Vascular resistance concepts US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Vascular resistance concepts. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Vascular resistance concepts US Medical PG Question 1: What is the primary mechanism for maintaining constant cerebral blood flow despite changes in systemic blood pressure?
- A. Endothelial factors
- B. Baroreceptor reflex
- C. Myogenic autoregulation (Correct Answer)
- D. Metabolic control
Vascular resistance concepts Explanation: ***Myogenic autoregulation***
- **Myogenic autoregulation** is the intrinsic ability of vascular smooth muscle to contract when stretched by increased blood pressure, thereby maintaining a constant cerebral blood flow.
- This mechanism operates within a specific range of mean arterial pressures (typically **60-150 mmHg**) to prevent both hypoperfusion and hyperperfusion of the brain.
*Endothelial factors*
- Endothelial cells release various vasoactive substances like **nitric oxide** and **endothelin**, which influence vascular tone.
- While important for local blood flow regulation, these factors play a secondary role to myogenic autoregulation in maintaining constant cerebral blood flow against systemic pressure changes.
*Baroreceptor reflex*
- The **baroreceptor reflex** primarily controls systemic blood pressure by regulating heart rate and peripheral vascular resistance.
- It does not directly regulate cerebral blood flow stability in response to systemic pressure changes; its main role is to stabilize the overall systemic arterial pressure.
*Metabolic control*
- **Metabolic control** regulates cerebral blood flow in response to the brain's metabolic demands, primarily by sensing local concentrations of **CO2**, **pH**, and **oxygen**.
- While essential for matching blood supply to neuronal activity, it is not the primary mechanism for maintaining cerebral blood flow despite changes in systemic blood pressure.
Vascular resistance concepts US Medical PG Question 2: Which of the following physiologic changes decreases pulmonary vascular resistance (PVR)?
- A. Inhaling the inspiratory reserve volume (IRV)
- B. Exhaling the entire vital capacity (VC)
- C. Exhaling the expiratory reserve volume (ERV)
- D. Breath holding maneuver at functional residual capacity (FRC)
- E. Inhaling the entire vital capacity (VC) (Correct Answer)
Vascular resistance concepts Explanation: ***Inhaling the entire vital capacity (VC)***
- As lung volume increases from FRC to TLC (which includes inhaling the entire VC), alveolar vessels are **stretched open**, and extra-alveolar vessels are **pulled open** by the increased radial traction, leading to a decrease in PVR.
- This **maximizes the cross-sectional area** of the pulmonary vascular bed, lowering resistance.
*Inhaling the inspiratory reserve volume (IRV)*
- While inhaling IRV increases lung volume, it's not the maximal inspiration of the entire VC where **PVR is typically at its lowest**.
- PVR continues to decrease as lung volume approaches total lung capacity (TLC).
*Exhaling the entire vital capacity (VC)*
- Exhaling the entire vital capacity leads to very low lung volumes, where PVR significantly **increases**.
- At low lung volumes, **alveolar vessels become compressed** and extra-alveolar vessels **narrow**, increasing resistance.
*Exhaling the expiratory reserve volume (ERV)*
- Exhaling the ERV results in a lung volume below FRC, which causes a **marked increase in PVR**.
- This is due to the **compression of alveolar vessels** and decreased radial traction on extra-alveolar vessels.
*Breath holding maneuver at functional residual capacity (FRC)*
- At FRC, the PVR is at an **intermediate level**, not its lowest.
- This is the point where the opposing forces affecting alveolar and extra-alveolar vessels are somewhat balanced, but not optimized for minimal resistance.
Vascular resistance concepts US Medical PG Question 3: A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system?
Stroke volume | Heart rate | Peripheral vascular resistance
- A. ↓ ↓ ↓
- B. ↓ ↓ ↑ (Correct Answer)
- C. ↓ ↑ ↑
- D. ↑ ↑ ↑
- E. ↑ ↑ ↓
Vascular resistance concepts Explanation: ***↓ ↓ ↑***
- This patient likely has **essential tremor**, which is characterized by **bilateral hand tremors** that improve with alcohol and worsen with intention (postural tremor). The prescribed medication is a **beta-blocker** (e.g., propranolol), which is associated with an increased risk of bronchospasms due to blocking **beta-2 receptors** in the airways.
- Beta-blockers **decrease heart rate** (negative chronotropic effect) and **stroke volume** (negative inotropic effect) by blocking beta-1 receptors in the heart, reducing cardiac output.
- **Peripheral vascular resistance increases** acutely due to: (1) **unopposed alpha-1 adrenergic tone** in blood vessels (loss of beta-2 mediated vasodilation), and (2) baroreceptor-mediated reflex vasoconstriction in response to decreased cardiac output. This helps maintain blood pressure despite reduced cardiac output.
*↓ ↓ ↓*
- While beta-blockers decrease **heart rate** and **stroke volume**, peripheral vascular resistance does not decrease acutely. A decrease in all three parameters would cause severe hypotension.
- The loss of beta-2 receptor-mediated vasodilation and baroreceptor reflexes lead to increased, not decreased, peripheral vascular resistance.
*↓ ↑ ↑*
- Beta-blockers **decrease heart rate** through beta-1 blockade, not increase it. This is their primary cardiac mechanism of action.
- An increase in heart rate would be expected with sympathomimetic drugs or anticholinergics, not beta-blockers.
*↑ ↑ ↑*
- This combination indicates increased cardiovascular activity, which is the opposite effect of **beta-blockers**.
- Beta-blockers reduce heart rate and stroke volume by blocking beta-1 receptors; they do not increase these parameters.
- This pattern would suggest sympathetic activation or administration of an adrenergic agonist.
*↑ ↑ ↓*
- Beta-blockers **decrease** (not increase) both heart rate and stroke volume through beta-1 receptor blockade.
- While decreased peripheral vascular resistance occurs with vasodilators, beta-blockers acutely **increase** PVR due to unopposed alpha-adrenergic tone.
Vascular resistance concepts US Medical PG Question 4: Which factor most strongly influences coronary blood flow during exercise?
- A. Endothelin release
- B. Metabolic demand (Correct Answer)
- C. Myogenic response
- D. Neural regulation
- E. Baroreceptor reflex
Vascular resistance concepts Explanation: **Metabolic demand**
- During exercise, increased **myocardial activity** leads to a higher demand for oxygen and nutrients, prompting a significant increase in coronary blood flow.
- Local release of **metabolites** such as adenosine, nitric oxide, and hydrogen ions causes powerful vasodilation of coronary arteries, closely matching blood supply to demand.
*Endothelin release*
- **Endothelin** is a potent vasoconstrictor and plays a role in regulating vascular tone, but its primary influence is not the immediate or strongest factor dictating increased coronary flow during exercise.
- While it can modulate flow, metabolic changes are the dominant driver for the rapid and substantial increases needed during exertion.
*Myogenic response*
- The **myogenic response** is an intrinsic property of vascular smooth muscle cells to contract when stretched (due to increased pressure) and relax when pressure decreases, helping to maintain relatively constant blood flow.
- This mechanism primarily contributes to **autoregulation** and flow stability, but it does not account for the massive increase in flow required by the heart during exercise.
*Neural regulation*
- **Neural regulation**, primarily sympathetic stimulation, increases heart rate and contractility, which indirectly increases metabolic demand.
- However, direct neural effects on coronary arteries can be complex (both vasodilation and vasoconstriction depending on receptor type), and the overriding control during exercise is typically metabolic.
Vascular resistance concepts US Medical PG Question 5: A 46-year-old male was found unconscious in the field and brought to the emergency department by EMS. The patient was intubated in transit and given a 2 liter bolus of normal saline. On arrival, the patient's blood pressure is 80/60 mmHg and temperature is 37.5°C. Jugular veins are flat and capillary refill time is 4 seconds.
Vascular parameters are measured and are as follows:
Cardiac index - Low
Pulmonary capillary wedge pressure (PCWP) - Low
Systemic vascular resistance - High
Which of the following is the most likely diagnosis?
- A. Septic shock
- B. Anaphylactic shock
- C. Cardiogenic shock
- D. Hypovolemic shock (Correct Answer)
- E. Neurogenic shock
Vascular resistance concepts Explanation: ***Hypovolemic shock***
- The patient presents with **hypotension**, **flat jugular veins**, **prolonged capillary refill**, and a **low cardiac index** and **low pulmonary capillary wedge pressure (PCWP)**, all indicative of inadequate intravascular volume.
- The **high systemic vascular resistance** is a compensatory mechanism to maintain blood pressure in the setting of decreased circulating volume.
*Septic shock*
- Septic shock typically presents with **vasodilation**, leading to a **low systemic vascular resistance**, which contradicts the findings in this patient.
- While patients can be hypotensive, the vascular parameters, especially SVR, do not align with septic shock.
*Anaphylactic shock*
- This type of shock is characterized by widespread **vasodilation** and increased capillary permeability, leading to a **low systemic vascular resistance** and often significant **edema** or **urticaria**, none of which are suggested here.
- While it can cause hypotension and low PCWP due to fluid shifts, the high SVR makes it less likely.
*Cardiogenic shock*
- Cardiogenic shock is characterized by **pump failure**, leading to a **low cardiac index** but a **high PCWP** due to fluid backup in the pulmonary circulation.
- This directly contrasts the patient's low PCWP.
*Neurogenic shock*
- Neurogenic shock involves a loss of **sympathetic tone**, resulting in widespread **vasodilation** and a **low systemic vascular resistance**, often accompanied by **bradycardia**.
- The high SVR in this patient rules out neurogenic shock.
Vascular resistance concepts US Medical PG Question 6: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?
- A. Norepinephrine causes increased glucose absorption within the intestines.
- B. Without epinephrine, insulin cannot act on the liver.
- C. Peripheral tissues require epinephrine to take up glucose.
- D. Epinephrine increases liver glycogenolysis. (Correct Answer)
- E. Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.
Vascular resistance concepts Explanation: ***Epinephrine increases liver glycogenolysis.***
- **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy.
- It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**.
*Norepinephrine causes increased glucose absorption within the intestines.*
- **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress.
- Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine.
*Without epinephrine, insulin cannot act on the liver.*
- **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**.
- Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it.
*Peripheral tissues require epinephrine to take up glucose.*
- **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**.
- Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress.
*Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.*
- Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**.
- This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.
Vascular resistance concepts US Medical PG Question 7: A 69-year-old woman is admitted to the hospital with substernal, crushing chest pain. She is emergently moved to the cardiac catheterization lab where she undergoes cardiac angiography. Angiography reveals that the diameter of her left anterior descending artery (LAD) is 50% of normal. If her blood pressure, LAD length, and blood viscosity have not changed, which of the following represents the most likely change in LAD flow from baseline?
- A. Decreased by 93.75% (Correct Answer)
- B. Increased by 6.25%
- C. Decreased by 25%
- D. Decreased by 87.5%
- E. Increased by 25%
Vascular resistance concepts Explanation: ***Decreased by 93.75%***
- This option is correct based on Poiseuille's Law, which states that flow is proportional to the **fourth power of the radius (r^4)**. A 50% decrease in diameter means a 50% decrease in radius (0.5r).
- The new flow would be (0.5)^4 = 0.0625 times the original flow. Therefore, the decrease in flow is 1 - 0.0625 = 0.9375, or **93.75%**.
*Increased by 6.25%*
- This answer incorrectly suggests an **increase** in flow, which is contrary to the effect of a narrowed artery.
- While 6.25% represents the new flow as a percentage of baseline (since 0.0625 = 6.25%), the vessel stenosis causes a **decrease**, not an increase in flow.
*Decreased by 25%*
- This calculation might arise from considering a linear relationship (e.g., radius decreases by 50%, so flow decreases by 50% of 50%, which is incorrect).
- It does not account for the **fourth power relationship** between radius and flow according to Poiseuille's Law.
*Decreased by 87.5%*
- This percentage represents a calculation error, likely from misapplying the fourth power relationship or confusing the calculation steps.
- It does not accurately reflect the dramatic reduction in flow caused by a 50% reduction in vessel diameter.
*Increased by 25%*
- This option implies a significant increase in blood flow, which would not happen with a **stenosed artery**.
- It completely contradicts the physiological response to a **narrowed vessel**.
Vascular resistance concepts US Medical PG Question 8: 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: ↔
Vascular resistance concepts 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.
Vascular resistance concepts US Medical PG Question 9: An 8-year-old boy presents to your office for a routine well-child visit. Upon physical examination, he is found to have a harsh-sounding, holosystolic murmur that is best appreciated at the left sternal border. The murmur becomes louder when you ask him to make fists with his hands. Which of the following is the most likely explanation for these findings?
- A. Aortic stenosis
- B. Ventricular septal defect (Correct Answer)
- C. Left ventricular hypertrophy
- D. Pulmonary hypertension
- E. Tricuspid atresia
Vascular resistance concepts Explanation: ***Ventricular septal defect***
- A **holosystolic murmur** heard best at the **left sternal border** is characteristic of a VSD, caused by blood shunting from the left to the right ventricle during systole.
- The murmur becoming louder with a maneuver that increases **afterload** (like making fists, which increases systemic vascular resistance) is consistent with a VSD, as it enhances the pressure gradient and shunting.
*Aortic stenosis*
- An aortic stenosis murmur is typically a **systolic ejection murmur**, not holosystolic, and is often heard best at the right upper sternal border with radiation to the carotids.
- While it can be affected by maneuvers that change cardiac output, the description of a harsh, holosystolic murmur at the left sternal border is not typical for aortic stenosis.
*Left ventricular hypertrophy*
- **Left ventricular hypertrophy** (LVH) is an anatomical change in the heart muscle and is not a direct cause of a primary murmur itself. It is usually a consequence of other conditions like aortic stenosis or hypertension.
- While significant LVH can alter heart sounds or be associated with murmurs from underlying conditions, it does not directly produce a harsh, holosystolic murmur with these specific characteristics.
*Pulmonary hypertension*
- Pulmonary hypertension can cause murmurs related to pulmonary regurgitation (a diastolic murmur) or tricuspid regurgitation (a holosystolic murmur), but these are usually associated with symptoms like dyspnea and fatigue, and a holosystolic murmur from **tricuspid regurgitation** is typically louder at the xiphoid process rather than the left sternal border and is often associated with venous distension.
- An increase in systemic afterload (making fists) would generally decrease the intensity of a murmur due to tricuspid regurgitation, not increase it.
*Tricuspid atresia*
- **Tricuspid atresia** is a severe congenital heart defect where the tricuspid valve fails to form, resulting in no direct communication between the right atrium and right ventricle. It typically presents with cyanosis and severe symptoms early in life.
- While it often coexists with a VSD (which would produce a murmur), the primary defect itself is not directly associated with the specific holosystolic murmur description that becomes louder with increased afterload in an otherwise apparently well 8-year-old.
Vascular resistance concepts US Medical PG Question 10: A 21-year-old lacrosse player comes to the doctor for an annual health assessment. She does not smoke or drink alcohol. She is 160 cm (5 ft 3 in) tall and weighs 57 kg (125 lb); BMI is 22 kg/m2. Pulmonary function tests show an FEV1 of 90% and an FVC of 3600 mL. Whole body plethysmography is performed to measure airway resistance. Which of the following structures of the respiratory tree is likely to have the highest contribution to total airway resistance?
- A. Conducting bronchioles
- B. Terminal bronchioles
- C. Segmental bronchi (Correct Answer)
- D. Respiratory bronchioles
- E. Mainstem bronchi
Vascular resistance concepts Explanation: ***Segmental bronchi***
- In healthy individuals, **medium-sized bronchi** (including segmental and subsegmental bronchi, approximately generations 4-8) contribute approximately **80% of total airway resistance**.
- While **Poiseuille's Law** states resistance is inversely proportional to radius to the fourth power (R ∝ 1/r⁴), the key factor is the **total cross-sectional area** and **degree of branching**.
- Medium-sized bronchi have moderate individual resistance and **limited parallel branching**, making them the dominant site of resistance.
- This is why diseases affecting medium-sized airways (e.g., asthma, bronchitis) cause significant increases in airway resistance.
*Terminal bronchioles*
- Although individual terminal bronchioles have small radii and high individual resistance, there are **millions of them arranged in parallel**.
- With parallel resistances, total resistance decreases: 1/R_total = 1/R₁ + 1/R₂ + 1/R₃...
- The **massive number** of small airways means their collective resistance is actually quite **low** (~10-20% of total).
- This is why small airways disease is called the "**silent zone**" - significant pathology can occur before detection.
*Conducting bronchioles*
- These airways also benefit from extensive **parallel branching**, reducing their contribution to total resistance.
- They contribute less than medium-sized bronchi due to their large cumulative cross-sectional area.
*Respiratory bronchioles*
- Part of the **respiratory zone** with the largest total cross-sectional area in the lungs.
- Minimal contribution to airway resistance due to enormous parallel arrangement.
- Primary function is **gas exchange**, not air conduction.
*Mainstem bronchi*
- These large airways have **low individual resistance** due to large diameter.
- Together with the trachea, they contribute approximately **20% of total airway resistance**.
- Not the primary site despite being early in the airway tree.
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