CRNA Exam

The chapters move from the cardiovascular system to the airway and lungs, then to the nervous system and neuromuscular junction, and finish with the renal, hepatic, endocrine, hematologic, thermoregulatory and immune systems plus the changes of aging and pregnancy. Every value used here is a mainstream teaching value; when sources differ, the commonly accepted range is given.

This chapter covers coronary anatomy and dominance, the conduction system, the cardiac cycle and pressure-volume loops, the determinants of cardiac output, myocardial oxygen balance, cardiovascular reflexes and vascular physiology.

The left main coronary artery arises from the left aortic sinus and divides into the left anterior descending (LAD) and circumflex arteries. The LAD supplies the anterior left ventricle, the anterior two-thirds of the interventricular septum and the apex. The circumflex supplies the lateral wall. The right coronary artery (RCA) supplies the right ventricle, the right atrium and, in most people, the inferior wall of the left ventricle.

Dominance is defined by which artery gives rise to the posterior descending artery (PDA). About 70-85% of people are right dominant, about 5-10% are left dominant (PDA from the circumflex) and the rest are codominant. In a right-dominant heart the RCA supplies the AV node in about 85-90% of people; the SA node is supplied by the RCA in about 60% and by the circumflex in about 40%.

The left ventricle is perfused mainly during diastole because systolic wall tension compresses the subendocardial vessels. The right ventricle, with its lower wall pressure, is perfused in both systole and diastole. The subendocardium of the left ventricle is the most vulnerable region for ischemia. Venous blood returns mainly through the coronary sinus into the right atrium; a small amount drains directly into the chambers through Thebesian veins, which contributes to normal anatomic shunt.

Coronary perfusion pressure (CPP) = aortic diastolic pressure - LVEDP

Worked example: a patient has an arterial pressure of 118/52 mmHg and a pulmonary artery occlusion pressure (an estimate of LVEDP) of 22 mmHg. CPP = 52 - 22 = 30 mmHg. If phenylephrine raises diastolic pressure to 64 mmHg and diuresis lowers the LVEDP to 14 mmHg, CPP = 64 - 14 = 50 mmHg. Both raising diastolic pressure and lowering filling pressure improve coronary perfusion.

The SA node in the right atrium near the superior vena cava is the normal pacemaker (60-100 beats per minute). Impulses travel through the atria to the AV node, where conduction is slowed to allow atrial emptying (the PR interval, normally 0.12-0.20 s). The bundle of His divides into right and left bundle branches, and the left divides into anterior and posterior fascicles before the Purkinje fibers. Intrinsic rates fall as you move down the system: AV junction about 40-60 per minute, ventricular escape about 20-40 per minute.

Pacemaker cells depolarize spontaneously during phase 4 because of the funny current (If) and calcium entry; their upstroke (phase 0) depends on L-type calcium channels. Ventricular myocytes have a fast sodium-dependent phase 0, a plateau (phase 2) from calcium entry, and repolarization (phase 3) from potassium efflux. Calcium entering during the plateau triggers calcium release from the sarcoplasmic reticulum through the ryanodine receptor, which is the basis of excitation-contraction coupling.

The left ventricular pressure-volume loop runs counterclockwise through four phases: filling (mitral valve open), isovolumetric contraction (all valves closed), ejection (aortic valve open) and isovolumetric relaxation (all valves closed). The width of the loop is stroke volume. The lower right corner is end-diastolic volume and pressure; the upper left corner is end-systolic volume and pressure.

The atrial contraction (atrial kick) contributes about 20-30% of ventricular filling in healthy patients and more in stiff, hypertrophied ventricles. This is why loss of sinus rhythm causes sudden hypotension in aortic stenosis and hypertrophic cardiomyopathy.

Cardiac output = heart rate x stroke volume. Stroke volume depends on preload, afterload and contractility. Normal cardiac output is about 4-8 L/min, and cardiac index (output divided by body surface area) is about 2.5-4.0 L/min/m2.

Worked example: heart rate 80 per minute, stroke volume 70 mL. Cardiac output = 80 x 70 = 5,600 mL/min, or 5.6 L/min. With a body surface area of 1.9 m2, cardiac index = 5.6 / 1.9 = 2.9 L/min/m2.

Preload is ventricular wall stretch at end-diastole, best reflected by end-diastolic volume. The Frank-Starling relationship states that, within physiologic limits, greater stretch produces greater stroke volume because of optimal actin-myosin overlap and increased calcium sensitivity. A failing ventricle sits on a flatter curve, so added volume raises filling pressure with little gain in output.

Afterload is the wall tension the ventricle must develop to eject. By the Laplace relationship, wall tension = (pressure x radius) / (2 x wall thickness). A dilated ventricle has higher wall tension at the same pressure; a hypertrophied wall reduces tension but raises oxygen demand and stiffness. Systemic vascular resistance is the clinical surrogate for left ventricular afterload.

Contractility (inotropy) is the intrinsic strength of contraction independent of loading conditions. It is increased by sympathetic stimulation, calcium and inotropes and decreased by volatile anesthetics, beta blockade, acidosis, hypoxemia and hypocalcemia.

The heart extracts about 70-75% of delivered oxygen at rest, so coronary sinus saturation is only about 30%. Because extraction is nearly maximal, increased demand must be met by increased coronary flow.

Heart rate is the single most important factor because tachycardia both raises demand and shortens diastole, the time of left ventricular perfusion.

The baroreceptor reflex is the main short-term regulator of blood pressure. Stretch receptors in the carotid sinus send signals through the glossopharyngeal nerve (via the nerve of Hering), and receptors in the aortic arch send signals through the vagus nerve to the nucleus tractus solitarius in the medulla. A rise in pressure increases vagal tone and decreases sympathetic tone, causing bradycardia and vasodilation. Volatile anesthetics, propofol and chronic hypertension blunt the reflex.

The oculocardiac reflex uses the trigeminal nerve (ophthalmic division, through the ciliary ganglion) as the afferent limb and the vagus nerve as the efferent limb. The Bezold-Jarisch reflex explains sudden bradycardia and hypotension after spinal anesthesia or in the beach chair position with an empty, hypercontractile ventricle.

Clinical Scenario: During strabismus surgery on a 6-year-old, the heart rate drops from 110 to 48 beats per minute as the surgeon pulls on the medial rectus. The CRNA should ask the surgeon to release traction first. If bradycardia persists or recurs, give atropine (about 0.01-0.02 mg/kg IV) and make sure anesthetic depth and ventilation are adequate, because light anesthesia and hypercarbia make the reflex worse. The reflex fatigues with repeated traction.

Mean arterial pressure (MAP) = diastolic pressure + 1/3 (systolic - diastolic)

SVR = 80 x (MAP - CVP) / cardiac output, normal about 800-1,200 dynes-s-cm-5

PVR = 80 x (mean PA pressure - PAOP) / cardiac output, normal about 150-250 dynes-s-cm-5

Worked example: blood pressure 120/60 mmHg, CVP 8 mmHg, cardiac output 5 L/min. MAP = 60 + (60/3) = 80 mmHg. SVR = 80 x (80 - 8) / 5 = 80 x 72 / 5 = 1,152 dynes-s-cm-5, which is in the normal range.

Resistance to flow is inversely related to the fourth power of vessel radius (Poiseuille), so small changes in arteriolar tone produce large changes in SVR. Veins are about 20-30 times more compliant than arteries and hold about 65-70% of blood volume, which makes them the main reservoir that sympathetic tone, anesthetics and positioning shift toward or away from the heart. Venodilation from general or neuraxial anesthesia lowers preload, which is why induction hypotension is worse in the hypovolemic patient.

• Dominance is defined by which artery gives off the PDA; most hearts are right dominant, and the RCA usually supplies the AV node and inferior wall.
• CPP = aortic diastolic pressure minus LVEDP; the left ventricle is perfused mainly in diastole.
• Cardiac output = heart rate x stroke volume; stroke volume depends on preload, afterload and contractility.
• Tachycardia is the most harmful change for myocardial oxygen balance because it raises demand and shortens diastolic perfusion time.
• Oculocardiac reflex: trigeminal afferent, vagal efferent; stop traction first, then atropine.
• SVR = 80 x (MAP - CVP) / CO, normal about 800-1,200 dynes-s-cm-5.