Shock Study Guide What is shock?

Shock is syndrome characterized by tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply and demand for O2 and nutrients which are essential to life. Types of Shock: Cardiogenic: occurs when the pump mechanism of the heart fails = o2 to body and results in CO; o Caused by: Systolic dysfunction: heart cannot pump blood forward Diastolic dysfunction: heart doesnt fill Dysrhythmias Structural problems o Manifestations: Anxiety, agitation, altered LOC (poor brain perfusion) Oliguria-less than 30ml/hr. (decreased perfusion to kidneys) Cold, clammy skin, mottled extremities, profound diuresis (blood shunted from periphery to be able to perfuse vital organs) Weak, thready pulses, hypotension (inadequate CO) Dyspnea, tachypnea, cyanosis (pulmonary congestion r/t elevation of left atrial & pulmonary pressures) Dysrhythmias, angina (lack of O2 to myocardium) Sinus tachycardia (compensatory mechanism for CO) bowel sounds ( paralytic ileus as a result of blood shunting to vital organs) o Diagnostic: Altered hemodynamics: Pulmonary capillary wedge pressure (PCWP) 18mmHg or Cardiac index: 1.8 Systemic vascular resistance (SVR) mixed venous O2 sats. CXR: pulmonary congestion Abnormal labs: BUN & creatinine liver enzymes serum lactate BNP EKG- (acute injury r/t MI) Echo: structural damage or tamponade o Treatment: GOAL IS TO RESTORE BLOOD FLOW & RESTORE O2 SUPPLY/DEMAND ABCS take priority with any type of shock!!!!!!!!!!! Pharmacological: Positive inotropes- to stimulate cardiac contractility (Dopamine, dobutamine)

Vasodilators- decreased workload of the heart, improves CO, O2 consumption, LV pressure , pulmonary congestion (nitroprusside, epi) MAY WORSEN HYPOTENSION Diuretics- fluid vol., relieves congestion, (Lasix) WATCH FOR ELECTROLYTE IMBALANCES ***Watch for adverse reactions and responses to drug therapy and titrate as necessary Meds should be admin. via CENTRAL LINE

Interventions: Continuous EKG monitoring Monitor hemodynamics: Pulm. Arterial Pressure (PAP) Central Venous pressure (CVP) Pulm. Cap. Wedge Pressure (PCWP) CO Cardiac Index SVR Maintain MAP greater than mmHg Watch for electrolyte imbalances Give high flow O2 Elevate HOB Glasgow Coma Scale Monitor VS

Hypovolemic: Rapid fluid loss resulting in tissue perfusion. Can be internal or external o Causes: External hemorrhage Internal fluid shifting Dehydration, burns, GI losses, DKA o Manifestations: o Early signs-can compensate for loss up to 15% of blood vol Hypotension Thread pulse Restlessness/agitation urine output preload stroke vol o Late signs-loss of 15-30% total vol=activation of SNS response Lethargy leading to coma MAP less than 60 mmHg hypotension CO pulses

 capillary refill Tachypnea Pallor, cool clammy skin absent sounds Diagnostic Labs: H&H serum Lactate urine specific gravity Electrolyte imbalances Blood gases Central venous oxygenation (ScvO2) Treatment/Interventions: GOAL IS TO RESTORE TISSURE PERFUSION Assess ABCs including: Vitals SaO2 MAP ABGs (all to determine circulatory status) Elevate lower extremities to blood return and venous pooling Administer O2 to prevent hypoxia *****Fluid resuscitation (to increase circulating vol.) Insert 2 lg bore IVs Administer WARMED crystalloids (NS/LR) and colloids (D5/albumin) quickly If pt doesnt respond, blood admin can begin (watch for transfusion reactions) WARM BLOOD Admin clotting factors (Plasma) Serial Monitoring of CVP (normal is 8-12) & BP Insert Foley to monitor output every hour Medications: If pt has persistent hypotension after fluid resuscitation, vasopressor may be added to maintain MAP of 65 or greater Levophed: o BP & MAP o Renal vasoconstriction o CVP/PAWP o SVR (increases workload of the heart Dobutamine: o BP o CO Monitor for fluid overload (crackles/dyspnea) Assess vitals every 15 min Assess perfusion (urine output, cap refill, neuro status) Assess labs & electrolytes

Distributive: Inadequate vascular tone o Neurogenic-occurs within 30 min of spinal injury@ T5 or above (temporary, up to 6 wks.), anesthesia, pain, insulin shock o Massive vasodilation without compensation due to loss of SNS vasoconstrictor tone o Leads to pooling of blood, tissue hypoperfusion, and impaired cellular metabolism o o Bradycardia o Unable to regulate temp Poikilothermia-takes on temp of environment o Dry skin o Absence of reflexes below level of injury (spinal shock) o Anaphylactic-acute, life threatening hypersensitivity reaction to substance o Usually immediate o capillary permeability, fluid leaks into interstitial space o Can lead to resp distress Laryngeal edema Bronchospasm Massive vasodilation Circulatory failure o Manifestations: o Dizziness, itching o Chest pain, hypotension o Swelling of lips, tongue o Wheezing, stridor o Anxiety, confusion, impending sense of doom o Treatment: MAINTAIN AIRWAY-intubation Epinephrine!!! Antihistamines Treat hypotension w/fluid vol. expanders Vasopressors to counteract vasodilation O2 Teach pt to avoid allergen and get an Epi-Pen o Septic: o Sepsis: systemic s/s of severe infection o Septicemia: blood infection in which bacteria multiply rapidly & release toxins o Septic shock: syndrome marked by altered hemodynamics, decreased tissue perfusion and loss of cellular energy Criteria:

o Presence of sepsis along with hypotension despite fluid resuscitation along w/ presence of inadequate tissue perfusion

First, SIRS (systemic inflammatory response syndrome) must be diagnosed by finding at least any two of the following: Tachypnea (high respiratory rate) > 20 breaths per minute, or on blood gas, a PCO2 less than 32 mmHg signifying hyperventilation. White blood cell count either significantly low, < 4000 cells/mm or elevated > 12000 cells/mm. Heart rate > 90 beats per minute Temperature: Fever > 101.3 or hypothermia < 95.0 F Second, there must be sepsis and not an alternative form cause of SIRS. Sepsis requires evidence of infection, which may include positive blood culture, signs of pneumonia on chest x-ray, or other radiologic or laboratory evidence of infection. Third, signs of end-organ dysfunction are required such as renal failure, liver dysfunction, changes in mental status, or elevated serum lactate. Finally, septic shock is diagnosed if there is refractory hypotension (low blood pressure that does not respond to treatment). This signifies that intravenous fluid administration alone is insufficient to maintain a patient's blood pressure from becoming hypotensive.

Diagnostics: o ABGs- pH indicates acidosis o platelets (risk for DIC) o lactate o glucose o BUN/creatinine- due to decreased circulating blood vol o CBC w/ differential-abnormal WBC count indicating infection o Alteration in neuro status, GI dysfunction, GI bleeding, urine output, paralytic ileus o GFR Treatment: Immediate Antibiotics-broad spectrum until organism is identified IV fluids and plasma expanders to restore circulating vol Clot stim factors to neutrophil count Vasopressors to support BP O2 as needed to prevent hypoxia Monitor vitals and bleeding carefully Watch for complications (ARDS, MODS, DIC, acidosis) Watch for respiratory failure. Can develop into ARDS=intubation and mechanically ventilation.

1. (Early)Hyperdynamic Shock (warm shock): characterized by CO and peripheral resistance. Vasodilation =cap perm.=fluid shifts a. Vascular fluid loss-fever b. resp rate c. Profound diuresis d. Small clots plug up capillaries=Petichiae, mottling in the feet up to knees 2. (Ominous) Hypodynamic Shock (cold shock): characterized by CO and peripheral resistance. This stage of septic shock is irreversible and indistinguishable from hypovolemic shock. a. Subnormal temp b. Low WBC count with bands c. Hypotension and hypoperfusion are profound d. Skin is cold/mottled above the knees e. pulse, resps f. Crackles/gurgling g. CO h. Leads to coma, MODS and hemorrhaging from DIC. Obstructive: develops when a physical obstruction to blood flow occurs w/ CO. Caused by: o Abdominal compartment syndrome o Pulmonary embolism o Cardiac tamponade, tension pneumothorax, superior vena cava syndrome o Manifestations: CO afterload JVD Pulsus paradoxus o Treatment: Rapid assessment and tx are critical to prevent cardiac arrest and other problems

Stages of Shock ***These stages can overlap*** Initial: o Compensatory mechanisms are triggered o Blood loss is minimal (less than 10%) Pressure can be maintained CO is usually normal production of ADH Compensatory: o Blood vol by 15-25% o Blood shunted away from non-vital organs o Decompensation begins

Marked in CO Arterial pressure Tachycardia, tachypnea, vasoconstriction and oliguria present cerebral perfusion Progressive: o Rapid circulatory deterioration CO blood vol.= extremely BP= perfusion Edema Dysrhythmias, ischemia, MI Weak, thready or absent pulses Irreversible: o Cell destruction so severe that death is inevitable o Multiple organ failure o Profound hypotension o Unresponsiveness to drug therapy o Severe hypoxemia, unresponsive to O2 o Anuria (renal failure) o HR, BP fall =cardiac & resp. arrest

Systemic Inflammatory Response Syndrome (SIRS) SIRS a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines. . The clinical condition may lead to renal failure, respiratory distress syndrome, central nervous system dysfunction and possible gastrointestinal bleeding.

Systemic inflammatory response syndrome[2] Finding Value Temperature < 96.8 F or > 100.4 F Heart rate >90/min Respiratory rate >20/min or PaCO2<32 mmHg 9 WBC <4x10 /L (<4000/mm), >12x109/L (>12,000/mm), or 10% bands

Multiple Organ Dysfunction Syndrome (MODS) MODS is Multiple organ dysfunction syndrome (MODS), previously known as multiple organ failure (MOF) or multisystem organ failure (MSOF), is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis. Failure of 2 or more organ systems in an acutely ill pt. Stage 1 the patient has increased volume requirements and mild respiratory alkalosis which is accompanied by oliguria, hyperglycemia and increased insulin requirements. Stage 2 the patient is tachypneic, hypocapnic and hypoxemic. Moderate liver dysfunction and possible hematologic abnormalities.

Stage 3 the patient develops shock with azotemia and acid-base disturbances. Significant coagulation abnormalities. Stage 4 the patient is vasopressor dependent and oliguric or anuric. Ischemic colitis and lactic acidosis follow.