Shock Flashcards
What is the general definition of shock?
Shock is defined as low tissue perfusion resulting in cellular injury and tissue hypoxia.
What laboratory finding is commonly seen in all types of shock?
Elevated lactate dehydrogenase.
What clinical symptoms are commonly seen in patients with shock?
- Hypotension with a mean arterial pressure less than 70 mmHg.
- Clinical signs of hypoperfusion including cold skin.
- Altered mental status.
- Low urine output.
What is the normal urine output rate?
Greater than or equal to 0.5 milliliters per kilogram per hour in adults.
What is cardiac index and its normal value?
Cardiac output corrected for body surface area. Normal cardiac index is between 2.8 to 4.2 liters per minute per meter squared.
What is central venous oxygen saturation and its normal value?
A measure of oxygen delivery and utilization. Normal central venous oxygen saturation is between sixty five and seventy five percent.
What are the most common causes of hypovolemic shock?
Hemorrhage, dehydration, and burns.
How do patients with hypovolemic shock present?
Cold and clammy skin, hypotension, tachycardia, weak pulses, and decreased urine output.
What are the hemodynamic parameters in hypovolemic shock?
- Decreased central venous pressure.
- Decreased pulmonary capillary wedge pressure.
- Decreased cardiac output and cardiac index.
- Increased systemic vascular resistance.
- Decreased central venous oxygen saturation.
What is the pulse pressure in hypovolemic shock?
narrow.
What is the management for hypovolemic shock?
- Fluid resuscitation with crystalloids such as normal saline or lactated Ringer’s solution.
- Blood transfusion if hemorrhagic shock is present.
What are the most common causes of cardiogenic shock?
Acute myocardial infarction, heart failure, valvular disease, and arrhythmias.
How do patients with cardiogenic shock present?
Chest pain, tachycardia, hypotension, pulmonary congestion, and cool extremities.
What are the hemodynamic parameters in cardiogenic shock?
- Increased central venous pressure.
- Increased pulmonary capillary wedge pressure.
- Decreased cardiac index.
- Increased systemic vascular resistance.
- Decreased central venous oxygen saturation.
What is the management of cardiogenic shock?
- Inotropes such as dobutamine (perferred when the cardiac index is low but the BP is normal) or milrinone (is a PDE3 inhibitor that increases cardiac output).
- Vasopressors if hypotensive such as norepinephrine
- Mechanical support including intra-aortic balloon pump or extracorporeal membrane oxygenation.
What are the most common causes of obstructive shock?
- Cardiac tamponade
- Tension pneumothorax
- Pulmonary embolism
How do patients with obstructive shock secondary to cardiac tamponade present?
- Hypotension
- Distended neck veins also known as jugular venous distension
- Pulsus paradoxus in cardiac tamponade
- In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased due to external compression by pericardial fluid.
- Respiratory distress in pulmonary embolism or pneumothorax
What are the hemodynamic parameters in obstructive shock secondary to pulmonary embolism?
- Increased central venous pressure
- Pulmonary capillary wedge pressure is decreased in acute PE because less blood is pevented from going to lungs from the right atrium to the lungs.
- Decreased cardiac index due to obstructed flow from the lungs to the left atrium and left ventricle.
- Increased systemic vascular resistance.
- Decreased central venous oxygen saturation
What is PCWP in tension pneumothorax and pulmonary embolism?
Decreased.
How does cardiac tamponade affect pulmonary capillary wedge pressure?
Pulmonary capillary wedge pressure is paradoxically increased due to external compression of pericardial fluid, despite decreased left-sided preload.
What would be the hemodynamics of PCWP in PE?
This will be decreased due to low blood delivery.
What is the management of obstructive shock?
Relieve the obstruction. Perform pericardiocentesis for tamponade, thrombolysis or embolectomy for pulmonary embolism, and needle decompression for tension pneumothorax.
What are the most common causes of distributive shock?
Sepsis, anaphylaxis, and neurogenic shock.
How do patients with distributive shock present?
Warm, flushed skin early on, hypotension, tachycardia, wide pulse pressure, and bounding pulses.
What are the hemodynamic parameters in distributive shock?
- Decreased central venous pressure
- Decreased pulmonary capillary wedge pressure
- Increased cardiac index
- Decreased systemic vascular resistance
- Increased/normal central venous oxygen saturation (ScvO₂)
What is SVR in septic shock?
Low.
What is the management of distributive shock?
- Intravenous fluids.
- Vasopressors such as norepinephrine if MAP <65 mmHg.
- Give antibiotics for sepsis.
(Ceftriaxone for adults, Cefotaximine for children) - Give epinephrine for anaphylaxis.
What is the unique feature of neurogenic shock compared to other types of shock?
Everything is decreased including central venous pressure, pulmonary capillary wedge pressure, cardiac index, systemic vascular resistance, and in neurogenic shock, central venous oxygen saturation (ScvO₂) is typically increased or normal.
How does neurogenic shock present?
- Hypotension.
- Warm skin.
- Bradycardia due to a lack of compensatory tachycardia due to autonomic dysfunction.
What is the management of neurogenic shock?
- Intravenous fluids
- vasopressors such as norepinephrine
- atropine for bradycardia
What is the first-line vasopressor for septic, cardiogenic, and hypovolemic shock?
Norepinephrine, which acts on alpha one receptors more than alpha two and beta one receptors.
Which vasopressor is used if norepinephrine causes tachyarrhythmias?
Phenylephrine, which acts only on alpha one receptors.
What is the role of vasopressin in shock management?
Adjunctive vasopressor that increases systemic vascular resistance via vasopressin one and vasopressin two receptors.
What is the primary agent of choice for anaphylaxis?
Epinephrine, which has stronger effects on beta receptors than alpha receptors.
Which vasopressor is a second-line agent for bradycardia refractory to atropine?
Dopamine, which acts on dopamine one receptors at low doses, beta one receptors at moderate doses, and alpha one receptors at high doses.
Which oral agent is used for chronic hypotension in shock?
Midodrine, which is an alpha one agonist.
What is the initial inotropic agent for cardiogenic shock with low cardiac output and normal blood pressure?
Dobutamine, which acts on beta one receptors more than beta two and alpha receptors.
Which inotropic agent is a phosphodiesterase three inhibitor used in cardiogenic shock?
Milrinone, which increases cardiac output and causes vasodilation.
What are the preferred agents for rapid sequence intubation in hemodynamically stable patients vs unstable patients?
Ketamine is best used for patients with asthma, sepsis, or hemodynamically unstable patients due to its bronchodilatory and catecholamine-releasing effects. Ketamine, a phencyclidine derivative, is the preferred agent to use for awake intubations because it provides dissociation, amnesia, and analgesia (ie, dissociative anesthesia) while maintaining upper airway tone, protective airway reflexes, and respiratory drive. It also causes a sympathetic surge (by inhibiting reuptake of catecholamines) that increases blood pressure and causes bronchial smooth muscle relaxation, which are additional benefits in this patient with hypotension and bronchospasm.
Etomidate is most commonly used due to its rapid onset, hemodynamic stability, and minimal cardiovascular depression.
Propofol can provide rapid-onset sedation and amnesia. It typically causes deep sedation, respiratory depression, and loss of airway reflexes, which would be dangerous in patients with respiratory diseases. In addition, it can worsen hypotension.
When endotracheal intubation has failed, what is the best alternative?
Management of the failed airway (ie, airway that cannot be intubated on initial attempts) is determined by the ability to oxygenate the patient using mask ventilation. In patients who cannot be adequately oxygenated (“can’t intubate, can’t oxygenate”) due to upper airway obstruction, a surgical airway (ie, cricothyrotomy) should be performed. In contrast, patients who can be oxygenated via bag valve mask ventilation (“can’t intubate, can oxygenate”) may tolerate further intubation attempts. Adjunctive airway techniques (eg, video laryngoscopy) may increase the chance of success. After several attempts to secure a definitive airway via awake intubation have failed, and when the patient is threatened with severe hypoxia with signs concerning for impending cardiac arrest (eg, severe hypotension, falling heart rate), cricothyrotomy should be performed immediately to bypass the upper airway obstruction and restore ventilation and oxygenation. The procedure involves incising the cricothyroid membrane and inserting an endotracheal or tracheostomy tube, which can be used for mechanical ventilation. Especially if there is rapidly progressive airway edema (which further airway instrumentation will only increase), additional intubation attempts are unlikely to succeed and will only increase the risk of deterioration.
