Events of the Cardiac Cycle
Which node initiates atrial contraction?
→ SA node (Slide 4)
What is the term for the volume of blood in the ventricles at the end of filling?
→ End-diastolic volume (EDV) (Slide 9)
What is the formula for cardiac output?
→ CO = HR × SV (Slide 23)
What are chronotropic agents?
→ Factors that change HR (Slide 17)
What is preload?
→ Stretch of heart wall before contraction (Slide 20)
If HR = 75 bpm and SV = 80 ml, what is cardiac output?
→ 6000 ml/min (Slide 23)
Define bradycardia in adults.
→ HR < 60 bpm (Slide 18)
What is the function of the foramen ovale in fetal circulation?
→ Shunts RA → LA (Slide 26)
During which phase are the AV valves closed but semilunar valves still closed as well?
→ Isovolumetric contraction (Slide 5)
What is stroke volume?
→ Volume of blood ejected per beat (Slide 12)
What is a normal resting cardiac output for an adult?
→ ~5.25 L/min (5,250 ml/min) (Slide 15)
Name two positive chronotropic agents.
→ Thyroid hormone, caffeine, nicotine, cocaine (Slide 17)
What does the Frank-Starling law describe?
→ ↑ Venous return → ↑ SV (Slide 20)
If EDV = 120 ml and ESV = 50 ml, what is stroke volume?
→ 70 ml (Slide 23)
Define tachycardia in adults.
→ HR > 100 bpm (Slide 18)
What is the function of the ductus arteriosus?
→ Shunts pulmonary artery → aorta (Slide 26)
What happens to the semilunar valves during ventricular ejection?
→ They open to allow blood ejection (Slide 9)
What is end-systolic volume?
→ Volume remaining after contraction (Slide 9)
Define cardiac reserve.
→ Max CO − Resting CO (Slide 14; examples Slide 15)
Name one negative chronotropic agent.
→ Parasympathetic activity or beta-blockers (Slide 17)
What is afterload?
→ Resistance in arteries opposing ventricular ejection (Slide 20)
If HR = 100 bpm and SV = 50 ml, what is cardiac output?
→ 5000 ml/min (Slide 23)
Name one abnormal cause of bradycardia.
→ Hypothyroidism (others: electrolyte imbalance, CHF) (Slide 18)
Why are the lungs bypassed in fetal circulation?
→ Nonfunctional, high resistance (Slide 25)
What event causes the dicrotic notch in the aortic pressure trace?
→ Closure of the aortic semilunar valve (Slide 9)
Why must left and right ventricles eject the same volume of blood?
→ To maintain balance; imbalance causes edema (Slides 10)
A healthy non-athlete can increase CO about four-fold. How does this compare to an athlete?
→ Athlete up to ~7-fold (Slide 14)
What does parasympathetic activity do to heart rate?
→ Slows SA node and increases AV node delay, slows heart rate (Slide 17)
How does venous return affect stroke volume?
→ ↑ Venous return → ↑ preload → ↑ SV (Slide 20)
If EDV = 140 ml and SV = 90 ml, what is ESV?
→ 50 ml (Slide 23)
Name one cause of tachycardia.
→ Heart disease (others: fever, anxiety) (Slide 18)
What event at birth causes the foramen ovale to close?
→ First breath → pressure shift closes it (Slide 27)
Which phase occurs when all heart chambers are relaxed and AV valves open?
→ Atrial relaxation & ventricular filling (Slide 8)
What happens if the right ventricle pumps more blood than the left?
→ Pulmonary edema develops (Slides 10 + Supplemental)
Compare resting heart rate and stroke volume in endurance athletes vs non-athletes.
→ Athletes: high SV, low HR; Non-athletes: low SV, high HR (Slides 13 & 15)
Why might athletes exhibit bradycardia without it being abnormal?
→ Stronger heart pumps more per beat (Slides 13 & 18)
How do positive inotropic agents influence stroke volume?
→ Increase contractility → ↑ SV (Slide 21)
If HR = 60 bpm and SV = 90 ml, what is cardiac output?
→ 5400 ml/min (Slide 23)
Why can chronic tachycardia be dangerous for the heart?
→ ↑ O₂ demand, weakens heart (Slide 18 + Supplemental)
What event at birth causes the ductus arteriosus to collapse?
→ Pressure change after lung expansion (Slide 27)
Why is the isovolumetric contraction phase considered “isovolumetric”?
→ All valves closed → no volume change (Slides 5 & 7)
How does left ventricular wall thickness relate to its pumping function?
→ Left ventricle is stronger to pump blood farther (Slides 10)
A woman with a smaller heart has a stroke volume of 55 ml and a heart rate of 95 bpm at rest. Calculate her cardiac output and explain why her resting HR is higher than average.
→ CO = 5.23 L/min; smaller hearts have smaller SV, so HR runs higher to maintain CO. (Slides 23, 13)
Compare causes of abnormal bradycardia vs tachycardia.
→ Bradycardia: hypothyroidism, electrolyte imbalance, CHF; Tachycardia: heart disease, fever, anxiety (Slide 18)
Why does increased afterload reduce stroke volume?
→ Harder ejection → ↓ SV (Slide 22)
Compare cardiac output between 50 × 105 ml and 105 × 50 ml — what do you notice?
→ Both = 5250 ml/min → different HR/SV can yield same CO (Slide 23)
Why is cardiac output often reduced in congestive heart failure?
→ Weak pump → ↓ SV → ↓ CO (Slide 20 + Supplemental)
Compare blood flow through the fetal heart vs adult heart.
→ Fetal: bypasses lungs; Adult: full pulmonary circulation (Slides 25–27)
Predict what happens to blood flow if the AV valves fail to close properly during isovolumetric contraction.
→ Blood regurgitates into atria → ↓ stroke volume (5, Supplemental)
A patient has an end-diastolic volume (EDV) of 140 ml and an end-systolic volume (ESV) of 90 ml. Their heart rate is 80 bpm. Calculate their cardiac output, and predict how this would affect their activity tolerance.
→ SV = 50 ml; CO = 4.0 L/min → below typical rest, so reduced activity tolerance. (Slides 23, 15)
A man has a resting cardiac output of 5.2 L/min and a maximum cardiac output of 7.0 L/min. Calculate his cardiac reserve and predict how this limitation would affect his ability to exercise compared to a healthy individual.
→ Reserve = 1.8 L/min → low reserve → reduced exercise tolerance vs healthy (and much less than athletes). (Slides 14, 15)
A patient presents with a resting heart rate of 115 bpm. Calculate how much higher this is compared to the upper limit of a normal resting rate, and propose at least two possible underlying causes.
→ Normal = 60–100 bpm; 115 bpm = 15 bpm above normal. Possible causes: fever, heart disease, anxiety, stimulant use. (Slide 18)
Predict how dehydration would affect preload and therefore stroke volume.
→ ↓ Venous return → ↓ preload → ↓ SV (Slide 20 + Supplemental)
An athlete’s HR = 45 bpm and SV = 120 ml. Calculate cardiac output and explain how it is maintained.
→ 5400 ml/min; high SV maintains CO despite low HR (Slide 23)
Predict what happens to tissue perfusion if cardiac output is inadequate.
→ Inadequate O₂ delivery → organ dysfunction (Slide 13 + Supplemental)
Predict what would happen if the foramen ovale failed to close after birth.
→ Blood mixing → congenital defect (Slide 27 + Supplemental)
Compare atrial contraction’s role in ventricular filling to passive filling — which contributes more blood volume and why?
→ Passive filling ~70–80%; atrial contraction adds ~20–30% (Slide 4 + Supplemental)
A patient’s left ventricle is weakened, resulting in an ejection fraction of only 30%. Analyze how this imbalance would affect pressures and fluid buildup in the lungs versus the systemic circuit.
→ LV systolic failure → ↑ LA/pulmonary venous pressures → pulmonary edema; ↓ systemic perfusion; long-term strain may produce systemic edema. (Slides 10–11; Supplemental for EF mechanism)
A patient has resting CO = 5250 ml/min and max CO = 5750 ml/min. What does this indicate about their heart condition?
→ Very low reserve → severe cardiac dysfunction (Slide 15)
A patient is given both a beta-blocker and thyroid hormone. Analyze how each of these drugs would affect their heart rate, and predict the overall outcome when both are active at the same time.
→ Beta-blocker ↓ HR, thyroid hormone ↑ HR → combined effect depends on balance; may partially cancel out. (Slides 17–18)
Analyze how heart failure affects preload, contractility, and afterload simultaneously.
→ Preload ↑, contractility ↓, afterload ↑ (Slide 20 + Supplemental)
A patient has HR = 180 bpm and SV = 90 ml. Calculate cardiac output and analyze risks at this level.
→ 16,200 ml/min; risks = arrhythmia, failure (Slide 23)
Analyze how chronic hypertension (increased afterload) can eventually cause heart failure.
→ ↑ Afterload → LV hypertrophy → eventual failure (Slide 20 + Supplemental)
Analyze how persistent ductus arteriosus would affect pulmonary vs systemic circulation in a newborn.
→ Pulmonary hypertension & systemic underperfusion (Slide 27 + Supplemental)