The blood supply to the AV node almost always comes from the AV nodal artery, which typically branches off the right coronary artery. In about 90% of individuals, this RCA-derived supply perfuses the AV node, making that location the most common source. The SA node has its own nodal artery that often comes from the RCA in roughly half to two-thirds of people, with variation, and the inferior LV or RV walls are supplied by other branches depending on coronary dominance. Because the AV nodal artery is most often RCA-derived and provides the AV node’s blood supply in about 90% of cases, that option best matches the usual anatomy.

When a VAD is set to a high pump speed, the device can pull on the ventricle more than it can fill, creating suction and unstable flow. The best first move is gentle fluid resuscitation to boost preload and improve LVAD filling, which often resolves suction by restoring enough blood to meet the pump’s demand. This approach directly addresses inadequate volume status that can accompany high-speed settings. If preload is now adequate but suction or instability persists, you would then consider adjusting the pump speed downward. Other options, such as increasing vasopressors or giving diuretics, tend to worsen preload or volume status and are not the initial step. Ramping down the speed immediately without assessing preload may be necessary later, but the starting step is to improve volume status with careful fluid administration.

The QRS axis in the frontal plane is the average direction of ventricular depolarization, measured from −180° to +180°. Normal is about −30° to +90°. If the axis shifts further left beyond −90°, you’re into left-axis territory; when it reaches the far left end toward −180°, that region is called extreme axis deviation (often called the northwest axis). The range from 180° (which equals −180°) down to −90° thus lies in this extreme left-directed category, making Extreme Axis Deviation the best match. The other categories describe less extreme leftward tilt or rightward tilt, so they don’t fit this far-left range.

Aortic dissection occurs when the aortic wall is either structurally weakened or subjected to sudden, high wall stress. Diabetes mellitus does not belong to the usual list of risk factors for dissection; in fact, it’s not typically associated with this condition and some data suggest it may even have a neutral or protective association. Hypertension is the most common modifiable risk factor because chronic high blood pressure increases shear stress on the aortic wall, promoting an intimal tear and dissection. Pregnancy adds risk due to the cardiovascular changes—higher blood volume and cardiac output, along with hormonal effects—that can strain the aorta, especially in the presence of a dilated or weakened root. Connective tissue disorders, such as Marfan or Ehlers-Danlos syndromes, predispose to dissection through intrinsic weakness of the aortic media, making it prone to tearing under normal or increased stress. So diabetes mellitus is not listed as a risk factor, whereas hypertension, pregnancy, and connective tissue disorders are.

Left bundle branch block shows delayed activation of the left ventricle, which makes the QRS complex widen. The defining feature is a QRS duration of 120 milliseconds or more, indicating intraventricular conduction delay. Other patterns described aren’t used to define LBBB: Q waves in lateral leads aren’t a required criterion and are often absent in LBBB; a broad terminal R wave in V1–V3 is more typical of a right bundle branch block pattern; and a prolonged PR interval points to first-degree AV block, not LBBB.