Heart Anatomy
What is the sac that encloses the heart within the thoracic cavity?
→ The pericardium. (Slide 6)
What are the two main circuits of blood flow in the body?
→ Systemic circulation and pulmonary circulation. (Slide 18)
What heart sound is associated with the closing of the AV valves?
→ S1 (“lubb”) — closing of AV valves. (Slide 21)
What vessel carries oxygenated blood to the heart wall?
→ Coronary arteries. (Slide 24)
What is the normal pacemaker of the heart?
→ SA node. (Slide 30)
What law explains the relationship between stretch of the heart and contraction strength?
→ The Frank-Starling law. (Slide 32)
What does the P wave represent?
→ Atrial depolarization. (Slide 43)
What chamber of the heart has the thickest wall and why?
→ The left ventricle, because it must generate higher pressure for systemic circulation. (Slide 10-11)
What side of the heart pumps blood to the lungs?
→ The right side of the heart. (Slides 12, 16)
What heart sound is associated with the closing of the semilunar valves?
→ S2 (“dupp”) — closing of semilunar valves. (Slide 21)
Name the two major coronary arteries and where they come from.
→ The right and left coronary arteries. The aorta. (Slide 25)
What is the function of the AV node?
→ Slows conduction to allow atria to contract before ventricles. (Slide 37)
What is the plateau phase of a cardiac action potential caused by?
→ Influx of calcium ions. (Slides 33–34, 40)
What does the QRS complex represent?
→ Ventricular depolarization (and atrial repolarization). (Slide 44)
What structure separates the left and right atria?
→ The interatrial septum. (Slide 12)
What side of the heart pumps blood to the systemic circulation?
→ The left side of the heart. (Slide 14)
What is a heart murmur?
→ An abnormal heart sound due to turbulent blood flow. (Slide 21)
What is atherosclerosis?
→ plaques narrow coronary arteries. (Slide 27)
What conduction fibers rapidly deliver impulses to the ventricles?
→ Purkinje fibers. (Slide 38)
Why can’t cardiac muscle cells exhibit tetany?
→ Refractory period prevents tetany. (Slide 32)
What does the T wave represent?
→ Ventricular repolarization. (Slide 44)
How does pericarditis affect the function of the heart?
→ Inflammation increases fluid in pericardial cavity, restricting filling (cardiac tamponade). (Slide 7)
Explain why right ventricular failure leads to systemic edema.
→ Right ventricle failure → systemic venous backup → systemic edema. (Slide 18)
Describe the difference between valvular insufficiency and valvular stenosis.
→ Insufficiency = valves leak; stenosis = valves stiff/narrow. (Slides 22)
hich coronary artery supplies most of the interventricular septum?
→ Anterior interventricular artery (LAD). (Slide 25)
How does parasympathetic stimulation affect the heart rate?
→ Parasympathetic stimulation decreases HR (vagus nerve). (Slide 30)
Explain how calcium ions contribute to the contraction of cardiac muscle cells.
→ Calcium triggers cross-bridge cycling in cardiac muscle. (Slides 32)
What is happening during the S-T segment of an ECG?
→ Plateau phase of ventricular AP (ventricular contraction). (Slide 45)
Compare the anterior and posterior external features of the heart.
→ Anterior shows right atrium/ventricle more prominently; posterior shows left atrium/ventricle. (Slides 8-9)
Explain why left ventricular failure leads to pulmonary edema.
→ Left ventricle failure → pulmonary venous backup → pulmonary edema. (Slide 18)
Why might valvular insufficiency cause the heart to enlarge?
→ Backflow increases chamber volume, leading to enlargement. (Slide 22)
Why is myocardial infarction often described as producing referred pain in the left arm and jaw?
→ Pain signals travel along shared spinal nerves, producing referred pain. (Slide 29)
How does sympathetic stimulation affect the heart?
→ Sympathetic stimulation increases HR, contractility, and coronary flow. (Slide 30)
Why does the long refractory period of cardiac muscle protect heart function?
→ Ensures full contraction-relaxation cycle before next beat. (Slide 42)
How is a first-degree AV block identified on an ECG?
→ Prolonged PR interval. (Slide 47)
Explain how the structure of papillary muscles and chordae tendineae prevents valve prolapse.
→ Papillary muscles contract, tightening chordae tendineae, preventing valve prolapse. (Slide 13, 20)
Trace the flow of blood through the heart, starting at the superior vena cava.
→ SVC and IVC → RA → tricuspid AV valve→ RV →Pulmonary semilunar valve→ Pulmonary trunk→ Pulmonary ARTERIES → Lungs → LA → bicuspid AV valve→ LV → aortic semilunar valve→ Aorta. (Slides 15-16)
Explain how turbulent blood flow leads to an abnormal heart sound.
→ Turbulent flow causes vibrations detected as murmurs. (Slide 21)
Explain why sudden occlusion of the left coronary artery can be fatal.
→ It supplies most of the left ventricle/interventricular septum; occlusion = massive infarct. (Slides 27)
Explain why the SA node is considered “autorhythmic.”
→ Nodal cells depolarize spontaneously without external stimulus. (Slides 34
Compare action potentials in nodal cells vs. cardiac muscle cells.
→ Nodal = pacemaker, unstable RMP; Muscle = stable RMP, plateau. (Slides 34-35)
Why is ventricular fibrillation immediately life-threatening?
→ No coordinated ventricular contraction → no cardiac output. (Slide 48)
Predict what might happen if the interventricular septum did not develop properly.
→ Improper septum development → mixing of oxygenated and deoxygenated blood. (Slide 12)
Compare the efficiency of systemic vs. pulmonary circulation pressures and explain why they differ.
→ Systemic pressure is higher because blood must travel farther against greater resistance; pulmonary is lower. (Slides 10)
Predict the effect of severe aortic valve stenosis on left ventricular workload.
→ LV must generate greater pressure to push blood through narrowed valve, leading to hypertrophy. (Slide 21-22)
Predict what happens to cardiac muscle tissue downstream of a blocked coronary artery.
→ Ischemia (deprived of oxygen) → tissue death of the left ventricle (necrosis). (Slide 27)
Compare the outcomes if the SA node is damaged versus if the AV node is damaged.
→ SA node damage → slower AV node pacing (40–50 bpm); AV node damage → ventricles paced at 20–40 bpm. (Slide 34-35)
Predict what would happen if sodium channels in nodal cells were blocked.
→ Nodal cells could not depolarize → bradycardia/asystole. (Slide 33)
Predict how atrial fibrillation would affect blood filling of the ventricles.
→ Loss of atrial “kick” → reduced ventricular filling. (Slide 48)
A patient has a congenital defect that leaves the foramen ovale open after birth. What effect would this have on circulation?
→ Foramen ovale allows right-to-left shunting, reducing oxygen delivery to tissues. (Slide 12)
A patient presents with shortness of breath and swollen ankles. Analyze whether left or right heart failure is more likely the cause and justify.
→ Shortness of breath = pulmonary edema (LV failure); swollen ankles = systemic edema (RV failure). Could be combined. (Slide 18)
What is the fibrous skeleton of the heart?
→ It surrounds the valves of the heart and provides support and stability. (Slide 23)
→ It surrounds the valves of the heart and provides support and stability. (Slide 23)
Compare how atherosclerosis and coronary spasm each contribute to myocardial infarction risk.
→ Atherosclerosis = gradual narrowing; spasm = sudden constriction; both reduce blood flow. (Slide 27)
A patient has an ectopic pacemaker. Predict how this would affect heart rhythm compared to normal SA node control.
→ Ectopic pacemaker depolarizes abnormally → irregular rhythm. (Slide 39)
A drug prolongs the plateau phase of cardiac muscle action potentials. Analyze how this would affect contraction and rhythm.
→ Longer plateau = prolonged contraction, could disrupt rhythm. (Slide 38)
A patient presents with prolonged PR intervals and missed QRS complexes. What type of arrhythmia does this suggest?
→ Second-degree AV block (missed beats) or progressing to third-degree. (Slides 47)