Pressure-volume relationships US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Pressure-volume relationships. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Pressure-volume relationships 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
Pressure-volume relationships 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.
Pressure-volume relationships US Medical PG Question 2: A 76-year-old male with a history of chronic uncontrolled hypertension presents to the emergency room following an episode of syncope. He reports that he felt lightheaded and experienced chest pain while walking his dog earlier in the morning. He notes that he has experienced multiple similar episodes over the past year. A trans-esophageal echocardiogram demonstrates a thickened, calcified aortic valve with left ventricular hypertrophy. Which of the following heart sounds would likely be heard on auscultation of this patient?
- A. Crescendo-decrescendo murmur radiating to the carotids that is loudest at the right upper sternal border (Correct Answer)
- B. Diastolic rumble following an opening snap with an accentuated S1
- C. Early diastolic high-pitched blowing decrescendo murmur that is loudest at the left sternal border
- D. Holosystolic murmur radiating to the axilla that is loudest at the apex
- E. Midsystolic click that is loudest at the apex
Pressure-volume relationships Explanation: ***Crescendo-decrescendo murmur radiating to the carotids that is loudest at the right upper sternal border***
- The patient's symptoms of **syncope**, **chest pain**, and findings of a **thickened, calcified aortic valve** with **left ventricular hypertrophy** are classic for **aortic stenosis**.
- Aortic stenosis classically presents with a **systolic ejecting crescendo-decrescendo murmur** which is loudest at the **right upper sternal border**, and often **radiates to the carotids**.
*Diastolic rumble following an opening snap with an accentuated S1*
- This description is characteristic of **mitral stenosis**, which is typically caused by **rheumatic fever**.
- Mitral stenosis would present with dyspnea and fatigue, unlike the syncope and chest pain seen in this patient.
*Early diastolic high-pitched blowing decrescendo murmur that is loudest at the left sternal border*
- This murmur describes **aortic regurgitation**, where blood flows back into the left ventricle during diastole.
- While aortic regurgitation can cause heart failure symptoms, the echocardiogram shows a thickened, calcified valve more consistent with stenosis.
*Midsystolic click that is most prominent that is loudest at the apex*
- A **midsystolic click** followed by a **late systolic murmur** is characteristic of **mitral valve prolapse**.
- Symptoms of mitral valve prolapse can include atypical chest pain and palpitations, but not generally exertional syncope or the severe structural changes seen in the aortic valve.
*Holosystolic murmur radiating to the axilla that is loudest at the apex*
- This is the classic description of **mitral regurgitation**, indicating blood flow back into the left atrium during systole.
- Mitral regurgitation is associated with symptoms of heart failure and fatigue, but not usually the anginal chest pain and syncope in a patient with a calcified aortic valve.
Pressure-volume relationships US Medical PG Question 3: A 37-year-old man is brought to the emergency department by ambulance after a motor vehicle accident. He suffered multiple deep lacerations and experienced significant blood loss during transport. In the emergency department, his temperature is 98.6°F (37°C), blood pressure is 102/68 mmHg, pulse is 112/min, and respirations are 22/min. His lacerations are sutured and he is given 2 liters of saline by large bore intravenous lines. Which of the following changes will occur in this patient's cardiac physiology due to this intervention?
- A. Increased cardiac output and unchanged right atrial pressure
- B. Decreased cardiac output and increased right atrial pressure
- C. Increased cardiac output and decreased right atrial pressure
- D. Increased cardiac output and increased right atrial pressure (Correct Answer)
- E. Decreased cardiac output and decreased right atrial pressure
Pressure-volume relationships Explanation: ***Increased cardiac output and increased right atrial pressure***
- The patient experienced significant blood loss, leading to a **decreased preload** and subsequent **reduced cardiac output**. Volume resuscitation with saline directly increases the **intravascular volume** which bolsters **venous return** and **right atrial pressure**.
- According to the **Frank-Starling mechanism**, increased right atrial pressure (a measure of preload) results in an increase in ventricular stretch and a more forceful contraction, thereby increasing **stroke volume** and **cardiac output**.
*Increased cardiac output and unchanged right atrial pressure*
- While fluid administration will increase **cardiac output** by improving preload, it will also directly lead to an increase in **right atrial pressure** due to the augmented venous return.
- An unchanged right atrial pressure would imply no significant increase in central venous volume, which contradicts the effect of a large volume fluid resuscitation.
*Decreased cardiac output and increased right atrial pressure*
- This scenario is unlikely because increasing **intravascular volume** through fluid resuscitation typically aims to raise **cardiac output** by optimizing preload, not decrease it.
- A decrease in cardiac output despite increased right atrial pressure could indicate **cardiac pump failure**, which is not suggested by the clinical picture of hypovolemic shock treated with fluids.
*Increased cardiac output and decreased right atrial pressure*
- An increase in **cardiac output** as a result of fluid resuscitation is expected, but a **decreased right atrial pressure** would contradict the mechanism of increased venous return and volume expansion.
- Decreased right atrial pressure would typically indicate ongoing volume loss or inadequate fluid resuscitation to restore central venous volume.
*Decreased cardiac output and decreased right atrial pressure*
- Both decreasing **cardiac output** and decreasing **right atrial pressure** indicate a worsening state of **hypovolemia** or an inadequate response to fluid resuscitation.
- The administration of 2 liters of saline is intended to correct the hypovolemia and improve cardiodynamics, not to worsen them.
Pressure-volume relationships US Medical PG Question 4: A 19-year-old man presents to the clinic with a complaint of increasing shortness of breath for the past 2 years. His shortness of breath is associated with mild chest pain and occasional syncopal attacks during strenuous activity. There is no history of significant illness in the past, however, one of his uncles had similar symptoms when he was his age and died while playing basketball a few years later. He denies alcohol use, tobacco consumption, and the use of recreational drugs. On examination, pulse rate is 76/min and is regular and bounding; blood pressure is 130/70 mm Hg. A triple apical impulse is observed on the precordium and a systolic ejection crescendo-decrescendo murmur is audible between the apex and the left sternal border along with a prominent fourth heart sound. The physician then asks the patient to take a deep breath, close his mouth, and pinch his nose and try to breathe out without allowing his cheeks to bulge out. In doing so, the intensity of the murmur increases. Which of the following hemodynamic changes would be observed first during this maneuver?
- A. ↓ Mean Arterial Pressure, ↑ Heart rate, ↑ Baroreceptor activity, ↓ Parasympathetic Outflow
- B. ↑ Mean Arterial Pressure, ↓ Heart rate, ↑ Baroreceptor activity, ↑ Parasympathetic Outflow (Correct Answer)
- C. ↑ Mean Arterial Pressure, ↓ Heart rate, ↓ Baroreceptor activity, ↑ Parasympathetic Outflow
- D. ↑ Mean Arterial Pressure, ↑ Heart rate, ↓ Baroreceptor activity, ↓ Parasympathetic Outflow
- E. ↑ Mean Arterial Pressure, ↑ Heart rate, ↑ Baroreceptor activity, ↑ Parasympathetic Outflow
Pressure-volume relationships Explanation: **↑ Mean Arterial Pressure, ↓ Heart rate, ↑ Baroreceptor activity, ↑ Parasympathetic Outflow**
- This maneuver is the **Valsalva Maneuver**, which involves forced expiration against a closed glottis. It causes a transient increase in **intrathoracic pressure**, compressing the great vessels and temporarily increasing **mean arterial pressure**.
- The initial rise in blood pressure is detected by **baroreceptors**, leading to a reflex decrease in **heart rate** via increased **parasympathetic outflow**.
*↓ Mean Arterial Pressure, ↑ Heart rate, ↑ Baroreceptor activity, ↓ Parasympathetic Outflow*
- This option describes changes more typical of the **later phases** of a Valsalva maneuver (Phase 2), where venous return and cardiac output decrease, leading to a fall in MAP and a compensatory increase in heart rate.
- It does not represent the **immediate hemodynamic changes** (Phase 1) that occur during the initial strain of the maneuver.
*↑ Mean Arterial Pressure, ↓ Heart rate, ↓ Baroreceptor activity, ↑ Parasympathetic Outflow*
- A decrease in **baroreceptor activity** would typically lead to an *increase* in heart rate and a *decrease* in parasympathetic outflow, contrary to the initial response to increased blood pressure.
- The initial increase in MAP correctly leads to *increased* baroreceptor activity.
*↑ Mean Arterial Pressure, ↑ Heart rate, ↓ Baroreceptor activity, ↓ Parasympathetic Outflow*
- An increase in **mean arterial pressure** (MAP) would reflexively cause a *decrease* in heart rate and an *increase* in parasympathetic outflow, mediated by *increased* baroreceptor activity, not decreased activity.
- Therefore, the proposed changes in heart rate, baroreceptor activity, and parasympathetic outflow are inconsistent with an initial increase in MAP.
*↑ Mean Arterial Pressure, ↑ Heart rate, ↑ Baroreceptor activity, ↑ Parasympathetic Outflow*
- While an increase in **mean arterial pressure** does lead to an increase in **baroreceptor activity** and **parasympathetic outflow**, the reflexive response to this increased pressure is a *decrease* in **heart rate**, not an increase.
- An increased heart rate combined with increased parasympathetic outflow is contradictory, as sympathetic and parasympathetic systems typically exert opposing effects on heart rate.
Pressure-volume relationships US Medical PG Question 5: 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
Pressure-volume relationships 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.
Pressure-volume relationships US Medical PG Question 6: A previously healthy 52-year-old woman comes to the physician because of a 3-month history of chest pain on exertion. She takes no medications. Cardiopulmonary examination shows no abnormalities. Cardiac stress ECG shows inducible ST-segment depressions in the precordial leads that coincide with the patient's report of chest pain and resolve upon cessation of exercise. Pharmacotherapy with verapamil is initiated. This drug is most likely to have which of the following sets of effects?
$$$ End-diastolic volume (EDV) %%% Blood pressure (BP) %%% Contractility %%% Heart rate (HR) $$$
- A. No change no change no change no change
- B. ↓ ↓ no change ↑
- C. ↓ ↓ ↓ ↑
- D. ↓ ↓ ↓ no change
- E. ↑ ↓ ↓ ↓ (Correct Answer)
Pressure-volume relationships Explanation: ***↑ ↓ ↓ ↓***
- **Verapamil**, a **non-dihydropyridine calcium channel blocker**, reduces **cardiac contractility**, leading to decreased **heart rate** and **blood pressure**, while increasing **end-diastolic volume**.
- Its therapeutic effect in **exertional angina** is primarily due to reduced myocardial oxygen demand, achieved by decreasing **heart rate**, **contractility** (both leading to reduced work of heart), and **afterload** (due to vasodilation which decreases blood pressure).
*No change no change no change no change*
- This option is incorrect because verapamil has significant **pharmacological effects** on the cardiovascular system.
- Verapamil is prescribed to treat the patient's symptoms, implying a need for **hemodynamic changes**, not stasis.
*↓ ↓ no change ↑*
- Verapamil typically **decreases heart rate** due to its action on the sinoatrial (SA) node, making an increase unlikely.
- While it decreases **blood pressure** and **contractility**, the absence of an effect on heart rate and an increase in heart rate are inconsistent with verapamil's known pharmacology.
*↓ ↓ ↓ ↑*
- This option incorrectly suggests an **increase in heart rate**, whereas verapamil is known to cause a dose-dependent **decrease in heart rate**.
- The other parameters (decreased EDV, BP, contractility) are also not fully aligned with verapamil's effects; EDV tends to increase due to better filling time and reduced contractility.
*↓ ↓ ↓ no change*
- This option suggests a **decrease in EDV**, which is generally incorrect; verapamil tends to allow for **increased ventricular filling** due to a reduced heart rate and prolonged diastole.
- The absence of a change in heart rate is also incorrect, as verapamil is a known **negative chronotropic agent**.
Pressure-volume relationships US Medical PG Question 7: A 21-year-old man presents to his physician for a routine checkup. His doctor asks him if he has had any particular concerns since his last visit and if he has taken any new medications. He says that he has not been ill over the past year, except for one episode of the flu. He has been training excessively for his intercollege football tournament, which is supposed to be a huge event. His blood pressure is 110/70 mm Hg, pulse is 69/min, and respirations are 17/min. He has a heart sound coinciding with the rapid filling of the ventricles and no murmurs. He does not have any other significant physical findings. Which of the following best describes the heart sound heard in this patient?
- A. Fourth heart sound (S4)
- B. Opening snap
- C. Third heart sound (S3) (Correct Answer)
- D. Second heart sound (S2)
- E. Mid-systolic click
Pressure-volume relationships Explanation: ***Third heart sound (S3)***
- An **S3 heart sound** is a low-pitched sound heard during **rapid ventricular filling** in early diastole, immediately after S2.
- In young, healthy individuals, especially athletes, an S3 can be a normal physiological finding, representing rapid filling of a **compliant ventricle**.
*Fourth heart sound (S4)*
- An **S4 heart sound** occurs during **atrial contraction** against a stiff or non-compliant ventricle, just before S1.
- It is typically associated with conditions like **ventricular hypertrophy** or **ischemia** and is less likely to be a normal finding in a young, healthy individual.
*Opening snap*
- An **opening snap** is a high-pitched, crisp sound heard after S2, caused by the sudden opening of a **stenotic mitral** or **tricuspid valve**.
- It indicates valvular pathology, specifically **mitral stenosis**, and is not related to ventricular filling in a healthy heart.
*Second heart sound (S2)*
- The **S2 heart sound** represents the **closure of the aortic and pulmonary valves** at the end of ventricular systole.
- While it marks the beginning of diastole, it does not coincide with the rapid filling of the ventricles itself.
*Mid-systolic click*
- A **mid-systolic click** is typically associated with **mitral valve prolapse**, caused by the sudden tensing of the chordae tendineae or valve leaflets.
- It occurs during systole, not diastole, and is not related to ventricular filling.
Pressure-volume relationships US Medical PG Question 8: A 27-year-old man presents to the emergency department after being hit by a car while riding his bike. The patient was brought in with his airway intact, vitals stable, and with a C-collar on. Physical exam is notable for bruising over the patient’s head and a confused man with a Glasgow coma scale of 11. It is noticed that the patient has a very irregular pattern of breathing. Repeat vitals demonstrate his temperature is 97.5°F (36.4°C), blood pressure is 172/102 mmHg, pulse is 55/min, respirations are 22/min and irregular, and oxygen saturation is 94% on room air. Which of the following interventions are most likely to improve this patient's vital signs?
- A. Head elevation, sedation, hypertonic saline, hypoventilation
- B. Lower head, sedation, hypertonic saline, hypoventilation
- C. Head elevation, sedation, mannitol, hyperventilation (Correct Answer)
- D. Head elevation, norepinephrine, mannitol, hyperventilation
- E. Lower head, sedation, hypertonic saline, hyperventilation
Pressure-volume relationships Explanation: ***Head elevation, sedation, mannitol, hyperventilation***
- This patient presents with signs of **increased intracranial pressure (ICP)**, indicated by **Cushing's triad** (hypertension, bradycardia, irregular respirations) and a decreased Glasgow Coma Scale (GCS) after head trauma. **Head elevation** to 30 degrees promotes venous outflow from the brain, reducing ICP.
- **Sedation** lowers metabolic demand and reduces agitation, which can otherwise increase ICP. **Mannitol** is an osmotic diuretic that rapidly draws fluid from the brain, decreasing cerebral edema. **Hyperventilation** temporarily reduces ICP by causing cerebral vasoconstriction through decreased pCO2.
*Head elevation, sedation, hypertonic saline, hypoventilation*
- While **head elevation**, **sedation**, and **hypertonic saline** (an alternative osmotic agent to mannitol) are appropriate for ICP management, **hypoventilation** would increase pCO2, causing cerebral vasodilation and worsening ICP.
- The combination of effective and ineffective ICP-reducing strategies makes this an incorrect option.
*Lower head, sedation, hypertonic saline, hypoventilation*
- **Lowering the head** would impede venous drainage from the brain and increase ICP, which is detrimental in this scenario.
- As mentioned, **hypoventilation** is contraindicated as it exacerbates cerebral edema and elevated ICP.
*Head elevation, norepinephrine, mannitol, hyperventilation*
- While **head elevation**, **mannitol**, and **hyperventilation** are appropriate, **norepinephrine** is primarily used to treat hypotension and maintain cerebral perfusion pressure (CPP) if blood pressure is dangerously low.
- In this case, the patient is hypertensive (**blood pressure 172/102 mmHg**), so norepinephrine would further increase blood pressure and ICP.
*Lower head, sedation, hypertonic saline, hyperventilation*
- **Lowering the head** is contraindicated as it directly increases ICP by hindering venous outflow from the brain.
- Although **sedation**, **hypertonic saline**, and **hyperventilation** are useful for ICP control, the incorrect positioning makes this option less suitable.
Pressure-volume relationships US Medical PG Question 9: 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
Pressure-volume relationships 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.
Pressure-volume relationships US Medical PG Question 10: 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
Pressure-volume relationships 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**.
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