Shock Em

Front 1

Define Shock

Back 1

circulatory insufficiency that creates and imbalance between tissue oxygen supply and oxygen demand.

Front 2

Identify the consequence of decreased venous oxygen content

Back 2

global tissue hypoperfusion associated with decreased venous oxygen content and metabolic acidosis (lactic acidosis).

Front 3

List the 4 categories of shock by etiology

Back 3

1. hypovolemic: inadequate circulating volume 2. cardiogenic: inadequate cardiac pump function 3. distributive: peripheral vasodilatation & maldistribution of blood flow 4. obstructive: extra cardiac obstruction to blood flow

Front 4

Identify the first compensatory mechanism that occurs in shock, what happens when this is not sufficient and identify the marker of the severity of the tissue oxygen supply-to-demand imbalance.

Back 4

1)Increase in cardiac output
2)Amount of O2 extracted from Hg by tissues increases, which decreases the mixed venous O2 saturation. 3)Lactic acid levels used to measure this, also O2 sat,(pulmonary artery)

Front 5

List the autonomic responses that occur during shock

Back 5

1.arteriolar vasoconstriction 2.increase heart rate & contractility increasing cardiac output 3. constriction of venous capacitance vessels augmenting venous return 4. release of the vasoactive hormones epinephrine, norepinephrine, dopamine, & cortisol increasing arteriolar/venous tone 5. release antidiuretic hormone & activation of renin-angiotensin

Front 6

Identify important elements of a patient’s history that are important in assessing for possible shock

Back 6

Hx: cardiovascular disease, CP, CHF, neurologic diseases, Rx's, anaphylactic rxn to new med, drug toxicity

Front 7

Identify the most common categories of significant hemorrhage, and give a few examples of each.

Back 7

Common nontraumatic causes of hemorrhage include gastrointestinal bleeding, vascular aneurysm rupture, and ruptured ectopic pregnancy

Front 8

Explain what happens to the cardiovascular system during acute hemorrhage

Back 8

causes decreased cardiac output & vital organ perfusion only maintained at expense of nonvital organs. Progressive vasoconstriction in splenic, musculoskeletal, & cutaneous vascular beds allow sustained critical perfusion to heart, brain, & kidneys. Renal perfusion also sacrificed in severe states.

Front 9

Differentiate hemorrhage and shock caused by cardiac tamponade, tension pneumothorax, and spinal cord injury.

Back 9

Cardiac Tamponade: increased central venous pressure.
Tension Pneumothorax: unilaterally diminished breath sounds
Spinal Cord Injury: presence of neurologic deficits, warm skin, and lower than expected pulse rate

Front 10

Identify the features of acute hemorrhage and how this can differ in the elderly

Back 10

those with preexisting cardiac dz may show more severe S/S with less blood loss

Front 11

Identify the features of acute hemorrhage and how this can differ in the patients on beta-blockers,

Back 11

can mask some early S/S

Front 12

Identify the features of acute hemorrhage and how this can differ in the athletic patients

Back 12

can lose considerable amounts of blood before they appear ill

Front 13

Identify the features of acute hemorrhage and how this can differ in patient with intra-abdominal hemorrhage

Back 13

up to 1/3 who sustain intra-abd hemorrhage severe enough to develop hypotesnion (systolic < 90) will not develop tachycardia b/c of vagal stimulation from blood in peritoneal cavity

Front 14

Identify the classic features of acute hemorrhage

Back 14

tachycardia; tachypnea; narrow pulse pressure; decreased urine output; cool clammy skin; poor capillary refill; low central venous pressure and later stages: hypotension & altered mental status.

Front 15

Identify those groups of people most susceptible to septic shock.

Back 15

ID of systemic inflammatory response syndrome (SIRS) doesn't confirm Dx of infection or sepsis cause the features of SIRS can be seen in many other conditions like trauma, pancreatitis, burns, or infection. SIRS isn't a Dx, or good indicator of outcome

Front 16

Describe how clinical features change as blood loss progresses from < 20%

Back 16

Cool, clammy skin, Delayed capillary refill; ↓ pulse pressure; Maybe tachycardia. Generally normal BP though narrow pulse pressure

Front 17

Describe how clinical features change as blood loss progresses from less than 20-40%

Back 17

Tachycardic. Tachypneic. Postural changes in BP. confused. Agitated. If not resuscitated: hypotension & oligouria; respirations quicken & become deeper; tachycardia worsens; skin becomes mottled

Front 18

Describe how clinical features change as blood loss progresses from less than >40%

Back 18

Tachycardia; profound hypotession; either tachypnea or irregular respirations; markedly ↓ urine output; ↓ or absent peripheral pulses; pallor; lethargy and obtundation

Front 19

Identify the fluids of choice in resuscitation and for the hemodynamically unstable patient

Back 19

Rapid Infusion of 20–40 ml/kg as fast as possible, typically over 10–20 min

Front 20

Identify the fluids of choice in resuscitation for the management of acute hemorrhage

Back 20

Isotonic crystalloid, either 0.9% NaCl [normal saline (NS)] or ringer’s lactate (RL)

Front 21

For blood transfusion therapy, explain the following: Who can wait for fully cross-matched blood

Back 21

patient who appears to be stable

Front 22

For blood transfusion therapy, explain the following: When early transfusion is particularly important

Back 22

in elderly and those with significant respiratory and/or cardiac disease

Front 23

For blood transfusion therapy, explain the following: When aggressive therapy is mandated

Back 23

hemorrhaging pt exhibiting any degree of hemodynamic instability or signs of end-organ hypoperfusion

Front 24

For blood transfusion therapy, explain the following: Treatment of the moribund patient

Back 24

(quickly approaching death) type O immediately if available

Front 25

Identify the most frequent sites for infection

Back 25

lungs, abdomen and urinary tract

Front 26

List risk factors for gram-negative bacteremia

Back 26

DM, lymph diseases, cirrhosis, burns, invasive procedures and/or devices, chemotherapy

Front 27

List risk factors for gram-positive bacteremia

Back 27

vascular catheters, indwelling devices, burns, IV drugs

Front 28

List risk factor for fungemia

Back 28

immunocompromised

Front 29

Explain how sepsis starts and its effects on hypotension and multiple organ system failure.

Back 29

Starts as focus infection (uti, pneumonia, cellulites, abscess) resulting in bl strea invasion or proliferation of organisms at infected site, growing
organisms release exogenous toxins, hosts rxn to toxins result in release of endogenous mediators including complement, kinins, & coag factors,
release myocardial depressant substances results in depression of myocardial fxn, dilation of ventricles & vasodilation, result in generalized
cardiovascular insufficiency leading to refractory hypotension & multiple organ system failure & death

Front 30

Describe the causes of cardiogenic shock.

Back 30

impairment of heart’s pumping action to the degree that there is insufficient blood flow to the tissues to meet resting metabolic demands. The usual cause is contractile failure of the myocardium

Front 31

Identify the following regarding cardiogenic shock from acute MI: How frequently it occurs

Back 31

50,000 to 70,000 deaths/year in U.S. Reported incidence of cardiogenic shock after acute MI is 5-7%

Front 32

Identify the following regarding cardiogenic shock from acute MI: When it usually occurs

Back 32

occurs early in course of acute MI, typically in 7 hours from onset after symptoms to recognition of shock

Front 33

Identify the following regarding cardiogenicshock from acute MI: Independent risk factors

Back 33

advanced age, female gender, large MI as indicated by marked increases in creatinine kinase, anterior wall infarction, previous MI, previous CHF, multivessel disease, proximal occlusion of left anterior descending coronary artery, and DM

Front 34

Briefly identify treatment for cardiogenic shock regarding the following: Pain control and what to pay attention to:

Back 34

using IV notro or morphine; monitor and maintain systemic BP

Front 35

Briefly identify treatment for cardiogenic shock regarding the following: What to give if there is no pulmonary edema

Back 35

boluses of NS (100-250 mL)

Front 36

Briefly identify treatment for cardiogenic shock regarding the following: When fluid administration should be the first action

Back 36

RV infarct

Front 37

Briefly identify treatment for cardiogenic shock regarding the following: Initial drug to be given in the absence of profound hypotension:

Back 37

dobutamine initially

Front 38

Briefly identify treatment for cardiogenic shock regarding the following: Initial drug to be given with profound hypotension:

Back 38

dopamine if systolic is <70 mmHg

Front 39

Briefly identify treatment for cardiogenic shock regarding the following: When an intraaortic balloon pump should be used

Back 39

when above measures have failed to reverse shock

Front 40

Briefly identify treatment for cardiogenic shock regarding the following: Reperfusion modality of choice

Back 40

percutaneous transluminal coronary angioplasty if available within 60 minutes; if not available then fibrinolytics

Front 41

Define anaphylaxis and identify the most common causes.

Back 41

severe systemic hypersensitivity rxn characterized by hypotension or airway compromise that's potentially life threatening and caused by chemical and IgE mediators released from mast cells

Front 42

Identify the following regarding anaphylaxis: Type of hypersensitivity reaction

Back 42

The “classic” anaphylaxis (type I hypersensitivity) pathway involves the production of IgE and requires two separate exposures to either an antigen or a hapten-protein antigenic complex.

Front 43

Identify the following regarding anaphylaxis: Type of Ig involved

Back 43

IgE

Front 44

Describe how anaphylaxis presents, how soon it begins, and when most fatalities occur.

Back 44

pruritis, cutaneous flushing, & urticaria. Next: fullness in throat, anxiety, chest tightness, SOB, lightheaded, LOC, lump in throat & hoarseness signal life threatening laryngeal edema in pt with symptoms of anaphylaxis. Onset: within 60 minutes of exposure. faster onset = more severe rxn, with 1/2 fatalities in 1st hour

Front 45

Identify the patient who may require intubation when presenting with anaphylaxis.

Back 45

If the patient is beginning to experience respiratory distress and/or 100% O2 therapy is not resolving hypoxemia

Front 46

Identify when epinephrine can be given subcutaneously and when IV administration is indicated.

Back 46

SQ: less severe sx'x: decreasing blood pressure without hypotenstion (systolic >90mmHg) symptomatic dyspnea, abdominal cramps, urticaria. IV: SQ nonresponsive or severe symptoms (severe bronchospasm, laryngeal edema, sx's upper airway obstruction, respiratory arrest, or signs of shock)

Front 47

Identify the second-line drug Antihistamines which is used in anaphylaxis and their indications for use

Back 47

all patients with anaphylaxis should receive antihistamines particularly an H1 blocker such as diphenhydramine

Front 48

Identify the second-line drug Corticosteroids which is used in anaphylaxis and their indications for use

Back 48

all patients with anaphylaxis should receive corticosteroids such as methylprednisone

Front 49

Identify the second-line drug Glucagon which is used in anaphylaxis and their indications for use

Back 49

For patients taking beta blockers with hypotension refractory to fluids and epinephrine

Front 50

Identify the second-line drug Albuterol which is used in anaphylaxis and their indications for use

Back 50

If wheezing or tightness is part of patient’s presentation, a bronchodilator, such as a continuous albuterol nebulizer should be instituted

Front 51

Identify the second-line drug Aminophylline which is used in anaphylaxis and their indications for use

Back 51

for severe bronchospasm refractory to bronchodilator treatments

Front 52

Discuss the medications that might be given to a patient on beta-blockers.

Back 52

Pt's taking BB with hypotension refractory to fluids & epinephrine, glucagons should be used in a dose of 1 mg IV every 5 min. until hypotension resolves, followed by an infusion of 15 ug/min

Front 53

Describe the treatment of a minor allergic reaction

Back 53

ID and remove causative agent. give oral, intramuscular, or IV diphenhydramine 25-50 mg and observed at least 1 hour. If the pt stable, he/she can be discharged with antihistamine & prednisone 20 mg bid or 40 mg qd for 4 days.

Front 54

Describe the characteristics and treatment of neurogenic shock, identify the spinal cord injury level where this is most likely to occur.

Back 54

injury above T1 should be capable of disrupting spinal tracts that control entire sympathetic system. T1-L3 has potential to disrupt sympathetic outflow; the higher the injury in this zone, more likely or more severe the resulting neurogenic shock. cervical region is most commonly injured, followed by thoracolumbar junction, thoracic region, and lumbar segments.

Front 55

EM: Shock

Back 55

EM: Shock