Study Guide: The Heart (Chapter 20) – Structure, Function, and Clinical Aspects

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Heart Anatomy and Physiology

Mediastinum and Position of the Heart in the Thorax

The mediastinum is the central compartment of the thoracic cavity, located between the lungs. The heart is situated within the mediastinum, slightly left of the midline, and rests on the diaphragm. This position protects the heart and allows for efficient circulation.

Superior border: At the level of the second rib
Apex: Points downward, left, and anteriorly
Base: Directed toward the right shoulder

Clinical relevance: The mediastinal position is important for interpreting chest X-rays and understanding trauma impacts.

Pericardium: Structure and Function

The pericardium is a double-walled sac that surrounds and protects the heart. It consists of two main layers:

Fibrous pericardium: Tough, outer layer that anchors the heart and prevents overfilling.
Serous pericardium: Thin, inner layer with two parts: parietal (lines the fibrous pericardium) and visceral (epicardium, covers the heart surface).

The pericardial cavity between these layers contains fluid to reduce friction during heartbeats.

Pericarditis: Definition and Etiology

Pericarditis is inflammation of the pericardium, often caused by infection, autoimmune disorders, or trauma. It can lead to chest pain and, in severe cases, pericardial effusion or cardiac tamponade.

Etiology: Viral infections (most common), bacterial infections, post-MI, or idiopathic causes.

Structure and Function of Heart Wall Layers

The heart wall is composed of three layers, each with distinct functions:

Epicardium: Outer layer, also known as the visceral pericardium; provides protection and reduces friction.
Myocardium: Middle, muscular layer responsible for contraction and pumping blood.
Endocardium: Inner layer lining the chambers and valves; smooth surface minimizes resistance to blood flow.

Heart Muscle Histology: Intercalated Discs

Cardiac muscle cells are connected by intercalated discs, which contain gap junctions and desmosomes. These structures allow rapid electrical communication and strong mechanical connections, enabling the heart to contract as a unit.

Gap junctions: Permit ion flow for synchronized contraction.
Desmosomes: Provide structural stability during contraction.

Cardiac Hypertrophy: Definition, Causes, and Risk Factors

Cardiac hypertrophy is the thickening of the heart muscle, usually in response to increased workload. It can be physiological (athletic training) or pathological (hypertension, valve disease).

Causes: Chronic high blood pressure, valve disorders, genetic factors.
Risks: Heart failure, arrhythmias, sudden cardiac death.

Heart Anatomy and Circulation

Internal and External Anatomy of the Heart

The heart has four chambers (right/left atria, right/left ventricles) and is divided by septa. Major external features include the coronary sulcus, anterior/posterior interventricular sulci, and auricles.

Valves: Ensure unidirectional blood flow (tricuspid, pulmonary, mitral, aortic).
Major vessels: Superior/inferior vena cava, pulmonary arteries/veins, aorta.

Blood Flow Through the Heart

Blood flows through the heart in a specific sequence to ensure oxygenation and systemic delivery:

Deoxygenated blood enters right atrium via vena cavae.
Passes through tricuspid valve to right ventricle.
Pumped through pulmonary valve to pulmonary arteries and lungs.
Oxygenated blood returns via pulmonary veins to left atrium.
Passes through mitral valve to left ventricle.
Pumped through aortic valve to aorta and systemic circulation.

Heart Sounds: S1 and S2

Heart sounds are produced by the closing of valves:

S1 ("lub"): Closure of AV valves (tricuspid and mitral) at the start of ventricular systole.
S2 ("dub"): Closure of semilunar valves (aortic and pulmonary) at the start of ventricular diastole.

Valve Disorders: MVP and AVS

Mitral Valve Prolapse (MVP): The mitral valve bulges into the left atrium during systole, sometimes causing regurgitation. Etiology includes connective tissue disorders or idiopathic causes.

Aortic Valve Stenosis (AVS): Narrowing of the aortic valve, often due to age-related calcification or congenital defects, leading to increased left ventricular workload.

Coronary Artery Disease (CAD)

CAD is the narrowing or blockage of coronary arteries due to atherosclerosis, reducing blood flow to the myocardium and increasing risk of angina, MI, and heart failure.

Blood Tests for Myocardial Infarction (MI)

Key blood tests for MI diagnosis include:

Troponin I/T: Most specific and sensitive markers for myocardial injury.
CK-MB: Rises within 4-6 hours, peaks at 24 hours.
Myoglobin: Early marker but less specific.

Electrical Activity and Cardiac Function

Conduction System Pathway

The heart's conduction system ensures coordinated contraction:

Sinoatrial (SA) node: Pacemaker, initiates impulse.
Atrioventricular (AV) node: Delays impulse, allowing atrial contraction.
Bundle of His: Conducts impulse to ventricles.
Right and left bundle branches: Carry impulse through interventricular septum.
Purkinje fibers: Distribute impulse to ventricular myocardium.

Electrocardiogram (ECG) Interpretation

An ECG records the heart's electrical activity:

P wave: Atrial depolarization
QRS complex: Ventricular depolarization
T wave: Ventricular repolarization

Calcium Channels in Myocardium vs. Skeletal Muscle

Slow calcium channels in cardiac muscle prolong the action potential, allowing sustained contraction and preventing tetanus. Skeletal muscle lacks this plateau phase, enabling rapid, repeated contractions.

ST Elevation in MI

ST elevation on ECG indicates acute myocardial injury, often due to complete coronary artery occlusion. It is a key sign of ST-elevation myocardial infarction (STEMI).

Blood Pressure: Diastole and Systole

Systolic pressure: Maximum pressure during ventricular contraction. Diastolic pressure: Minimum pressure during ventricular relaxation.

Normal adult BP: ~120/80 mmHg.

ANP/BNP Hormones: Origin and Actions

Atrial Natriuretic Peptide (ANP): Released from atria in response to stretch; promotes sodium and water excretion, lowering blood volume and pressure.

Brain Natriuretic Peptide (BNP): Released from ventricles; similar actions to ANP, used clinically to assess heart failure severity.

Cardiodynamics and Clinical Calculations

Cardiodynamics: CO, SV, Preload, Afterload

Cardiodynamics refers to the forces and factors affecting cardiac output (CO):

Cardiac Output (CO): Volume of blood pumped per minute.
Stroke Volume (SV): Volume of blood ejected per beat.
Preload: Degree of ventricular stretch before contraction.
Afterload: Resistance the ventricle must overcome to eject blood.

Example: If HR = 70 bpm and SV = 70 mL, then mL/min.

Ejection Fraction and Congestive Heart Failure (CHF)

Ejection Fraction (EF): Percentage of end-diastolic volume ejected per beat. Normal EF is 55-70%.

Formula:

CHF: Occurs when EF is significantly reduced, indicating poor ventricular function.

Example: If SV = 60 mL and EDV = 120 mL,