anatomy circulatory system: heart

What are the great vessels connected to the heart, and which chambers do they connect to?

Superior & inferior vena cava → right atrium.

Pulmonary trunk (arteries) → right ventricle.

Pulmonary veins → left atrium.

Aorta → left ventricle.

Where is the heart located, what is its size, and where are its base and apex?

Located in mediastinum, between lungs.

About the size of a fist (≈ 300 g).

Base → superior, wide part at great vessels.

Apex → pointed tip at inferior left side.

What are the anatomy and function of the pericardium and pericardial fluid?

Fibrous pericardium → outer tough layer, anchors heart.

Serous pericardium (parietal & visceral/epicardium).

Pericardial cavity contains pericardial fluid → reduces friction.

What are the three layers of the heart wall, and how do they differ histologically?

Epicardium (visceral pericardium) → thin outer layer.

Myocardium → thick muscular middle layer.

Endocardium → smooth inner lining of chambers & valves.

How does the myocardium differ in thickness among chambers, and why?

Thicker in ventricles (esp. left) → pumps blood farther.

Thinner in atria → only push blood to ventricles.

Vortex pattern → twisting contraction for efficient ejection.

What is the fibrous skeleton of the heart, and what are its functions?

Dense connective tissue framework. Functions: structural support, anchor for valves, electrical insulation between atria & ventricles.

What are the anatomy and functions of atria and ventricles?

Atria → thin-walled, receive blood.

Ventricles → thick-walled, pump blood.

Internal septa (interatrial & interventricular) separate chambers.

External sulci (coronary & interventricular sulci) mark boundaries.

What are the names/synonyms for the four valves of the heart?

• Right AV valve = tricuspid.

• Left AV valve = bicuspid / mitral.

• Pulmonary semilunar valve.

• Aortic semilunar valve.

What structural differences exist between valves, and what roles do papillary muscles & tendinous cords play?

• AV valves → have cusps attached to tendinous cords & papillary muscles (prevent backflow).

• Semilunar valves → simple cusps, no cords.

What is the path of blood through the heart?

Body → vena cava → RA → tricuspid → RV → pulmonary valve → lungs → pulmonary veins → LA → mitral valve → LV → aortic valve → aorta → body.

What are the coronary arteries and their main branches?

• Left coronary artery → anterior interventricular (LAD) + circumflex.

• Right coronary artery → right marginal + posterior interventricular.

What causes myocardial infarction (MI), and how does collateral circulation help?

• Cause → blockage of coronary artery.

• Collateral circulation → alternate routes reduce tissue death risk.

Why is coronary blood flow greater when the heart relaxes than when it contracts?

• During systole, contraction compresses coronary vessels.

• During diastole, relaxation allows blood flow.

What veins drain the myocardium, and where does this blood go?

• Great cardiac vein, middle cardiac vein, left marginal vein → coronary sinus → right atrium.

• Supplemented by small cardiac veins → drain directly into right atrium.

What are the structural properties of cardiomyocytes?

• Short, branched cells with one central nucleus.

• Connected by intercalated discs (desmosomes + gap junctions).

• Striated like skeletal muscle, but cells are smaller and branched.

How do cardiomyocytes differ from skeletal muscle?

• Cardiomyocytes: involuntary, branched, single nucleus, intercalated discs, connected in a functional syncytium.

• Skeletal muscle: voluntary, long cylindrical fibers, multinucleated, no intercalated discs.

How do these structural differences relate to cardiac muscle function?

• Intercalated discs → mechanical strength & synchronized contraction.

• Branched structure → ensures rapid, uniform spread of contraction.

• Syncytium → heart beats as one coordinated unit.

What properties of cardiac muscle relate to its nearly exclusive reliance on aerobic respiration?

• High mitochondrial density → continuous ATP production.

• Rich blood supply → constant oxygen delivery.

• Fatigue-resistant → supports lifelong continuous contraction.

What are the components of the cardiac conduction system?

• Sinoatrial (SA) node → natural pacemaker.

• Atrioventricular (AV) node → delays signal.

• Atrioventricular (AV) bundle / Bundle of His → conducts signal to ventricles.

• Right and left bundle branches → spread signal down septum.

• Purkinje fibers → deliver signal to ventricular myocardium.

What is the path of electrical signals through the heart

SA node → atrial myocardium → AV node → AV bundle → bundle branches → Purkinje fibers → ventricular myocardium → coordinated ventricular contraction.

What do systole and diastole mean?

• Systole → contraction phase (chambers eject blood).

• Diastole → relaxation phase (chambers fill with blood).

What is sinus rhythm, and what are some causes of premature ventricular contractions (PVCs)?

• Sinus rhythm → normal heartbeat initiated by SA node.

• PVC causes → caffeine, stress, ischemia.

What is an ectopic focus, and how does it affect heart rhythm

Ectopic focus → abnormal pacemaker outside SA node; can take over rhythm if SA node fails or slows.

What is a nodal rhythm, and how does it differ from sinus rhythm

Nodal rhythm → AV node drives heartbeat (~40–50 bpm) if SA node fails; slower than normal sinus rhythm (~60–100 bpm).

What is the general term for abnormal cardiac rhythm?

Arrhythmia

How do SA node cells depolarize rhythmically?

• Pacemaker potentials → gradual depolarization caused by:

  • Na⁺ inflow (funny channels), Ca²⁺ inflow (T-type channels), K⁺ outflow.

• Depolarization repeats ~60–100 times/min at rest.

Describe the spread of excitation through the heart.

SA node → atrial myocardium → AV node (slow conduction) → AV bundle → bundle branches → Purkinje fibers → ventricular myocardium.

Why does conduction slow at the AV node?

Allows atria to complete contraction and ventricles to fill before ventricular systole.

How does the twisting contraction of ventricles help cardiac function?

Wrings blood out efficiently; tendinous cords prevent valve prolapse.

What is the resting potential of cardiomyocytes, and how does an action potential occur?

• Resting potential ~ -90 mV.

• Depolarization: Na⁺ inflow.

• Plateau: Ca²⁺ inflow balances K⁺ outflow.

• Repolarization: K⁺ outflow.

• Long refractory period prevents tetanus, ensures effective pumping.

What happens in the ECG waves?

• P wave: atrial depolarization.

• QRS complex: ventricular depolarization (atria repolarize simultaneously).

• T wave: ventricular repolarization.

How does a sphygmomanometer measure blood pressure?

Pressure required to stop blood flow; measured in mm Hg (height of mercury column).

How are fluid volume, pressure, and flow related in the heart?

Blood flows from high pressure → low pressure; chamber contraction increases pressure, ejecting blood.

How do heart valves open and close?

Pressure differences across valves; valves open toward lower pressure, close against backflow.

What are the four phases of the cardiac cycle?

• Atrial systole

• Isovolumetric ventricular contraction

• Ventricular ejection

• Isovolumetric ventricular relaxation

What occurs in each phase regarding chamber contraction, valve movement, ECG, and heart sounds?

• Atrial systole: atria contract, AV valves open, P wave, first heart sound.

• Isovolumetric ventricular contraction: ventricles contract, all valves closed, QRS, first heart sound.

• Ventricular ejection: semilunar valves open, blood ejected, pressure peaks.

• Isovolumetric relaxation: ventricles relax, semilunar valves close, T wave, second heart sound.

How is heart rate calculated from cardiac cycle duration?

HR = 60 / total duration of one cardiac cycle (seconds)

What are typical volumes in the ventricle?

• End-diastolic volume (EDV): ~130 mL

• Stroke volume (SV): ~70 mL

• Ejection fraction (EF): SV/EDV ≈ 54%

• End-systolic volume (ESV): ~60 mL

Why must both ventricles eject the same average volume?

Prevent blood accumulation in either systemic or pulmonary circuits → edema or congestion.

What are the sympathetic and parasympathetic pathways to the heart?

• Sympathetic: T1–T5 → SA/AV nodes & myocardium → ↑HR & contractility

• Parasympathetic: Vagus nerve → SA/AV nodes → ↓HR

What is cardiac output (CO) and how is it calculated?

CO = HR × SV

Typical resting HR and age changes?

~70 bpm; higher in infants, declines with age.

Terms for abnormal resting heart rates?

• Tachycardia: abnormally fast (>100 bpm)

• Bradycardia: abnormally slow (<60 bpm)

What are positive and negative chronotropic agents?

• Positive: ↑ HR (e.g., norepinephrine, epinephrine)

• Negative: ↓ HR (e.g., acetylcholine, beta-blockers)

Sympathetic vs parasympathetic effects on heart rate?

• Sympathetic → ↑ HR and contractility

• Parasympathetic → ↓ HR

Intrinsic SA node firing rate and vagal tone?

SA node fires ~100 bpm intrinsically; vagal tone keeps resting HR ~70 bpm.

How do proprioceptors, baroreceptors, and chemoreceptors affect HR?

• Proprioceptors: ↑ HR with movement

• Baroreceptors: adjust HR to maintain BP

• Chemoreceptors: ↑ HR if CO₂ ↑ or O₂ ↓

Effects of potassium and calcium on HR?

• ↑ K⁺ → slows HR or stops heart

• ↑ Ca²⁺ → ↑ HR and contractility

Define preload, contractility, afterload, and their effects on SV.

• Preload: EDV → ↑SV via Frank–Starling law

• Contractility: myocardial strength → ↑SV

• Afterload: resistance to ejection → ↑afterload ↓SV

How do positive/negative inotropic agents affect the heart?

• Positive: ↑ contractility (norepinephrine, digitalis)

• Negative: ↓ contractility (beta-blockers)

How does exercise affect cardiac output?

↑ HR and SV → ↑CO; well-conditioned athletes often have lower resting HR due to more efficient heart function.

Why well-conditioned athletes may have unusually low resting heart rates

Well-conditioned athletes have a higher stroke volume due to a larger, more powerful heart muscle (myocardial hypertrophy). Because cardiac output is the product of heart rate and stroke volume, their hearts can pump the same amount of blood per minute with fewer beats. This results in a lower resting heart rate (bradycardia).