Shock and Multiple Organ Dysfunction Syndrome PDF

Summary

This document provides an overview of shock and multiple organ dysfunction syndrome, explaining the causes, symptoms, and classifications of different shock types. It also highlights the importance of immediate medical intervention.

Full Transcript

**Chapter 11: Shock and Multiple Organ Dysfunction Syndrome, pg. 876 ONLY FOR THIS CHP, PINK HIGHLIGHT = ZOOM** **What is shock?** Life threatening condition in which the body is not getting enough blood flow - Circulatory failure that leads to **hypoperfusion to tissue, preventing adequate...

**Chapter 11: Shock and Multiple Organ Dysfunction Syndrome, pg. 876 ONLY FOR THIS CHP, PINK HIGHLIGHT = ZOOM** **What is shock?** Life threatening condition in which the body is not getting enough blood flow - Circulatory failure that leads to **hypoperfusion to tissue, preventing adequate oxygen delivery to cells,** and can lead to death. - Physiologic response include hypoperfusion of tissues, hypermetabolism, & activation of the inflammatory response \[book\] = **SNS ACTIVATED** - Not enough oxygen, cells switch to anaerobic metabolism which **produces lactic acid \[a sign of shock\]** - What does this mean for the body? - Can affect all body systems. Requires immediate medical treatment/worsens rapidly - If shock isn't effectively treated, **multiple organ dysfunction syndrome \[MODS\]** can occur leading to death - What is the first step in treating shock? **Identify the cause** - **Examples** - First thing to do when there's a pt who comes in with potential shock to know how to treat them? **Take vitals, find out what they're fighting and treat the source** - Home health pt with chronic foley comes in and is confused, has UTI, HR is going up, got fever = do a sepsis workup (check ABGs, type and cross): Take foley out, culture it, give abx, get blood/urine cultures, find out the source and figure out how to treat **Classification of Shock:** Hypovolemic, Cardiogenic, Septic, Neurogenic, Anaphylactic (distributive) **Pathophysiology in Shock,** Figure 11-2 p. 882 - Cells lack adequate blood supply & are deprived of O2 & nutrients = produce energy via **anaerobic metabolism** resulting in acidotic intracellular environment \[book\] - The body attempts to restore normal working order - BP drops, baroreceptors alerted, catecholamine released, increased HR and vasoconstriction = restored BP **Stages of Shock table 11-1 (know all the stages of shock): Initial/Compensatory, Progressive, Irreversible** **KNOW Compensatory/Initial Stage (same thing, used interchangeably)** - Body system is still perfused because of reflex compensatory mechanisms activated & pt presents as \[lecture\]: - SNS: increase BP, tachycardic \[not concerning\] - **Main organs to worry about for perfusion are brain & heart** - PNS: decrease peristalsis, decrease UOP - **THIS** is the optimal time to treat them. The further along they get through the rest of the stages, the less likely to save them or if they are saved, they'll have long term issues \[lecture\] - **Understand the sympathetic nervous system response and RAAS system\*\*** - **BP still within normal range** - **RAAS** - Renin released from kidneys. Renin converts ATN \[from liver\] → AG I. AG I → AG II via ACE in lungs. AG II causes vasoconstriction, aldosterone & ADH release = BP is restored - **S/sx:** cool clammy skin, hypoactive bowel sounds, tachycardic, UOP decreased, mild AMS/confusion, tachypnea, anxious - Aldosterone & ADH released = decrease UOP - Rapid RR raises blood pH causing compensatory respiratory alkalosis. - **Nursing Management:** Assess; Monitor tissue perfusion, Pulse pressure; Reduce anxiety, Safety **KNOW Progressive Stage, pg. 890** - **Severe tissue hypoperfusion ensues.** BP can no longer be regulated and decreases = **clinically hypotensive** - **MAP= perfusion pressure; falls below 65 mmHg** - Vasoconstriction: Prognosis worsens with this state - **S/s: Hypotension, increased HR \> 150, increased RR \[rapid & shallow\], crackles, pulmonary edema, arrhythmias, ischemia, mottling, petechiae, lethargy, metabolic acidosis, declining mental status, jaundice, GI ulcers** - Presents w/ metabolic acidosis. RR increases due to compensation for metabolic acidosis & high O2 demand. - Necrotic mucosa and DIC, edema, ascites, ischemic bowel or poor GI motility (blood diverted away from GI tract - **Nursing management**: preventing complications, promote rest & comfort, support family members **KNOW Irreversible/Refractory Stage, pg. 896 \***Point of no return\* - **BP is critically low 80/45 and HR is erratic; pt does NOT respond to tx & cannot survive** - **s/s: Worsening metabolic acidosis, pulmonary dysfunction leads to respiratory arrest & cardiac arrest** - Tachypneic, rapid shallow respirations, crackles, alveoli stop producing surfactant (atelectasis), pulmonary edema, skin is cool and clammy, petechiae, shunting, acute lung injury, progressive kidney injury anuria, poor cardiac perfusion - increased cerebral perfusion w/ hypoxia causes progressive deterioration in mental status. - Anaerobic metabolism worsens lactic acidosis \[acute metabolic acidosis\] - MODS has occurred & death is imminent - Realization of this stage is in hindsight - Body is trying to save vital organs and kills off the kidneys, liver, brain - If you're trying to keep them out of MODS and the end stage of shock, you want to do whatever it takes to reach adequate organ function - Depends on type of shock, won't give cardiogenic a bunch of fluids - Don't sedate them bc that'll slow it down more and they can't say if something hurts - Organs are shutting down = MODS **General Management of Shock, pg 885** - **Supplement O2 and/or mechanical ventilation for resp system may be required to increase the delivery of oxygen in the blood.** - **Monitoring tissue perfusion: (if they have at least 2 of these, report it immediately)** - **Changes in LOC/altered mental status (pg. 885) , Vital signs (RR \>/equal to 22)** - **Report SBP \< 100; MAP 65mm/Hg or \< (book, pg. 885)** - **Monitor hemodynamic stability; BP is an indirect measure of tissue hypoxia** - **Narrowing pulse pressure is an earlier indication of shock than a drop in systolic BP** - Pulse pressure is the difference b/t the systolic and diastolic blood pressure - Ex: BP = 120/80 so the pulse pressure would be 120 - 80 = 40 mmHg - Normal pulse pressure is between 40-60 - UOP/renal function, Skin color, temp, condition - Lab values: lactate, CO2, Na+, BUN/Cr, K+, BG - **Administration of IV fluids and medications supports BP and cardiac output, and the transfusion of packed red blood cells enhances oxygen transport. Make sure to reduce anxiety and clarify advance directives (book)** - **Fluid replacement for intravascular volume, pg. 898** - **Blood components \[packed RBCs, fresh-frozen plasma, & platelets\]** - **Crystalloids: electrolyte solution that move freely b/t intravascular compartment & interstitial spaces; typically stays in the system for \< 1 hour** - Start with crystalloids (LR) to expand volume b/c it has electrolytes & most closely resembles plasma (can cause volume overload, only used for short time) - Ex.: Isotonic (NS and LR), Hypertonic (3% sodium chloride) - **Colloids \[large-molecule IV solution\]: Albumin, plasmanate**, hetastarch - **Colloids given second b/c they are large protein molecules and they stay in the system longer (they don\'t leak across the vascular membrane)** - Most times will use albumin b/c hetastarch and dextran are not indicated b/c they interfere with platelet aggregation - **Vasoactive medications for improving cardiac function \[table 11-2\]** - Inotropic Agents (ex: dobutamine), Vasodilators, Vasopressor Agents - Check VS every 5-15 min with dobutamine to make sure the amount of med is correct - **These meds help increase strength of myocardial contractility, regulate HR, reduce myocardial resistance, & initiate vasoconstriction. Also maximize tissue perfusion \[book\]** - \[NOT IN BOOK\] Safety guideline: HAVE to titrate them down, has to be central line and pump. No peripheral line - **Nutritional support for metabolic requirements** - Pts in shock may require more than 3000 cal/daily \[book\] - Enteral (NG tube) or parenteral - Antacids (famotidine), H2 blockers, PPIs for ulcer prevention - Identify signs/symptoms of compensation **BEFORE** the development of hypotension and report to provider - Correct the underlying disorder **Hypovolemic Shock, \*\*MOST COMMON CAUSE OF SHOCK\*\* pg. 907** - Loss of at least 15-30% of circulating volume, approx. 750-1500 mLs - **Causes:** - External **fluid losses: traumatic blood loss** - Internal fluid shifts: severe dehydration, severe edema, or ascites - **Pathophysiology:** **decreased intravascular volume** leads to **decreased ventricular filling which** results in decreased stroke volume (amount of blood ejected from the heart) and **decreased cardiac output**. When cardiac output drops, BP drops and tissues cannot be **adequately perfused** - **Risk factors** ![](media/image2.png) - Clinical Manifestations: **decreased CO**, **cool skin,** **tachypnea, sweating, hypotension, confusion, agitation**, anxiety, decreased or no urine output, pallor, - Considerations - Proper patient positioning (do NOT position them in Trendelenburg) - Need to monitor for fluid volume overload s/sx: crackles, edema, SOB, bounding pulses, JVD - Monitor body temp during fluid administration - **Complications** - **TRALI:** transfusion related acute lung injury which causes pulmonary edema, hypoxemia, resp distress, & ground glass opacities on CXR - **TACO**: Transfusion associated circulatory overload which causes cardiogenic edema, dyspnea, crackles, cyanosis, elevated BNP (has mild diuretic fixations) **What is the goal of treatment? Pg. 912** - Treat the underlying cause. Fluid or blood replacement - **Fluid replacement**: two large-gauge IV lines, **use normal saline + lactated ringers, blood products, and colloids (albumin)** - Redistribution of fluid. Medications. Monitor administration of fluids and medications closely - Labs, VS, ABGs, Physical assessment, oxygen, comfort/safety, **strict I&Os** **Cardiogenic Shock, pg. 913** - Patho.: Failure of the heart as an effective pump when **blood volume is adequate. Supply of O2 is inadequate for heart & tissues.** - **Decreased cardiac contractility → decreased stroke volume and CO → pulmonary congestion, decreases systemic tissue perfusion, and decreased coronary artery perfusion** - Cardiac output, which is a function of both stroke volume and heart rate, **is compromised.** - When stroke volume and heart rate decrease or become erratic, BP falls and tissue perfusion is reduced. - Most Common Cause: **anterior wall MI (heart attack),** hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax, cardiomyopathies, valvular damage, cardiac tamponade, and arrhythmias - S/sx: **tachycardia**, **hypotension**, **oliguria** (\ - Patho: **widespread infection or sepsis**; life-threatening organ dysfunction - **Septic shock**: a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality \[book\] - **Dysregulation of the immune system** - BP is typically normal in the beginning OR slightly hypotensive - Triggers coagulation cascade + inflammatory response. Increased capillary permeability + vasodilation - Maldistribution of intravascular volume - Decreased venous return (d/t pooling) which puts them at risk for DVTs. Decreased CO - Decreased tissue perfusion - **Risk factors chart 11-5:** - **Immunosuppression**, **Elderly, Infants/Very young**, **Invasive Procedures,** Malnourishment, Chronic illness, Emergent and/or multiple surgeries - **Chronic illness that have increased risk for infection: DM**, HIV, CKD, steroid use, and liver disease - Diabetic with wounds, pt with urinary catheter, pt with AIDS - **S/s, pg. 928: fever, tachypnea, low BP, tachycardia, chills, low UOP,** C-reactive protein, UOP is normal to slightly decreased, Confused, hyperthermia, RR is elevated, N/V/D, altered loc - **As sepsis progresses the cardiovascular system also begins to fail, the BP does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (HALLMARK, zoom)** - **SIRS**: **"SIRS can septically shock you"** - **SIRS \[systemic inflammatory response syndrome\]**: widespread inflammation response. There is a cytokine release syndrome resulting from clinical insult that initiates a systemic inflammatory response \[book\] - **Criteria to ID (2 or more)** - **Temp \101.3 F (38.5 C) or \< 95 F (35 C)** - **Heart rate: \> 90/min, tachycardia** - **Tachypnea \> 22** - **WBC: \>12,000, \ - **Anaphylactic Shock, pg. 937** - Caused by a severe allergic reaction when patients who have already produced antibodies to an antigen develop a systemic antigen-antibody reaction - **RF:** hx of **medication sensitivity, hx or reaction to insect bites, food allergies**, transfusion rxn, and latex sensitivity - **Three defining characteristics**: acute onset of s/s, presence of two or more s/s that include resp compromise, reduced BP, GI distress, skin/mucosal tissue irritation); CV compromise after exposure - **s/sx**: **rapid swelling of throat tissues, decreased CO**, **bronchospasm,** headache, lightheadedness, N/V, acute abdominal pain/discomfort, pruritus, feeling of impending doom, generalized flushing, dyspnea (laryngeal edema), cardiac arrhythmias, and hypotension - Loss of consciousness, hives, swelling of tongue and inability to swallow, laryngeal edema - **Management**: - **ABCs. Remove the causative antigen. Obtain IV access**. Assess for allergies. Educate patients - Meds \[**antihistamines/diphenhydramine, albuterol, corticosteroids, epinephrine\]**, IVFs, life saving measures - **Monitor**: O2 and VS, serial ABGs, and hemodynamics **Multiple Organ Dysfunction Syndrome, pg. 939** - An altered organ function in acutely ill patients that requires medical intervention to support continued organ function (book) - Most commonly seen in pts with sepsis as a result of inadequate tissue perfusion - **s/s** \[pg. 940\]: dyspnea and resp failure, hyperglycemia, increased BUN - **Management**: early detection, control the initiating event, promote adequate organ persuasion, providing nutritional support, and maximizing pt comfort - **Education** - Preventing further infections/injury. S/s to monitor. Continuing/transitional care - Long-term care facility/rehab. Hospice/End of life -

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