NURS-400 Exam 2: Shock/Sepsis/Mods (A Crisis in Tissue Perfusion/Oxygenation)

What Really Counts: Tissue Perfusion - FLOW!

1.) Blood Flow = Pressure gradient/Resistance → So BP looks good, but downstream tissues are flow-starved. 2.) Critical Closing Pressure: Point at which vessel collapse and flow stops. → Normal: 20 mmHg. → Sympathetic stimulation: 60 mmHg.

Hypo-dynamic Phase: What does it look like?

1.) Vasoconstriction, Ventricular Failure: → Low CO/CI - Low LVSWI and High RAP/PAP. → Low BP, Low pulse pressure, weak pulse - High SVR. → Pale, cool, clammy skin. → Low paO2/SaO2, rales, rhonchi, wheezes - respiratory acidosis. 2.) Compensation: → HR. → Or low temperature. 3.) Inadequate tissue oxygenation: → Or low SVO2, high lactate, high base deficit, low HCO3^-, and metabolic acidosis.

Cellular Oxygen Use (2)

% increase with nursing activities: 1.) Dressing change - 10% 2.) Electrocardiogram - 16% 3.) Agitation - 18% 4.) Physical Examination - 20% 5.) Visitor (prob. restriction) - 22% 6.) Linen change - 22% 7.) Bath - 23% 8.) Chest x-ray examination - 25% 9.) Suctioning ETT - 27% 10.) Position change - 31% 11.) Chest physiotherapy - 35% 12.) Weighing on sling scale - 36% Clustering care is the worst thing you can do for these patients as it puts an incredible high oxygen demand on their system, and they can already not meet the demands of there body because that is the very definition of shock. We need to space out our care. It will not be obvious what the effects of these activities are as it happens at the cellular level, so you just have to be aware of it.

Cellular Oxygen Use (1)

% increase with various conditions: 1.) Fever - 10% 2.) Skeletal injuries - 10-30% 3.) Work of breathing - 40% 4.) Severe infection - 60% 5.) Chest trauma - 60% 6.) MODS - 20-80% 7.) Shivering - 50-100% 8.) Sepsis - 50-100% 9.) Head injury sedated - 89% 10.) Burns - 100% 11.) Head injury not sedated - 138%

Guidelines: Setting Goals of Care

1.) Address goals of care no later than within 72 hours of ICU admission. 2.) Discuss goals of care and prognosis with patients and families. 3.) Incorporate goals of care into tx and end-of-life planning, utilizing palliative care principles where appropriate.

Guidelines: Antibiotics (Need to Know!)

1.) Begin IV antibiotics therapy within 1st hour. → After 1st hour, each hour delay x6hrs associated with average decrease in survival of 7.6%. 2.) Empiric broad-spectrum therapy: 1 or more drug(s) to cover all likely pathogens. → Narrow therapy once culture and sensitivities completed or clinical improvement. 3.) Empiric combination therapy (2 different classes) aimed at most likely pathogens for shock only. → De-escalation to single tx within first few days in response to improvement.

How do we know?

... if our interventions to support DO2 are effectively restoring adequate cellular oxygenation. We cannot just provide intervention and assume it is working you need to re assess!

Guidelines: Vasoactive Meds (Need to Know!)

1.) 1st choice: Norepinephrine (Levophed). 2.) May add vasopressin or epinephrine if needed. 3.) Dopamine as alternative only in highly selected pts (low risk of tachy arrhythmias and absolute or relative bradycardia). 4.) Dobutamine if persistent hypoperfusion despite adequate fluid and vasopressors. 5.) Arterial line placement in all pts requiring vasopressors. 6.) Do NOT use low dose dopamine for renal protection. FDA approval of first new drug for use in septic shock in over a decade: Angiotensin II (Giapreza).

Sepsis: Post-Discharge Outcomes

1.) 2 years and beyond: → Higher morality and pooper quality of life. 2.) 2 years after hospital discharge: → Higher mortality, pain, readmissions, functioning decline.

Trendelenburg: Latest Research Review

1.) 20 studies - Primarily observational. 2.) Predominant effects: → Increased preload, SV & CO/CI lasting about 1-3 minutes in healthy population and 3-5 min in acutely ill. → No change in BO. 3.) Negative effects: → Pounding vascular headache. → Progressive dyspnea - decreased resp expansion. Take Home Message: Probably not useful - effects small and unsustained.

Compensation

1.) ANS Stimulation: Activation of the alpha and beta receptors. → Increased sympathetic tone leads to increased HR/contractility. → This is why you see the symptoms of tachycardia, increased DBP, cool & clammy, mottling, and decreased capillary refill. 2.) Hormonal Stimulation: → Epi and norepi leads to and augments the ANS response. → ACTH leads to glucocorticoids leads to increased glucose. → Renin-angiotensin-aldosterone leads to ?? → This leads to all the same symptoms that you have above plus fluid retention, decreased urine output, and decreased K+. 3.) Chemical Stimulation: → Hyperventilation leads to respiratory alkalosis. → This is to try and increase the oxygen level in the blood. Notice: Many of the early "S&S" of shock are actually signs of attempted compensation. They do not tell you what the problem is, they tell you that your patient is in trouble.

MODS: Specific Signs & Symptoms

1.) CV: Cardiovascular Failure → Hypotension despite adequate volume status - "vasopressor dependent." → S&S of Congestive HF (Increased CVP/PAOP). → Metabolic acidosis: Lactate levels 1.5 x nl. This is because it is evidence of inadequate tissue perfusion. 2.) Pulmonary: Acute Respiratory Failure or ARDS → PaO2/FiO2 (p/F) ratio less than or equal to 250. 3.) Renal: Acute Renal Failure → UO < 0.5 ml/kg/hr x 2hr despite fluid resuscitation. → Increased creatinine and BUN, decreased GFR.

Progressive Organ Dysfunction

1.) CV: Endothelial injury ▻ Microvascular thrombosis. Cardiovascular failure. 2.) Pulmonary: Acute respiratory failure & ARDS. 3.) Renal: Acute kidney injury (AKI). 4.) Neuro: CNS dysfunction, SNS & thermoregulatory failure, cardiac & respiratory depression. 5.) Hemat: DIC, thrombocytopenia. 6.) GI: GI failure, liver failure, pancreatic failure.

Pathophysiologic Consequences (continued again)

1.) Coagulopathy (consumptive coagulopathy - if you clot a lot you are not going to have much clouting factors left so you are going to start bleeding out. 2.) Cellular Metabolic Derangement. → Mitochondrial dysfunction (bioenergetic failure). → Apoptosis - propagates cycle (becomes this storm that propagates itself that we cannot stop). 3.) Cellular hypoxia - failure of ion transport. → Cellular functional impairment. → Cell swelling and cell death - MODS. 4.) Intractable depletion of ATP - irreversible shock.

Latest Research Findings: Type of Fluid

1.) Colloids (IV fluids that have an osmotic pressure to them; they should draw in fluid back into the intravascular space and good for third spacing; albumin and plasmanade) vs. Crystalloids (IV solution that do not have osmotic pressure NS, ½NS, LR): → Safe study: Similar outcomes, regardless of baseline albumin. → Why give colloid if they are more expensive and have more complications so crystalloids won! 2.) Colloid vs. Colloid: → No difference. 3.) Hypertonic saline or Hyperoncotic fluids: → No benefit. Take Home Message: Crystalloids work

Pathophysiologic Consequences

1.) Diffuse endothelial injury. → Your vasculature is one continuous sheath so once you activate the endothelium in one place it can quickly spread to the rest of the body. 2.) Microvascular thrombosis. 3.) Massive vasodilation (due to cytokines) - relative hypovolemia. 4.) Increased capillary permeability. → Absolute intravascular hypovolemia. → Interstitial edema - lungs and tissue. Inadequate O2 delivery (DO2) to the cells.

Guidelines: Nutrition (continued)

1.) Do not use routine GRV monitoring unless feeding intolerance or high risk of aspiration. 2.) Post-pyloric feeding tube if feeding intolerance or high risk of aspiration. 3.) Pro-kinetic agents if feeding intolerance.

Guidelines: Nutrition

1.) Early oral or enteral feedings (trophic or full) rather than either complete fasting or only IV glucose. 2.) Do NOT use TPN if can be fed enterally. 3.) 1st 7 days: Use enteral feeds and IV glucose rather than TPN alone or in conjunction with enteral when early enteral feeding not feasible. 4.) Do NOT use omega-3 fatty acids, arginine, glutamine, or IV selenium.

Progressive Stage

1.) Endothelial (walls of the blood vessel; takes them oxygen to maintain vascular tone and they cannot do this is shock so the patient vasodilates) and epithelial hypoxia leads to vasodilation and increased vascular permeability which leads to intravascular hypovolemia. 2.) Tissue hypoxia → Release Inflammatory mediators → Systemic Inflammatory Response Syndrome (SIRS). → Vasodilation and increased vascular permeability leads to tissue edema and decreased tissue perfusion. → Microcirculatory impairment and cell damage leads to perpetuation of shock cycle.

Guidelines: Fluid Therapy (Need to Know!)

1.) Fluid of Choice = Crystalloids. 2.) Continue fluid challenge technique as long as hemodynamic factors continue to improve. 3.) Add albumin when substantial amounts of crystalloids necessary. 4.) Do not use hydroxethyl starches (cause coagulopathy).

Other S&S of Sepsis From Earlier Diagnostic Criteria for Sepsis

1.) General variables: → Temp >38.3C or <36C. → HR >90. → Significant edema or + fluid balance (>20 ml/kg in 24h). → Hyperglycemia (>140mg/dl) if no diabetes. → Tachypnea. → Altered mental status. 2.) Inflammatory variables: → Leukocytosis (>12,000 uL^-1), Leukopenia (<4,000) or normal WBC count with >10% bands. → Increased plasma C-reactive protein (lab test that indicates inflammation; people that have elevated CRP that is as high of a risk factor for cardiac disease as high cholesterol; isn't that valuable in sepsis). → Increased plasma procalcitonin (biomarker of bacterial infection). Now we know if the infection is bacterial, viral, or fungal. 3.) Tissue perfusion variable: → Decreased capillary refill or mottling.

Pathophysiologic Consequences (continued)

1.) Gut injury (endothelial & epithelial injury with increased permeability; cytokines; hypoperfusion). → Disruption of intestinal mucosal barrier releases pro-inflammatory substances - propagates inflammatory response and shock syndrome (SIRS). → Most of your immune tissue is in the gut. So, there are pro-inflammatory substances the get into the blood stream and propagate and septic shock reaction throughout the entire body . 2.) Myocyte dysfunction (secondary to cytokines and hypoxia) - impaired ventricular contractility. 3.) CNS activation: At a time when your O2 delivery is impaired you O2 demand goes sky high! → Hypermetabolism. → Selective vasoconstriction of splanchnic bed.

MODS: Signs & Symptoms

1.) Hematologic: Coagulation Abnormalities → Thrombocytopenia (platelets < 100,000). → DIC - Increased D-dimers, APTT, PT, INR, etc. → Bleeding or bruising. 2.) Neuro: CNS dysfunction, cerebral edema → Lethargy, confusion, psychosis. → Decreased LOC, coma. → Thermoregulatory failure. 3.) GI/Hepatic: → Increased LFTs, Jaundice, decreased albumin/transferrin. → Hyperbilirubinemia (> 4 mg/dl or 70 mmol/l). → Cholecystitis/Pancreatitis. → Ileus; Intestinal ischemia or infarction; GI bleed.

Types of Shock

1.) Hypovolemic. 2.) Cardiogenic. 3.) Distributive.

Guidelines: Source Control

1.) Identify specific anatomic site of infection and intervene as rapidly as possible. 2.) If intravascular devices are potentially the source, promptly remove after establishing other vascular access.

Septic Shock: Hyper-dynamic Phase

1.) Vascular response to the biochemical mediators is primarily vasodilation. 2.) Cardiac output rises significantly.

Pathophysiology of Sepsis

1.) In response to this infection the macrophages and the white cells get activated and start adhering to the endothelium of the blood vessels. The white cells stick and roll along the blood vessels. 2.) The macrophages and white cells release biochemical mediators, also called cytokines into the blood stream (countless cytokines). 3.) Once they get released they cause the monocytes and the endothelial tissue of the blood vessels to release tissue factor, and tissue factor makes you clot! This is the major pathway that is going to cause many of the problems we see. Now the immune response is going to cause a coagulation response and form clots everywhere in your body. 4.) It also releases stuff that suppresses fibrinolysis so that we don't break down the clots.

Shock Syndrome: Etiology

1.) Inadequate volume: Hypovolemic ("Cold [ineffective tissue perfusion] & Dry [dry in intravascular space]"). 2.) Inadequate pump: Cardiogenic ("Cold [ineffective tissue perfusion] & Wet [intravascular hypervolemia]". 3.) Maldistribution of Volume: Distributive ("Warm") → We have adequate volume inside the body but it is in the wrong place. It is out in the third space or interstitium instead of the vascular space. → Caused primarily by vasodilation so they are actually warm! Notice that both hypovolemic and cardiogenic are "cold" while distributive is warm - a very distinctively different type of shock.

Sepsis

1.) Incidence = >700,000 admissions/yr. 2.) 11th leading cause of death in the US. 3.) 250,000 deaths per year in the US 4.) 11 million deaths worldwide; 20% of all global deaths. Bacteremia is if you have bacteria in the blood which is not sepsis. If you have the presence of bacteria or virus in the blood it is not sepsis, sepsis is a different animal.

Mortality in Sepsis

1.) Leading cause of in-hospital death in the US. 2.) 1 in 3 patients who die in the hospital have sepsis at the time of death. 3.) Account for 50-80% of ICU deaths. 4.) Current mortality rate of 23-50% (dependent on where you get care).

Hypoperfusion w/o hypotension - how can that be?

1.) Macro-circulation: → Arteries, veins. → Assessment: BP is a determinant (MAP; you have to have an adequate MAP in order to achieve peripheral tissue perfusion, but just because you have an adequate MAP it does not mean adequate peripheral perfusion is guaranteed), but not an indicator of peripheral perfusion. ⤷ BP. 2.) Micro-circulation: This is where gas exchange takes place. This helps you know if the patient converts from aerobic to anaerobic metabolism. → Arterioles, capillaries, venules. → Assessment: Indicator of the adequacy of tissue O2. ⤷ Lactate. ⤷ Base deficit. ⤷ HCO3- ⤷ SvO2/ScvO2 (direct measures of tissue oxygenation; indicators of the adequacy of tissue O2).

Pathophysiology of Sepsis (continued)

1.) Macrophages and neutrophils synthesize inflammatory and regulatory cytokines. 2.) Neutrophil-endothelial cell adhesion. 3.) Inflammatory cytokines (TNF-a, IL-1, IL-6) - stimulate monocytes and endothelium to release tissue factor. 4.) Tissue factor initiates clotting cascade and release of thrombin to form a fibrin clot. 5.) Thrombin impairs fibrinolysis. → With cytokines stimulates platelets and endothelium to release plasminogen-activator inhibitor (PAI-1). → Activates thrombin - activatable fibrinolysis inhibitor (TAFI). 6.) Thrombin stimulates multiple inflammatory pathways. 7.) Endothelial injury - decreased thrombomodulin levels - impaired conversation of protein C to activated form.

Guidelines: Sedation and Analgesia

1.) Minimized sedation in mechanically ventilated patients, intermittent or continuous, with specific titration end points.

Sepsis: Pathophysiology

1.) Multifaceted, dysregulated host response to an infecting pathogen (may be amplified by endogenous factors - patient characteristics [obesity, age, immune function, history]). 2.) Early activation of pro and anti inflammatory responses. → This is why we do not run for steroids! → The immune system has a pro and anti inflammatory response that usually play in balance of each other much like the SNS and ANS. When we jump in with something like steroids it worsens this balances and increases mortality rates. → We do not totally understand this response and when we go and muck it up it ends up worse! 3.) Major changes in non immunologic pathways: → CV, neuronal, autonomic, hormonal, bioenergetics, metabolic, coagulation. 4.) Significant biological & clinical heterogeneity in those affected (acts differently and looks differently in different people). → Age, gender, race, genetics, comorbidities, concurrent injuries/surgeries, meds, source of infection.

Sepsis: Key Nursing Priorities (Need to Know!)

1.) Prevention: EBP to reduce nosocomial infection. 2.) Early identification. 3.) Continual observation for progression. 4.) EBP to prevent further infection. → Immunosuppression - resurgence in opportunistic infections at 15 days and beyond. 5.) EBP to prevent complications of immobility, etc. 6.) Early rehab to reduce duration of delirium (sepsis-associated encephalopathy).

MODS - Multiple Organ Dysfunction Syndrome

1.) Progressive physiologic failure of 2 or more separate organ systems. 2.) Results form either direct insult (primary MODS) or SIRS (secondary MODS). Often is a combination of the two! 3.) Mortality is related to number of organ systems. These organs are not failing independently. This is death that is occurring on a gradual level when organs are failing simultaneously. This shows that the organs are not being adequately oxygenated throughout the body and is showing by organs beginning to fail. → 2 or more = 54%. → 5 = 100% The major cause of death in ICUs. Because of the global ineffective tissue perfusion that is taking place!

Guidelines: Glucose Control

1.) Protocalized approach commencing when 2 consecutive BG levels are >180 mg/dl. 2.) Target BG: less than or equal to 180 mg/dl. 3.) Monitor sugars q1-2h, then q4h when stable. 4.) Use caution interpreting point-of-care testing of capillary blood as may not be accurate. 5.) If arterial catheter present, use arterial blood rather than capillary blood for testing.

Guidelines: Blood Products

1.) RBC transfusion only when hgb <7.0 g/l (unless myocardial ischemia, severe hypoxemia, acute hemorrhage). 2.) Platelet administration of count </= 10,000mm^3 in absence of apparent bleeding or </= 20,000 if significant risk of bleeding. → Higher counts (>50,000) advised for active bleeding, surgery, or invasive procedures. 3.) Do NOT use: → Erythropoietin. → FFP to correct lab clotting abnormalities. → Antithrombin therapy.

Guidelines: Antibiotics

1.) Reassess therapy daily for potential de-escalation. → When the culture comes back we need to realize what antibiotic will be more helpful! Leaving them on an antibiotic that is ineffective or they have a fungal infection instead is harmful! 2.) Duration 7-10 days for most. 3.) Use procalcitonin levels to support shortening duration or discontinuation in patients with no subsequent evidence of infection. 4.) Do not use in patients with severe inflammatory states of noninfectious origin.

Guidelines: Screening/Diagnosis

1.) Screening: → Hospital-based performance improvement program for sepsis, including sepsis screening for acutely ill, high risk patients. 2.) Diagnosis: → Obtain cultures before beginning antibiotics if doing so results in no substantial delay in start of antimicrobials. → Always include at least two blood cultures (aerobic and anaerobic).

Surviving Sepsis Campaign (SSC): An International Effort (1991-2018)

1.) Sepsis is defined as life-threatening organ dysfunction (difference between bacteremia and sepsis) caused by a dysregulated host response to infection. 2.) In lay terms, sepsis is a life-threatening condition that arises when the body's response to an infection injures its own tissues and organs.

Criteria for Sepsis-Induced Organ Dysfunction (Still Recommended for Use)

1.) Sepsis-induced hypotension (SBP <90, MAP <70, or decrease in SBP >40mm).* 2.) Lactate >2mmol/L.* 3.) Acute Lung Injury with paO2/FiO2 <250 in absence of PNA as infection source or <200 in presence of PNA as infection source. 4.) UO <0.5ml/kg/hr x greater than or equal to 2hr despite adequate fluid resuscitation. 5.) Creatinine >2.0mg/dl (176.8 umol/L). 6.) Platelets <100,000 uL. 7.) Bilirubin >2mg/dl (34.2 umol/L). 8.) Coagulopathy (INR >1.5).

The Third International Consensus Definitions for Sepsis and Septic Shock

1.) Sepsis-induced organ dysfunction may be occult so it's presence should be considered in any patient presenting with infection. 2.) EARLY ID - Patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital can be promptly identified at the bedside with qSOFA, i.e., alteration in mental status (brain failure), systolic blood pressure less than or equal to 100mmHg, or respiratory rate greater than or equal to 22/min. SSC: qSOFA does not define sepsis! Simply identifies those at high risk for ICU >3 days or death.

The Third International Consensus Definitions for Sepsis and Septic Shock (continued)

1.) Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. 2.) Patients with septic shock can be identified with a clinical construct of sepsis with persisting hypertension requiring vasopressors to maintain MAP >/= 65 mmHg and having a serum lactate level >2 mmol/L (18 mg/dL) despite adequate volume resuscitation. With these criteria, hospital mortality is in excess of 40%.

Shock: Management (continued)

1.) Support cellular O2 supply (delivery). 2.) Assess adequacy of tissue perfusion DO2 & VO2: → Lactic acidosis (shows that our interventions are failing; use it as a measurement for the effectiveness of our interventions). → SvO2/ScvO2. → Organ function (a little late in the game; this is why we measure UO so closely because if it drops we know we are losing the battle of cellular oxygenation). The bottom-line: Are we succeeding at the very basic level of sustaining life - tissue oxygenation? Sodium bicarbonate is not the answer and is not recommended. We have not been able to develop a way to measure VO2, but have figured out a way to measure what is coming back! SO if we know what we sent down we can measure what came back and we can know what got used.

Guidelines: Mechanical Ventilation of Sepsis-Induced ARDS

1.) Target Vt = 6ml/kg/predicted body weight. 2.) Plateau pressures less than or equal to 30cm H2O. 3.) Higher vs. lower PEEP if mod-severe ARDS. 4.) Prone positioning if paO2/FiO2 ratio <150. 5.) HOB elevated 30-45 degrees to decrease aspiration and VAP. 6.) NMB x 48 hours or less for established ARDS and paO2/FiO2 < 150.

Cellular O2 Supply (continued)

1.) The arterial oxygen content (CaO2) is the amount of O2 per 100ml of blood (dl) available to the tissues. → We carry oxygen dissolved (paO2) and bound. → Both are absolutely essential because what is dissolved in necessary for perfusion across the capillary cellular membrane so that oxygen can diffuse across the capillary and into the cell itself. The bound oxygen is all that oxygen storage that can then jump off the hemoglobin to resupply the diffused oxygen so we have enough for the next time. 2.) If we want to quantify the dissolved O2 take the paO2 x .003 and for bound O2 it is SaO2 x hgb x 1.34. → We know that a gram of hgb is capable of carrying 1.34 mls of oxygen. → Look at equation on the picture. Normal = 16-22 ml/100ml blood (vol %)

RBC Transfusion Concerns

1.) Transfusion-associated immunodulation: Transfusion is going to affect the immune system. → Activation of SIRS: Decreased microcirculatory flow, increased pulmonary vascular resistance, and coagulopathy. → Immunosuppression - Infection. ⤷ Higher nosocomial infection rate in transfused vs. non transfused patients (6x more likely). ⤷ Number of transfusions independently associated with nosocomial infection. 2.) Transfusion related lung injury (TRALI): Leading cause of transfusion-related death. → Nurses assume that this respiratory distress is due to fluid overload (TACO). The problem is, if there is no evidence of fluid overload it is TRALI! → Leads to an inflammatory response much like ARDS. 3.) Lack of effect on oxygen consumption: → Impaired deformability of RBCs (often these RBCs are unable to change shape to get through tight circulation which is a problem in shock when someone is vasoconstricted. → Decreased ability to offload O2 to tissue (normally O2 and RBCs have a healthy relationship in that they love each other, but know when to let go; however, in transfused RBCs they have an increased oxygen affinity so they do not let go - pathological toxic relationship). Take home message: Restrictive transfusion practice lowers mortality.

Preventing Sepsis

1.) VAP. 2.) CLABSI (Central Line Associated Blood Stream Infection). 3.) CAUTI (Catheter Associated UTI). 4.) Hand-washing. 5.) Proper use of PPE. Sources of Cross-Contamination: Long sleeves, stethoscopes**, artificial nails, neck-ties, reusable ECG leads, and nail polish.

Other

1.) VTE prophylaxis: LMWH (preferred) or UFH - mechanical device if heparin contraindicated - both when possible. 2.) Stress Ulcer Prophylaxis (H2 antagonist or PPI) only if bleeding risk factors. 3.) Acute Kidney Injury: CRRT or intermittent hemodialysis - CRRT if hemodynamically unstable - only if indicated (not just for oliguria or increased creatinine). 4.) Do NOT use bicarbonate therapy for treating hypoperfusion induced lactic academia (pH >/= 7.15). 5.) Do NOT use immunoglobulins.

Hyper-dynamic Phase: What does it look like?

1.) Vasodilation & Increased capillary permeability. → Low SVR (decreased DBP & decreased MAP with variable SBP). → Warm, pink skin. → Low preload (flat neck veins, decreased RAP, PAOP). → Tissue edema & pulmonary edema. 2.) Hypermetabolism & Compensation. → Tachycardia. → Increased CO/CI (if adequate volume & before contractility decreased). Increased or decreased ScvO2/SVO2, increased lactate, increased base deficit, decreased HCO3- & metabolic acidosis. WARM SHOCK

Guidelines: Mechanical Ventilation of Sepsis-Induced ARDS (continued)

1.) Weaning protocols and spontaneous breathing trials. 2.) Conservative fluid strategy if tissue perfusion adequate. 3.) Do NOT use: → High frequency oscillatory ventilation. → Pulmonary artery catheter routinely. → Beta 20agonists without broncho spasm.

What Does Sepsis Look Like?

1.) What does this process "look" like clinically. 2.) How do we recognize that it is happening so we can respond?

Shock - A Syndrome

A physiologic state of inadequate cellular oxygenation (O2 demand exceeds O2 supply). 1.) Resulting from ineffective tissue perfusion. 2.) Resulting in widespread cellular dysfunction and death. Shock is a SYNDROME as there is not a single clinical test that can tell us one has this disease. This is a cellular phenomenon that occurs when we have higher oxygen demand than we have oxygen supply.

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

All of the critically ill patients are being scored by our equipment that predict mortality. 1.) These scores also help the hospital rating as since they have a really high score they were going to die anyways and no one can blame the hospital. 2.) You have to take into account how severe their cases are.

What does it really look like?

As a nurse, how will I know my patient is septic?

Progressive Stage (continued)

Cell Death: 1.) Ischemic necrosis: Inadequate oxygenation → Na/K pump fails ▻ cells and organelles swell and rupture. → Mitochondria ▻ loss of cell energy production even if O2 present (bioenergetic failure). → Digestive organelles ▻ leak destructive enzymes. 2.) Apoptosis: Injury-activated preprogrammed cellular suicide (about half of the cells die this way). → Triggered into suicide.

Compensated Shock

Compensatory mechanisms may produce normal hemodynamic values even when tissue perfusion is compromised! Hypotension is a late sign!

Shock: Management (continued again and again)

Considering the fact that shock is a state of inadequate cellular oxygenation resulting from ineffective tissue perfusion, the appropriate management of shock it to restore effective tissue perfusion - support cellular O2 supply (DO2).

Shock: Management (continued again)

Hypovolemic shock is pretty straightforward - you've already learned how to treat low preload and cardiogenic shock you have already learned how to treat. So, is that all there is to it? Only in the early stages.

SOFA Score

If you get new onset organ function in response to a suspected or known infection, that is sepsis.

Shock Syndrome (continued)

Initial threat to perfusion (decreased CO) → Compensation (ANS, hormonal, and chemical stimulation) → Progressive Stage (compensatory mechanism failure) → Refractory shock (unresponsive to treatment and MODS) → Death.

Shock Syndrome

Initial threat to perfusion (decreased CO) → Compensation (ANS, hormonal, and chemical stimulation) → Progressive stage (compensatory mechanism failure). Inadequate tissue perfusion → anaerobic metabolism → worsening lactic academia and tissue hypoxia. Really important stage because this is going to set off a cycle that is very difficult to stop. If we can help the patient during the initial threat to perfusion or early in the compensation stage we can stop everything, threat them and they are fine. Once you enter the progressive stage ...

Is that It?

Is that the "fix"? All we have to do is to return CO2 to normal values? How much DO2 is "adequate" for your patient?

Cellular O2 Supply (continued again)

Know normals!

Distributive Shock

Maldistribution of circulating volume due to: 1.) Vasodilation. 2.) 3rd Spacing (when your fluid is leaking out of your vascular system into your interstitium and this happens throughout the whole body especially the abdomen). → It is in the body, but in all the wrong places. → It is not only not in the vascular space where it needs to be, this is going to interfere with tissue oxygenation. The capillaries need to be right by the tissue they are providing oxygen to and if you have a lot of 3rd spacing, the gas exchange has to also cross all of that fluid! → You are also getting cerebral edema, lung edema producing ARDS, and in the myocardium where it is going to swell and not function. 3.) Three types of distributive shock: → Neurogenic. → Anaphylactic. → Septic.

Case Study: Mrs. Leaf

Mrs. Leaf is a 56 year old women admitted to the ED with a diagnosis of UGI bleed after being found in a pool of blood, unconscious, and hypotensive. She is intubated and placed on a ventilator, an arterial line and CVC are inserted and fluid is administered. She is transferred to the ICU with these VS and lab: BP 106/88, HR 115, RR 18, Temp 97, CVP 2, SVR 1478, Hgb 8.4

Guidelines: Steroids

Not used for anti-inflammatory prosperities - only to tx adrenal insufficiency (because they were in a catecholamine storm). 1.) Do NOT use unless unable to restore hemodynamic stability with fluids and vasopressors. 2.) IV hydrocortisone 200mg/day as a continuous infusion.

Cellular Oxygen Use (4)

O2 Consumption (V dot O2): How much are they actually using. 1.) Normal: → Determined by O2 demand - Influenced by internal metabolic environment. → 2 compensatory mechanisms to meet the demand. ⤷ Increased O2 supply (DO2) via increased CO (this is why your patients become tachycardic when you take them out of bed as their oxygen demand increases and HR increases in order to increase CO). ⬩ Normal oxygen consumption is 250ml and normal oxygen delivery is 1000 so normally we are only using about 25% and you have 75% reserved, this is good cause when your oxygen demand jumps up to 500ml because of the SNS stimulation the oxygen delivery can jump to 2000 and you are still only using 25%. ⤷ Increased O2 extraction (back up mechanism if this increase CO cannot meet the demand like you have a bad heart or you are on beta blockers; the body will extract a higher percentage) ⬩ If the demand goes from 250 to 500ml and you cannot increase your CO and it stays at 1000 your body will extract 50%. 2.) Critically Ill: "Bioenergetic Failure." → O2 extraction as compensatory response is limited - regardless of need. → Consumption may be less than demand. We need oxygen in order to produce ATP, our energy, for our body to keep functioning! A dot over something is a quantity or volume.

Cellular Oxygen Use (5)

O2 Consumption (VO2) = amount of O2 used by the tissue per minute. 1.) O2 Delivery - O2 Return → CO x (CaO2 x 10) - CO x (CvO2 x 10). → = CO x (CaO2 - CvO2) x 10 → Calculations are identical except instead of SaO2, you use SvO2. → You have to look at mixed venous blood to know what the WHOLE body is using. Normal VO2 is about 250ml/min VIO2 is about 110-160ml/min^2

Cellular Oxygen Use (6)

O2 Consumptions (VO2): 1.) Normal is about 250ml O2/min out of the normal DO2 of 1000ml/min = O2 extraction ratio is about 25% (22-32). 2.) O2 extraction ratio will tell you if you pt's CO is keeping pace with his demands. 3.) ... or if he is resorting to increased extraction. 4.) ... or if he is no longer able to extract O2.

Cellular Oxygen Use (7)

O2 Consumptions (VO2): 1.) SVO2 Measurement: → Mixed venous blood gases from the pulmonary artery. This is why you have a right ventricle. It is the mixing chamber! → PA catheter with SVO2 monitoring capability. ⤷ You draw blood from the Swann and the arterial line at the same time. From those numbers you can figure out oxygen consumption and even CO! ⤷ Continuous monitoring of oxygen consumption Swann has been developed. Not used frequently as it is expensive. → CVP catheter with ScvO2 monitoring capability* ⤷ You can also monitor it through a CVP line and is now the preferred method because it does not require placement of a PA catheter! ⤷ Triple lumen catheter with a plug that will give you continued monitor of ScvO2. *CVP Preferred because it does not require PAC placement.

Giapreza

Provides a new approach for increasing blood pressure in distributive shock. 1.) First one to target the RAAS system in order to increase blood pressure. 2.) However, it is super expensive so it isn't really used.

Cellular O2 Supply (continued again and again)

Refer to Photo!

Surviving Sepsis Campaign (SSC): An International Effort (1991-2018) (continued again)

Renewed examination of our current understanding ... 1.) A "syndrome," not a specific illness. 2.) Uncertain pathobiology (means we still do not clearly understand it). 3.) No gold standard diagnostic test. 4.) Identified by constellation of S&S in patient with suspected infection. 5.) Primary cause of death from infection (all ages die from sepsis).

Guidelines: Initial Resuscitation (Need to Know!)

Sepsis & Septic shock are medical emergencies - initiate treatment and resuscitation immediately. 1.) At least 30 ml/kg IV crystalloid fluid within first three hours (over 2L, but you have to do it a lot and fast cause they will die before this is bad for them). 2.) Guide additional fluid resuscitation by hemodynamic reassessment. → Clinical exam, HR, BP, SaO2, RR, temp, UO, and others (invasive or noninvasive). → Want a CVP greater than or equal to 8. 3.) If vasopressors needed, target = MAP greater than or equal to 65 mmHg. 4.) Normalize lactate as a marker of tissue perfusion (are we doing this well enough).

Focus on Hypovolemic & Cardiogenic Shock

Shock Syndrome: Initial threat to perfusion (decreased CO; in hypovolemic decreased preload and cardiogenic inadequate SV) → Compensation (ANS, hormonal & chemical stimulation). 1.) Despite the what is causing the threat, the body is going to respond to try and stay alive. → In hypovolemic shock our preload is too low, causing a stroke volume that is too low. → In cardiogenic shock we have an inadequate stroke volume resulting in an inadequate CO which is accompanied by a high preload because of the neurohormonal activation which will contribute to a drop in SV.

Shock: Management

Support Cellular O2 supply (DO2) 1.) Maximize SaO2 (pul gas exchange). 2.) Optimize Hgb (about 7-9GM%). 3.) Optimize CO. → HR (WNL - no dysrhythmias). → Preload (preload responsiveness or CVP about 8-12 [12-15 if vent] [do not want it too high because we do not want it to push into the interstitium] or PAOP about 12-15). → Afterload (SVR = 800-1400). → Contractility (after all above). Nutritional support and glucose control.

SIRS/Septic Shock: Management

Support cellular O2 supply: 1.) Maximize SaO2. 2.) Optimize Hgb. 3.) Optimize CO. → HR. → Preload. → Afterload. → Contractility.

Cellular Oxygen Use (3)

What would decrease it? 1.) Therapeutic: → Hypothermia. → Anesthesia (sedation) - reducing metabolic demands. → Neuromuscular blockade. (NMBs - paralytics; we have devices you have to use to monitor how much you are blocking the neuromuscular system; only do this in the most extreme circumstances as they have many complications). 2.) Pathologic: Bioenergetic failure → We're delivering O2, but the cells are unable to "use" it ... Mitochondrial dysfunction! → If we get patients early enough in shock, we can reserve it, but once they get too deep into it it's super hard to pull them out (because even if they are giving more oxygen, they will not use it).

Pathogens

The vast majority of sepsis is caused by single pathogens that are NOT superbugs that have been around forever. 1.) Most common single pathogens: → Staphylococcus aureus. → Pseudomonas aeruginosa. → E. coli. → Streptococcus. → Fungi. → Klebsiella pneumoniae. 2.) Blood culture positive in only 30-50% of patients with sepsis. 3.) 10-30% - Source of infection is not identified. ⅓ of sepsis patients start with a lung infection! ¼ are UTIs, 11% is gut infection, and 11% is skin infection.

Update: Renewed Emphasis on Returning to Noninvasive Measures of Peripheral Perfusion

This can be done anywhere! 1.) Capillary refill time. 2.) Skin mottling score.

Low Perfused Vessel Density (OPS in Septic Shock)

This is because you have clotted off all of your microvasculature.

Septic Shock: Hypo-dynamic Phase

Typically, very late (pre-terminal) or in a very young.old unable to mount a hyper-dynamic response. 1.) Vascular response to the biochemical mediators is primarily vasoconstriction. 2.) Cardiac output fails.

Shock - A Syndrome (continued)

What exactly is "ineffective tissue perfusion?" 1.) The purpose of tissue perfusion is to supply (deliver) oxygen (O2) to the cells → Oxygen Delivery (DO2). 2.) So that the cells can "use" the O2 to create energy (aerobic metabolism) → Oxygen consumption (VO2).