Cardiac

Question 1

Risk factors for AKI in cardiac surgery

Answer 1

pre-existing renal dysfunction anemia blood transfusion

Question 2

Baroreceptor reflex aka carotid sinus reflex

Answer 2

(Miller Ch 20)

• Stretch receptors located in carotid sinus and aortic arch.
• If systemic BP >170 then decreased sympathetic activity and activation of parasympathetic activity leading to decreased HR, contractility and vascular.
• Reverse effect if patient hypotensive. Reflex arch is lost if BP less than 50.
• Volatile anesthetics, CCB, ACEi, PDI will lessen CV response via baroreceptor reflex.
• Chronic HTN can reset preset value and can have decreased baroreceptor reflex response.

Question 3

Chemoreceptor reflex

Answer 3

Miller Ch 20

• Chemoreceptors in the carotid bodies and the aortic body respond to changes in pH status and blood O2. At PaO2 of less than 50 mm Hg or in acidosis, the chemoreceptors send afferent signals to the medulla.
• This area responds by stimulating the respiratory centers and thereby increasing ventilatory drive. Also activation of the parasympathetic system ensues and leads to a reduction in heart rate and myocardial contractility.
• In the case of persistent hypoxia, the CNS will be directly stimulated, with a resultant increase in sympathetic activity.

Question 4

Bezold-Jarisch reflex

Answer 4

(Barasch p.935)

• Bezold-Jarisch reflex responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the left ventricular wall by inducing the triad of hypotension, bradycardia, and coronary artery dilatation.
• Usually seen with neuraxial anesthesia and hypotension with accompanying bradycardia.
• This reflex is mediated by 5HT-3 serotonin receptors located in the vagus nerve and in ventricular myocardium.
• Activation of these receptors in response to systemic hypotension increases efferent vagal signaling, producing bradycardia, reduced cardiac output, and worsened hypotension.
• 5HT-3 receptor antagonists like ondansetron may mitigate the hemodynamic effects of neuraxial anesthesia

Question 5

Vagal maneuvers

Answer 5

(Miller Ch 20)

• Forced expiration against a closed glottis -> increased intrathoracic pressure, increased central venous pressure, and decreased venous return ->Cardiac output and blood pressure decreased initially.
• Low BP sensed by baroreceptors and will reflexively result in an increase in heart rate and myocardial contractility through sympathetic stimulation.
• When the glottis opens, venous return increases and causes the heart to respond by vigorous contraction and an increase in blood pressure.
• This increase in arterial blood pressure will then be sensed by baroreceptors, thereby stimulating the parasympathetic efferent pathways to the heart.

Question 6

Cushing’s reflex

Answer 6

(Miller Ch 20)

• Cerebral ischemia due to raise ICP will induce activation of sympathetic system -> increase in heart rate, arterial blood pressure, and myocardial contractility (to improve CPP).
• Due to high vascular tone, reflex bradycardia mediated by baroreceptors.

Question 7

Oculocardic reflex

Answer 7

(Barasch p1379)

• This reflex is triggered by pressure on the globe (or left over tissue from enuclation) and by traction on the extraocular muscles as well as on the conjunctiva or the orbital structures.
• Also be elicited by performance of an eye block and by ocular trauma.
• The afferent limb is trigeminal and the efferent limb is vagal.
• Although the most common manifestation of the oculocardiac reflex is sinus bradycardia. Cardiac dysrhythmias may occur (junctional rhythm, ectopic atrial rhythm, AV blockade, multifocal premature ventricular contractions, wandering pacemaker, asystole, and ventricular tachycardia).
• This reflex may appear during either local or general anesthesia; augmented by, hypercarbia and hypoxemia

Question 8

Bainbridge reflex

Answer 8

(Miller Ch 20)

• It is elicited by stretch receptors located in the right atrial wall and the cavoatrial junction. An increase in right-sided filling pressure sends vagal afferent signals to the cardiovascular center in the medulla.
• These afferent signals inhibit parasympathetic activity, thereby increasing the heart rate. Acceleration of the heart rate also results from a direct effect on the SA node by stretching the atrium.
• The changes in heart rate are dependent on the underlying heart rate before stimulation.