Cardiac Autonomic Neuropathy
1. The earliest autonomic abnormality in Cardiac Autonomic Neuropathy is:
Parasympathetic dysfunction occurs first in CAN, leading to early loss of beat-to-beat HR variability.
2. The strongest prognostic implication of CAN is increased risk of:
CAN independently predicts sudden cardiac death due to malignant arrhythmias and silent ischemia.
3. Gold-standard tests for diagnosing CAN are:
CARTs (Ewing tests) assess parasympathetic and sympathetic autonomic function and remain the diagnostic standard.
4. Resting tachycardia in CAN is primarily due to:
Early parasympathetic denervation leads to unopposed sympathetic influence and resting tachycardia.
5. Diagnosis of definite CAN requires:
Definite CAN is diagnosed when two or more autonomic reflex tests are abnormal.
1. The earliest ECG-based manifestation of CAN is best reflected by:
Loss of parasympathetic modulation manifests earliest as reduced RR variability, often years before symptoms.
2. DCCT/EDIC data established that intensive glycemic control in Type 1 DM reduces CAN primarily by:
DCCT showed benefit mainly in preventing early autonomic damage, not reversing advanced CAN.
3. In CAN, silent myocardial ischemia is most directly explained by dysfunction of:
Denervation of afferent pain pathways leads to ischemia without anginal perception.
4. QT prolongation in CAN primarily reflects:
Sympathetic–parasympathetic imbalance alters dispersion of repolarization, predisposing to arrhythmia.
5. Fixed heart rate during exercise in a diabetic patient indicates:
Loss of both autonomic limbs prevents appropriate chronotropic response to exertion.
6. Among CARTs, the most sensitive early test for CAN is:
Respiratory sinus arrhythmia testing detects early parasympathetic loss.
7. Orthostatic hypotension in CAN results primarily from:
Sympathetic efferent failure prevents compensatory increase in SVR on standing.
8. Peri-operative risk in CAN is MOST related to:
Autonomic failure blunts cardiovascular reflexes during induction and volume shifts.
9. CAN is an independent predictor of all-cause mortality because it predisposes to:
QT prolongation, impaired HRV, and ischemic denervation increase sudden cardiac death risk.
10. Best pharmacologic agent for symptomatic orthostatic hypotension in CAN:
Alpha-1 agonism restores peripheral vascular tone in autonomic failure.
11. A diabetic patient with CAN undergoing spinal anesthesia is MOST likely to develop:
Loss of sympathetic vasoconstrictor tone in CAN leads to severe hypotension after neuraxial blockade.
12. A Holter ECG in early CAN will MOST characteristically show:
Reduced SDNN (standard deviation of NN intervals) reflects loss of HRV—earliest ECG marker of CAN.
13. QT dispersion in CAN correlates MOST strongly with:
QT dispersion reflects heterogeneity of repolarization and predicts malignant ventricular arrhythmias.
14. During induction of general anesthesia, a patient with advanced CAN fails to mount tachycardia because of:
Advanced CAN involves sympathetic denervation, abolishing chronotropic response to hypotension or stress.
15. Which ECG finding in CAN indicates the HIGHEST arrhythmic risk?
Combination of QT prolongation and autonomic imbalance markedly increases ventricular arrhythmia risk.
16. A diabetic patient with CAN is MOST likely to experience silent ischemia because of dysfunction in:
Loss of afferent autonomic pain pathways explains painless MI in diabetics with CAN.
17. In peri-operative risk stratification, CAN is MOST comparable to:
Peri-operative instability in CAN mirrors pure autonomic failure physiology.
18. Which anesthetic agent requires PARTICULAR caution in CAN?
Loss of autonomic compensation makes CAN patients extremely sensitive to vasodilatory hypotension.
19. CAN-related resting tachycardia reflects:
Early CAN is dominated by vagal withdrawal, not sympathetic overactivity.
20. A CAN patient with unexplained syncope should FIRST be evaluated for:
Autonomic failure with postural BP drop is a common but overlooked cause of syncope in CAN.
