013.