Vasodilators in Cardiac Anesthesia — MCQs
Most potent cerebral vasodilator is
All are vasodilators except –
Which of the following anaesthetic agent causes bone marrow suppression?
Which calcium channel blocker has the shortest duration of action?
Which of the following drugs acts as a direct vasodilator on blood vessels?
Anesthetic agent (s) safe to use in ICP
A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
An inhalation anaesthetic agent was used in a surgery which caused high output renal failure. The agent is:
Which of the following is NOT a treatment for supraventricular tachycardia with hypotension in a patient under general anesthesia?
What is the component of Advanced Cardiovascular Life Support (ACLS) in accordance with AHA 2015 guidelines?
Vasodilators in Cardiac Anesthesia Indian Medical PG Practice Questions and MCQs
Question 1: Most potent cerebral vasodilator is
- A. Nitroprusside
- B. Nitro-glycerine
- C. Hypercarbia (Correct Answer)
- D. Beta blocker
Explanation: ***Hypercarbia*** - **Hypercapnia** (increased arterial carbon dioxide tension, PaCO2) is the most potent physiological cerebral vasodilator. - An increase in PaCO2 directly causes cerebral arterioles to dilate, leading to a significant increase in **cerebral blood flow (CBF)** to help clear excess CO2. *Nitroprusside* - **Sodium nitroprusside** is a powerful systemic vasodilator that also affects cerebral vessels, but its primary action is not selectively cerebral. - Its effects on CBF are complex and can be inconsistent in comparison to CO2, and it carries risks like **cyanide toxicity**. *Nitroglycerin* - **Nitroglycerin** primarily causes venodilation and has some arterial vasodilating effects, mainly in vascular beds like the coronary arteries. - While it can cause some cerebral vasodilation, it is not as potent or direct in modulating CBF as CO2. *Beta blocker* - **Beta-blockers** (e.g., propranolol, metoprolol) are primarily used to reduce heart rate, blood pressure, and myocardial contractility. - They generally have **minimal or no direct vasodilatory effect** on cerebral blood vessels; some may even cause vasoconstriction.
Question 2: All are vasodilators except –
- A. Lidocaine
- B. Procaine
- C. Bupivacaine
- D. Cocaine (Correct Answer)
Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics because it causes **vasoconstriction** rather than vasodilation. - This vasoconstrictive effect is due to its blocking of **norepinephrine reuptake** at adrenergic nerve terminals, leading to an accumulation of norepinephrine and subsequent adrenergic stimulation. *Lidocaine* - Lidocaine is a common **amide-type local anesthetic** known for its vasodilatory properties that contribute to its systemic absorption. - Its vasodilatory effect can lead to a **flushing** sensation and increased blood flow in the area of injection. *Procaine* - Procaine is an **ester-type local anesthetic** that causes vasodilation, which results in a relatively short duration of action. - This vasodilation increases **local blood flow**, speeding up the systemic absorption and metabolism of the drug. *Bupivacaine* - Bupivacaine is an **amide-type local anesthetic** with longer duration of action compared to lidocaine, and like most local anesthetics, it causes vasodilation. - The vasodilatory effect of bupivacaine can lead to increased **systemic absorption** and potential for systemic toxicity if not managed carefully.
Question 3: Which of the following anaesthetic agent causes bone marrow suppression?
- A. Isoflurane
- B. Halothane
- C. Ketamine
- D. Nitrous Oxide (Correct Answer)
Explanation: ***Nitrous Oxide*** - **Nitrous oxide** can cause **bone marrow suppression** due to its ability to irreversibly oxidize the **cobalamin cofactor** of **methionine synthase**. - This inactivation leads to reduced DNA synthesis and impacts rapidly dividing cells like those in the bone marrow, potentially causing **megaloblastic anemia** with prolonged or repeated exposure. *Isoflurane* - **Isoflurane** is a volatile anesthetic known for its minimal effects on bone marrow function. - It primarily acts on the central nervous system to induce anesthesia and muscle relaxation with limited systemic toxicities. *Halothane* - **Halothane** is associated with **hepatotoxicity** (halothane hepatitis) in some susceptible individuals, but not bone marrow suppression. - Its use has largely been replaced by newer, safer volatile anesthetics due to this risk. *Ketamine* - **Ketamine** is a dissociative anesthetic that primarily affects the central nervous system, causing analgesia and amnesia. - It does not significantly impact bone marrow function or hematopoiesis.
Question 4: Which calcium channel blocker has the shortest duration of action?
- A. Diltiazem
- B. Amlodipine
- C. Nimodipine (Correct Answer)
- D. Verapamil
Explanation: ***Nimodipine*** - Nimodipine is a **dihydropyridine calcium channel blocker** specifically formulated for cerebral vasodilation and used in conditions like **subarachnoid hemorrhage**. - It has a relatively **short half-life** and rapid onset, making its duration of action shorter compared to other commonly used calcium channel blockers. *Amlodipine* - Amlodipine is known for its **long duration of action** and once-daily dosing due to its slow absorption and high bioavailability. - Its prolonged action is beneficial for conditions like **hypertension and angina**, where sustained vasodilation is desired. *Diltiazem* - Diltiazem's duration of action is **intermediate** compared to other calcium channel blockers, often requiring BID to TID dosing for immediate-release formulations. - It's a **non-dihydropyridine calcium channel blocker** with effects on both vascular smooth muscle and cardiac conduction. *Verapamil* - Verapamil also has an **intermediate duration of action**, similar to diltiazem, with immediate-release forms requiring multiple daily doses. - As a **non-dihydropyridine calcium channel blocker**, it has significant effects on myocardial contractility and AV nodal conduction.
Question 5: Which of the following drugs acts as a direct vasodilator on blood vessels?
- A. Verapamil
- B. Propranolol
- C. Methyldopa
- D. Hydralazine (Correct Answer)
Explanation: ***Hydralazine*** - **Hydralazine** is a **direct-acting vasodilator** that works by directly relaxing the smooth muscle of **arterioles**. - Unlike drugs that work through receptors or central mechanisms, hydralazine acts **directly on vascular smooth muscle** to cause relaxation. - This direct relaxation leads to a decrease in **peripheral vascular resistance**, which lowers blood pressure. - It is a prototype drug for understanding direct vasodilator mechanisms. *Verapamil* - **Verapamil** is a **non-dihydropyridine calcium channel blocker** that works by blocking L-type calcium channels. - Its vasodilatory effects are **indirect**, mediated through calcium channel blockade rather than direct smooth muscle relaxation. - Its main actions are to reduce **heart rate** and **myocardial contractility**, with secondary vasodilation. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that primarily reduces blood pressure by decreasing heart rate and myocardial contractility. - Its effects on blood vessels are **indirect**, mainly by blocking **beta-1 receptors** in the heart and **beta-2 receptors** in the vasculature. - It is not a direct vasodilator and may even cause vasoconstriction due to unopposed alpha-adrenergic effects. *Methyldopa* - **Methyldopa** is an **alpha-2 adrenergic agonist** that acts **centrally** in the brainstem to reduce sympathetic outflow. - It does not directly act on blood vessels but rather reduces peripheral vascular tone through its **central nervous system effects**. - Its mechanism is indirect, working through the CNS rather than peripheral vascular tissue.
Question 6: Anesthetic agent (s) safe to use in ICP
- A. Ketamine
- B. Thiopentone (Correct Answer)
- C. Halothane
- D. Ether
Explanation: ***Thiopentone*** - **Thiopentone** is an ultrashort-acting barbiturate that reduces cerebral blood flow and cerebral metabolic rate, leading to a decrease in **intracranial pressure (ICP)**. - It rapidly depresses brain activity, which directly lowers the demand for oxygen and nutrients, thus decreasing the blood volume within the cranium. *Ketamine* - **Ketamine** is known to increase cerebral blood flow and cerebral metabolic rate, which can lead to an undesirable **increase in ICP**. - It causes cerebral vasodilation, which in patients with compromised intracranial compliance can worsen cerebral edema and raise ICP. *Halothane* - **Halothane** is a potent volatile anesthetic that causes significant **cerebral vasodilation**, leading to an increase in cerebral blood flow and potentially elevated **ICP**. - Its use has largely declined due to its dose-dependent cerebral vasodilation and potential for myocardial depression. *Ether* - **Ether** is an old inhaled anesthetic agent that causes marked **cerebral vasodilation** and increased cerebral blood flow, thereby elevating **ICP**. - It also has a slow onset and offset of action and is highly flammable, making it unsuitable for modern anesthesia, especially in neurosurgical contexts.
Question 7: A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
- A. Bradycardia
- B. Dysrhythmia
- C. Increased peripheral vascular resistance
- D. Hypotension (Correct Answer)
Explanation: ***Hypotension*** - **Hypotension** is a hallmark cardiovascular sign of anaphylaxis, occurring due to widespread **vasodilation** and increased vascular permeability. - This symptom is often profound and unresponsive to initial fluid resuscitation due to the ongoing systemic release of inflammatory mediators. *Bradycardia* - While bradycardia can occur in some rare cases of anaphylaxis (e.g., **vasovagal response**), **tachycardia** is the more common cardiac response due to compensatory mechanisms. - It is not a primary or consistent indicator of anaphylaxis, making it less helpful for diagnosis in this context. *Dysrhythmia* - **Dysrhythmias** can occur during anaphylaxis due to myocardial ischemia or electrolyte imbalances, but they are not a direct or consistent diagnostic feature. - Their presence often reflects severe compromise or co-existing conditions rather than being a primary anaphylactic sign. *Increased peripheral vascular resistance* - Anaphylaxis is characterized by a significant **decrease in peripheral vascular resistance** due to mast cell and basophil degranulation releasing vasodilatory mediators like histamine. - Therefore, an increase in peripheral vascular resistance would contradict the pathophysiology of anaphylaxis.
Question 8: An inhalation anaesthetic agent was used in a surgery which caused high output renal failure. The agent is:
- A. Enflurane
- B. Methoxyflurane (Correct Answer)
- C. Diethyl ether
- D. Halothane
Explanation: ***Methoxyflurane*** - **Methoxyflurane** is extensively metabolized, releasing a significant amount of **free fluoride ions**. - These **fluoride ions** are toxic to the renal tubules, leading to **high-output renal failure** by impairing the kidney's ability to concentrate urine. *Enflurane* - While enflurane also undergoes some metabolism to **fluoride ions**, the amount produced is generally lower than with methoxyflurane and is less likely to cause significant **renal toxicity** in common clinical use. - Its renal effects are typically milder and usually self-limiting, not leading to the severe **high-output renal failure** seen with methoxyflurane. *Diethyl ether* - Diethyl ether is primarily eliminated via the lungs, with very little metabolism, hence it is not associated with **renal toxicity** from fluoride ions. - Its main concerns include flammability and slower induction and emergence, not **renal impairment**. *Halothane* - Halothane is associated with **halothane hepatitis** (liver toxicity) due to its metabolism producing reactive trifluoroacetyl adducts. - It is not known to cause significant **high-output renal failure** due to fluoride toxicity.
Question 9: Which of the following is NOT a treatment for supraventricular tachycardia with hypotension in a patient under general anesthesia?
- A. Carotid sinus massage
- B. Adenosine 3-12 mg IV
- C. Direct current cardioversion
- D. Verapamil 5 mg IV (Correct Answer)
Explanation: ### Explanation The management of intraoperative supraventricular tachycardia (SVT) depends primarily on the patient's **hemodynamic stability**. **1. Why Verapamil is the Correct Answer (The "NOT" treatment):** In a patient with SVT and **hypotension** (hemodynamic instability), calcium channel blockers like Verapamil are **contraindicated**. Verapamil has potent negative inotropic and vasodilator properties. Administering it to a hypotensive patient can cause a further drop in systemic vascular resistance and myocardial contractility, potentially leading to cardiovascular collapse or cardiac arrest. **2. Analysis of Other Options:** * **Direct Current (DC) Cardioversion (Option C):** This is the **treatment of choice** for any tachyarrhythmia causing hemodynamic instability (hypotension, altered mentation, or pulmonary edema) under general anesthesia. Synchronized cardioversion (starting at 50-100J) provides immediate rhythm correction. * **Adenosine (Option B):** If the patient is unstable but IV access is immediately available, Adenosine (6mg, then 12mg) can be attempted as it has an ultra-short half-life and may terminate the reentry circuit without prolonged hemodynamic depression. * **Carotid Sinus Massage (Option A):** This is a non-invasive vagal maneuver that can be attempted quickly to increase vagal tone and slow AV node conduction while preparing for cardioversion. **Clinical Pearls for NEET-PG:** * **Unstable Tachycardia:** Always choose **Synchronized DC Cardioversion**. * **Stable SVT:** First-line is Vagal maneuvers, followed by Adenosine (Drug of Choice). * **Verapamil Warning:** Never give Verapamil in wide-complex tachycardias of unknown origin or in patients with WPW syndrome + Atrial Fibrillation, as it can lead to ventricular fibrillation. * **Amiodarone:** Preferred for stable ventricular tachycardia or refractory SVT.
Question 10: What is the component of Advanced Cardiovascular Life Support (ACLS) in accordance with AHA 2015 guidelines?
- A. Chest compression 100-150 per minute
- B. Chest compression at least 5 cm/2 inch (Correct Answer)
- C. Vasopressors are used to maintain MAP > 70 mmHg in non-responsive to fluids
- D. 1 Breath every 8 seconds
Explanation: This question tests knowledge of the **AHA 2015 Guidelines for CPR and Emergency Cardiovascular Care**, which emphasize high-quality chest compressions as the cornerstone of ACLS. ### **Explanation of the Correct Answer** **Option B** is correct. According to the 2015 guidelines, for an average adult, the chest should be compressed to a depth of **at least 2 inches (5 cm)** but should not exceed 2.4 inches (6 cm). Adequate depth is critical to create enough intrathoracic pressure and direct cardiac compression to maintain vital organ perfusion during cardiac arrest. ### **Analysis of Incorrect Options** * **Option A:** The recommended compression rate is **100–120 per minute**. A rate exceeding 150/min is incorrect as it prevents adequate ventricular filling and reduces cardiac output. * **Option C:** While vasopressors (like Epinephrine) are used in ACLS, the primary goal during active resuscitation is achieving **ROSC** (Return of Spontaneous Circulation), not titrating to a specific MAP of 70 mmHg. MAP targets are more relevant in post-cardiac arrest care. * **Option D:** Once an advanced airway is in place, the ventilation rate is **1 breath every 6 seconds** (10 breaths per minute). A rate of 1 breath every 8 seconds is too slow. ### **High-Yield Clinical Pearls for NEET-PG** * **Compression-to-Ventilation Ratio:** 30:2 (for all adults) until an advanced airway is placed. * **Chest Recoil:** Allow complete chest recoil after each compression; do not "lean" on the chest. * **Minimize Interruptions:** Limit pauses in compressions to less than 10 seconds. * **Capnography (ETCO2):** If ETCO2 is **<10 mmHg**, it indicates poor quality CPR; aim for >20 mmHg. * **Defibrillation:** For shockable rhythms (VF/pVT), the initial dose for a biphasic defibrillator is typically **120–200 J**.
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