Week 11: Sepsis & Shock

What is cardiogenic shock?Systolic or diastolic dysfunction that leads to a compromised cardiac outputWhat causes cardiogenic shock?-myocardial infarction -cardiomyopathy -blunt cardiac injury -severe systemic or pulmonary HTN -cardiac tamponade -myocardial depression from metabolic problemsWhat is the pathophysiology behind cardiogenic shock?*Whether the initiating event is myocardial dysfunction, a structural problem (e.g., valvular disorder, ventricular septal rupture), or dysrhythmias, the physiologic responses are similar. **The patient experiences impaired tissue perfusion and cellular metabolism because of cardiogenic shock.What is the primary problem in cardiogenic shock:preload? increased contractility? decreased**** afterload? increased heart rate? increasedHow is cardiogenic shock treated: preload? contractility? afterload? heart rate?preload? diuresis contractility? increased contractility with inotropes (dobutamine and milrinone; increase contractility without increasing afterload); do not give levophed; balloon pump (decreases afterload and will eventually increase contractility); inotropes can increase HR so watch for it afterload? decrease with ACEI or ARB heart rate? decrease HR, but don't give beta blockers or dopamineWhat is obstructive shock?Develops when physical obstruction to blood flow occurs with decreased CO: -tension pneumothorax -pneumopericardium -cardiac tamponade -pulmonary embolism *Pulmonary embolism and right ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. This leads to decreased blood flow to the lungs, as well as decreased blood return to the left atrium.What type of shock occurs with a pulmonary embolism?obstructive shockWhat causes a pulmonary embolism?-usually caused by DVT, but can also be due to an air embolus, fat embolus, or amniotic fluid embolusWhat does a pulmonary embolism lead to?-lung injury -infarct -right sided heart failure (increased PVR) *Right side of heart is not nearly as muscular as the left side and when it has to overcome pressures it fails and dilates out quickly; fatigues quicklyWhat are the clinical manifestations (s/sx) of pulmonary embolism?-Tachypnea* -Dyspnea* -Chest pain (inspiration)* -wheezing, cough, hemoptysis -palpitations -cyanosis and low O2 saturation -altered VS -pleural friction rub -elevated JVD -restlessness and apprehensionWhat diagnostic testing is done for a patient with a suspected pulmonary embolism?1) Test D-Dimer (looks for clots being broken up; if positive then there could be a PE; if negative then there is not a PE or any other clot) 2) CT angiography or venogram (if negative then no treatment and may do an MRI; if positive then further testing is needed) 3) Repeat CT; MRI; ultrasound; pulmonary scintigraphy; digital subtraction angiography; serial ultrasoundWhat is Well's criteria for pulmonary embolism?-risk approximation score for PE; not diagnostic but may guide treatment -factors in: clinical s/sx of DVT; PE is #1 diagnosis or equally likely; HR >100; immbolization at least 3 days or surgery in previous 4 weeks; previous objectively diagnosed PE or DVT; hemoptysis; malignancy with treatment within 6 months or palliativeWhat other diagnostic tests are done for pulmonary embolism?-lab tests (D-dimer) -VQ scan (less commonly done now; usually done for ppl with Hx of PE) (radioactive dye injected and look at perfusion in the lungs of that dye; patient inhales radioactive isotope and observe ventilation by comparing one film to another to determine if there is a defect and associated with a PE) -CT pulmonary angiography vs pulmonary angiography (gold standard test; visualizing blood vessels going thru the lungs) -EKG (look at S1, Q3, T3) -Leg doppler (see if cause was DVT)What do you look for in an EKG for pulmonary embolism?-look for an S-wave in lead I -look for a Q wave in lead III -look for an inverted T-wave in lead III *just screening test; not diagnosticWhat are the collaborative treatments for pulmonary embolism?1) Anticoagulation-- (low dose IV heparin and then warfarin for 6 months; prevents further clotting) 2) Fibrinolytics-- to dissolve the PE (TPA, RNK, streptokinase) (come with risks, so we only give to those with PE that is causing hemodynamic instability) 3) Surgery-- pulmonary thrombectomy (last ditch effort; take out part of lung with the PE; high mortality rate) and/or inferior vena cava filter (if patient has repeated PEs; umbrella of mesh in inferior vena cava and as clots are dislodged they catch in the filter and the body breaks the clots over time)What are 3 things that occur with obstructive shock?1) decreased CO 2) increased afterload (PVR) (ineffective tissue perfusion and impaired gas exchange) 3) variable left ventricular filling pressure **Blood is not getting thru to left side of the heart; right sided backupWhat is the main problem in obstructive shock (pulmonary embolism): preload? contractility? afterload? heart rate?preload? high on R; low on L contractility? low on Right side afterload? high*** heart rate? high *Preload high on R side because blood backed up; low on L side because not enough blood going to itHow is a pulmonary embolism treated?break down the clotWhat is the main problem in obstructive shock (cardiac tamponade): preload? contractility? afterload? heart rate?preload? low*** contractility? low afterload? high heart rate? high *Fluid around heart and the heart cannot expand **Amount of volume of blood in heart itself is low, but pressure around the heart is high ***CVP of 18 (high because it is a reflection of pressure and not volume)How is cardiac tamponade treated?relieve pressure around the heartWhat are goals for the patient with pulmonary embolism in terms of O2 saturations?keep O2 saturation above 90%Those with pulmonary embolism experience what respiratory imbalance?-respiratory alkalosis or acidosis -most patients come in with alkalosis first due to SOB and pain causing tachypnea and hyperventilationWhat are respiratory interventions for patients with pulmonary embolism?-positioning (affected side up and good side down b/c blood flow will go to where it can get the most perfusion; otherwise use high fowlers) -O2 suctioning -Bedrest; pace activities -pain relief; relieve anxiety -angicoagulation for 3-6 months or indefinitelyWhat is distributive shock?-arteries and veins both lose tone and responsiveness to the SNS; no vasoconstrictive ability (loss of afterload is main problem due to massive vasodilation) -blood pools in the venous system -loss of preload causes CO and arterial pressure to decreaseWhat are the causes of distributive shock?-anaphylaxis -drugs/toxins -tissue injury -prolonged hypoxia or ischemia -septic shock -neurogenic shock (injury to spinal cord above T5; causesWhat is neurogenic shock, a type of distributive shock?-hemodynamic phenomenon; any factor that stimulates parasympathetic activity or inhibits sympathetic activity of vascular smooth muscles -results in massive, widespread vasodilation -imbalance between sympathetic and parasympathetic stimulation --> massive vasodilation --> decreased vascular tone --> decreased systemic vascular resistance --> inadequate cardiac output --> decreased tissue perfusion --> impaired cellular metabolism -low SVR, bradycardia -can occur within 30 minutes of a spinal cord injury at the 5th thoracic vertebra or above; can be caused by spinal anesthesia; can be caused by vasomotor center depression from drugs, pain, hypoglycemia -can last up to 6 weeksWhat is the pathophysiology behind neurogenic shock?What is the main issue in neurogenic shock: preload? contractility? afterload? heart rate?preload? low contractility? low afterload? low*** heart rate? lowHow is neurogenic shock treated?raise afterload to restore vascular tone -levophed -vasopressors -dopamineWhat are the diagnostic criteria for SIRS (systemic inflammatory response syndrome)?Can result from any shock state previously mentioned Diagnosis requires two or more of the following: -temperature of >38 C or <36 C -heart rate of >90 -respiratory rate of >20 or PaCO2 less than 32mmHg -WBC count >12000 or <4000 (or 10% immature neutrophils)What are the diagnostic criteria for sepsis?SIRS plus a culture-documented infectionWhat are the diagnostic criteria for severe sepsis?sepsis plus organ dysfunction, hypotension, or hypoperfusion (including but not limited to lactic acidosis, oliguria, or acute mental status changes)What are the diagnostic criteria for septic shock?hypotension (despite fluid resuscitation) hypoperfusionWhat is the end result of SIRS, sepsis, severe sepsis, and septic shock?MODS (multiple organ dysfunction syndrome)What is SIRS?systemic inflammatory response syndrome -systemic inflammatory response to a variety of insults -generalized inflammation in organs remote from the initial insult causing cytokine releaseWhat is the progression from SIRS to septic shock?As it progresses, the % of mortality is higher and higherWhat are the causes of SIRS?-mechanical tissue trauma (r/t burns, crush injury, surgical procedures) -abscess formation (intraabdominal, extremities) -Ischemic or necrotic tissue (pancreatitis, vascular disease, MI) -Microbial invasion (bacteria, viruses, fungi) -Endotoxin release (gram negative bacteria) -Global perfusion deficits (postcardiac resuscitation, shock states) -Regional perfusion deficits: distal perfusion deficitsWhat is the pathophysiology of SIRS inflammatory response? (chart)How does shock lead to SIRS and MODs? (picture)What is the relationship between sepsis and SIRS? (picture)You can have an infection and develop Sepsis You can have a person with trauma (SIRS) and develop SepsisWhat is septic shock, a type of distributive shock?Systemic inflammatory response to documented or suspected infection -presence of sepsis with hypotension (despite fluid resuscitation) -presence of inadequate tissue perfusion resulting in hypoxia -clinically identified (vasopressor requirement to maintain a MAP of 65mmHg or greater AND serum lactate >2mmol/L in absence of hypovolemia)How is septic shock 1st recognized (quick and easy ways to assess for distributive shock)?1) SOFA score (sequential organ failure assessment): PaO2, FiO2, platelet count, GCS, bilirubin, etc 2) HAT score: hypotension, altered menta status, tachypneaWhat is a HAT score based on?Adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have >2 clinical criteria -Hypotension: SBP </= 100mmHg -Altered mental status: GCS <15 -Tachypnea: RR >/= 22What is the pathophysiology of septic shock? (chart)What is the main issue in septic shock: preload? contractility? afterload? heart rate?preload? low contractility? low afterload? low*** heart rate? highWhat is done in the treatment of septic shock?1: fluids 2: vasopressors (levophed)What is MODS?multiple organ dysfunction syndrome -failure of 2+ organ systems -hemostasis cannot be maintained without intervention -results from SIRS and septic shock -90% mortality rate for 3 organ involvementMODS (patho chart)What is the pathophysiology of SIRS and MODS: -consequences of inflammatory response -organ and metabolic dysfunctionConsequences of inflammatory response: -release of inflammatory mediators -direct damage to the endothelium -hypermetabolism -increase in vascular permeability -activation of coagulation cascade Organ and metabolic dysfunction: -hypotension (r.t vasodilation) -decreased perfusion -formation of microemboli (r/t inflammation; causes petechiae) -redistribution or shunting of bloodEnd Organ Damage in Sepsis (picture)What is the pathophysiology of SIRS and MODS: -Respiratory system-alveolar edema -decrease in surfactant -increase in shunt -V/Q mismatch -end result --> ARDS (bilateral infiltrates, no cardiomegaly, vascular redistribution) *****usually is the first system to failWhat is the pathophysiology of SIRS and MODS: -Cardiovascular system-myocardial depression -massive vasodilation -results in decreased SVR and BP -baroreceptors respond to enhance CO (increase HR) -treatment: give albumin and fluids to replace blood lost in the vesselsWhat is the pathophysiology of SIRS and MODS: -Neurologic System-mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion -often early sign of MODSWhat is the pathophysiology of SIRS and MODS: Renal systemAKI (acute kidney injury) -hypoperfusion -release of mediators -activation of RAAS -can be caused by nephrotoxic drugs (esp ABx)What is the pathophysiology of SIRS and MODS: GI system-decreased motility (abdominal distention and paralytic ileus) -decreased perfusion (risk for ulceration and GI bleeding) -potential for bacterial translocationWhat is the pathophysiology of SIRS and MODS: Hypermetabolic state-hyperglycemia/hypoglycemia -insulin resistance -catabolic state -liver dysfunction -lactic acidosisWhat is the pathophysiology of SIRS and MODS: Hematologic system-DICWhat is the pathophysiology of SIRS and MODS: Electrolyte and pH Imbalancesmetabolic acidosisWhat is the recommendation for initial resuscitation in Sepsis? (CVP, MAP, UOP, ScvO2)In the 1st 6 hours of resuscitation, the goals of resuscitation include -CVP 8-12 mmHg -MAP >/= 65 mmHg -UOP >/ 0.5 mL/kg/hr -ScvO2 >/= 70%After initial resuscitation, what are the next steps in the surviving sepsis campaign?1) Supplemental oxygen (perhaps endotracheal intubation and/or mechanical ventilation) 2) Central venous and arterial catheterization (early insertion of ScvO2 catheter) 3) Sedation or paralysis (if intubated) 4) Therapy titrated to CVP, MAP, ScvO2After initial resuscitation, what are the next steps in the surviving sepsis campaign? (chart)In sepsis management, how is therapy titrated to CVP, MAP, and ScvO2?1) CVP (8-12 mmHg): <8, give crystalloid or colloid fluids 2) MAP (65-90 mmHg): <65 or >90, give vasoactive agents (levophed) 3) ScvO2 (>/= 70%): <70%, give transfusion or red cells until Hct is >/= 30% and then give inotropic agentsTrue or False: Sepsis and septic shock are medical emergencies and we recommend that treatment and resuscitation begin immediately.trueWhat is the best practice statement on sepsis regarding drawing labs?Draw blood cultures within an hour of onset *We recommend that a specific anatomic diagnosis of infection requiring emergent source control be identified or excluded as rapidly as possible in patients with sepsis or septic shock, and that any required source control intervention be implemented as soon as medically and logistically practical after the diagnosis is made.What is the best practice statement on sepsis regarding antibiotics?-administration of IV antimicrobials be initiated as soon as possible after recognition and within 1 hour for both sepsis and septic shock -empiric broad spectrum therapy with one or more antimicrobials to cover all likely pathogensWhat is the best practice statement on sepsis regarding initial resuscitation?-It is recommended that in the resuscitation from sepsis-induced hypoperfusion, at least 30 mL/kg of IV crystalloid fluid be given within the first 3 hours -following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hyemodynamic statusWhat is the best practice statement on sepsis regarding fluid therapy?-Crystalloids are recommended as the fluid of choice for initial resuscitation and subsequent intravascular volume replacement in patients with sepsis and septic shock -Suggested that albumin, in addition to crystalloids, be used when patients require substantial amounts of crystalloids.What is the best practice statement on sepsis regarding blood pressures?-initial target MAP of 65 mmHg in patients requiring vasopressorsWhat is the best practice statement on sepsis regarding vasoactive agents?-Norepinephrine (levophed) is 1st choice vasopressor -Add vasopressin (up to 0.03 U/min) or epinephrine to norepinephrine with the intent of raising MAP to target; or adding vasopressin (up to 0.03 U/min) to decrease norepinephrine dosageWhat is the best practice statement on sepsis if shock is not resolving quickly?-Recommend further hemodynamic assessment (assess cardiac functioning) to determine the type of shock if the clinical examination dose not lead to a clear diagnosis -Suggest that dynamic over static variables be used to predict fluid responsiveness, when availableWhat is the best practice statement on sepsis regarding lactate levels?-Guide resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion -high lactate = increased risk of mortalityWhat is the best practice statement on sepsis: SUMMARY?-Start resuscitation early with source control, intravenous fluids and antibiotics. -Frequent assessment of the patients' volume status is crucial throughout the resuscitation period. -We suggest guiding resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion.What is the best practice statement on sepsis: prevention?We recommend that hospitals and hospital systems have a performance improvement program for sepsis including sepsis screening for acutely ill, high-risk patients. (BPS)What is the best practice statement on sepsis: diagnosis?We recommend that appropriate routine microbiologic cultures (including blood) be obtained before starting antimicrobial therapy in patients with suspected sepsis and septic shock if doing so results in no substantial delay in the start of antimicrobials. (BPS) ***Appropriate routine microbiologic cultures always include at least two sets of blood cultures (aerobic and anaerobic).What is the best practice statement on sepsis: ABX?We suggest empiric combination therapy (using at least two antibiotics of different antimicrobial classes) aimed at the most likely bacterial pathogen(s) for the initial management of septic shock.What is the best practice statement on sepsis: corticosteroids?We suggest against using intravenous hydrocortisone to treat septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability. If this is not achievable, we suggest intravenous hydrocortisone at a dose of 200 mg per day. (weak recommendation; used as last source of treatment; not routinely given)What is the best practice statement on sepsis: mechanical ventilation?-We suggest using higher PEEP over lower PEEP in adult patients with sepsis-induced moderate to severe ARDS. -We recommend using prone over supine position in adult patients with sepsis-induced ARDS and a PaO2/FIO2 ratio <150. -We recommend against the use of HFOV (high frequency oscillating ventilation) in adult patients with sepsis-induced ARDS. -We recommend against the use of beta-2 agonists for the treatment of patients with sepsis- induced ARDS without bronchospasm. -We suggest using lower tidal volumes over higher tidal volumes in adult patients with sepsis-induced respiratory failure without ARDS.What is the best practice statement on sepsis: glucose control?-We recommend a protocolized approach to blood glucose management in ICU patients with sepsis, commencing insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL. This approach should target an upper blood glucose level ≤180 mg/dL rather than an upper target blood glucose ≤110 mg/dL. *We recommend that blood glucose values be monitored every 1 to 2 hrs until glucose values and insulin infusion rates are stable, then every 4 hrs thereafter in patients receiving insulin infusions. (BPS)What is the best practice statement on sepsis: renal replacement therapy?-We suggest against the use of renal replacement therapy in patients with sepsis and acute kidney injury for increase in creatinine or oliguria without other definitive indications for dialysis. (pulling off of fluid lead to hypovolemia, didn't help)What is the best practice statement on sepsis: nutrition?-We recommend against the administration of early parenteral nutrition alone or parenteral nutrition in combination with enteral feedings (but rather initiate early enteral nutrition) in critically ill patients with sepsis or septic shock who can be fed enterally. -We suggest the use of prokinetic agents in critically ill patients with sepsis or septic shock and feeding intolerance. (Initially give bicarb (only works for 30 min) and then correct metabolic state; Do not stop feeds (they are hypermetabolic), even if residuals are high) Pyloric tube Start feeds at a low dose within 24 hours Villi within gut need energey or else they will shrivel up and dieWhat is the best practice statement on sepsis: goals of care?-We recommend that goals of care and prognosis be discussed with patients and families. (BPS) -We recommend that the goals of care be incorporated into treatment and end-of-life care planning, utilizing palliative care principles where appropriate. -We suggest that goals of care be addressed as early as feasible, but no later than within 72 hours of ICU admission.A patient with a history of alcoholism is admitted to the ICU with hemorrhage from esophageal varices. Admission VS are BP 84/58 mm Hg, HR 105, and RR 32 breaths/min. The nurse recognizes the onset of systemic inflammatory response syndrome (SIRS) upon finding: pulmonary edema. cardiac dysrhythmias. absent bowel sounds. decreasing blood pressure.pulmonary edemaA patient admitted to the hospital from a long-term care facility appears to be in the late stage of shock with systemic inflammatory response syndrome (SIRS). Which order implemented by the nurse has the highest priority? Insert an indwelling urinary catheter. Insert two large-bore intravenous catheters. Administer 0.9% normal saline at 100 ml/hr. Administer 100% oxygen by non-rebreather mask.Administer 100% oxygen by non-rebreather mask.

Week 11: Sepsis & Shock

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