Vasopressors and inotropes US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Vasopressors and inotropes. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Vasopressors and inotropes US Medical PG Question 1: A patient presents with periods of severe headaches and flushing however every time they have come to the physician they have not experienced any symptoms. The only abnormal finding is a blood pressure of 175 mmHg/100 mmHg. It is determined that the optimal treatment for this patient is surgical. Prior to surgery which of the following noncompetitive inhibitors should be administered?
- A. Phentolamine
- B. Isoproterenol
- C. Atropine
- D. Propranolol
- E. Phenoxybenzamine (Correct Answer)
Vasopressors and inotropes Explanation: ***Phenoxybenzamine***
- This patient likely has a **pheochromocytoma**, which explains the episodic headaches, flushing, and hypertension. **Phenoxybenzamine** is a **non-competitive, irreversible alpha-adrenergic blocker** that is crucial for preoperative preparation to prevent a **hypertensive crisis** during surgery.
- Its **irreversible binding** provides sustained alpha blockade, essential to control blood pressure and avoid catecholamine-induced surges during tumor manipulation.
*Phentolamine*
- **Phentolamine** is a **competitive alpha-adrenergic blocker** used to manage acute hypertensive episodes, but it has a shorter duration of action.
- It is not preferred for sustained preoperative alpha blockade due to its **reversible nature** and potential for drug washout during surgery, which could lead to catecholamine surges.
*Isoproterenol*
- **Isoproterenol** is a **beta-adrenergic agonist** that increases heart rate and contractility, and causes bronchodilation.
- It would be contraindicated in a patient with pheochromocytoma as it could worsen hypertension and cardiac symptoms by stimulating beta receptors that are already overly sensitive to endogenous catecholamines.
*Atropine*
- **Atropine** is a **muscarinic acetylcholine receptor antagonist** that blocks parasympathetic effects, like bradycardia and salivation.
- It has no role in managing hypertension or the catecholamine excess seen in pheochromocytoma.
*Propranolol*
- **Propranolol** is a **non-selective beta-adrenergic blocker** that can be used to control tachycardia and arrhythmias in pheochromocytoma, but only *after* adequate alpha-blockade has been established.
- Using **propranolol alone** or before alpha-blockade can lead to **unopposed alpha-adrenergic stimulation**, resulting in a severe, life-threatening hypertensive crisis.
Vasopressors and inotropes US Medical PG Question 2: A 57-year-old man is admitted to the burn unit after he was brought to the emergency room following an accidental fire in his house. His past medical history is unknown due to his current clinical condition. Currently, his blood pressure is 75/40 mmHg, pulse rate is 140/min, and respiratory rate is 17/min. The patient is subsequently intubated and started on aggressive fluid resuscitation. A Swan-Ganz catheter is inserted to clarify his volume status. Which of the following hemodynamic parameters would you expect to see in this patient?
- A. Cardiac output: ↓, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔
- B. Cardiac output: ↑, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↔
- C. Cardiac output: ↑, systemic vascular resistance: ↓, pulmonary artery wedge pressure: ↔
- D. Cardiac output: ↓, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↓ (Correct Answer)
- E. Cardiac output: ↔, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔
Vasopressors and inotropes Explanation: ***Cardiac output: ↓, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↓***
- The patient's **hypotension (75/40 mmHg)** and **tachycardia (140/min)**, combined with severe burns, indicate **hypovolemic shock** due to massive fluid loss from damaged capillaries.
- In response to decreased cardiac output and hypovolemia, the body compensates by increasing **systemic vascular resistance (SVR)** to maintain perfusion to vital organs, and **pulmonary artery wedge pressure (PAWP)** will be low due to reduced intravascular volume.
*Cardiac output: ↓, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔*
- This option incorrectly suggests that systemic vascular resistance and pulmonary artery wedge pressure would be normal, which is inconsistent with **hypovolemic shock**.
- In shock, the body's compensatory mechanisms would lead to significant changes in SVR and PAWP, not maintain them at baseline.
*Cardiac output: ↑, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↔*
- Increased cardiac output is usually seen in **distributive shock** (e.g., septic shock) where vasodilation leads to reduced SVR, not increased SVR as suggested here.
- An elevated SVR coupled with an increased cardiac output would typically result in a higher blood pressure unless there is a compensatory drop in other parameters.
*Cardiac output: ↑, systemic vascular resistance: ↓, pulmonary artery wedge pressure: ↔*
- This pattern (high cardiac output, low SVR) is characteristic of **distributive shock**, such as **septic shock** or anaphylactic shock, rather than the hypovolemic shock expected in a burn patient.
- Severe burns primarily cause massive fluid shifts, leading to hypovolemia and a reduced cardiac output, not an elevated one.
*Cardiac output: ↔, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔*
- This scenario represents **normal hemodynamic parameters**, which would not be expected in a patient experiencing severe shock from extensive burns.
- The patient's clinical presentation (hypotension, tachycardia) clearly indicates a state of hemodynamic instability.
Vasopressors and inotropes US Medical PG Question 3: A 53-year-old man presents to the office for a routine examination. The medical history is significant for diabetes mellitus, for which he is taking metformin. The medical records show blood pressure readings from three separate visits to fall in the 130–160 mm Hg range for systolic and 90–100 mm Hg range for diastolic. Prazosin is prescribed. Which of the following are effects of this drug?
- A. Vasodilation, decreased heart rate, bronchial constriction
- B. Vasodilation, increased peristalsis, bronchial dilation
- C. Vasoconstriction, bladder sphincter constriction, mydriasis
- D. Vasoconstriction, increase in AV conduction rate, bronchial dilation
- E. Vasodilation, bladder sphincter relaxation (Correct Answer)
Vasopressors and inotropes Explanation: ***Vasodilation, bladder sphincter relaxation***
- **Prazosin** is an **alpha-1 adrenergic receptor antagonist**, which blocks the effects of norepinephrine on vascular smooth muscle, leading to **vasodilation** and decreased blood pressure.
- Blocking alpha-1 receptors in the bladder neck and prostate causes **bladder sphincter relaxation**, which can improve urine flow and is also useful in benign prostatic hyperplasia (BPH).
- These are the two primary clinically relevant effects of alpha-1 blockade with prazosin.
*Vasodilation, decreased heart rate, bronchial constriction*
- While prazosin causes **vasodilation**, it does not typically decrease heart rate directly; alpha-1 blockade can lead to **reflex tachycardia** due to decreased blood pressure.
- Prazosin has no significant effect on bronchial smooth muscle and does not cause **bronchial constriction**; bronchial effects are primarily mediated by beta-2 receptors or muscarinic (M3) receptors.
*Vasodilation, increased peristalsis, bronchial dilation*
- Prazosin does cause **vasodilation** but does not directly cause **increased peristalsis**; gastrointestinal motility is mainly regulated by the autonomic nervous system via muscarinic receptors and the enteric nervous system.
- Prazosin does not cause **bronchial dilation**; this effect is mediated by beta-2 adrenergic receptor stimulation.
*Vasoconstriction, bladder sphincter constriction, mydriasis*
- Prazosin is an alpha-1 antagonist, meaning it *blocks* **vasoconstriction** and instead causes vasodilation.
- Similarly, it causes **bladder sphincter relaxation**, not constriction.
- Prazosin has minimal effects on pupil size; mydriasis would be caused by alpha-1 agonists or muscarinic antagonists, not alpha-1 antagonists.
*Vasoconstriction, increase in AV conduction rate, bronchial dilation*
- Prazosin causes **vasodilation**, not vasoconstriction.
- It does not significantly affect **AV conduction rate** or directly cause **bronchial dilation**.
Vasopressors and inotropes US Medical PG Question 4: A 65-year-old male with a history of CHF presents to the emergency room with shortness of breath, lower leg edema, and fatigue. He is diagnosed with acute decompensated congestive heart failure, was admitted to the CCU, and treated with a medication that targets beta-1 adrenergic receptors preferentially over beta-2 adrenergic receptors. The prescribing physician explained that this medication would only be used temporarily as its efficacy decreases within 2-3 days due to receptor downregulation. Which of the following was prescribed?
- A. Epinephrine
- B. Norepinephrine
- C. Milrinone
- D. Isoproterenol
- E. Dobutamine (Correct Answer)
Vasopressors and inotropes Explanation: ***Dobutamine***
- **Dobutamine** is a beta-1 adrenergic agonist preferentially acting on beta-1 receptors in the heart, increasing contractility and heart rate during acute decompensated heart failure.
- Its efficacy reduces over time due to **receptor downregulation**, making it effective for only short-term use, typically less than 72 hours.
*Epinephrine*
- **Epinephrine** is a non-selective adrenergic agonist acting on both alpha and beta receptors, causing vasoconstriction and bronchodilation in addition to cardiac stimulation.
- It is typically used in emergency situations like **cardiac arrest** and **anaphylaxis**, not primarily for acute CHF exacerbation in this manner.
*Norepinephrine*
- **Norepinephrine** primarily acts on alpha-1 adrenergic receptors, causing significant vasoconstriction, and has some beta-1 agonistic effects.
- It is mainly used as a **vasopressor** in septic shock or severe hypotension to increase systemic vascular resistance, rather than directly improving cardiac output in decompensated CHF.
*Milrinone*
- **Milrinone** is a phosphodiesterase-3 inhibitor, increasing intracellular cAMP levels and leading to positive inotropy and vasodilation.
- While used in acute heart failure, its mechanism is distinct from adrenergic agonists, and its efficacy is not limited by a rapid receptor downregulation mechanism as described.
*Isoproterenol*
- **Isoproterenol** is a non-selective beta-adrenergic agonist, stimulating both beta-1 and beta-2 receptors, leading to increased heart rate and contractility, as well as bronchodilation and vasodilation.
- Due to its strong chronotropic effects and potential for severe arrhythmias and hypotension, it is rarely used in CHF and is primarily reserved for conditions like **bradycardia** or **torsades de pointes**.
Vasopressors and inotropes US Medical PG Question 5: A 77-year-old man with refractory shock has been under treatment in an intensive care unit for last 7 days. Despite the best possible management by the team of physicians and intensivists, he fails to show improvement. After discussion with his relatives and obtaining informed consent from them, the team administers to him a novel drug, an adrenergic agonist that produces positive chronotropic effects and inotropic effects and stimulates the release of renin from the kidneys. The drug does not have any other adrenergic effects. Which of the following second messengers is most likely to be responsible for the actions of the novel drug?
- A. Calcium ion
- B. Cyclic adenosine monophosphate (cAMP) (Correct Answer)
- C. Cyclic guanosine monophosphate (cGMP)
- D. Diacylglycerol (DAG)
- E. Inositol 1,4,5-triphosphate (IP3)
Vasopressors and inotropes Explanation: **Cyclic adenosine monophosphate (cAMP)**
- The drug described is an **adrenergic agonist** with **positive chronotropic** and **inotropic effects**, and it stimulates **renin release**. These actions are characteristic of **beta-1 (β1) adrenergic receptor** activation.
- Activation of β1 receptors is coupled to **G protein-coupled receptors (GPCRs)** that activate **adenylyl cyclase**, leading to an increase in intracellular **cAMP**, which acts as the second messenger.
*Calcium ion*
- While **calcium ions** are crucial for cardiac contractility and renin release, they are often directly modulated downstream by events initiated by second messengers like **cAMP** or **IP3/DAG**, rather than being the primary direct second messenger for β1-adrenergic stimulation.
- For example, increased cAMP in cardiac cells leads to **phosphorylation of L-type calcium channels**, increasing calcium influx, but cAMP itself is the direct initiating second messenger.
*Cyclic guanosine monophosphate (cGMP)*
- **cGMP** is typically associated with pathways activated by **nitric oxide** and **natriuretic peptides**, leading to vasodilation and smooth muscle relaxation, which are not the primary effects described for this drug.
- Drugs that activate **guanylyl cyclase** to increase cGMP would generally have opposite effects to the cardiotonic and renin-releasing actions mentioned.
*Diacylglycerol (DAG)*
- **DAG** is a second messenger produced along with **IP3** by the activation of **phospholipase C**, typically initiated by **alpha-1 (α1) adrenergic receptors** or other Gq-coupled GPCRs.
- α1 adrenergic activation causes **vasoconstriction** and other effects, which are distinct from the positive chronotropic and inotropic actions of a β1 agonist.
*Inositol 1,4,5-triphosphate (IP3)*
- **IP3** is generated alongside **DAG** through the activation of **phospholipase C**, following the binding of agonists to **Gq-coupled receptors** like the α1 adrenergic receptor.
- Its primary role is to trigger the release of **calcium from intracellular stores**, which, while important for muscle contraction, is not the direct second messenger pathway for the described β1-adrenergic actions.
Vasopressors and inotropes US Medical PG Question 6: A 72-year-old man presents to the emergency department after a fall. The patient was found lying down on the floor in his room in his retirement community. The patient has a past medical history of Alzheimer dementia and a prosthetic valve. His current medications include donepezil and warfarin. His temperature is 97.7°F (36.5°C), blood pressure is 85/50 mmHg, pulse is 160/min, respirations are 13/min, and oxygen saturation is 97% on room air. The patient is started on IV fluids and a type and screen is performed. Laboratory values are ordered as seen below.
Hemoglobin: 13 g/dL
Hematocrit: 39%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 225,000/mm^3
INR: 2.5
AST: 10 U/L
ALT: 12 U/L
A chest radiograph and EKG are performed and are within normal limits. A full physical exam is within normal limits. The patient's vitals are repeated. His temperature is 99.5°F (37.5°C), blood pressure is 110/70 mmHg, pulse is 90/min, respirations are 10/min, and oxygen saturation is 98% on room air. Which of the following is the best next step in management?
- A. CT scan (Correct Answer)
- B. Urgent blood transfusion
- C. Fresh frozen plasma
- D. Exploratory laparoscopy
- E. Exploratory laparotomy
Vasopressors and inotropes Explanation: ***CT scan***
- A patient with a **prosthetic valve** on **warfarin** and a fall is at high risk for **intracranial hemorrhage**, even without focal neurological deficits.
- While initial vitals improved after IV fluids, the mechanism of injury (fall) and medication profile warrant a **CT scan** of the head to rule out serious internal injury, especially given the history of dementia which might mask symptoms.
*Urgent blood transfusion*
- The patient's **hemoglobin (13 g/dL)** and **hematocrit (39%)** are within normal limits, indicating no acute need for blood transfusion due to hemorrhage.
- Transfusions are typically reserved for patients with significant blood loss or severe symptomatic anemia.
*Fresh frozen plasma*
- The patient's **INR of 2.5** is within the therapeutic range for a patient with a prosthetic valve on warfarin.
- There is no evidence of active bleeding or supratherapeutic anticoagulation that would necessitate the administration of **fresh frozen plasma (FFP)** to reverse anticoagulation.
*Exploratory laparoscopy*
- There are no clinical signs or symptoms, such as abdominal pain, distension, or evidence of intra-abdominal bleeding (e.g., declining hemoglobin, peritoneal signs), to suggest an indication for an **exploratory laparoscopy**.
- The patient's physical exam was described as normal.
*Exploratory laparotomy*
- Similar to laparoscopy, there is no clinical evidence of acute abdominal injury or hemorrhage, which would necessitate an **exploratory laparotomy**.
- This invasive procedure is reserved for cases with strong suspicion of significant intra-abdominal pathology or trauma.
Vasopressors and inotropes US Medical PG Question 7: A previously healthy 44-year-old man is brought by his coworkers to the emergency department 45 minutes after he became light-headed and collapsed while working in the boiler room of a factory. He did not lose consciousness. His coworkers report that 30 minutes prior to collapsing, he told them he was nauseous and had a headache. The patient appears sweaty and lethargic. He is not oriented to time, place, or person. The patient’s vital signs are as follows: temperature 41°C (105.8°F); heart rate 133/min; respiratory rate 22/min; and blood pressure 90/52 mm Hg. Examination shows equal and reactive pupils. Deep tendon reflexes are 2+ bilaterally. His neck is supple. A 0.9% saline infusion is administered. A urinary catheter is inserted and dark brown urine is collected. The patient’s laboratory test results are as follows:
Laboratory test
Blood
Hemoglobin 15 g/dL
Leukocyte count 18,000/mm3
Platelet count 51,000/mm3
Serum
Na+ 149 mEq/L
K+ 5.0 mEq/L
Cl- 98 mEq/L
Urea nitrogen 42 mg/dL
Glucose 88 mg/dL
Creatinine 1.8 mg/dL
Aspartate aminotransferase (AST, GOT) 210
Alanine aminotransferase (ALT, GPT) 250
Creatine kinase 86,000 U/mL
Which of the following is the most appropriate next step in patient management?
- A. Dantrolene
- B. Acetaminophen therapy
- C. Hemodialysis
- D. Ice water immersion (Correct Answer)
- E. Evaporative cooling
Vasopressors and inotropes Explanation: ***Ice water immersion***
- This patient presents with signs and symptoms consistent with **heat stroke**, including high body temperature (41°C), altered mental status, and a history of working in a hot environment (boiler room). **Rapid aggressive cooling** is the most critical immediate intervention to prevent organ damage.
- **Ice water immersion** is the fastest and most effective cooling method for heat stroke, aiming to reduce core body temperature to less than 39°C (102.2°F) within 30 minutes.
*Dantrolene*
- **Dantrolene** is primarily used to treat **malignant hyperthermia** and **neuroleptic malignant syndrome**, conditions caused by abnormal calcium release in muscle cells, not environmental heat exposure.
- While both conditions involve hyperthermia, the underlying pathophysiology and triggers are different from heat stroke.
*Acetaminophen therapy*
- **Acetaminophen** is an antipyretic that works by inhibiting prostaglandin synthesis in the central nervous system, affecting the hypothalamic thermoregulatory center.
- It is **ineffective** for the hyperthermia seen in heat stroke, which is due to a failure of thermoregulation rather than an altered hypothalamic set point, and could potentially worsen liver injury.
*Hemodialysis*
- **Hemodialysis** is indicated for severe **renal failure**, drug overdose, or certain electrolyte imbalances. Although this patient has acute kidney injury (elevated BUN and creatinine, dark urine suggestive of rhabdomyolysis), aggressive cooling is the immediate life-saving intervention for heat stroke.
- While renal support might be necessary later if kidney injury progresses, it is not the most appropriate *initial* next step for hyperthermia and altered mental status.
*Evaporative cooling*
- **Evaporative cooling** (e.g., spraying with lukewarm water and using fans) is a cooling method that can be effective, particularly in environments with low humidity.
- However, for severe heat stroke with a temperature as high as 41°C, **ice water immersion** provides a more rapid and aggressive temperature reduction, which is crucial for improving outcomes.
Vasopressors and inotropes US Medical PG Question 8: A 72-year-old man is brought to the emergency room by his daughter with complaints of a productive cough, rust-colored sputum, and fever for 1 week. He denies any breathlessness or chest pain. The past medical history is unremarkable. The vital signs include a pulse rate of 103/min, respiratory rate of 34/min, and blood pressure of 136/94 mm Hg, with an axillary temperature of 38.9°C (102.0°F). The SaO2 is 86% on room air. The chest examination revealed a dull percussion note and coarse crepitations over the left mid-chest. The patient was admitted to the medical unit and intravenous antibiotics were started. He responded well, but after 2 days an elevated temperature was noted. The patient deteriorated and he was transferred to the intensive care unit. A few days later, his temperature was 39.0°C (103.2°F), the respiratory rate was 23/min, the blood pressure was 78/56 mm Hg, and the SaO2 was 78%. He also had a delayed capillary refill time with a pulse of 141/min. Blood was drawn for the white cell count, which revealed a total count of 17,000/µL. The attending physician decides to begin therapy for the low blood pressure. After administration of the medication, hemodynamic monitoring reveals an increase in mean arterial pressure, increased venous return (reflected by increased central venous pressure), and increased cardiac output. Which of the following medications was most likely administered to the patient?
- A. Captopril
- B. Norepinephrine (Correct Answer)
- C. Low-dose dopamine
- D. Phenoxybenzamine
- E. Isoproterenol
Vasopressors and inotropes Explanation: ***Norepinephrine***
- The graph shows an increase in both **mean arterial pressure (MAP)** and **venous return** (indicated by an increase in central venous pressure and right atrial pressure proxy), as well as an increase in **cardiac output**. This pattern is consistent with the effects of **norepinephrine**, a potent vasoconstrictor and inotropic agent used in **septic shock**.
- **Norepinephrine** primarily acts on **alpha-1 adrenergic receptors** to cause widespread **vasoconstriction**, increasing systemic vascular resistance (SVR) and thus MAP. It also has **beta-1 adrenergic effects**, increasing myocardial contractility and heart rate, which contributes to increased cardiac output.
*Captopril*
- **Captopril** is an **ACE inhibitor** that causes **vasodilation** by preventing the conversion of angiotensin I to angiotensin II, leading to a decrease in blood pressure.
- Administering captopril in a patient with **hypotension** and **septic shock** would worsen the condition by further lowering blood pressure, which is contradictory to the graph showing an increase.
*Low-dose dopamine*
- **Low-dose dopamine** (renal-dose) primarily acts on **dopamine D1 receptors** in the renal, mesenteric, and coronary beds, causing **vasodilation** and increasing blood flow to these organs.
- While it might increase renal perfusion, it is not effective in significantly increasing **mean arterial pressure** or venous return in septic shock, and in higher doses, it can increase heart rate excessively.
*Phenoxybenzamine*
- **Phenoxybenzamine** is an **irreversible alpha-adrenergic blocker**. It causes **vasodilation** by inhibiting the vasoconstrictive effects of catecholamines on alpha-receptors.
- Administering phenoxybenzamine in a hypotensive patient would further **decrease blood pressure** and overall vascular resistance, which is the opposite of the desired effect shown in the graph.
*Isoproterenol*
- **Isoproterenol** is a **pure beta-adrenergic agonist** that stimulates both **beta-1 and beta-2 receptors**. It causes increased heart rate and contractility (beta-1) but also significant **vasodilation** (beta-2).
- While it would increase cardiac output, its strong **vasodilatory effects** would likely lead to a decrease in mean arterial pressure, making it unsuitable for treating hypotension in septic shock, which contradicts the graph.
Vasopressors and inotropes US Medical PG Question 9: A 73-year-old man presents to his primary care physician with chest pain. He noticed the pain after walking several blocks, and the pain is relieved by sitting. On exam, he has a BP 155/89 mmHg, HR 79 bpm, and T 98.9 F. The physician refers the patient to a cardiologist and offers prescriptions for carvedilol and nitroglycerin. Which of the following describes the mechanism or effects of each of these medications, respectively?
- A. Increased contractility; Decreased endothelial nitric oxide
- B. Decreased cAMP; Increased cGMP (Correct Answer)
- C. Increased cAMP; Increased cAMP
- D. Decreased cGMP; Increased venous resistance
- E. Increased heart rate; Decreased arterial resistance
Vasopressors and inotropes Explanation: ***Decreased cAMP; Increased cGMP***
- **Carvedilol** is a beta-blocker that *blocks β1 and β2 adrenergic receptors*, leading to a **decrease in intracellular cAMP**, which in turn reduces heart rate, contractility, and blood pressure.
- **Nitroglycerin** acts by releasing **nitric oxide**, which activates **guanylate cyclase** to convert GTP to **cGMP**, leading to smooth muscle relaxation and vasodilation.
*Increased contractility; Decreased endothelial nitric oxide*
- **Carvedilol** (a beta-blocker) causes a **decrease in contractility**, not an increase, by blocking beta-adrenergic receptors.
- **Nitroglycerin** works by **increasing** the production of nitric oxide, not decreasing it.
*Increased cAMP; Increased cAMP*
- **Carvedilol** (a beta-blocker) functions by **decreasing** cAMP, not increasing it.
- While other agents might increase cAMP, this is not the mechanism for nitroglycerin.
*Decreased cGMP; Increased venous resistance*
- **Nitroglycerin** works by **increasing cGMP**, which promotes vasodilation, rather than decreasing it.
- Nitroglycerin causes **decreased venous resistance** (venous dilation) to reduce preload, not increased resistance.
*Increased heart rate; Decreased arterial resistance*
- **Carvedilol** (a beta-blocker) primarily **decreases heart rate**, not increases it.
- While nitroglycerin does cause some arterial dilation, its primary effect at therapeutic doses is **venous dilation** to reduce preload, not just decreased arterial resistance.
Vasopressors and inotropes US Medical PG Question 10: A 70-year-old man comes to the physician for the evaluation of pain, cramps, and tingling in his lower extremities over the past 6 months. The patient reports that the symptoms worsen with walking more than two blocks and are completely relieved by rest. Over the past 3 months, his symptoms have not improved despite his participating in supervised exercise therapy. He has type 2 diabetes mellitus. He had smoked one pack of cigarettes daily for the past 50 years, but quit 3 months ago. He does not drink alcohol. His current medications include metformin, atorvastatin, and aspirin. Examination shows loss of hair and decreased skin temperature in the lower legs. Femoral pulses are palpable; pedal pulses are absent. Which of the following is the most appropriate treatment for this patient?
- A. Compression stockings
- B. Endarterectomy
- C. Bypass surgery
- D. Percutaneous transluminal angioplasty
- E. Administration of cilostazol (Correct Answer)
Vasopressors and inotropes Explanation: ***Administration of cilostazol***
- The patient presents with classic symptoms of **peripheral artery disease (PAD)**, including **intermittent claudication** (pain with exertion, relieved by rest), **loss of hair**, **decreased skin temperature**, and **absent pedal pulses**.
- **Cilostazol** is a phosphodiesterase inhibitor that improves walking distance and reduces symptoms of claudication by causing **vasodilation** and inhibiting **platelet aggregation**.
*Compression stockings*
- Compression stockings are primarily used for conditions like **venous insufficiency** or **lymphedema**, which involve problems with venous return or lymphatic drainage.
- They are **contraindicated** in patients with significant PAD because they can further occlude already compromised arterial flow and worsen tissue ischemia.
*Endarterectomy*
- **Endarterectomy** is a surgical procedure to remove plaque from the inner lining of an artery. It is indicated for **localized, severe arterial stenosis** and is more invasive than other revascularization options.
- While it can be considered for PAD, less invasive options are usually tried first, especially in a patient who has not yet received optimal medical therapy.
*Bypass surgery*
- **Bypass surgery** involves rerouting blood flow around a blocked artery using a graft (vein or synthetic material). It is a more invasive revascularization procedure for PAD with significant, extensive arterial occlusions.
- It is typically reserved for **severe symptoms** refractory to medical management and less invasive procedures, or for critical limb ischemia.
*Percutaneous transluminal angioplasty*
- **Percutaneous transluminal angioplasty (PTA)** is a minimally invasive procedure that uses a balloon to widen a narrowed artery, often with stent placement.
- It is an effective revascularization option for PAD but is generally considered after lifestyle modifications and pharmacotherapy (like cilostazol) have failed to improve symptoms sufficiently.
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