1. The SA node is located at the junction of the superior vena cava (SVC) and right atrium (RA).

2. Enlargement of the left atrium (LA) on chest x-ray appears as follows:

3. The first three major branches of the aorta are listed:

The innominate divides into the right subclavian and carotid arteries.

4. The two coronary arteries originate from the sinuses of Valsalva in the aortic valve. Occlusion in the anterior descending branch produces ischemic electrocardiogram (ECG) changes in leads V₃ to V₅. Circumflex occlusion is seen in leads I and aVL. Two main branches of the right coronary artery (RCA) are the sinus node artery and the atrioventricular (AV) nodal artery.

5. The blood supply to the AV node and common bundle of His is the AV branch of the RCA (90% of hearts) and the septal perforators of the left anterior descending coronary artery (10% of patients).

6. RCA occlusion produces changes in leads II, III, and aVF on the ECG.

7. The abdominal branches of the aorta include the following:

The kidneys receive 20% of cardiac output (CO) from a single renal artery. The aorta bifurcates into right and left iliac arteries in the lower torso. At the level of the inguinal ligament the iliacs bifurcate into the superficial (profunda) femoral artery and the deep femoral artery. Just below the knee, the femoral artery divides into the anterior and posterior tibial arteries.

8. The blood supply to the spinal cord consists of the anterior spinal arteries (75%) (from the vertebral arteries) and posterior spinal artery (25%) (from the terminal portion of the anterior spinal artery). There are also several radicular branches (from the intercostal and lumbar arteries) that anastomose with the anterior spinal artery. The largest of these is called the arteria radicularis magna (artery of Adamkiewicz) in the lower thoracic/upper lumbar region.

The liver is supplied by both the hepatic artery (25% of CO) and the portal vein. The portal vein supplies 65% to 80% of the total hepatic blood flow.

9. Thebesian, bronchial, and pleural venous flows contribute the normal 1% to 3% of arteriovenous shunt.

1. The AV node is located in the floor of the RA near the ostium of the coronary sinus.

2. The sympathetic innervation to the heart and blood vessels comes from the thoracolumbar region; the three major nerves from the stellate and middle cervical ganglia are listed here:

The end result of sympathetic stimulation is beta-1-adrenergic receptor activation.

3. The parasympathetic neurons arise in the cervical region and from the medulla oblongata and the nucleus ambiguus. These fibers from the latter two enter the thorax as branches from the recurrent laryngeal and thoracic vagus nerves (the motor efferents).

4. The innervation of the peripheral circulation originates from the thoracolumbar sympathetic fibers. Alpha-adrenergic stimulation causes constriction in the arterial vascular beds of the skin, skeletal muscle, splanchnic organs, kidneys, and systemic veins. Beta-2-receptor stimulation dilates systemic veins and arteries of the muscle, splanchnic, and renal circulations.

5. Oxygen (O₂) saturation (SaO₂) is greater in the inferior vena cava than in the SVC because of the contribution of blood from the renal veins.

6. The total amount of contrast should not exceed 5 mL/kg because contrast media are hyperosmolar substances that depress the myocardium, dilate the coronary arteries, decrease blood pH, increase serum osmolarity, and cause allergic reactions.

7. Ventricular systole occurs immediately following the QRS complex.

8. Coronary arteriography occasionally causes ventricular ectopy, asystole, or fibrillation. Injection in the RCA produces T-wave inversion in lead II, and injection in the left coronary artery (LCA) produces a peaked T wave in lead II.

1. The Fick equation measures O₂ consumption by measuring the arteriovenous O₂ concentration difference (× CO × 100). Arterial and mixed-venous O₂ contents are calculated using (0.00031 × PO₂) + (1.34 × Hgb × SaO₂%)

2. Thermodilution outputs are subject to inaccuracies because of the following:

3. The v wave on the venous pressure tracing corresponds to the gradual increase in atrial blood volume as blood returns from the periphery. It crests when the atria are filled, and the tricuspid and mitral valves open to initiate ventricular filling.

The y wave results from the opening of the AV valves combined with ventricular relaxation.

4. Acute atrial fibrillation (AF) increases atrial pressures, reduces atrial compliance, increases atrial O₂ consumption, and eliminates the contribution of the atria to ventricular filling (there is no a wave on the venous pressure tracing).

5. An S₃ heart sound occurs at the point of transition from rapid ventricular filling to reduced ventricular filling. An S₄, which occurs 0.04 second after the P wave, results from the vibrations of the left ventricular (LV) muscle and mitral valve. It is most likely to occur with vigorous atrial contraction.

6. The c wave marks the isovolumetric phase of ventricular contraction. It is the period between closure of the AV valves and opening of the semilunar (aortopulmonary) valves. These valves open at the summit of the c wave.

7. S₁ notes the closure of the AV valves. Since right ventricular (RV) and LV contractions are normally slightly asynchronous, S₁ is usually split. S₂ results from rapid deceleration of blood, causing vibration of the outflow tracks and great vessels and closure of the semilunar valves.

1. In automatic cells of the SA and AV nodes, slow, spontaneous depolarization occurs during phase 4. The rate of automatic cells depends on the following:

Other factors include decrease or increase in the resting membrane potential, hypothermia, hypoxia, and ischemia.

2. The inhibitory parasympathetic system usually predominates in the heart over the sympathetic system. Parasympathetic stimulation (particularly of the right vagus nerve) decreases heart rate (HR) by slowing the SA node and tends to suppress ventricular automaticity. It may facilitate termination of ventricular dysrhythmias.

3. Effects of receptors in the heart include the following:

The effects of norepinephrine (NE) on contractility are mediated by calcium.

4. Types of ventricular receptors in the heart include the following:

5. The majority of LCA flow occurs during diastole. In the RCA, the majority of flow occurs during both systole and diastole because intramyocardial pressure is lower in the thinner RV.

6. O₂ extraction in the heart cannot be increased further; therefore, coronary flow must increase if the heart requires additional O₂. Coronary venous blood is only 30% saturated, with a PO₂ of 18 to 20 mm Hg.

7. Coronary pressure is autoregulated between 50 and 120 mm Hg.

1. Factors affecting coronary autoregulation include myocardial O₂, coronary venous O₂, decreased HR, pharmacologic coronary constriction, metabolic regulators (e.g., adenosine), O₂, potassium, pH, carbon dioxide (CO₂), endothelium-derived relaxing factor, prostaglandins, prostacyclin, histamine, and adenosine triphosphate.

2. Coronary flow reserve is the difference between resting and maximal coronary flow. It can be decreased by decreased maximal flow or increased regulated coronary flow.

3. Arteriolar vasodilation occurs in the face of coronary artery stenosis to maintain flow at normal levels. Once the vasodilator reserve is exhausted (stenosis >90%), an increase in stenosis will decrease flow. Coronary steal occurs when a vasodilator is administered to a vascular bed supplied by both a normal and a stenosed artery connected by collaterals. The vasodilator will dilate the normal arterioles but will produce little change in arterioles served by the stenotic artery because they are already maximally dilated. Blood will be “stolen” from the ischemic area to perfuse the dilated normal arterioles.

4. Sympathetic stimulation causes coronary dilatation as a result of the metabolic factors produced by increased myocardial O₂ demand (MVO₂) and direct beta-receptor stimulation.

5. CO is the volume of blood pumped by the heart each minute: CO = HR × stroke volume (SV). CO increases with increased HR, preload or contractility, and with decreased afterload. CO is decreased by decreased HR, contractility, or preload and increased afterload. CO is also affected by ventricular compliance.

6. Preload can be defined as all of the factors that contribute to passive ventricular wall stress (or tension) at the end of diastole. Determinants of preload include the following:

SV is the difference between the ventricular end-diastolic volume (EDV) and the endsystolic volume (ESV).

7. Afterload is all the factors that contribute to total myocardial wall stress (or tension) during systolic ejection. It depends upon the following:

Systemic vascular resistance (SVR) is frequently used to approximate afterload. SVR underestimates afterload when afterload is increased or decreased or contractility is improved.

1. CO can be increased by the following:

2. Contractility is decreased by the following:

3. Compliance is the ability of a blood vessel or a cardiac chamber to change its volume in response to changes in pressure.

4. According to Starling’s law, contractility depends on muscle fiber length. Increased preload or initial fiber length leads to increased resting tension, velocity of tension development, and peak tension. An increased venous return stretches muscle fibers to increase contractility and improve CO. Peak ventricular output occurs at normal filling pressures of approximately 10 mm Hg.

5. Pressure-volume loops are a more accurate index of contractility and compliance because they are less affected by preload, afterload, or other conditions; performance is difficult to measure and not immediately available for patient care. The values that can be determined from the pressure-volume loop include the following:

6. In pressure-length loops, ventricular segment length is plotted on the x-axis and ventricular pressure on the y-axis. They have four segments:

These loops are altered by changes in preload, afterload, and inotropic state and by ischemia.

7. Force-velocity curves are sensitive evaluators of contractility that ultimately demonstrate that there is an inverse relationship between shortening velocity and afterload. A passively stretched muscle is stimulated to contract against either no load or an afterload, which is measured as the tension that develops.

1. Myocardial metabolism includes both substrate utilization and O₂ consumption. The energy supply of the heart is derived primarily from fatty acids and carbohydrates (lactate). During fasting, energy is derived from fatty acids, and postprandially from glucose (glucose is used only during high glucose levels, insulin secretion, or hypoxia).

2. Myocardial O₂ consumption at rest is 8 to 10 mL/100 g myocardium per minute. The subendocardium requires approximately 20% more O₂ than the epicardium; therefore, it is more vulnerable to ischemia. Myocardial O₂ consumption is determined by the following:

Less important factors include O₂ costs of shortening muscle fibers, electrical activation, catecholamines, basal O₂ requirements, and level of arterial oxygenation.

3. Wall-tension components include the following:

4. Myocardial O₂ supply depends on the following:

O₂ content is due to PaO₂, hemoglobin, and 2,3-diphosphoglycerate (2,3-DPG), as well as pH, PCO₂, or temperature effects on the oxy-hemoglobin dissociation curve.

5. Coronary perfusion pressure is the difference between the aortic diastolic pressure and the LVEDP. This relationship does not hold in coronary occlusive disease because the pressure distal to a coronary stenosis is lower than the aortic diastolic pressure.

6. Normal O₂ extraction by the heart is 60% to 70% (it changes very little with increased cardiac work due to decreases in coronary vascular resistance). If the coronary vascular response is limited, O₂ extraction can be increased to >90%. An increase in O₂ extraction and coronary vasodilation constitutes the metabolic reserve of the heart during increased demand.

7. The CO is distributed to the following organs:

The organ circulations that autoregulate (maintain a constant blood flow) include cerebral, renal, coronary, hepatic arterial, intestinal, and muscle vascular beds.

1. The carotid sinus reflex (pressoreceptor/baroreceptor reflex) occurs when an increase in blood pressure (BP) stretches pressoreceptors in the carotid sinus or arch of the aorta to increase their frequency of discharge, which increases parasympathetic activity (decreased sympathetic activity). This leads to decreased cardiac contractility, HR, and vasoconstrictor tone.

2. The Valsalva maneuver can be used to assess autonomic reflex control of cardiovascular function. It is a forced expiration against a closed glottis, holding this for at least 10 seconds. It decreases venous return to the right ventricle, which causes a decreased CO and BP, with a reflex increase in HR. With glottic opening, venous return suddenly increases and elicits the pressoreceptor response to produce transient bradycardia.

3. The Bezold-Jarisch reflex causes hypotension, bradycardia, and parasympathetically induced coronary vasodilation in response to noxious stimuli to the ventricular wall.

4. Cushing’s reflex is severe hypertension associated with reflex bradycardia to maintain perfusion of (or reperfuse) the brain. Increases in intracranial pressure compress the cerebral arteries, causing cerebral ischemia and resultant increased sympathetic activity. The increased sympathetic activity leads to severe peripheral vasoconstriction. The ensuing hypertension is associated with a reflex bradycardia.

5. The Bainbridge reflex causes an increased HR when vagal tone is high and the RA or central veins are distended. It is primarily mediated through vagal myelinated fibers. Global atrial distention in response to high pressures causes bradycardia, hypotension, and decreased SVR.

6. Peripheral chemoreceptors are located in the carotid and aortic bodies and are sensitive to decreasing O₂ tension or increased hydrogen ion concentrations. The effects of stimulation of the carotid bodies are increased pulmonary ventilation and BP while HR is decreased. Stimulation of the aortic bodies causes tachycardia.

7. The oculocardiac reflex is caused by traction or pressure on the globe, leading to bradycardia and hypotension. Traction on the medial rectus muscle is likely to elicit this reflex, involving the ciliary ganglion through the ophthalmic division of the trigeminal nerve through the gasserian ganglion. It is usually abolished by cessation of the stimulating event, and attenuated by intravenous atropine administration.

8. The celiac reflex stimulates afferent vagal nerve endings to cause bradycardia, apnea, and hypotension (vasovagal reflex).

1. The arterial pulse waveform is the result of the combined effects of the forward-propagating pressure wave and its reflectance back toward the heart from various parts of the vasculature. Systolic pressure is higher, whereas mean and diastolic pressures are slightly lower in the periphery. The contour of the pressure wave depends on the velocity of the pressure wave, the duration of the pulse, and the length of the tube.

2. Mean BP is

DBP + (SBP-DBP/3)

Mean BP remains constant, while pulse and SBP increase peripherally. BP decreases by <6 mm Hg with respiration because pulmonary venous capacitance increases during inspiration to a greater extent than the increase in right-sided heart venous return and output, causing a decrease in LV stroke output and pressure.

3. Factors controlling BP and peripheral vascular tone include the following:

Brain natriuretic peptide, related to ANF, is a hormone secreted specifically by the left ventricular myocytes. Its concentration is correlated with the severity of symptomatic or asymptomatic left ventricular dysfunction.

4. Endothelium-derived relaxing factor causes relaxation of vascular smooth muscle and inhibits platelet adhesion and aggregation. It activates soluble guanylate cyclase to increase intracellular cyclic guanosine monophosphate. Endothelium-derived relaxing factor is nitric oxide.

5. ANF is released in response to increased vascular volume (atrial distention), epinephrine, vasopressin, acetylcholine, morphine, and increased atrial pressure.

Effects of ANF include the following:

ANF is increased in congestive heart failure (CHF) and atrial tachydysrhythmias.