Comprehensive Introduction to Internal Medicine: Cardiology

Anatomy of the Heart and Adjacent Structures

  • Superior Vessels: Left common carotid artery, Left subclavian artery, Brachiocephalic artery, and the Aorta.

  • Ligamentum arteriosum: A remnant structure connecting the aorta and the pulmonary artery.

  • Pulmonary Circulation Structures: Right pulmonary artery, Left pulmonary artery, Pulmonary trunk, Right pulmonary veins (superior and inferior), and Left pulmonary veins (superior and inferior).

  • Venous Return Structures: Superior vena cava and Inferior vena cava.

  • Internal Heart Anatomy:

    • Atria: Right atrium (containing the opening of the coronary sinus) and Left atrium.

    • Ventricles: Right ventricle and Left ventricle.

    • Septum: Interventricular septum.

    • Septal and Ventricular Markers: Tendinous cords (chordae tendineae) and Papillary muscles.

Valvular Structure and the Subvalvular Apparatus

  • Atrioventricular (AV) Valves:

    • Tricuspid Valve: Consists of three leaflets and is located between the right atrium and the right ventricle. Similar to the three-lobed right lung, it is situated on the right side of the heart.

    • Mitral Valve (Bicuspid Valve): Consists of two leaflets and is located between the left atrium and the left ventricle. Similar to the two-lobed left lung, it is situated on the left side of the heart.

  • Subvalvular Apparatus Components:

    • Chordae tendineae: Fibrous cords that provide support to the AV valves by connecting them to the papillary muscles.

    • Papillary muscles: These structures derive from the myocardium and extend from the anterior and posterior ventricular walls as well as the septum. There are three papillary muscles in the right ventricle and two in the left ventricle. Their apices attach to the chordae tendineae. During systole, they contract to tighten the chordae tendineae, thereby preventing valve leaflet prolapse and regurgitation into the atria as ventricular pressure rises.

  • Semilunar Valves:

    • Pulmonary Valve: Composed of three crescent-shaped cusps without a subvalvular apparatus; located between the right ventricle and the pulmonary trunk.

    • Aortic Valve: Composed of three crescent-shaped cusps without a subvalvular apparatus; located between the left ventricle and the aorta.

  • Aortic Root and Sinuses:

    • Aortic Sinuses: Spaces located immediately above the aortic valve, situated between an aortic valve leaflet and the wall of the ascending aorta. There are three sinuses: the left, right, and posterior aortic sinuses.

    • Left and Right Aortic Sinuses: Give rise to the left and right coronary arteries, respectively.

    • Aortic Bulb: A dilation at the root of the aorta formed collectively by the three aortic sinuses and the aortic valve leaflets.

Cardiac Hemodynamics and Physiological Indices

  • Heart Rate (HR): The number of heart contractions per minute, with a normal range of 60−100 bpm60-100\,\text{bpm}.

  • Stroke Volume (SV): The volume of blood ejected by the left or right ventricle during a single heartbeat. It is calculated as: SV=EDV−ESVSV = EDV - ESV.

  • Ejection Fraction (EF): The proportion of end-diastolic volume ejected from the ventricle. It serves as a primary index of myocardial contractility. It is calculated as: EF=SVEDV=EDV−ESVEDVEF = \frac{SV}{EDV} = \frac{EDV - ESV}{EDV}.

    • Normal range: 50−70%50-70\%.

    • Clinical significance: A decrease in myocardial contractility leading to an EF<40%EF < 40\% is characteristic of systolic heart failure. In diastolic heart failure, the EF is usually normal.

  • Venous Return: The rate at which blood flows back to the heart, which normally equals cardiac output.

  • Cardiac Output (CO): The volume of blood pumped through the circulatory system per minute. It is calculated as: CO=HR×SVCO = HR \times SV.

    • Normal rest value: 5 L/min5\,L/min.

    • During physical activity, once SV becomes constant, increases in CO are achieved by increasing the HR.

  • Preload: The degree to which heart muscle fibers are stretched before systole begins. It is dependent on the end-diastolic ventricular volume (EDV), which is influenced by:

    • Venous constriction: Increased venous tone leads to increased venous return, increasing EDV and preload.

    • Circulating blood volume: Increased blood volume leads to increased venous return, increasing EDV and preload.

  • Afterload: The force against which the ventricle must contract to eject blood during systole. It is primarily determined by the mean arterial pressure (MAP) in the aorta, which is influenced by total peripheral resistance.

    • An increase in afterload results in higher left ventricular pressure and increased left ventricular wall stress.

Clinical Picture and Symptomology of Heart Disease

  • Pulmonary Congestion (Common in Left-Sided Heart Failure): Occurs due to the failure of the heart to accept pulmonary venous return. Symptoms include:

    • Dyspnea

    • Cough

    • Hemoptysis

    • Confusion and Insomnia

  • Systemic Congestion (Common in Right-Sided Heart Failure): Occurs due to the failure of the heart to accept systemic venous return. Symptoms include:

    • Right hypochondrial pain

    • Anorexia, nausea, and vomiting

    • Dyspepsia and epigastric pain

    • Edema of dependent parts

    • Abdominal swelling due to ascites

  • Low Cardiac Output Symptoms: Result from the failure of the heart to eject sufficient cardiac output in left-sided, right-sided, or biventricular failure. Affects include:

    • Brain: Dizziness, headache, syncope.

    • Eyes: Blurring of vision.

    • Heart: Angina pectoris.

    • Kidneys: Oliguria.

    • Muscles: Easy fatigability and intermittent claudication.

    • Skin: Pallor, coldness, and peripheral cyanosis in severe cases.

  • Palpitation: An unpleasant awareness of the heartbeat. Possible etiologies include changes in rate (tachycardia or bradycardia), rhythm (arrhythmia), force of contraction, or psychoneurosis.

  • Chest Pain: Cardiac-derived pain can arise from the pericardium (pericarditis), myocardium (angina pectoris or myocardial infarction), endocardium (mitral valve prolapse), aorta (aortic aneurysm), or pulmonary structures (pulmonary embolism). Evaluation must cover seven items: site, character, radiation, duration, precipitating factors, relieving factors, and associated symptoms.

  • Pressure Symptoms: Caused by enlarged cardiac chambers or vessels pressing on surrounding structures:

    • Esophagus: Dysphagia.

    • Tracheobronchial tree: Dyspnea and cough.

    • Left Recurrent Laryngeal Nerve (RLN): Hoarseness of voice.

    • Superior Vena Cava (SVC): Facial swelling and eyelid puffiness.

    • Spine: Back pain.

  • Cyanosis: A bluish discoloration of the skin and mucous membranes caused by the presence of more than 5 g5\,g of reduced hemoglobin per 100 cc100\,cc of blood.

Generalized Physical Signs in Cardiology

  • Respiratory and Congestive Signs: Tachypnea, bilateral fine basal crepitations, and pleural effusion. Right-sided signs include congested pulsating neck veins, lower limb edema followed by ascites, and an enlarged, tender liver (which may exhibit pulsation or hepatojugular reflux).

  • Vitals and Skin: Rapid, weak pulse and low systolic blood pressure. Skin may be cold or exhibit peripheral cyanosis.

  • Differential Causes of Pallor in Cardiac Disease: Anemia, rheumatic activity, infective endocarditis, low cardiac output, and shock.

  • Differential Causes of Jaundice in Cardiac Disease: Severe right-sided heart failure and pulmonary embolism.

  • Clinical Postures:

    • Orthopnea: Associated with left-sided heart failure.

    • Prayer's position (sitting up and leaning forward): Characteristic of pericardial effusion.

    • Squatting: Associated with Tetralogy of Fallot.

  • Fever in Cardiac Patients: Can indicate rheumatic activity, infective endocarditis, pericarditis, myocarditis, myocardial infarction, pulmonary infarction, or pulmonary infection.

  • Finger Clubbing: Occurs as pale clubbing in infective endocarditis and as cyanotic clubbing in cyanotic cardiac conditions.

Precordial Examination: Inspection and Palpation

  • Assessment criteria follow the SECRT mnemonic:

    • Site: Left Ventricular Enlargement (LVE) shifts the apex outwards and downwards. Right Ventricular Enlargement (RVE) shifts it outwards only.

    • Extent: LVE is typically localized, while RVE is diffuse.

    • Character: Pressure overload causes a heaving apex. Volume overload causes a hyperdynamic apex. Mitral stenosis (MS) produces a slapping apex.

    • Relation to Systole: LVE shows systolic bulge; RVE shows systolic retraction.

    • Thrill and Pulsation specificities:

      • Mitral area: Diastolic thrill (MS) or systolic thrill (MR).

      • Tricuspid area: RVE pulsation or VSD thrill.

      • Pulmonary area: Pulmonary hypertension pulsation or PS thrill.

      • Aortic area: Aortic aneurysm pulsation or AS thrill.

      • Epigastric area: Pulsations from RVE, the liver (hepatic), or the aorta.

Auscultation: Heart Sounds and Murmurs

  • Main Heart Sounds:

    • First Heart Sound (S1S_1): Caused by the closure of mitral and tricuspid valves at the beginning of systole. Increased in MS, TS, and tachycardia; decreased in TR, MR, and bradycardia. Best heard at the apex and tricuspid areas.

    • Second Heart Sound (S2S_2): Caused by the closure of aortic and pulmonary valves at the beginning of diastole. Increased in systemic and pulmonary hypertension; decreased in AS, AR, PS, and PR. Found at the aortic and pulmonary areas. Splitting is increased in PS, ASD, and RBBB; decreased in AS, PDA, and LBBB.

    • Third Heart Sound (S3S_3): Occurs in diastole after the isometric relaxation phase. Caused by increased flow from atrium to ventricle or a flabby myocardium (Heart Failure, ischemic heart disease). Best heard at the apex or tricuspid area.

    • Fourth Heart Sound (S4S_4): A presystolic sound before S1S_1 caused by powerful atrial contraction. Best heard at the apex or tricuspid area.

  • Additional Sounds:

    • Opening Snap: Diastolic sound following the isometric relaxation phase; caused by opening of a rigid mitral or tricuspid valve (MS, TS).

    • Ejection Click: Systolic sound following the isometric contraction phase; caused by opening of rigid aortic or pulmonary valves or opening against high pressure.

  • Murmur Characteristics and Propagation:

    • Mitral Stenosis (MS): Mitral area; localized; rumbling character; increases in left lateral position.

    • Mitral Regurgitation (MR): Mitral area; propagates to the axilla (anterior leaflet) or back/sternum (posterior leaflet); soft character.

    • Aortic Stenosis (AS): 1st aortic area; propagates to the apex and carotids; harsh character; increases leaning forward.

    • Aortic Regurgitation (AR): 2nd aortic area; propagates to the apex; increases leaning forward.

    • Tricuspid and Pulmonary murmurs: Increase with inspiration (Carvallo’s sign).

    • Patent Ductus Arteriosus (PDA): Continuous machinery-like murmur, loudest in the 2nd left interspace.

    • Carey Coomb's murmur: A functional MS murmur heard in Rheumatic Fever.

    • Graham Steell murmur: An early diastolic murmur of pulmonary regurgitation (PR).

  • Murmur Grading:

    • A thrill indicates a palpable, loud murmur (comparable to a purring cat).

    • A thrill requires a minimum grade of 4/64/6.

    • Systolic murmurs are harsh with a marked thrill; functional murmurs are soft with no thrill.

Diagnostic Investigations and Management

  • Imaging and Technical Investigations:

    • X-ray: Detects chamber enlargement, pulmonary congestion, and pleural effusion.

    • ECG and Echo: Used for identifying the cause of disease, chamber enlargement, and detecting paradoxical movement of the myocardium.

    • Catheterization: Used for definitive cause detection and chamber size verification.

    • Other: Radio-isotope studies, CT, and MRI.

  • Laboratory Tests:

    • General: CBC, Lipid profile, blood glucose, liver and renal function tests.

    • Myocardial Infarction: Cardiac enzymes.

    • Infective Endocarditis: Blood culture.

    • Pulmonary Embolism: Pulmonary angiography, spiral CT, and D-dimer.

    • Cardiomyopathy: Biopsy.

  • Treatment Strategies:

    • Primary: Treat the underlying cause and precipitating factors.

    • Hyperlipidemia Management:

      • Statins: Dosage of 20−80 mg/d20-80\,mg/d; side effect includes myositis.

      • Fenofibrate: Dosage of 300 mg/d300\,mg/d.

      • Omega 3: Derived from fish oil.