Shock, Sepsis, MODS Flashcards

Question

Vasopressor agents

Answer 1

* Increase blood flow by vasoconstriction * However, it increases afterload, increasing cardiac workload, which can limit perfusion to skin, kidney, lungs and GI * Examples * Norepi * Dopamine * Phenylephrine * Vasopressin * Epi * Angiotensin II

Answer 2

* Causes constriction of the cardiopulmonary, GI , Skin and Kidney

Answer 3

Causes increased heart rate and myocardial contraction

Answer 4

Causes vasodilation in the heart and skeletal muscles as the bronchioles relax

Answer 5

* **Refractory to all treatment** * BP not sustainable with life (No perfusion) * Respiratory, needs max support with massive hypoxemia * Multiple pressors * Metabolic acidosis * MODS * Anaerobic metabolism worsens and elevated lactate levels * All reserves are depleted (no mo ATP) and any potential of new energy stores are destroyed (Cells have no energy and no way to get more) * Death is immanent

Answer 6

* Hemostasis **cannot** be maintained * Progressive and potential reversible physiological dysfunction of two or more organs * Each organ involved increases mortality rate * Mortality rate is 27-100% depending on organs involved

Answer 7

1. Increase blood volume 2. Causes kidneys to keep sodium and water RAAS system, increases your blood volume by preventing the excretion of urine. This causes retention of sodium. This in turn causes the urine to have a high osmolarity as it is much more concentrated

Answer 8

ALL options are correct. All these conditions can occur in the progressive stage of shock

Answer 9

The answer is B. This is the progressive stage. There are four stages of shock (in order): initial, compensatory, progressive, and refractory. The patient’s body is experiencing major signs and symptoms of shock. This is not found in the initial stage of shock because the signs and symptoms are subtle. During the compensatory stage, the body (for a while) can compensate so major organs are not showing major signs and symptoms of failure as they are in this scenario (the kidneys are starting to fail based on the BUN, creatinine, urinary output). In addition, the body is no longer compensating because the blood pressure is very low along with the MAP (mean arterial pressure). A big sign is that the patient’s mental status is altered. This represents that the brain is not being perfused very well. The MAP should be 60 or greater to provide adequate perfusion. The MAP here is 50 and this shows us the body is NOT perfusing the organs, so the cells will experience hypoxic injury. The patient is also starting to show early signs and symptoms of DIC due to the slight oozing of blood around puncture sites. The next stage (which is the last) is the refractory and this is where organs have failed or are about too. Death is imminent. This patient is not at that point but is getting close. This patient needs very dynamic treatment in order to survive

Answer 10

Compensatory

Answer 11

* Hypovolemic * Cardiogenic * Obstructive * Distributive

Answer 12

* Sudden loss of intravascular volume, whether externally or interstitially

Answer 13

* Trauma * Surgery * Vomiting * Diarrhea * Diuresis * DKA * DI

Answer 14

* Hemorrhage * Burns * Ascites * Peritonitis * Dehydration * Necrotizing pancreatitis

Answer 15

* Decreased intravascular volume * Decreased venous return * Decreased Filling pressures (PAD,PCWP), decreased blood in the heart * Decreased Stroke volume * decreased CO * Decreased Tissue perfusion> Starving cell

Answer 16

* Primary prevention: Closely monitoring a patient at risk * safe admin of meds: Vasopressors * Safe admin of fluid and or blood replacement * O2 admin

Answer 17

* LR * Buffers metabolic acidosis * Can cause pulmonary edema and abdominal compartment syndrome, may need central * 0.9% NS * Can cause hypernatremia * Hypokalemia * Hyperchloremic metabolic acidosis * ALI * ACS

Answer 18

* Albumin * Plasma expander: Rapidly expands plasma volume * Can cause HF * Expensive

Answer 19

* Rapidly replaces volume due to hemorrhage * Can consider MTP * TRALI or TACO

Answer 20

* Hearts inability to contract and pump * O2 is inadequate for heart and tissue

Answer 21

* Coronary * Noncoronary

Answer 22

* Acute MI with dmg to the LV * Anterior wall MI most common for cardiogenic shock due to dmg to the left ventricle and occlusion to the left anterior descending CA

Answer 23

* Stess to the myocardium * From hypoxia, acidosis , hypoglycemia, tension pneumo, Cardiomyopathies, valvular dmg, cardiac tamponade, arrhythmia

Answer 24

* Tachycardia * Dysrhythmias * Pulsus alternans: poor prognosis * Tachypnea * S3 * Crackles

Answer 25

* JVD * Peripheral edema * Hepatosplenomegaly

Answer 26

* Prevention: Decrease work demand of pt, admin O2 * Monitoring Hemodynamics * Intra-aortic balloon pump * Administering meds and fluids: need to see how they tolerate them **Fluids arent as effective as other forms of shock** * Maintaining safety and comfort

Answer 27

* Vital organs and tissue do not get enough blood flow * Blood can't get in or out * No CO, but the heart muscle is usually ok * Rare type * Highest rate of survival if identified and treated early

Answer 28

* Large blood clot in the PA * Pericardial tamponade * aortic stenosis * Aortic dissection * Constrictive pericarditis * Vena cava compression syndrome * Tension pneumo * Tension hemothorax * Tumors * High PEEP (Barotrauma)

Answer 29

* Pulmonary Vascular * Mechanical

Answer 30

* RV fails, can't pump into the lungs because it doesn't have enough pressure to go against pulmonary resistance * PE * Pulmonary hypertension * Severe stenosis, acute obstruction of the pulmonary or tricuspid valve

Answer 31

* Presents as hypovolemic shock, with decreased preload * Tension Pneumo * Pericardial tamponade * Constrictive pericarditis * Restrictive cardiomyopathy

Answer 32

* Assess: With stethoscope, both resp and cardio * Obtain medical assistance immediately (**Medical emergency**) * Prepare: IV insertion and O2 * Prepare: bedside ultrasound, echo and ekg * Prepare: med admin (fluids, blood, vasoactive meds)

Answer 33

1. A precipitating event causes **massive vasodilation, ** 2. which triggers the inflammatory response to try and fix it (it doesn't). 3. leading to the maldistribution of intravascular volume. 4. Less volume means less venous return 5. Less venous return return means less preload leading to reduced CO 6. No CO means no tissue perfusion

Answer 34

* Neurogenic * Anaphylactic * Septic

Answer 35

* Type of distributive shock * loss of the parasympathetic and sympathetic stimulation * Caused by * Spinal cord injury * Spinal anesthesia * Nervous system dmg * Meds * Hypoglycemia

Answer 36

* Usually with forms of shock with the hypotension, it is accompanied with tachycardia and cool moist skin. * With neurogenic shock your sympathetic nervous system is unable to react leading to **hypotension, with bradycardia and dry warm skin** (Idk about hypoglycemia tho)

Answer 37

* Restore sympathetic tone * Stabilize the spine * Patient proper positioning * Define underlying cause

Answer 38

* Support cardiovascular and neuro function until the shock resolves * HOB 30 degrees * Immobilization of pt * Assess for any lower extremity pain, redness, tenderness and warmth * Complete passive rom to increase circulation * Application of pneumatic compression devices * Antithrombotic agents * Prepare to assist provider with stabilization of the spine

Answer 39

* Form of distributive shock * Ig-E mediated allergic reactions * Drug and toxin induced * SIRS like syndromes * Narcotics, snake and insect bites, transfusion reactions * Heavy metal poisoning , toxic shock * Endocrine * Addisonian crisis (Adrenal failure due to mineralocorticoid deficiency)

Answer 40

* Onset of 2-30 min * S+S include resp distress, decreased BP, GI, skin and mucosal tissue irritation * Feeling of impending doom

Answer 41

* Know the cause, and stop it! remove the antigen * IV access * IV fluids * Epinephrine (Epi pen) * Diphenhydramine IV (benadryl) * Albuterol * CPR

Answer 42

* Prevention and early intervention is key * Being aware of S+S anaphylactic shock * Asking about any allergies * Knowing how the patient has reacted in the past to any reactions * Being aware of all risk factors * Meds * Foods * Contrast

Answer 43

4 2 1 3 6 5

Answer 44

The classic pattern for the development of MODS begins with the lungs as the client experiences progressive dyspnea and respiratory failure. Increasing amounts of IV fluids and vasoactive agents are then needed to support blood pressure and cardiac output. Signs of a hypermetabolic state occur next, which is characterized by hyperglycemia, hyper lactic acidemia, and an increased blood urea nitrogen level. After 7 to 10 days, signs of liver dysfunction (elevated bilirubin and liver function tests) and kidney dysfunction (elevated creatinine and anuria) develop. As the lack of tissue perfusion continues, the hematologic system becomes dysfunctional, which increases the risk of bleeding. The cardiovascular system becomes unstable and unresponsive to vasoactive medications, and the neurologic system deteriorates to a state of unresponsiveness or coma. 5 2 6 8 3 1 4

Answer 45

Anaphylactic shock EPI IV fluids Albuterol

Answer 46

In the irreversible stage of shock, significant cells and organs are damaged. The client’s condition reaches a “point of no return” despite treatment efforts. Death occurs from multiple system failure as the kidneys, heart, lungs, liver, and brain cease to function. 4

Answer 47

Increased myocardial contractility

Answer 48

* Most common type of distributive shock * Dmged capillaries * maldistribution of blood flow * Vasodilation * Poor O2 utilization * High mortality risk

Answer 49

* Age under 1, over 65 * Malnutrition * Debilitation * Immunocompromise * Hepatic dysfunction, CD, DM, renal disease, ETOH abuse, HIV cancer * Pregnancy

Answer 50

* Invasive procedures and cath (Central line, cath, dialysis, advanced airway, surgical procedures * Immunosuppression meds: Steroids, chemo, biologics * Wounds * Traumatic injury * Antibiotic resistance

Answer 51

* E coli * Klebsiella: Mouth and intestines * Pseudomonas aeruginosa * Bacteroids * Proteus

Answer 52

* Staph aureus * Strep pyogenes * Strep Pneumoniae * Pneumococcus * Clostridium

Answer 53

* Physiologic response to an insult or injury from an infectious or noninfectious source * Temp greater than 38 or less than 36 * HR greater than 90 * RR greater than 20, or PaCO2 less than 32, or need for mechanical venting due to resp failure * White blood cells: greater than 12k or less than 4k

Answer 54

* Physical barriers * Skin, organ mucosal layers

Answer 55

Stomach acid, lysozymes in eye

Answer 56

Inflammatory response cells (Mast, neutrophils, macrophages, Natural killer cells)

Answer 57

* Cell mediated response+ humoral response * Cell mediated * T lymphocytes: to CD4 and CD8 cells * Humoral response * B-lymphocytes: antibodies

Answer 58

* Immune system responds to invading microorganism without causing dmg to its own tissue * Limited number of microbes, local responses are sufficient to clear the pathogen and the body returns to homeostasis * High microbial load, host genetics and other issues can lead to an exaggerated response, which can lead to collateral tissue dmg and cell death (Starts to be an issue) * Necrotic cell death causes a release of DAMP that act on the pRR that were triggered by initial pathogens * Inflammatory process continues * Complex array of intersecting pathways become dysfunctional * Excessive function * Depressed function * Results in a self destructive process that can be fatal

Answer 59

* Activation of the complement system and subsequent release of vasoactive substances * Activation of kinin system * Histamine release

Answer 60

* Activation of the clotting system * Aggregation of neutrophils due to increased C5 * Plt aggregation due to increased Thromboxane A2 and Prostacyclin

Answer 61

* Increased prostaglandin F * Decreased Prostacyclin * Norepi, Epi, Angiotensin release * Myocardial depressant factor released

Answer 62

* Activation of the complement system * Release of myocardial depressant factor * Endorphin release secondary to LEM * Histamine release

Answer 63

* Venous * Dilation of the veins and venules * Venous pooling * Decreased Venous return * Decreased Filling pressure * Decreased Preload * Arterial * Dilation of arterioles * Increased lumen diameter * Decreased SVR * Decreased afterload

Answer 64

* Select vasoconstriction * Blood vessels in the pulmonary renal and gut constrict * This occurs as a result of increased catecholamines and angiotensin release myocardial depressant factor * This causes increased pulmonary vascular resistance, causing pulmonary hypertension (oh no) * Decreased renal blood flow, increased GFR and urine output

Answer 65

* Any two of the 2 criteria for both a new or existing pt * Temp <36 or >38 * HR over 90 * RR over 20 or PaCO2 under 32 * WBC under 4000 or over 12k

Answer 66

* **All or nothing** in order to be compliant you need to meet the measures. for severe sepsis

Answer 67

* Measure serum lactate * Obtain blood cultures prior to antibiotics * Admin antibiotics

Answer 68

* Repeat serum lactate if initial lactate is **>2**

Answer 69

* Measure serum lactate * Obtain blood cultures prior to antibiotics * Admin antibiotics * Resuscitation with 30ml/kg crystalloid fluids

Answer 70

* Repeat column status and tissue perfusion assessment * Vasopressor admin (If hypotension persist after fluid)

Answer 71

* Repeat assessment of volume status and tissue perfusion is **required** for patients with septic shock * This is done when a pt has persistent hypotension after fluid resuscitation (Can be done with a **focused assessment or using physiologic parameters**) * Pts who are **transferred** from another acute care facility are not included in this

Answer 72

* Vitals * Cardiopulmonary exam * Cap refill * Peripheral pulse eval * Skin exam

Answer 73

* Can be done instead of a physical exam but it must include 2 of the following * Central venous pressure * Central venous oxygen * Bedside cardiovascular ultrasound * Passive leg raise or fluid challenge

Answer 74

* Leukopenia, occurs **early** during septicemia * Resultant of the coherence of the endotoxins to the walls of the circulatory white blood cells (Neutrophils or PMN) * Leukocytes are sequestered in the spleen and removed from circulation * As immune defenses are mobilized a rebound leukocytosis (**Increased WBC**) occurs.

Answer 75

* Indirect identification of tissue perfusion * Increase can indicate hypoxia * **>2mmol/L remeasure in 2-4 hours** * Lactate guided resuscitation is shown to decrease mortality

Answer 76

* **Obtain prior to antibiotics** * Sterilization of cultures can occur within min of first dose of antibiotic * Optimize pathogen identification and improve outcomes * Obtain 2 sets of blood cultures (anaerobic and aerobic) * Admin of appropriate antibiotics should not be delayed in order to obtain cultures

Answer 77

* Should be started asap to cover all possible pathogens * Therapy should be narrowed once pathogen is established * Discontinue if pt does not have an infection * Potent antibiotics can cause large amount of exotoxins from dying bacteria, this can make the hypotension and vasodilation worse

Answer 78

* Sepsis induced hypoperfusion or septic shock is a medical emergency, need to start effective fluid resuscitation immediately * Hypotension and elevated lactate * 30ml/kg IV crystalloid * Fluid admin beyond initial resuscitation requires careful assessment and patient fluid responsiveness should be eval (FVE) * Some evidence says sustained positive fluid balance during icu is harmful

Answer 79

* Restore adequate perfusion pressure to the vital organs * Start vasopressors within the first hour to achieve MAP> 65 * Norepinephrine is pressor of choice

Answer 80

* Initial resuscitation for sepsis and septic shock 1. Measure lactate level (Remeasure if >2) 2. Obtain blood cultures before antibiotics 3. Admin broad spectrum antibiotics 4. Begin rapid admin of 30ml/kg crystalloid for hypotension or lactate greater than 4 5. Apply vasopressors if hypotensive during or after to maintain a map of greater than 65

Answer 81

3. Shallow, rapid respirations

Answer 82

As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the client begins to show signs of organ dysfunction. The cardiovascular system also begins to fail, the blood pressure does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., acute kidney injury, pulmonary failure, hepatic failure). As sepsis progresses to septic shock, the blood pressure drops, and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs. Adventitious lung sounds occur throughout the lung fields, not just in the upper fields of the lungs.

Answer 83

Just a guess but 4

Answer 84

1 3 5 The nurse should expect to administer oxygen therapy to support perfusion, monitor temperature to assess metabolic response, and obtain lactate levels, which serve as a critical predictor of the client's metabolic stress response. The nurse should not place a client with septicemia in a prone position because this would lead to further respiratory compromise. The nurse should not increase PO fluid intake because this would also lead to respiratory compromise and fluid volume overload

Answer 85

* Need to be able to critically think, there might be more than one source of the cause, or one may transfer to another * Look at the diagram in lecture it displays it well