Starling's law of the heart US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Starling's law of the heart. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Starling's law of the heart US Medical PG Question 1: A 40-year-old female volunteers for an invasive study to measure her cardiac function. She has no previous cardiovascular history and takes no medications. With the test subject at rest, the following data is collected using blood tests, intravascular probes, and a closed rebreathing circuit:
Blood hemoglobin concentration 14 g/dL
Arterial oxygen content 0.22 mL O2/mL
Arterial oxygen saturation 98%
Venous oxygen content 0.17 mL O2/mL
Venous oxygen saturation 78%
Oxygen consumption 250 mL/min
The patient's pulse is 75/min, respiratory rate is 14/ min, and blood pressure is 125/70 mm Hg. What is the cardiac output of this volunteer?
- A. Body surface area is required to calculate cardiac output.
- B. Stroke volume is required to calculate cardiac output.
- C. 250 mL/min
- D. 5.0 L/min (Correct Answer)
- E. 50 L/min
Starling's law of the heart Explanation: ***5.0 L/min***
- Cardiac output can be calculated using the **Fick principle**: Cardiac Output $(\text{CO}) = \frac{{\text{Oxygen Consumption}}}{{\text{Arterial } \text{O}_2 \text{ Content} - \text{Venous O}_2 \text{ Content}}}$.
- Given Oxygen Consumption = 250 mL/min, Arterial O$_2$ Content = 0.22 mL/mL, and Venous O$_2$ Content = 0.17 mL/mL. Thus, CO = $\frac{{250 \text{ mL/min}}}{{(0.22 - 0.17) \text{ mL } \text{O}_2/\text{mL blood}}} = \frac{{250 \text{ mL/min}}}{{0.05 \text{ mL } \text{O}_2/\text{mL blood}}} = 5000 \text{ mL/min } = 5.0 \text{ L/min}$.
*Body surface area is required to calculate cardiac output.*
- **Body surface area (BSA)** is used to calculate **cardiac index**, which is cardiac output normalized to body size, but not cardiac output directly.
- While a normal cardiac output might be compared to a patient's BSA for context, it is not a necessary component for calculating the absolute cardiac output.
*Stroke volume is required to calculate cardiac output.*
- Cardiac output can be calculated as **Stroke Volume (SV) x Heart Rate (HR)**. However, stroke volume is not provided directly in this question.
- The Fick principle allows for the calculation of cardiac output **without explicit knowledge of stroke volume** or heart rate, using oxygen consumption and arteriovenous oxygen difference.
*250 mL/min*
- 250 mL/min represents the **oxygen consumption**, not the cardiac output.
- Cardiac output is the volume of blood pumped by the heart per minute, which is influenced by both oxygen consumption and the difference in oxygen content between arterial and venous blood.
*50 L/min*
- A cardiac output of 50 L/min is an **extremely high and physiologically impossible** value for a resting individual.
- This value is 10 times higher than the calculated cardiac output and typically represents a calculation error.
Starling's law of the heart 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)
Starling's law of the heart 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.
Starling's law of the heart US Medical PG Question 3: A healthy 22-year-old male participates in a research study you are leading to compare the properties of skeletal and cardiac muscle. You conduct a 3-phased experiment with the participant. In the first phase, you get him to lift up a 2.3 kg (5 lb) weight off a table with his left hand. In the second phase, you get him to do 20 burpees, taking his heart rate to 150/min. In the third phase, you electrically stimulate his gastrocnemius with a frequency of 50 Hz. You are interested in the tension and electrical activity of specific muscles as follows: Biceps in phase 1, cardiac muscle in phase 2, and gastrocnemius in phase 3. What would you expect to be happening in the phases and the respective muscles of interest?
- A. Increase of tension in experiments 2 and 3, with the same underlying mechanism
- B. Increase of tension in all phases (Correct Answer)
- C. Recruitment of large motor units followed by small motor units in experiment 1
- D. Fused tetanic contraction at the end of all three experiments
- E. Recruitment of small motor units at the start of experiments 1 and 2
Starling's law of the heart Explanation: ***Increase of tension in all phases***
- In **phase 1**, lifting a 2.3 kg weight requires the **biceps** to contract, generating sufficient force (**tension**) to overcome gravity.
- In **phase 2**, the **cardiac muscle** increases its contractile force (**tension**) to meet the metabolic demands of **exercise**, leading to a heart rate of 150/min.
- In **phase 3**, electrical stimulation of the **gastrocnemius** at 50 Hz triggers muscle contraction, leading to an increase in **tension**.
*Increase of tension in experiments 2 and 3, with the same underlying mechanism*
- While tension increases in phases 2 and 3, the **underlying mechanisms differ**: cardiac muscle tension increases due to increased sympathetic stimulation and preload, while skeletal muscle tension increases due to unfused or fused tetanus from electrical stimulation.
- Cardiac muscle contraction is regulated by **calcium-induced calcium release**, while skeletal muscle involves direct coupling of DHP receptor and ryanodine receptor.
*Recruitment of large motor units followed by small motor units in experiment 1*
- **Motor unit recruitment** follows the **size principle**, meaning smaller, more easily excitable motor units are activated first, followed by larger ones as more force is needed.
- Therefore, in phase 1, **small motor units** would be recruited first, not large ones.
*Fused tetanic contraction at the end of all three experiments*
- **Fused tetanic contraction** occurs in **skeletal muscle** when stimulation frequency is high enough that individual twitches summate completely, leading to sustained contraction.
- This phenomenon is **not possible in cardiac muscle** due to its long **refractory period**, which prevents sustained contraction and allows for adequate filling time.
*Recruitment of small motor units at the start of experiments 1 and 2*
- **Motor unit recruitment** applies to **skeletal muscle** (phase 1) and involves recruiting small motor units first for fine or gentle movements.
- **Cardiac muscle** (phase 2) does not have motor units; instead, it relies on the **Frank-Starling mechanism** and hormonal/nervous regulation to adjust its contractile force as a syncytium.
Starling's law of the heart US Medical PG Question 4: An 83-year-old male presents with dyspnea, orthopnea, and a chest radiograph demonstrating pulmonary edema. A diagnosis of congestive heart failure is considered. The following clinical measurements are obtained: 100 bpm heart rate, 0.2 mL O2/mL systemic blood arterial oxygen content, 0.1 mL O2/mL pulmonary arterial oxygen content, and 400 mL O2/min oxygen consumption. Using the above information, which of the following values represents this patient's cardiac stroke volume?
- A. 30 mL/beat
- B. 70 mL/beat
- C. 40 mL/beat (Correct Answer)
- D. 60 mL/beat
- E. 50 mL/beat
Starling's law of the heart Explanation: ***40 mL/beat***
- First, calculate cardiac output (CO) using the **Fick principle**: CO = Oxygen Consumption / (Arterial O2 content - Venous O2 content). Here, CO = 400 mL O2/min / (0.2 mL O2/mL - 0.1 mL O2/mL) = 400 mL O2/min / 0.1 mL O2/mL = **4000 mL/min**.
- Next, calculate stroke volume (SV) using the formula: SV = CO / Heart Rate. Given a heart rate of 100 bpm, SV = 4000 mL/min / 100 beats/min = **40 mL/beat**.
*30 mL/beat*
- This answer would result if there was an error in calculating either the **cardiac output** or if the **arteriovenous oxygen difference** was overestimated.
- A stroke volume of 30 mL/beat with a heart rate of 100 bpm would yield a cardiac output of 3 L/min, which is sub-physiologic for an oxygen consumption of 400 mL/min given the provided oxygen content values.
*70 mL/beat*
- This stroke volume is higher than calculated and would imply either a significantly **lower heart rate** or a much **higher cardiac output** than derived from the Fick principle with the given values.
- A stroke volume of 70 mL/beat at a heart rate of 100 bpm would mean a cardiac output of 7 L/min, which is inconsistent with the provided oxygen consumption and arteriovenous oxygen difference.
*60 mL/beat*
- This value is higher than the correct calculation, suggesting an error in the initial calculation of **cardiac output** or the **avO2 difference**.
- To get 60 mL/beat, the cardiac output would need to be 6000 mL/min, which would mean an avO2 difference of 0.067 mL O2/mL, not 0.1 mL O2/mL.
*50 mL/beat*
- This stroke volume would result from an incorrect calculation of the **cardiac output**, potentially from a slight miscalculation of the **arteriovenous oxygen difference**.
- A stroke volume of 50 mL/beat at 100 bpm would mean a cardiac output of 5 L/min, requiring an avO2 difference of 0.08 mL O2/mL, which is not consistent with the given values.
Starling's law of the heart US Medical PG Question 5: A 60-year-old male engineer who complains of shortness of breath when walking a few blocks undergoes a cardiac stress test because of concern for coronary artery disease. During the test he asks his cardiologist about what variables are usually used to quantify the functioning of the heart. He learns that one of these variables is stroke volume. Which of the following scenarios would be most likely to lead to a decrease in stroke volume?
- A. Anxiety
- B. Heart failure (Correct Answer)
- C. Exercise
- D. Pregnancy
- E. Digitalis
Starling's law of the heart Explanation: ***Heart failure***
- In **heart failure**, the heart's pumping ability is impaired, leading to a reduced **ejection fraction** and thus a decreased **stroke volume**.
- The weakened myocardium cannot effectively contract to expel the normal volume of blood, resulting in lower blood output per beat.
*Anxiety*
- **Anxiety** typically causes an increase in **sympathetic nervous system** activity, leading to increased heart rate and myocardial contractility.
- This often results in a temporary **increase in stroke volume** due to enhanced cardiac performance, not a decrease.
*Exercise*
- During **exercise**, there is a significant **increase in venous return** and sympathetic stimulation, leading to increased **end-diastolic volume** and contractility.
- This physiological response causes a substantial **increase in stroke volume** to meet the body's higher oxygen demands.
*Pregnancy*
- **Pregnancy** leads to significant **physiological adaptations** to accommodate the growing fetus, including a substantial increase in **blood volume**.
- This increased blood volume and cardiac output result in an **increase in stroke volume** to maintain adequate perfusion for both mother and fetus.
*Digitalis*
- **Digitalis** is a cardiac glycoside that **increases intracellular calcium** in myocardial cells, enhancing the **force of contraction**.
- This positive inotropic effect leads to an **increased stroke volume** by improving the heart's pumping efficiency.
Starling's law of the heart US Medical PG Question 6: An 82-year-old male with congestive heart failure experiences rapid decompensation of his condition, manifesting as worsening dyspnea, edema, and increased fatigue. Labs reveal an increase in his serum creatinine from baseline. As part of the management of this acute change, the patient is given IV dobutamine to alleviate his symptoms. Which of the following effects occur as a result of this therapy?
- A. Decreased cardiac contractility
- B. Decreased heart rate
- C. Increased myocardial oxygen consumption (Correct Answer)
- D. Increased systemic vascular resistance due to systemic vasoconstriction
- E. Slowed atrioventricular conduction velocities
Starling's law of the heart Explanation: ***Increased myocardial oxygen consumption***
- Dobutamine is a **beta-1 adrenergic agonist** that increases **myocardial contractility** and **heart rate**.
- This enhanced cardiac workload directly leads to an **increased demand for oxygen** by the heart muscle.
*Decreased cardiac contractility*
- Dobutamine is primarily used in heart failure to **increase cardiac contractility** (positive inotropic effect), thus improving cardiac output.
- Decreased contractility would worsen the patient's condition, which is contrary to the therapeutic goal of dobutamine.
*Decreased heart rate*
- Dobutamine, through its beta-1 agonism, typically causes an **increase in heart rate**, not a decrease.
- A decreased heart rate would further compromise cardiac output in a decompensated heart failure patient.
*Increased systemic vascular resistance due to systemic vasoconstriction*
- Dobutamine has a relatively weak effect on alpha-1 adrenergic receptors, and its primary action is to cause **vasodilation**, which tends to **decrease systemic vascular resistance**.
- While other inotropes like norepinephrine can cause vasoconstriction, dobutamine's effect on SVR is generally minimal or mildly vasodilatory, which helps to reduce afterload.
*Slowed atrioventricular conduction velocities*
- Beta-1 agonists like dobutamine generally tend to **increase atrioventricular (AV) conduction velocity** and can even precipitate arrhythmias.
- Slowed AV conduction is characteristic of drugs like beta-blockers or calcium channel blockers, which would be contraindicated in this setting.
Starling's law of the heart US Medical PG Question 7: 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
Starling's law of the heart 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.
Starling's law of the heart US Medical PG Question 8: A researcher measures action potential propagation velocity in various regions of the heart in a 42-year-old Caucasian female. Which of the following set of measurements corresponds to the velocities found in the atrial muscle, AV Node, Purkinje system, and ventricular muscle, respectively?
- A. 0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s
- B. 2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s
- C. 0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s
- D. 0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s
- E. 1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s (Correct Answer)
Starling's law of the heart Explanation: ***1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s***
- This option correctly lists the approximate conduction velocities for the **atrial muscle (1.1 m/s)**, **AV node (0.05 m/s)**, **Purkinje system (2.2 m/s)**, and **ventricular muscle (0.3 m/s)**, respectively.
- The **AV node has the slowest conduction velocity (~0.05 m/s)**, which is crucial for delaying ventricular contraction and allowing complete ventricular filling.
- The **Purkinje system has the fastest conduction velocity (~2-4 m/s)**, ensuring rapid and coordinated ventricular depolarization.
- **Atrial muscle (~1 m/s)** and **ventricular muscle (~0.3-0.5 m/s)** have intermediate velocities.
*0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s*
- This sequence is incorrect because it places the **AV node's velocity (0.05 m/s)** first (as atrial muscle) and significantly overestimates ventricular muscle velocity (3.3 m/s).
- Atrial muscle conducts faster than 0.05 m/s, and ventricular muscle velocity should be approximately 0.3-0.5 m/s, not 3.3 m/s.
*2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s*
- This option incorrectly assigns the **highest velocity (2.2 m/s)** to atrial muscle, which is characteristic of the Purkinje system, and misplaces the **slowest velocity (0.05 m/s)** in the Purkinje system instead of the AV node.
- The values do not align with known physiological conduction speeds across cardiac tissues.
*0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s*
- This sequence incorrectly places the **slowest velocity (0.05 m/s)** in the Purkinje system, which is known for the most rapid conduction, and assigns an unrealistically high velocity (2.2 m/s) to the AV node.
- The arrangement directly contradicts the physiological function and relative speeds within the cardiac conduction system.
*0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s*
- This option underestimates the **atrial muscle velocity** (0.5 m/s instead of ~1 m/s) and significantly overestimates the **ventricular muscle velocity** (3 m/s instead of ~0.3-0.5 m/s).
- The provided values do not accurately represent the typical ranges of conduction velocities for each specified cardiac region.
Starling's law of the heart US Medical PG Question 9: A 73-year-old woman presents to clinic with a week of fatigue, headache, and swelling of her ankles bilaterally. She reports that she can no longer go on her daily walk around her neighborhood without stopping frequently to catch her breath. At night she gets short of breath and has found that she can only sleep well in her recliner. Her past medical history is significant for hypertension and a myocardial infarction three years ago for which she had a stent placed. She is currently on hydrochlorothiazide, aspirin, and clopidogrel. She smoked 1 pack per day for 30 years before quitting 10 years ago and socially drinks around 1 drink per month. She denies any illicit drug use. Her temperature is 99.0°F (37.2°C), pulse is 115/min, respirations are 18/min, and blood pressure is 108/78 mmHg. On physical exam there is marked elevations of her neck veins, bilateral pitting edema in the lower extremities, and a 3/6 holosystolic ejection murmur over the right sternal border. Echocardiography shows the following findings:
End systolic volume (ESV): 100 mL
End diastolic volume (EDV): 160 mL
How would cardiac output be determined in this patient?
- A. 108/3 + (2 * 78)/3
- B. (160 - 100) / 160
- C. 160 - 100
- D. (160 - 100) * 115 (Correct Answer)
- E. (100 - 160) * 115
Starling's law of the heart Explanation: ***(160 - 100) * 115***
- **Cardiac output (CO)** is calculated as **stroke volume (SV) multiplied by heart rate (HR)**.
- **Stroke volume** is determined by subtracting the **end-systolic volume (ESV)** from the **end-diastolic volume (EDV)** (SV = EDV - ESV).
*(108/3 + (2 * 78)/3)*
- This formula represents the calculation for **mean arterial pressure (MAP)**, which is not directly used to determine cardiac output.
- **MAP** is approximated as (Systolic BP + 2 * Diastolic BP) / 3.
*(160 - 100) / 160*
- This formula calculates the **ejection fraction (EF)**, which is the fraction of blood pumped out of the ventricle with each beat.
- While **ejection fraction** is a crucial measure of cardiac function, it does not directly determine cardiac output.
*160 - 100*
- This calculation represents the **stroke volume (SV)** (EDV - ESV), which is the amount of blood ejected from the ventricle per beat.
- However, to get the **cardiac output**, stroke volume must be multiplied by the heart rate.
*(100 – 160) * 115*
- This calculation would result in a **negative stroke volume**, which is physiologically incorrect as stroke volume must be a positive value.
- **Stroke volume** is always calculated as the **end-diastolic volume minus the end-systolic volume**.
Starling's law of the heart US Medical PG Question 10: A 33-year-old woman presents to her physician's office for a postpartum check-up. She gave birth to a full-term boy via an uncomplicated vaginal delivery 3 weeks ago and has been exclusively breastfeeding her son. The hormone most responsible for promoting milk let-down during lactation in this new mother would lead to the greatest change in the level of which of the following factors?
- A. Ras
- B. Phospholipase A
- C. cGMP
- D. cAMP
- E. IP3 (Correct Answer)
Starling's law of the heart Explanation: ***IP3***
- The hormone responsible for milk let-down is **oxytocin**, which acts via **Gq protein-coupled receptors**.
- Gq protein activation leads to the activation of **phospholipase C**, which hydrolyzes **PIP2** into **IP3** (inositol triphosphate) and DAG (diacylglycerol). IP3 then signals the release of intracellular calcium.
*Ras*
- **Ras** is a small GTPase involved in signal transduction pathways, typically associated with **receptor tyrosine kinases** and cell growth/differentiation, not primarily with oxytocin signaling for milk let-down.
- It plays a role in the **MAP kinase pathway**, distinct from the Gq protein pathway activated by oxytocin.
*Phospholipase A*
- **Phospholipase A** enzymes (PLA1, PLA2, PLC, PLD) hydrolyze phospholipids, but **phospholipase A2** is primarily known for producing **arachidonic acid**, a precursor to prostaglandins and leukotrienes, which is not the main downstream effector of oxytocin.
- While phospholipases are involved in lipid signaling, **phospholipase C** is the specific enzyme activated by oxytocin's Gq pathway leading to IP3 production.
*cGMP*
- **cGMP** (cyclic guanosine monophosphate) is a second messenger typically produced by **guanylyl cyclases** in response to nitric oxide or natriuretic peptides.
- It is involved in processes like **vasodilation** and smooth muscle relaxation, distinct from the oxytocin pathway for milk ejection.
*cAMP*
- **cAMP** (cyclic adenosine monophosphate) is a common second messenger generated by **adenylyl cyclase** following activation of **Gs protein-coupled receptors**.
- While important in many hormonal pathways, it is not the primary signaling molecule downstream of oxytocin's action on its receptors for milk let-down, which predominantly uses the Gq pathway.
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