Hypotension Flashcards

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1
Q

What class of antihypertensive agents is best known for severe, first-dose orthostatic hypotension?

A

Alpha1-antagonists such as terazosin.

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2
Q

Define shock.

A

Shock is a state in which blood flow to and perfusion of peripheral tissues are inadequate for sustaining life.

Although they are not included in a rigid definition of shock, hypotension, lactic acidosis (inadequate perfusion leading to anaerobic metabolism), and oliguria or anuria (inadequate renal perfusion) are associated findings for board purposes.

Tachycardia is also usually present as a compensatory response.

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3
Q

List the four primary categories of shock.

A

Hypovolemic shock (e.g., dehydration, hemorrhage),

cardiogenic shock,

distributive shock (e.g., septic shock, anaphylactic shock, neurogenic shock in which vasodilation causes poor distribution of blood flow)

obstructive shock (e.g., tension pneumothorax causing impeded venous return, cardiac tamponade with poor cardiac filling due to pressure from fluid in the pericardial space).

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4
Q

What should you do if a patient is in shock?

A

Keep the patient alive according to the ABC protocol (airway, breathing, and circulation) while you try to determine the cause of the shock.

Give oxygen and fluids while you are thinking unless the patient is in congestive heart failure (CHF).

If CHF is present, avoid fluids.

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5
Q

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

A

Many patients in shock need fluid.

The standard intravenous bolus is 10 to 20 mL/kg of normal saline or lactated Ringer solution;
infuse 1 to 2 L as fast as it will go.

Then reassess the patient to determine whether the bolus helped;

positive signs include increases in blood pressure and urine output.

Do not be afraid to give a second bolus if the first bolus leads to no improvement.

You should watch for fluid overload, which may cause CHF.

Make sure that no bilateral crackles can be heard on lung examination.

Place a Foley catheter to ensure accurate monitoring of urine output.

In the case of hemorrhagic shock, blood products are preferred over crystalloid solutions.

For septic and anaphylactic shock, resuscitation with a large amount of fluid is generally required;
the most recent sepsis guidelines recommend 30 mL/kg at a minimum.

Neurogenic shock is due to decreased sympathetic tone,
so fluids are usually not as effective as vasopressors but can be given initially

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6
Q

What should you do if fluid challenges fail to raise a patient’s blood pressure?

A

Consider the use of vasoactive agents to increase tissue perfusion.

Norepinephrine (Levophed) is the first-line treatment for septic and cardiogenic shock.

Epinephrine is the first line of treatment for anaphylactic shock.

Blood transfusions and source control are the mainstays of treatment for hemorrhagic shock.

The use of invasive hemodynamic monitoring (e.g., central venous catheter or Swan-Ganz catheter) can help to determine the cause of the shock and guide therapeutic decisions.

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7
Q

What are the classic parameters for each type of shock?

A

CO, Cardiac output;
PCWP, pulmonary capillary wedge pressure;
SVO2, systemic venous oxygen saturation;
SVR, systemic vascular resistance.

For anaphylactic shock, the cause is usually obvious because of a temporal relation to a common culprit.

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8
Q

Specify the usual findings in patients with neurogenic shock.

A

Patients usually have a history of severe central nervous system trauma or hemorrhage and flushed skin.

The heart rate may be normal.

These patients require early vasopressors as a substitute for their endogenous sympathetic tone, which they have lost.

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9
Q

How do you recognize septic shock?

A

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

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10
Q

What clues suggest cardiogenic shock?

A

Look for a history of myocardial infarction (MI), CHF, or chest pain.

Assess patients for risk factors for coronary artery disease.

Most patients have cold, clammy skin and look pale.

Distended neck veins and pulmonary congestion (as demonstrated by a physical exam and/or chest radiograph) are usually present.

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11
Q

How do you recognize hypovolemic shock?

A

Look for a 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 in the case of a ruptured abdominal or thoracic aortic aneurysm and obstruction or infarction of the spleen, pancreas, or bowel.

The postoperative state may also lead to hypovolemic shock.

Patients usually have orthostatic hypotension, tachycardia, sunken eyes, tenting of the skin, and a sunken fontanelle (young children).

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12
Q

What clues suggest anaphylactic shock?

A

Look for a history of recent exposure to the common culprits: bee stings, peanuts, shellfish, penicillins, sulfa drugs, or any new medication.

Treat with epinephrine and fluids.

Administer oxygen, and intubate if necessary.

A tracheostomy or cricothyroidotomy should be performed if laryngeal edema prevents intubation.

Antihistamines are helpful primarily when the reaction is mild, but will only treat the cutaneous symptoms.

Use corticosteroids, but understand that they take several hours to take effect.

Monitor all patients for at least 6 hours after the initial reaction.

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13
Q

What clues suggest pulmonary embolus as a cause of shock?

A

Look for deep venous thrombosis (DVT; positive Homan sign with a painful, swollen leg) or risk factors for DVT.

Remember the Virchow triad: endothelial damage, stasis, and hypercoagulable state.

Watch for postoperative status (especially 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, shortness of breath, hypoxia, right-axis shift on ECG, and a positive CT pulmonary angiography or ventilation/perfusion scan.

Heparin or its low–molecular-weight form should be administered to prevent further clotting and emboli.

Thrombolysis with tissue plasminogen activator (t-PA) is indicated in hemodynamically unstable patients.

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14
Q

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

A

Look for the Beck triad: hypotension, distended neck veins, and muffled heart sounds.

Look for a compatible history such as penetrating chest trauma or aortic dissection.

Also consider risk factors for pericardial effusion: malignancy, pericarditis, autoimmune disease, and uremia.

Perform emergent pericardiocentesis in the setting of tamponade and arrange for definitive surgical management.

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15
Q

Explain toxic shock syndrome.

A

Toxic shock syndrome classically occurs in a woman of reproductive age who leaves her tampon in too long.

Look for skin desquamation.

The syndrome is caused by a Staphylococcus aureus toxin.

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16
Q

What clues suggest Addison disease as a cause of shock?

A

Patients usually have a history of steroid use,
hyperkalemia, and
hyponatremia.

Treat with steroids and large volumes of normal saline.

17
Q

What is the most important point to remember if a patient is in shock?

A

The ABCs. Patients in shock often need heroic measures to survive and are among the exceptions to the “wait and see” and “be conservative” rules that are usually favored by USMLE examiners. Intubate at the drop of a hat, do not feed the patient, and avoid narcotics if possible. Mental status changes are often an important clue to impending doom. Also monitor the ECG, vital signs, Swan-Ganz parameters (although these are no longer being used as much), urine output, arterial blood gas, and hemoglobin/hematocrit.

18
Q

Discuss the use of norepinephrine, dobutamine, dopamine, and isoproterenol to support blood pressure in the setting of shock.

A

Norepinephrine is used for its alpha1-agonist effects, but it also has beta1-agonist effects. It is given primarily to patients with hypotension to increase peripheral resistance so that perfusion to vital organs can be maintained. It is the first line of therapy for septic and cardiogenic shock.

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

Dopamine affects dopamine receptors at low doses and results in selective vasodilation (the traditional use for renal perfusion has been disproven). At higher doses, its beta1-agonist effects increase contractility. At the highest doses, dopamine has alpha1-agonist effects and causes vasoconstriction. Note that this differential effect is debated but could still be tested. The beta1-agonist activity of dopamine makes it a first-line agent for many cases of symptomatic bradycardia.

Isoproterenol is used for its beta1-agonist and beta2-agonist effects in hypovolemic, septic, and cardiogenic shock.

19
Q

Norepinephrine

A

is used for its alpha1-agonist effects, but it also has beta1-agonist effects.

It is given primarily to patients with hypotension to increase peripheral resistance so that perfusion to vital organs can be maintained.

It is the first line of therapy for
septic and
cardiogenic shock.

20
Q

Dobutamine

A

is a beta1-agonist

used to increase cardiac output by increasing contractility;

it is the intensive care equivalent of digoxin.

21
Q

Dopamine

A

affects dopamine receptors at low doses and
results in selective vasodilation (the traditional use for renal perfusion has been disproven).

At higher doses, its beta1-agonist effects increase contractility.

At the highest doses, dopamine has alpha1-agonist effects and causes vasoconstriction.

Note that this differential effect is debated but could still be tested.

The beta1-agonist activity of dopamine makes it a first-line agent for many cases of symptomatic bradycardia.

22
Q

Isoproterenol

A

is used for its beta1-agonist and beta2-agonist effects in
hypovolemic,
septic, and
cardiogenic shock.

23
Q

What about the use of phenylephrine, epinephrine, and milrinone in the setting of shock?

A

Phenylephrine is used for its pure alpha1-agonist effects; it is similar to norepinephrine but has no beta effects.

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

Milrinone and amrinone are phosphodiesterase inhibitors.

They are used in patients with refractory heart failure (they are not first-line agents) because they have a positive inotropic effect via potentiation of cyclic adenosine monophosphate (cAMP), but they
CANNOT be used in hypotensive patients.

24
Q

Phenylephrine

A

is used for its pure alpha1-agonist effects;

it is similar to norepinephrine but has no beta effects.

25
Q

Epinephrine

A

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

26
Q

Milrinone and amrinone

A

are phosphodiesterase inhibitors.

They are used in patients with refractory heart failure (they are not first-line agents)

because they have a positive inotropic effect via potentiation of cyclic adenosine monophosphate (cAMP), but they

CANNOT be used in hypotensive patients