OXYGENATION, SHOCK STATES, and MODS

Today: Rapid response Shock states Septic shock case scenario

Homework for next week; Crit Care Case #3 Sepsis [cite references] EKG papers: 119, 160, 217 Answer questions on Sims Septic Scenario [cite refereneces]

Test question on the “when to call RRT” paper

Objectives: Upon completion of this class, the student will be able to:

1. Define pathological conditions that result in impaired oxygenation;

1. Ventilation impairment: (air in and out): inspiratory muscle weakness or trauma, dec LOC, obstructed airways, lungs, thorax, restrictive pulmonary d/o. Diffusion impairment: dec in alveolar-capillary membrane surface area (atelectasis, lung tumors, pneumonia), inc alveolar-cap membrane thickness (ARDS, pulm edema, pneumonia) Perfusion impairment: dec Hb (anemia, carbon monoxide poisoning), decreased perfusion (dec CO, hemorrhage, pulm emoblism), pulmonary vasoconstriction (pulmonary hypertension, hypoxemia) 2. Identify techniques to assess oxygenation status in relation to pulmonary gas exchange, oxygen delivery, and oxygen consumption; Assessing Pulmonary Gas Exchange: ABG (PaO2, PaCO2), Auscultation, End-tidal CO2, Assessment of respiratory muscle efficiency (VT, VC, RR, pulmonary function tests), calculation of intrapulmonary shunt (QS/QT), PaO2/FIO2 (fraction of inspired oxygen) ratio

3. Describe the mechanism of impaired oxygenation for each of the four functional classifications of shock states; 2. Hypovolemic: caused by not enough fluid circulating for adequate perfusion, or vasodilation [esp sepsis], or both 3. Transport: diminished Hb to carry O2 to tissues (CO2, for ex.) 4. Obstructive: mechanical barrier to blood flow that blocks O2 delivery to tissues 5. Cardiogenic: impaired O2 delivery due to cardiac dysfunction 6. Assessing O2 Delivery: Skin color, cap refill, temp, ABGs, pulse ox. CO can be assessed by HR, stroke vol, pulmonary artery catheter. 7. Assessing O2 consumption: measure lactate levels, base, base deficit, mixed venous O2 sat (SVO2): balance betw O2 supply and demand 4. Describe the compensatory mechanism that occur in response to shock states; Baroreeptors and chemoreceptors activates fight or flight response which results increased venous return, inc CO, inc O2 delivery (inc HR, vasoconstriction, etc.) Increased water retention by kidneys to inc blood volume and BP: compensatory mechanisms designed to restore O2 delivery by augmenting CO, redistributing blood flow and restoring blood volume

5. List the clinical manifestations of each of the four shock states; I think low BP and lactic acid should present in all of these, probably with tach and clammy skin, signs of poor perfusion to extremities, etc 8. hypovolemic: cool skin, poor cap refill, low BP, may have orthostatic BP changes. Tachycardia, low urine output. Less volume returned to right atrium. 0 HR increased, BP decreased, Preload decreased, Afterload increased 9. transport: if caused by anemia or hemorrhage, low Hct and Hb, but RAP and PAWP may be normal depending of fluid vol status 10. CO2 poisoning: hdache, malaise, nausea, difficulties with memory, personality changes, gross neurologic dysfunction. 11. Obstructive: cardiac tamponade causes obstruction: pulsus paradoxus (>10mm Hg dec of systolic BP) during inspiration classic sign. 12. Cardiogenic: depend on whether heart failure r or l side. 0 L-sided heart failure: hypoperfusion and pulmonary congestion: dypsnea, bilateral crackles, distant heart sounds, valve sounds, cough, frothy sputum, fatique. Elevated PAWP (>15), low cardiac index, systolic hypotension. 1 R-sided heart failure: systemic venous congestion: peripheral edema, jugular vein distention, liver enlargement (RUQ pain), ascites, fatigue, weight gain, elevated RAPs and normal or low PAWP 13. HR increased, BP decreased, Preload increased, Afterload increased 14. Septic: Fever, tachycardia, low bp, HR increased, BP decreased, Preload decreased, Afterload decreased

6. Describe management of shock states that optimize oxygen delivery and decrease oxygen consumption; 15. supplemental O2 (high flow nonrebreather mask), IV fluids, positive inotropic drugs (dopamine and dobutamine), vasoactive drugs (epinephrine, norepinephrine, dopamine, vasopressin). Vasodilators (nitroprusside, nitroglycerine). Trendelenberg or supine position if hypotensive 16. Decrease O2 consumption: (decrease body work, pain and anxiety, and dec temp): mechanical ventilation, neuromuscular blocking agents (vecuronium, pancuronium), propofol (deep sedation, short) analgesics and anxiolytics, antipyretics, physical cooling measures. Old people: -can’t stay in compensatory stage long. Have dec effectiveness of baroreceptors -more at risk for MI and cardiomyopathy -more prone to dehydration due to dec fluid intake, protein intake, meds such as diuretics. If vomiting and diarrhea will become dehydrated quickly -urosepsis more frequent. Have dim sensations of burning and urgency that recognizes infection. Also catheters 17. 7. State four pathophysiologic changes that occur with MODS; uncontrolled systemic inflammation tissue hypoxia unregulated apoptosis microvascular coagulopathy

8. Describe the collaborative management of the patient with MODS. Infection control measures, talk to cardiologist, urologist, pulmonologist; in other words, experts in specific organ systems.

know the septic shock protocol 4. septic: prevention!!; give antibiotics within one hour of MD order Goal: optimize O2 delivery and decrease O2 consumption A. Optimize oxygen delivery 1. O2 2. fluid resuscitation to optimize preload B. Drugs: 1.Positive inotropes: dopamine, dobutamine, milrinone 2.Afterload reduction C. Decrease O2 consumption: decrease total body work, decrease pain, anxiety, temperature

from SIM questions: 2.Nursing priorities in the care of the patient with sepsis and septic shock: 1. Eliminate infection. 2. Support tissue perfusion/circulatory volume. 3. Prevent complications. 4. Provide information about disease process, prognosis, and treatment needs.  Monitor neurological status, including mental state and LOC  Monitor BP, HR, rhythm, pulse quality, CVP, PAP, CO  Monitor color and character of skin  Monitor ABGs, blood counts, clotting times, platelet counts  Monitor RR, rhythm and breath sounds  Monitor temp Q2 hrs  Monitor I&O; report < 30 ml/h  Give antibiotics IV  Give fluids IV (NS, LR) to increase BP  Nutrition  Drugs, such as dopamine or norepinephrine (which cause blood vessels to narrow), may be needed to increase blood flow to the brain, heart, and other organs.  Oxygen given through a mask, through nasal cannula, or, if a breathing (endotracheal) tube has been inserted, through that tube. If needed, a mechanical ventilator is used to help with breathing. Referenced from LeMone and Burke

7. Identify the treatment guidelines currently recommended for the management of sepsis and septic shock. The stop sepsis campaign has a "6 hour bundle" that includes the following rapid treatment strategy. "A "bundle" is a group of interventions related to a disease process that, when executed together, result in better outcomes than when implemented individually. The individual bundle elements are built on upon evidence-based practices. The science behind the elements of a bundle is so well-established that their implementation should be considered a generally accepted practice: Bundle Element 1: Measure serum lactate. Bundle Element 2: Obtain blood cultures prior to antibiotic administration. Bundle Element 3: Administer broad-spectrum antibiotic within 3 hours of ED admission and within 1 hour of non-ED admission. Bundle Element 4: In the event of hypotension and/or serum lactate >4 mmol/L: a. Deliver an initial minimum of 20 mL/kg of crystalloid or an equivalent b. Apply vasopressors for hypotension not responding to initial fluid resuscitation to maintain mean arterial pressure (MAP) >65 mm Hg * Treat Hypotension and/or Elevated Lactate with Fluids * Apply Vasopressors for Ongoing Hypotension Bundle Element 5: In the event of persistent hyptension despite fluid resuscitation (septic shock) and/or lactate >4 mmol/L: a. Achieve a central venous pressure (CVP) of >8 mm Hg b. Achieve a central venous oxygen saturation (ScvO2) > 70% or mixed venous oxygen saturation (SvO2) > 65% " http://www.survivingsepsis.org/implement/bundles

12. Discuss the importance/rationale for central line placement in a patient with sepsis. A central line is an intravenous catheter or IV placed into a large vein. A central line is needed to give the medical team access to a large vein that can be used to give fluids, measure the amount of fluid in the body, or to give medication that might be irritating to smaller veins. Having a central line allows for the necessary interventions and monitoring needed for favorable outcomes for sepsis patients.

Case Scenarios 1. Your patient is a 67 yo male admitted with severe left flank pain. He has had pain for 3 weeks but it is now severe and sharp. His VS are: BP 84/52, HR 134, atrial fibrillation, RR 28, shallow, alert, anxious, c/o 8/10 pain. CT reveals left renal mass and large hematoma around left kidney. What oxygenation needs does he have? What type of shock state is present? What management is indicated? 2. Your patient is an 85 yo female admitted with sepsis. What is sepsis? What interventions are indicated? 3. You are caring for a 22 yo MVC multiple trauma injury patient. What life- threatening complications is he at risk to develop?

I. OXYGENATION: skipping this for now. A. Def: multisystem integration and coordination in intake, delivery, and consumption of oxygen for energy metabolism; which systems are involved?

B. Pulmonary gas exchange 1. ventilation, diffusion, perfusion 2. conditions that impair gas exchange a. ventilation impairment: examples? b. diffusion impairment: examples? c. Perfusion impairment: examples?

C. Oxygen Delivery: cardiac output

D. Oxygen Consumption

1. aerobic metabolism

2. anaerobic metabolism

3. conditions that alter: increased or decreased

II. SHOCK STATES: shock means inadequate perfusion/oxygenation, meaning both CV and resp systems. If your cells are w/o oxygen, they go into anerobic metabolism. That’s why we check lactic acid levels to assess sepsis—they check Q4 hrs until its less than 2. Lactic acid also means you’re in metabolic acidosis. Check lactic acid levels for anaerobic metabolism: prevent metabolic acidosis

A. Def: inadequate oxygen delivery to meet cellular oxygen demand

B. Hypovolemic Shock States: not enough volume, r/t hemorrhage, GI bleed, burns. Fill the tank!

1. causes: decreased fluid volume: hemorrhage, burns [b/c of evap of water without skin there, 3rd spacing], diarrhea, third spacing leads to decreased CO, impaired oxygen delivery, inflammation leads water into a certain area post damage, infection, etc. Lots of talk about inflammation, cardinal signs, mediators, purpose is healing, cell mediation, etc etc. If we don’t provide enough blood to a cell, it becomes ischemic—if we have a post op pt with inflammation that can lead to shock. ischemic means not enough blood supply and therefore O2, but it is still reversible [infarct is permanent]. 2. increased size of intravascular compartment means decreased venous return: vasodilation from neurogenic shock [spinal cord injury, low sympathetic tone], anaphylactic shock, and septic shock. Sepsis is the most common that we’ll see. Pg 372.

3. pathology of septic shock: know this! Pg 372. Cascade of events: microbe/infection. This is why we are pressured to minimize infex. Endotoxins [esp from gram negtive] cause immune rxn, holes are poked in the capillary walls, vasodilation, blood leaks out of the capillaries and you lose blood.

At risk: Hospitalized people b/c: Chronic illness dec immune function Exposed to other pathogens

 Sepsis: a serious bodywide response to bacteremia or another infection.  Severe sepsis: sepsis associated with acute organ dysfunction  Septic shock: life-threatening low blood pressure (shock) due to sepsis altered fluid volume r/t vasodilation, increased capillary permeability, and maldistribution of fluid volumer. [systemic response to gram -negative and gram -positive bacteria, fungi, or viruses. Endotoxins stimulate release of cytokines. This produces vasodilation and increased capillary permeability, which reduces venous return and CO. There is a maldistribution of circulating blood volume. Some organs get more blood than they need, others get less] 4. Why is myocardial depression almost always present in patient with septic shock despite initial rise in CO: The inflammatory response to sepsis and septic shock produces chemicals that depress the heart. Myocardial dysfunction is an important component in the hemodynamic collapse induced by sepsis and septic shock. A series of inflammatory cascades triggered by the inciting infection generate circulatory myocardial depressant substances, including TNF-α , IL-1 β , PAF, and lysozyme. Their effects are partly mediated through NO generation. How NO depresses cardiac contractility is largely unknown. The research into the pathophysiology of septic myocardial depression will hopefully yield potential therapies. Until then, volume resuscitation, with inotropic and vasopressor support, is the current standard of care to restore tissue perfusion (Wong & Kumar , 2006. Myocardial Depression in Sepsis and Septic Shock. Sepsis, 2nd Edition, Springer New York).

5. Discuss the cascade of host inflammatory responses that produce the major detrimental effects seen in sepsis due to gram-negative bacteria. Viruses and fungi can cause sepsis, but more often bacteria do. Gram (-) bacteria contain endotoxins [lipid A, within a lipopolysaccharide] just inside their membranes. As the host immune response lyses these cells, the endotoxin is released. The immune system responds to these events with the following cascade: 1: Cytokines are released [bradykinin, complement, interleukin, tumor necrosis factors, etc]--these cause endothelial cell damage and cause the blood vessels to 'leak' fluid. The endothelial cells are also 'activated' which causes these things: a; vasoconstriction [thromboxane, endothelin, angiotensin II, etc] b; vasodilation: [prostanoids, nitric oxide] Both these things impair vascular smooth muscle tone c; inc endothelial permeability, fluid leaks to the interstitial zone causing inc interstitial edema and less fluid in the blood vessels [intravascular hypovolemia] d; Coagulation cascade [platelet adhesion and aggregation, formation of microemboli-- meaning little clots in little capillaries and less clotting factors in other circulation.] e; Aggregation and adhesion of lympohcytes that damage healthy tissue--well that' not good, because your immune cells are globbing together and sticking to something and causing damage, instead of going out and fighting off bacteria. And then....that causes more clotting factors reacting to damage. And then you have a lot less circulating blood volume. You therefore have low CO, low perfusion, tissue hypoxia, which then begets anaerobic respiration and lactic acid buildup. You also get "maldistribution of circulating blood volume" meaning blood is shunted to certain vital organs and away from others (esp skin, lungs, and kidneys). (Wagner, p 372) In the end, the bacteria is not your problem-- it's the immune system freaking out and causing trouble that kills you.

C. Transport Shock States: problem w/ not enough ‘transport’, meaning hemoglobin. 1. decreased supply of Hb to carry O2 to tissues; 2. causes: anemia, hemorrhage, carbon monoxide toxicity We don’t transfuse pts too much b/c of risk of transfusion, but it’s a moment to get on the phone with the MD. Check H&H. Standard is to allow Hb to be low. Make sure getting enough O2 to maintain saturation. Give erythropoietin to stimulate RBC production.

D. Obstructive Shock States: beware of our trauma pts 1. mechanical barrier to blood flow that blocks O2 delivery 2. causes: pulmonary embolism, tension pneumothorax [(air in the pleural space, complication of chest tube: trauma pts) life threatening, secondary to ventilation], cardiac tamponade [fluid or blood in the pericardial shock], fractured ribs that injure the lungs---any thing that collapses the lungs….tension pneumo causes medastinal shift, something else, and then you have no room in the thorax for venous return—no blood going in or out.

E. Cardiogenic Shock States: happening less. 1. cardiac dysfunction causes impaired O2 delivery 2. causes: heart failure, AMI, cardiomyopathy [big ol heart, from HF or just regular cardiomyopathy], ruptured muscle, heart failure could lead to cardiogenic shock.

III. PHYSIOLOGIC RESONSE TO SHOCK: our body likes to not die, so it does a lot to avoid death—sometimes not enough. A. SNS flight or fight response B. Stages: Initial, Compensatory, progressive, refractory C. Clinical Findings: result of impaired oxygenation and neuroendocrine and CV compensatory mechanisms

Book Notes: Progression of Shock: p 375 initial: low CO and tissue perfusion result in cells starting anerobic respiration--leading to buildup of lactic acid and metabolic acidosis Compensatory: neuroendocrine response to increase CO and O2 delivery.

Sheet Margi Gave us Hypovol shock: post MVA with splenic rupture. Early signs: pale skin, thready pulses, low BP. HR incr to maintain CO, tachypnea too. Blood shunts to vital organs; so cool clammy skin, low UO, low bowel sounds. Yes, this can lead to ischemic renal failure. Rx: fill the tank, IVF, hopefully LR. Don’t give pressors, b/c vasodilation is not the problem. Send in blood transfusion. Oxygen: how about send it all via non re-breather. You might have to put him on a vent momentarily.

1. vs: 2. labs: lactate, ABGs, CBC Lactic acid: normally <2, septic shock looks like 7.5. 3. hypovolemic: what symptoms? 4. transport: what lab changes? 5. obstructive: pulses paradoxus, dyspnea with PE 6. cardiogenic: left heart vs right heart

Septic Shock: what is the requirement to qualify for sepsis? Temp >38 or <36 HR >90 RR >20 pCO2 <32 WBC > 12000 or <4000 This could be your pt, and you need to move quickly so that it doesn’t become severe sepsis: organ dysfunction. Severe sepsis is more of the same above.

Septic shock: hypoTNSn w/o response to fluids.

IV. MANAGEMENT OF SHOCK STATES: Goal: optimize O2 delivery and decrease O2 consumption A. Optimize oxygen delivery 1. O2 2. fluid resuscitation to optimize preload B. Drugs: 1.Positive inotropes: dopamine, dobutamine, milrinone 2.Afterload reduction

C. Decrease O2 consumption: decrease total body work, decrease pain, anxiety, temperature D. Hypovolemic shock: 1. restore fluid volume, find source of fluid loss 2. neurogenic-stabilize spine 3. anaphylactic: maintain airway, support BP, drugs 4. septic: prevention!!; give antibiotics within one hour of MD order 5. transport: restore O2-carrying capacity of RBCs 6. obstructive: remove mechanical barrier; heparin with PEs 7. cardiogenic: decrease MVO2 & improve O2 supply; thrombolytics, PTCA

Overressucitation: means you filled the tank too much—too many liters in field, in ER in ICU, and the RNs need to make sure to keep track of it.

Margis pt: had diverticulitis and went home on abx. Then the divurticulum ruptured, meaning the peritoneum/viscus ruptured, in ER in septic shock. They did a CT of abd and found a mass, sent her for a exploratory lap, and found a L of stool in her peritoneum. Her lactic acid was 7.5, 5.9 later in ICU, then 6.4. WBC 5.4 [5-10]—she’s immune comp b/c of her age, her WBC count should be through the roof after diverticulitis after 2 weeks. H and H high b/c of hypovolemia. ICU: was ventilated b/c we don’t want her to have to do the tedious work of breathing— she is too likely to die of septic shock. Septic: toxins poking holes in the vasculature, intravascularly hypovolemic. Fill her tank; IVF at 200/ hr. She was given sodium bicarb in the NS to manage the lactic acidosis. Her bicarb was 15; she was low. She did go into ARF w/ 15 mL UO per shift. Still need to address the abx and the infection. Pressors: fix the vasodilation with Levophed [norepinephrine] on a drip, she was at 16 mcg per minute. The goal was a systolic BP of >90. Needs: pain management, her abd was so edematous they couldn’t close the surgery, she needs morphine IVP, but make sure you don’t drop her blood pressure so give it slowly. Sedation: usually but she was too little O2 to the brain anyway and didn’t need it. ARF: yes we care that she’s in ARF, but the kidneys are not the priority. They are being cut off from blood. We need to fill the tank, so we don’t care about UO. Also need to know if the family is aware that she could die tonight. Bowel sounds? No we don’t expect them. I care about Lung Sounds, BP Q 15 mins. Lung sounds; I am on watch for crackles and pulm edema. Peripheral circulation, esp feet. Cold feet, mottled skin on LE’s, no palpable but Doppler pedal pulses, etc b/c of shunting blood to core. Also levophed will do that. Want to titrate down the levophed as much as possible b/c its such a potent vasoconstrictor. Arterial line did not agree with the BP cuff—Margi checked the art line and confirmed that the art line is really working. V. MODS: another way of looking at sepsis. A. Def: syndrome of progressive dysfunction of 2 or more organ systems Our example: this woman was in GI and Renal failure, CV. Lots of endothelial damage [inside blood vessels] sets off all these endothelial mediators. Endothelial damage starts this cascade of micro coagulation—bunched up cells in the micro circulation, but not enough clotting factors in the major circulation. DIC is part of this whole thing—also part of SIRS. Little bitty clots in the little bitty capillaries. Primary and secondary MODS;

B. Local inflammatory response 1. endothelial damage 2. mediators 3. coagulation

D. MODS: Multi Organ Dysfunction Syndrome ” Multiple organ dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. It usually involves two or more organ systems.[1]” {wiki} 1. characteristics: uncontrolled systemic inflammation, hypoxia, unregulated apoptosis, microvascular coagulopathy 2. two pathways: primary MODS & secondary MODS 3. organ failure: lungs, CV, neuro, renal, hepatic, GI 4. management:

C. Systemic Inflammatory Response Syndrome (SIRS) same criteria as sepsis but there’s no pathogen—sepsis is SIRS with a pathogen. “In medicine, systemic inflammatory response syndrome (SIRS) is an inflammatory state of the whole body (the "system") without a proven source of infection.” (wiki)

1. Def: systemic response to event: Causes of SIRS

* Severe trauma * Surgery, complication of * Adrenal insufficiency * Pulmonary embolism * Complicated aortic aneurysm * Myocardial infarction * Hemorrhage * Cardiac tamponade * Anaphylaxis * Drug overdose * Burns * Acute pancreatitis * Immunodeficiency (such as AIDS[6]) * Infected Skin lesion [7]

[edit] Relation to cytokine storm

SIRS can be considered to be a subset of cytokine storm, a general term (not commonly used in clinical medicine) for cytokine dysregulation.

2. what clinical findings are present? Criteria for SIRS were agreed upon in 1992.[1] SIRS can be diagnosed when two or more of the following are present:[2][3][4][5] * Heart rate > 90 beats per minute * Body temperature < 36 or > 38°C * Tachypnea (high respiratory rate) > 20 breaths per minute or, on blood gas, a PaCO2 < 4.3 kPa (32 mm Hg) * White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 109 or > 12 x 109 cells/L), or the presence of greater than 10% immature neutrophils. [wiki]