Shock Flashcards

1
Q

Define shock

A

State in which blood flow to and perfusion of peripheral tissues is inadequate to sustain life. Hypotension and oliguria or anuria are associated findings. Tachycardia is also usually present.

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2
Q

List the 5 primary clinical types of shock

A

Hypovolemic, cardiogenic, septic, anaphylactic, neurogenic

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3
Q

What should you do if a patient is in shock?

A

ABCs (airway, breathing, circulation). Give oxygen and fluids. Avoid fluids if congestive heart failure is present.

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4
Q

How should fluids be given if a patient is in shock?

A

Standard IV bolus is 10-20 mL/kg of NS or lactated Ringers; infuse 1-2 L as fast as it will go. Do not be afraid to give a second bolus if the first bolus leads to no improvement. Make sure that no bilateral crackles can be heard on lung exam. Place Foley catheter to ensure accurate monitoring of urine output.

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5
Q

What should you do if fluid challenges fail to raise the BP?

A

Use invasive hemodynamic monitoring (i.e. Swan-Ganz catheter) to help determine the cause of the shock and to guide therapeutic decisions.

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6
Q

What are the classic parameters (CO, PCWP, SVR, SVO2) of septic (early) shock?

A

CO - HIGH
PCWP - low
SVR - low
SVO2 - HIGH

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7
Q

What are the classic parameters (CO, PCWP, SVR, SVO2) of hypovolemic (or late septic) shock?

A

CO - low
PCWP - low
SVR - HIGH
SVO2 - low

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8
Q

What are the classic parameters (CO, PCWP, SVR, SVO2) of cardiogenic shock?

A

CO - low
PCWP - HIGH
SVR - high
SVO2 - low

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9
Q

What are the classic parameters (CO, PCWP, SVR, SVO2) of neurogenic shock?

A

CO - low
PCWP - low
SVR - LOW
SVO2 - low

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10
Q

Specify the usual findings in patients with neurogenic shock.

A

History of severe CNS trauma or hemorrhage and flushed skin. HR may be normal.

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11
Q

How do you recognize septic shock?

A

Look for fever, leukocytosis (unless patient is on chemotherapy or has an immunosuppressive condition), skin that is flushed and warm to the touch, and extremes of age.
Start broad-spectrum antibiotics after “pan-culturing” (blood, sputum, and urine plus others as dictated by history).

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12
Q

What clues suggest cardiogenic shock?

A

Look for history of MI, CHF, or chest pain. Assess patients for risk factors for CAD. Most patients have cold, clammy skin and look pale. Distended neck veins and pulmonary congestion (as demonstrated by physical exam or CXR) are usually present.

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13
Q

How do you recognize hypovolemic shock?

A

Look for history of fluid loss (hemorrhage, diarrhea, vomiting, sweating, use of diuretics, inability to drink water). Patients have cold, clammy skin and look pale. Fluid loss may be internal, as with a ruptured abdominal or thoracic aneurysm and obstruction or infarction of the spleen, pancreas, or bowel. The postoperative state also may lead to hypovolemic shock. Patients usually have orthostatic hypotension, tachycardia, sunken eyes, tenting of skin, and sunken fontanelle (young children).

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14
Q

What clues suggest anaphylactic shocks?

A

Look for a history of recent exposure to the common culprits (bee stings, peanuts, shellfish, penicillins, sulfa drugs, or new meds). Treat with epinephrine and fluids. Administer oxygen, and intubate if necessary. Tracheostomy or cricothyroidecomy should be performed if laryngeal edema prevents intubation. Antihistamines are helpful when reaction is mild. Use corticosteroids when reaction is prolonged or severe, but they are not first-line drugs for anaphylaxis. Monitor for at least 6 hours after initial reaction.

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15
Q

What clues suggest pulmonary embolus as a cause of shock?

A

Look for DVT or risk factors. Remember Virchow’s triad. Watch for posteroperative status (esp. after orthopedic or pelvic surgery) or a history of recent delivery (amniotic fluid embolus) or bone fractures (fat emboli). Patients classically have chest pain, tachypnea, SOB, right-axis shift on EKG, and positive V/Q scan or CT pulmonary angiography. Heparin or LMW heparin should be administered to prevent further clotting and emboli.

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16
Q

How do you recognize pericardial tamponade as a cause of shock?

A

Look for history of stab wound in left chest and distended neck veins. Do pericardiocentesis emergently in the setting of shock.

17
Q

Explain toxic shock syndrome

A

Presents in a woman of reproductive age who leaves her tampon in place too long. Look for skin desquamation. Caused by Staph aureus toxin.

18
Q

What clues suggest Addison disease as a cause of shock?

A

Usually have history of steroid use, hyperkalemia, and hyponatremia. Treat with steroids.

19
Q

Discuss the use of dobutamine to support BP in the setting of shock.

A

Dobutamine is a beta1-agonist used to increase cardiac output by increasing contractility; it is the intensive-care equivalent of digoxin

20
Q

Discuss the use of dopamine to support BP in the setting of shock.

A

Dopamine affects dopamine receptors at low doses and results in selective vasodilation (traditional use for renal perfusion is questionable). At higher doses, its beta1-agonist effects increase contractility. At the highest doses, dopamine has alpha1-agonist effects and causes vasoconstriction.

21
Q

Discuss the use of NE to support BP in the setting of shock.

A

NE is used for its alpha1-agonist effects, but it also has beta1 effects. It is given primarily to patients with hypotension to increase peripheral resistance so that perfusion to vital organs can be maintained.

22
Q

Discuss the use of isoproterenol to support BP in the setting of shock.

A

Isoproterenol is a beta1-agonist that has chronotropic effects (may help in case of bradycardia) and causes vasodilation. As such, its use in hypotensive patients is limited.

23
Q

Discuss the use of phenylephrine in the setting of shock.

A

Phenylephrine is used for its alpha1-agonist effects. It is similar to NE but has no beta effects.

24
Q

Discuss the use of epinephrine in the setting of shock.

A

Epinephrine is used in patients with cardiac arrest and anaphylaxis for its alpha and beta effects.

25
Q

Discuss the use of milrinone in the setting of shock.

A

Milrinone and amrinone are phosphodiesterase inhibitors. They are used in patients with refractory HF because they have a positive inotropic effect via potentiation of cAMP, but they cannot be used in hypotensive patients.