Cardiac Anatomy & Coronary Circulation

1. Quick Answer

Cardiac anatomy encompasses the four-chambered heart, its valvular apparatus, coronary circulation, conducting system, pericardium, and fibrous skeleton - all essential knowledge for intensive care practice.

Key Concepts:

• The heart consists of two atria (thin-walled receiving chambers) and two ventricles (thick-walled pumping chambers)
• Four valves ensure unidirectional blood flow: mitral and tricuspid (atrioventricular), aortic and pulmonary (semilunar)
• Coronary arteries arise from the aortic sinuses of Valsalva and supply the myocardium
• The conducting system initiates and propagates electrical impulses for coordinated contraction
• The pericardium provides mechanical protection and reduces friction during cardiac motion

ICU Relevance:

• Critical for pulmonary artery catheter placement and interpretation
• Essential for echocardiographic assessment of cardiac function
• Understanding coronary territories guides management of myocardial infarction
• Knowledge of conducting system blood supply predicts arrhythmia risk in coronary syndromes
• Pericardial anatomy is essential for pericardiocentesis and post-cardiac surgery care

Exam Focus:

• CICM First Part examiners commonly ask about coronary artery territories, conducting system blood supply, valve anatomy, and applied cardiac anatomy for procedures

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2. CICM First Part Exam Focus

What Examiners Expect

Written SAQ:

Common question stems:

• "Describe the anatomy of the coronary arteries, including the concept of coronary dominance"
• "Outline the blood supply to the cardiac conducting system"
• "Describe the anatomy of the mitral valve apparatus"
• "Draw and label a cross-section of the heart at the level of the ventricles"
• "Describe the anatomical considerations relevant to pericardiocentesis"
• "Outline the anatomy relevant to pulmonary artery catheter placement"

Expected depth:

• Origin, course, and territories of coronary arteries
• Concept of coronary dominance with prevalence figures
• Blood supply to SA and AV nodes
• Detailed valve anatomy including papillary muscles and chordae tendineae
• Clear diagrams with accurate labeling
• Explicit ICU application (echocardiography, hemodynamic monitoring)

Written MCQ:

Common topics tested:

• Coronary artery territories and dominance patterns
• Conducting system components and blood supply
• Valve anatomy and pathology
• Cardiac chamber anatomy and wall thickness ratios
• Surface anatomy and cardiac landmarks
• Pericardial anatomy and sinuses

Difficulty level:

• Applied anatomical scenarios (e.g., "Which artery supplies the AV node in most patients?")
• Identification of structures from echocardiographic or angiographic descriptions
• Clinical consequences of coronary occlusion at different sites

Oral Viva:

Expected discussion flow:

1. Define/Describe - Overview of cardiac chambers, orientation in thorax
2. Coronary Arteries - Origin, course, branches, territories, dominance
3. Conducting System - Components from SA node to Purkinje fibres, blood supply
4. Valvular Apparatus - Annuli, leaflets, supporting structures
5. Apply to ICU - PAC placement, echocardiography windows, pericardiocentesis
6. Compare - Normal variants, congenital anomalies, clinical implications

Common viva scenarios:

• "Walk me through the coronary artery anatomy and explain dominance"
• "A patient has an inferior STEMI - which conducting structures are at risk?"
• "Describe the anatomy relevant to inserting a pulmonary artery catheter"
• "What anatomical structures are relevant to performing a pericardiocentesis?"

Pass vs Fail Performance

Pass Standard:

• Accurate description of right and left coronary artery origins and main branches
• Correct understanding of coronary dominance (70-85% right dominant)
• Clear knowledge of SA node supply (60% RCA, 40% LCx)
• AV node supply predominantly from RCA (80-90%)
• Ability to relate coronary territories to ECG changes
• Draws clear diagrams of coronary anatomy

Common Reasons for Failure:

• Stating 50% right dominant (it's 70-85%)
• Not knowing the blood supply to the conducting system
• Confusing the mitral and tricuspid valve anatomy
• Inability to describe papillary muscle blood supply
• Poor understanding of coronary artery territories
• Cannot describe pericardiocentesis landmarks

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3. Key Points

Must-Know Facts

1. Coronary Artery Origins: Left coronary artery (LCA) arises from the left aortic sinus of Valsalva and bifurcates into left anterior descending (LAD) and left circumflex (LCx). Right coronary artery (RCA) arises from the right aortic sinus. Coronary ostia are located approximately 1-2cm above the aortic valve (PMID: 17210824).

2. Coronary Dominance: Right dominant (posterior descending artery from RCA) occurs in 70-85%, left dominant (PDA from LCx) in 8-10%, and co-dominant in 5-15% of hearts. Dominance determines the blood supply to the inferior wall and AV node (PMID: 22403395).

3. SA Node Blood Supply: The sinoatrial nodal artery arises from the RCA in 55-60% and from the LCx in 40-45% of cases. The SA node is a small structure (15-20mm long, 2-3mm wide) in the sulcus terminalis (PMID: 16046534).

4. AV Node Blood Supply: The AV nodal artery arises from the dominant coronary artery - RCA in right dominant hearts (80-90%), LCx in left dominant hearts. Inferior STEMI carries significant risk of AV nodal ischemia and heart block (PMID: 15837856).

5. Left Anterior Descending (LAD) Territory: Supplies the anterior two-thirds of interventricular septum, anterior wall of left ventricle, and apex. Occlusion causes anterior STEMI with the largest territory at risk - often called the "widow maker" (PMID: 26153014).

6. Right Coronary Artery (RCA) Territory: Supplies the right atrium, right ventricle, SA node (60%), AV node (80-90%), posterior one-third of interventricular septum (in right dominant hearts), and inferior wall of left ventricle. RCA occlusion causes inferior STEMI with risk of bradyarrhythmias (PMID: 28555623).

7. Ventricular Wall Thickness: Left ventricular free wall is 8-15mm thick; right ventricular free wall is 2-5mm thick. The interventricular septum is 8-11mm. LV:RV wall thickness ratio is approximately 3:1 (PMID: 26139504).

8. Mitral Valve Anatomy: Bicuspid valve with anterior (aortic) and posterior (mural) leaflets, annulus circumference 8-12cm, two papillary muscle groups (anterolateral and posteromedial), and multiple chordae tendineae connecting leaflets to papillary muscles (PMID: 27180020).

9. Pericardiocentesis Anatomy: Subxiphoid approach enters pericardial space 5-8cm deep, directed toward the left shoulder at 30-45 degrees. The pericardial space normally contains 15-50mL of serous fluid. Cardiac tamponade occurs when intrapericardial pressure exceeds filling pressures (PMID: 21884679).

10. Cardiac Conducting System: SA node (pacemaker, 60-100 bpm) → internodal pathways → AV node (0.05m/s conduction, 0.1s delay) → Bundle of His → right and left bundle branches → Purkinje fibres (4m/s conduction). The conducting system has dual blood supply, with the proximal system (SA, AV nodes) more vulnerable to ischemia (PMID: 25092578).

Normal Values Table

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4. Cardiac Chambers

4.1 Right Atrium (RA)

External Features

Surface Anatomy:

• Located in the right anterior aspect of the heart
• Receives venous return from superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus
• The sulcus terminalis is an external groove marking the junction of the smooth sinus venarum and trabeculated atrium

Anatomical Relations:

• Anteriorly: Sternum, right pleura
• Posteriorly: Right pulmonary veins, left atrium
• Superiorly: SVC, right pulmonary artery
• Inferiorly: IVC, tricuspid valve

Internal Features

Crista Terminalis:

• Internal muscular ridge corresponding to sulcus terminalis
• Separates smooth sinus venarum (posterior) from trabeculated right atrial appendage (anterior)
• Embryologically derived from junction of sinus venosus and primitive atrium
• Important landmark during catheter ablation procedures (PMID: 16945928)

Pectinate Muscles:

• Muscular ridges in the right atrial appendage
• Arranged like teeth of a comb (pecten = comb)
• Absent in the smooth sinus venarum

Openings and Structures:

• SVC orifice: No valve, receives blood from head, neck, upper limbs
• IVC orifice: Guarded by Eustachian valve (valve of inferior vena cava), embryological remnant directing oxygenated blood toward foramen ovale in fetal life
• Coronary sinus orifice: Located between IVC orifice and tricuspid annulus, guarded by Thebesian valve
• Fossa ovalis: Shallow depression on interatrial septum, remnant of foramen ovale; limbic margin forms the raised border

Triangle of Koch:

• Anatomical landmark containing the AV node
• Boundaries: Tendon of Todaro (fibrous extension of Eustachian valve), septal leaflet of tricuspid valve, coronary sinus orifice
• Apex points toward the central fibrous body and membranous septum
• Critical landmark to avoid during electrophysiology procedures (PMID: 16214567)

Sinoatrial (SA) Node Location:

• Situated at the junction of SVC and right atrium
• In the sulcus terminalis, approximately 1mm beneath the epicardium
• Spindle-shaped structure 15-20mm long, 2-3mm wide
• Contains pacemaker cells with highest intrinsic automaticity (PMID: 25092578)

Clinical Correlations

Right Atrium in ICU:

• Central venous catheter tip ideally positioned in SVC near RA junction
• PAC passes through RA, recognizable by pressure waveform (a-wave, v-wave)
• Right atrial pressure (RAP) reflects right ventricular preload
• Normal RAP: 2-8 mmHg; elevated in RV failure, tricuspid regurgitation, tamponade

Patent Foramen Ovale (PFO):

• Occurs in 25-30% of general population
• Potential for paradoxical embolism (venous thrombus crossing to arterial circulation)
• Diagnosed by bubble contrast echocardiography (PMID: 19228612)

4.2 Left Atrium (LA)

External Features

Surface Anatomy:

• Most posterior cardiac chamber, lying against esophagus and descending aorta
• Receives oxygenated blood from four pulmonary veins (typically)
• Left atrial appendage (LAA) is the most anterior portion

Anatomical Relations:

• Anteriorly: Right atrium, aortic root
• Posteriorly: Esophagus, descending thoracic aorta
• Superiorly: Pulmonary arteries
• Inferiorly: Coronary sinus, mitral valve

Internal Features

Smooth-Walled Chamber:

• Most of left atrium is smooth-walled (derived from pulmonary vein tissue)
• Only the left atrial appendage has pectinate muscles
• No crista terminalis (present only in right atrium)

Left Atrial Appendage (LAA):

• Tubular, finger-like structure anterolateral to left upper pulmonary vein
• Major site of thrombus formation in atrial fibrillation
• Variable morphology: "chicken wing" (48%), "cactus" (30%), "windsock" (19%), "cauliflower" (3%)
• "Cauliflower" morphology associated with highest stroke risk (PMID: 22749982)

Pulmonary Vein Orifices:

• Typically four: right superior, right inferior, left superior, left inferior
• Common variations: common left pulmonary vein trunk (10-25%), accessory right middle pulmonary vein (20%)
• Pulmonary vein ostia are important targets for atrial fibrillation ablation (PMID: 16214567)

Interatrial Septum from Left Side:

• Fossa ovalis visible as a slight concavity
• Septum primum forms the floor of fossa ovalis
• Important for transseptal puncture during left heart catheterization

Clinical Correlations

Left Atrium in ICU:

• LA pressure reflected by pulmonary artery wedge pressure (PAWP)
• LA dilation correlates with AF burden and stroke risk
• Transesophageal echocardiography (TOE) provides excellent LA/LAA views due to posterior position
• TOE screening for LAA thrombus before cardioversion

4.3 Right Ventricle (RV)

External Features

Surface Anatomy:

• Most anterior cardiac chamber, lying behind the sternum
• Forms the largest portion of the sternocostal (anterior) surface of the heart
• Extends from the tricuspid valve to the pulmonary valve

Anatomical Relations:

• Anteriorly: Sternum, costal cartilages
• Posteriorly: Interventricular septum
• Superiorly: Conus arteriosus, pulmonary trunk
• Inferiorly: Diaphragm (inferior aspect)

Internal Features

Wall Thickness:

• Normal RV free wall: 2-5mm
• Thickens to >5mm in RV hypertrophy (pulmonary hypertension, pulmonary stenosis)
• LV:RV wall thickness ratio approximately 3:1

Three Anatomical Components:

1. Inlet Component:

   • Extends from tricuspid annulus
   • Contains tricuspid valve apparatus and papillary muscles
   • Heavily trabeculated

2. Trabecular/Apical Component:

   • Coarse trabeculations (trabeculae carneae)
   • Moderator band (septomarginal trabecula) - muscular band crossing from septum to anterior papillary muscle, carries right bundle branch
   • Distinguishes RV from LV in congenital heart disease (PMID: 16626686)

3. Outlet Component (Conus Arteriosus/Infundibulum):

   • Smooth-walled muscular outflow tract
   • Leads to pulmonary valve
   • Crista supraventricularis (supraventricular crest) separates inlet from outlet

Papillary Muscles:

• Three main papillary muscles: anterior (largest), posterior, septal (variable)
• Anterior papillary muscle attached to moderator band
• Arise from ventricular wall and anchor chordae tendineae

Moderator Band (Septomarginal Trabecula):

• Muscular band extending from interventricular septum to base of anterior papillary muscle
• Contains the right bundle branch
• Important landmark on echocardiography to distinguish RV from LV
• Present in ~90% of hearts (PMID: 25092578)

Clinical Correlations

Right Ventricle in ICU:

• Sensitive to preload (Frank-Starling mechanism more important than in LV)
• Poorly tolerates acute afterload increase (massive PE causes acute RV failure)
• RV function assessed by TAPSE (tricuspid annular plane systolic excursion) >17mm normal
• RV dilation (RV:LV ratio >0.9 at base) in acute PE suggests poor prognosis (PMID: 24696312)

Right Ventricular Infarction:

• Occurs with proximal RCA occlusion (before RV marginal branches)
• Characterized by hypotension, elevated JVP, clear lung fields
• Managed with volume resuscitation (right-sided preload dependent)
• Avoid nitrates and diuretics (preload reduction worsens hemodynamics)

4.4 Left Ventricle (LV)

External Features

Surface Anatomy:

• Forms the apex of the heart (fifth intercostal space, midclavicular line)
• Cardiac apex beat palpable in thin individuals
• Comprises the left inferior and posterior cardiac surfaces

Anatomical Relations:

• Anteriorly: Right ventricle, anterior interventricular groove (containing LAD)
• Posteriorly: Left atrium, descending aorta
• Laterally: Left pleura, left phrenic nerve
• Inferiorly: Diaphragm

Internal Features

Wall Thickness:

• Normal LV free wall: 8-15mm

• 15mm = LV hypertrophy

• <7mm suggests dilated cardiomyopathy with wall thinning
• Interventricular septum: 8-11mm (normally equal to posterior wall)

Two Anatomical Components:

1. Inlet/Trabecular Component:

   • Fine trabeculations (cf. coarse RV trabeculations)
   • No moderator band
   • Two papillary muscle groups

2. Outlet Component:

   • Smooth-walled aortic vestibule
   • Continuous with mitral valve (aorto-mitral continuity)
   • No crista supraventricularis (cf. RV)

Papillary Muscles:

• Two groups: anterolateral and posteromedial
• Anterolateral papillary muscle: Dual blood supply from LAD (diagonal branches) and LCx (obtuse marginal branches) - rarely ruptures
• Posteromedial papillary muscle: Single blood supply from PDA (usually RCA) - more vulnerable to ischemic rupture (PMID: 27180020)

Interventricular Septum:

• Thickness: 8-11mm
• Two portions:
  • "Muscular septum: Thicker, comprises 85% of septum, supplied by LAD (anterior two-thirds) and PDA (posterior one-third)"
  • "Membranous septum: Thin fibrous portion, 2-4mm diameter, located beneath aortic valve, site of perimembranous VSD"

Trabecular Features:

• Trabeculae carneae: Finer than in RV
• False tendons: Fibrous or muscular bands crossing LV cavity, may be mistaken for thrombus on echo
• No moderator band (distinguishes LV from RV)

Clinical Correlations

Left Ventricle in ICU:

• LV function assessed by ejection fraction (normal 55-70%)
• Wall motion abnormalities localize coronary occlusion territory
• Diastolic dysfunction assessed by E/A ratio, E/e', deceleration time
• LVOT diameter essential for cardiac output calculation by echo

Papillary Muscle Rupture:

• Occurs 2-7 days post-MI (after myocardium softens)
• Posteromedial papillary muscle rupture more common (single blood supply)
• Presents with acute severe mitral regurgitation, pulmonary edema, cardiogenic shock
• Diagnosis by echo: flail leaflet, severe MR jet, possible hyperdynamic LV
• Mortality >70% without urgent surgical repair (PMID: 22554612)

4.5 Interventricular Septum

Anatomy

Muscular Septum:

• Forms 85% of the septum
• Thickness 8-11mm
• Supplied by septal perforators from LAD (anterior two-thirds) and PDA (posterior one-third)
• Composed of myocardium

Membranous Septum:

• Forms 15% of the septum (small 2-4mm fibrous area)
• Located in the outflow tract, beneath the aortic valve
• Divided into:
  • "Atrioventricular component: Between LV and RA"
  • "Interventricular component: Between LV and RV"
• Site of perimembranous ventricular septal defects
• Bundle of His passes through this region (PMID: 25092578)

Blood Supply

LAD Territory:

• Anterior two-thirds of septum
• Via 3-5 septal perforator branches
• First septal perforator often largest ("first septal perforator")

PDA Territory:

• Posterior one-third of septum
• In right dominant hearts, PDA from RCA
• In left dominant hearts, PDA from LCx

Clinical Correlations

Septal Anatomy in ICU:

• Septal motion abnormality indicates LAD or RCA/PDA territory infarction
• Paradoxical septal motion in RV volume/pressure overload
• Asymmetric septal hypertrophy (>1.3:1 septum:posterior wall ratio) suggests HCM
• Post-MI VSD typically occurs in muscular septum, 2-5 days after infarction

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5. Cardiac Valves

5.1 Mitral Valve (Bicuspid Valve)

Anatomical Position

• Left atrioventricular valve
• Separates left atrium from left ventricle
• Most frequently affected valve in rheumatic heart disease (PMID: 23462518)

Structural Components

Annulus:

• Saddle-shaped (highest points anteriorly and posteriorly, lowest points medially and laterally)
• Circumference: 8-12cm
• Dynamic structure that changes shape during cardiac cycle
• Calcification of annulus occurs with aging and reduces leaflet mobility (PMID: 27180020)

Leaflets:

• Anterior (Aortic/Anteromedial) Leaflet:

  • Larger, more mobile
  • In fibrous continuity with aortic valve (aorto-mitral curtain)
  • Two-thirds of surface area, one-third of annular circumference

• Posterior (Mural/Posterolateral) Leaflet:

  • Smaller, has three scallops (P1, P2, P3)
  • One-third of surface area, two-thirds of annular circumference
  • Commonly affected in myxomatous degeneration/prolapse

Nomenclature (Carpentier Classification):

• A1, A2, A3: Three segments of anterior leaflet
• P1 (lateral), P2 (middle), P3 (medial): Three scallops of posterior leaflet
• P2 most commonly prolapsing segment

Chordae Tendineae:

• Fibrous cords connecting leaflet edges to papillary muscles
• Types:
  • "Primary (marginal): Attach to leaflet free edge, prevent prolapse"
  • "Secondary (intermediate): Attach to ventricular surface of leaflet"
  • "Tertiary (basal): Only posterior leaflet, from ventricular wall"
• Rupture causes acute mitral regurgitation

Papillary Muscles:

• Anterolateral Papillary Muscle:

  • Attaches chordae to A1, A2, P1, P2
  • "Dual blood supply: LAD (diagonals) + LCx (obtuse marginals)"
  • Rarely ruptures due to redundant supply

• Posteromedial Papillary Muscle:

  • Attaches chordae to A3, P3, and portions of A2, P2
  • "Single blood supply: PDA (usually RCA in right dominant hearts)"
  • "More vulnerable to ischemic rupture (PMID: 22554612)"

Clinical Correlations

Mitral Valve in ICU:

• Mitral regurgitation assessed by color Doppler, vena contracta, PISA
• Acute MR (post-MI papillary rupture, endocarditis) causes hemodynamic collapse
• Severe mitral stenosis: Valve area <1.0cm², mean gradient >10mmHg
• RWMA of inferior/posterior wall suggests posteromedial papillary muscle at risk

5.2 Tricuspid Valve

Anatomical Position

• Right atrioventricular valve
• Separates right atrium from right ventricle
• Largest cardiac valve by orifice area
• Located more apically (closer to apex) than mitral valve

Structural Components

Annulus:

• Circumference: 10-14cm
• Larger and more circular than mitral annulus
• Dilates in RV failure, causing functional tricuspid regurgitation
• The AV node is located superior to the septal annulus (proximity matters for surgery)

Leaflets:

• Anterior Leaflet: Largest, most mobile
• Septal Leaflet: Smallest, attached to interventricular septum
• Posterior (Inferior) Leaflet: Variable size

Commissures:

• Anteroseptal, anteroposterior, posteroseptal commissures
• Named by adjacent leaflets

Chordae Tendineae:

• Similar arrangement to mitral valve
• Attach to three papillary muscles

Papillary Muscles:

• Anterior (largest): Connects to anterior papillary muscle from RV wall
• Posterior: Variable, may be multiple
• Septal: Small, may be absent; some chordae attach directly to septum

Clinical Correlations

Tricuspid Valve in ICU:

• Functional TR common in RV dilation (secondary to LV failure, pulmonary hypertension)
• TR severity graded by hepatic vein flow reversal, vena contracta, EROA
• Severe TR: Vena contracta >7mm, hepatic vein systolic reversal
• Central line/PPM leads can damage tricuspid valve
• Tricuspid annulus TAPSE reflects RV systolic function

5.3 Aortic Valve

Anatomical Position

• Left ventricular outflow valve
• Separates left ventricle from ascending aorta
• Located in the central fibrous body
• Three cusps corresponding to three sinuses of Valsalva

Structural Components

Annulus:

• Diameter: 21-26mm (men), 19-23mm (women)
• Crown-shaped rather than flat ring
• Fibrous continuity with mitral valve anteriorly (aorto-mitral curtain)

Cusps/Leaflets:

• Right Coronary Cusp: Overlies right coronary ostium
• Left Coronary Cusp: Overlies left coronary ostium
• Non-Coronary (Posterior) Cusp: No coronary ostium; related to right atrium

Each cusp has:

• Lunula: Thin, crescent-shaped edge
• Nodule of Arantius: Central nodular thickening at midpoint of free edge
• Body: Main portion of cusp

Sinuses of Valsalva:

• Dilated portions of aortic root above each cusp
• Right coronary sinus: Contains right coronary ostium
• Left coronary sinus: Contains left coronary ostium
• Non-coronary sinus: No coronary artery
• Aneurysm of sinus of Valsalva is a rare congenital anomaly

Sinotubular Junction:

• Transition between sinuses of Valsalva and tubular ascending aorta
• Normal diameter: 25-30mm
• Dilation causes aortic regurgitation (Marfan syndrome)

Bicuspid Aortic Valve

Prevalence: 1-2% of general population (PMID: 26153014) Configurations:

• Right-left cusp fusion (most common, 70-80%)
• Right-non cusp fusion (20-30%)
• Left-non cusp fusion (rare, 1%)

Associated Conditions:

• Aortic coarctation (present in 50-70% of coarctation patients)
• Aortopathy (dilated ascending aorta, dissection risk)
• Accelerated calcific aortic stenosis
• Turner syndrome

Clinical Correlations

Aortic Valve in ICU:

• Aortic stenosis: Valve area <1.0cm², mean gradient >40mmHg, Vmax >4m/s = severe
• Low-gradient severe AS in low EF states - dobutamine stress echo helpful
• Aortic regurgitation: Holodiastolic flow reversal in descending aorta = severe
• Post-TAVR monitoring: Paravalvular leak assessment, conduction abnormalities

5.4 Pulmonary Valve

Anatomical Position

• Right ventricular outflow valve
• Most anterior and superior of all cardiac valves
• Separated from tricuspid valve by infundibulum (no fibrous continuity)

Structural Components

Annulus:

• Diameter slightly larger than aortic valve: 22-27mm
• Fibrous ring supporting three cusps
• Located at base of pulmonary trunk

Cusps:

• Anterior Cusp
• Right Cusp
• Left Cusp
• Named by their position in the body (not by coronary arteries)
• Similar structure to aortic cusps: lunula, nodule, body

Pulmonary Sinuses:

• Three dilated areas above cusps (similar to sinuses of Valsalva)
• No coronary arteries arise from pulmonary sinuses

Clinical Correlations

Pulmonary Valve in ICU:

• Pulmonary regurgitation common in pulmonary hypertension
• Severe PR: Dense spectral Doppler signal, short pressure half-time
• Ross procedure: Pulmonary valve (autograft) replaces diseased aortic valve
• Carcinoid syndrome causes thickened, retracted pulmonary (and tricuspid) valve leaflets

5.5 Cardiac Skeleton and Fibrous Rings

Central Fibrous Body

Anatomy:

• Dense connective tissue at the junction of mitral, tricuspid, and aortic valves
• Provides structural support for valve annuli
• Contains the Bundle of His as it passes from AV node to ventricles
• Forms the atrioventricular septum

Components:

• Right Fibrous Trigone: Between aortic, mitral, and tricuspid valves; largest part of central fibrous body
• Left Fibrous Trigone: Between aortic and mitral valves
• Aorto-mitral Curtain: Fibrous continuity between aortic and mitral valves

Fibrous Rings (Annuli)

• Surround each valve orifice
• Provide attachment for valve leaflets/cusps
• Electrically isolate atria from ventricles (except at AV node/Bundle of His)
• Degenerative calcification causes conduction abnormalities

Clinical Correlations

Cardiac Skeleton in ICU:

• Fibrous skeleton provides electrical insulation between atria and ventricles
• Calcification can extend to conducting system (AV block, bundle branch block)
• Abscess of central fibrous body in endocarditis carries poor prognosis
• Structural support relevant for TAVR planning

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6. Coronary Arteries

6.1 Left Coronary Artery (LCA)

Origin and Main Trunk (Left Main Coronary Artery - LMCA)

Origin:

• Arises from left aortic sinus of Valsalva (left coronary sinus)
• Ostium located 1-2cm above aortic valve at the sinotubular junction
• Diameter: 3.5-5.0mm at origin

Course:

• Emerges between pulmonary trunk and left atrial appendage
• Length: 2-40mm (average 10-15mm)
• Bifurcates (or trifurcates) at end of left main trunk

Branches:

1. Left Anterior Descending (LAD)
2. Left Circumflex (LCx)
3. Ramus Intermedius (when present, 15-37% of hearts) - supplies lateral wall (PMID: 28555623)

Left Anterior Descending Artery (LAD)

Course:

• Descends in anterior interventricular groove (sulcus)
• Passes toward cardiac apex
• May wrap around apex to supply posterior apical region (long LAD)

Branches:

1. Septal Perforators:

   • 3-5 branches penetrating interventricular septum
   • Supply anterior two-thirds of septum
   • First septal perforator often largest

2. Diagonal Branches:

   • 1-3 branches coursing over anterolateral LV wall
   • D1 (first diagonal) is largest
   • Supply anterolateral left ventricular wall
   • Contribute to anterolateral papillary muscle supply

Territory:

• Anterior wall of left ventricle
• Anterior two-thirds of interventricular septum
• Cardiac apex
• Part of anterolateral papillary muscle

ECG Territory:

• V1-V6 (anteroseptal, anterior, lateral)
• I, aVL (high lateral)
• LAD occlusion = anterior STEMI

Left Circumflex Artery (LCx)

Course:

• Courses in left atrioventricular groove (coronary sulcus)
• Passes posteriorly toward the cardiac crux
• Variable length depending on dominance

Branches:

1. Obtuse Marginal Branches (OM1, OM2, OM3):

   • Course over lateral LV wall
   • Supply lateral and posterolateral LV wall
   • Contribute to anterolateral papillary muscle supply

2. Left Atrial Branches:

   • Supply left atrium

3. SA Nodal Artery (40% of hearts):

   • When SA node supplied by LCx (vs RCA 60%)

4. Posterior Descending Artery (PDA) (in left dominant hearts, 8-10%):

   • Arises from LCx instead of RCA

Territory:

• Lateral wall of left ventricle
• Posterolateral wall of left ventricle
• Part of anterolateral papillary muscle
• SA node (40%)
• AV node and posterior septum (in left dominant hearts only)

ECG Territory:

• I, aVL, V5, V6 (lateral)
• LCx occlusion may have minimal ECG changes (electrically silent territory)

6.2 Right Coronary Artery (RCA)

Origin

Origin:

• Arises from right aortic sinus of Valsalva (right coronary sinus)
• Ostium located 1-2cm above aortic valve
• Diameter: 2.5-4.5mm at origin

Course

Proximal RCA:

• Emerges between pulmonary trunk and right atrial appendage
• Descends in right atrioventricular groove

Mid RCA:

• Courses along inferior border of heart
• Gives off acute marginal branches

Distal RCA:

• Reaches posterior interventricular groove at cardiac crux
• In right dominant hearts, gives rise to posterior descending artery (PDA)

Major Branches

1. Conus Branch (Infundibular):

   • First branch, supplies RV outflow tract
   • May arise directly from aorta (10%)
   • Potential collateral to LAD territory (Vieussens' arterial ring)

2. SA Nodal Artery (55-60% of hearts):

   • Arises from proximal RCA
   • Courses posteriorly around SVC to reach SA node (PMID: 16046534)

3. Right Atrial Branches:

   • Supply right atrium

4. Acute Marginal Branches (AM1, AM2):

   • Supply right ventricular free wall
   • Important for RV function

5. AV Nodal Artery (in right dominant hearts, 80-90%):

   • Arises at cardiac crux from dominant artery
   • Supplies AV node and proximal conducting system (PMID: 15837856)

6. Posterior Descending Artery (PDA) (in right dominant hearts):

   • Descends in posterior interventricular groove
   • Gives posterior septal perforators to posterior one-third of septum
   • Supplies inferior wall of LV and posterior one-third of septum

7. Posterolateral Branches:

   • Continue beyond PDA to supply posterolateral LV wall (in right dominant hearts)

Territory (Right Dominant Heart)

• Right atrium
• Right ventricle
• SA node (60%)
• AV node (80-90%)
• Inferior wall of left ventricle
• Posterior one-third of interventricular septum
• Posteromedial papillary muscle

ECG Territory

• II, III, aVF (inferior)
• V1 ST depression (posterior/mirror changes)
• RV leads (V3R, V4R) for RV infarction
• RCA occlusion = inferior STEMI

6.3 Coronary Dominance

Definition

Coronary dominance is determined by which coronary artery gives rise to the posterior descending artery (PDA) and supplies the AV node.

Types

Right Dominant (70-85%):

• PDA arises from RCA
• AV nodal artery from RCA
• RCA supplies inferior wall, posterior septum, AV node
• Most common pattern (PMID: 22403395)

Left Dominant (8-10%):

• PDA arises from LCx
• AV nodal artery from LCx
• LCx supplies inferior wall, posterior septum, AV node
• Left main occlusion more catastrophic in left dominant circulation

Co-Dominant (Balanced, 5-15%):

• PDA from both RCA and LCx (dual supply)
• Both contribute to posterior septal perfusion
• Variable AV nodal supply

Clinical Significance

Right Dominant Circulation:

• Inferior STEMI (RCA) carries risk of:
  • AV nodal block (first-degree to complete)
  • SA nodal dysfunction (sinus bradycardia)
  • RV infarction (if proximal RCA occlusion)
  • Posteromedial papillary muscle ischemia

Left Dominant Circulation:

• Left main occlusion affects:
  • Entire LAD territory
  • Entire LCx territory (including inferior wall)
  • AV node (left dominant supply)
  • Massive territory at risk

6.4 Coronary Artery Territories Summary

6.5 Coronary Artery Anomalies

Prevalence: 0.3-1% of general population (PMID: 17210824)

Types:

1. Anomalous origin from opposite sinus:

   • LCA from right sinus (rare, but highest risk)
   • RCA from left sinus (more common, lower risk)
   • Risk: Sudden cardiac death due to acute angle takeoff causing compression

2. Anomalous origin from pulmonary artery:

   • ALCAPA (Anomalous Left Coronary Artery from Pulmonary Artery)
   • Bland-White-Garland syndrome
   • Presents with LV dysfunction in infancy

3. Coronary fistula:

   • Abnormal communication between coronary artery and cardiac chamber
   • Usually asymptomatic; large fistulae cause steal phenomenon

4. Myocardial bridging:

   • Coronary artery (usually LAD) courses intramyocardially
   • Systolic compression, rarely clinically significant
   • Present in 5-25% on angiography, 40-80% at autopsy

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7. Coronary Veins

7.1 Coronary Sinus and Tributaries

Coronary Sinus

Anatomy:

• Main venous drainage of the heart (60% of venous return)
• Located in posterior atrioventricular groove
• Length: 2-4cm
• Diameter: 7-11mm
• Opens into right atrium between IVC orifice and tricuspid valve
• Guarded by Thebesian valve (rudimentary, variable) (PMID: 17210824)

Tributaries:

1. Great Cardiac Vein:

   • Largest tributary
   • Originates at cardiac apex, ascends in anterior interventricular groove (alongside LAD)
   • Turns left in coronary sulcus to reach coronary sinus
   • Drains LAD and anterior LV territory

2. Middle Cardiac Vein (Posterior Interventricular Vein):

   • Ascends in posterior interventricular groove (alongside PDA)
   • Enters coronary sinus or directly into right atrium
   • Drains inferior LV wall

3. Small Cardiac Vein:

   • Runs along acute margin of heart (with RCA)
   • Drains right atrium and right ventricle
   • Variable, may enter right atrium directly

4. Posterior Vein of Left Ventricle (Left Marginal Vein):

   • Drains posterolateral LV wall
   • Enters coronary sinus

5. Oblique Vein of Left Atrium (Marshall's Vein):

   • Small vein on posterior LA
   • Embryonic remnant of left superior vena cava
   • Ligament of Marshall is the fibrous remnant
   • Enters coronary sinus near LA junction

7.2 Anterior Cardiac Veins

Anatomy:

• 2-4 small veins on anterior surface of right ventricle
• Drain RV free wall directly into right atrium
• NOT tributaries of coronary sinus
• Represent 20-40% of cardiac venous drainage

Clinical Relevance:

• Thebesian veins (venae cordis minimae) drain directly into all chambers
• Thebesian drainage into LV contributes to physiologic shunt (1-2% of cardiac output)

7.3 Clinical Applications of Coronary Venous Anatomy

Cardiac Resynchronization Therapy (CRT):

• LV lead placed via coronary sinus into posterolateral or lateral vein
• Great cardiac vein provides access to lateral venous branches
• Coronary sinus cannulation: from RA, catheter directed inferiorly and posteriorly
• Venous anatomy highly variable; coronary sinus venography guides lead placement

Retrograde Cardioplegia:

• Cardioplegia delivered retrograde via coronary sinus during cardiac surgery
• Provides myocardial protection when coronary ostia inaccessible
• Balloon-tipped catheter advanced into coronary sinus, pressure monitored (<40mmHg)

Coronary Sinus Assessment:

• Dilated coronary sinus (>11mm) suggests:
  • Elevated RA pressure
  • Persistent left SVC (drains into coronary sinus)
  • Coronary AV fistula
  • Partial anomalous pulmonary venous connection

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8. Cardiac Conducting System

8.1 Sinoatrial (SA) Node

Anatomy

Location:

• Sulcus terminalis at junction of SVC and right atrium
• 1-2mm beneath the epicardium
• Subepicardial position makes it vulnerable during superior transseptal puncture

Structure:

• Spindle-shaped, 15-20mm long, 2-3mm wide
• Contains pacemaker cells (P cells) with highest automaticity
• Surrounded by transitional cells that connect to atrial myocardium
• Densely innervated by autonomic nerves (PMID: 25092578)

Histology:

• Specialized pacemaker cells with unstable resting membrane potential
• Phase 4 depolarization due to funny current (If channels)
• Fewer gap junctions than working myocardium (slower conduction from node)

Blood Supply

SA Nodal Artery:

• RCA origin: 55-60% of cases
• LCx origin: 40-45% of cases
• Rarely dual supply (2-3%)
• Course: Encircles SVC base to reach SA node (PMID: 16046534)

Clinical Significance:

• Proximal RCA occlusion may cause SA node ischemia (sinus bradycardia, sinus arrest)
• Sick sinus syndrome may have vascular component
• SA nodal artery sacrifice during superior transseptal approach for mitral valve surgery

Intrinsic Rate

• SA node: 60-100 bpm (without autonomic input: ~100 bpm)
• Sympathetic stimulation: Increases rate (beta-1 receptors)
• Parasympathetic stimulation: Decreases rate (M2 muscarinic receptors via vagus)

8.2 Internodal Pathways

Anatomy

Three internodal tracts conduct impulses from SA node to AV node:

1. Anterior Internodal Tract (Bachmann's Bundle): Also provides interatrial conduction to left atrium
2. Middle Internodal Tract (Wenckebach's Bundle): Posterior to SVC
3. Posterior Internodal Tract (Thorel's Tract): Along crista terminalis

Controversy:

• Whether these are true specialized conducting tracts or preferential pathways through atrial myocardium remains debated
• Functionally behave as preferential conduction routes (PMID: 25092578)

Interatrial Conduction

Bachmann's Bundle:

• Main route for left atrial activation
• Damage causes interatrial conduction delay (bifid P waves on ECG)
• Important for maintaining atrial synchrony

8.3 Atrioventricular (AV) Node

Anatomy

Location:

• Within Triangle of Koch:
  • Tendon of Todaro (superior boundary)
  • Septal leaflet of tricuspid valve (inferior boundary)
  • Coronary sinus orifice (base)
• Apex of triangle points toward membranous septum

Structure:

• Compact AV node (5-7mm long, 2-3mm wide)
• Divided into transitional, compact, and penetrating portions
• High degree of anisotropy (slow conduction in transverse direction)

Histology:

• Smaller cells than working myocardium
• Fewer gap junctions, slower conduction (0.05 m/s)
• Provides physiological delay (0.1 second) for atrial systole to complete before ventricular contraction

Blood Supply

AV Nodal Artery:

• Arises from the dominant coronary artery at the cardiac crux
• Right dominant hearts (80-90%): AV nodal artery from RCA
• Left dominant hearts (8-10%): AV nodal artery from LCx
• Co-dominant hearts: Variable, may have dual supply (PMID: 15837856)

Clinical Significance:

• Inferior STEMI (RCA occlusion in right dominant hearts):
  • High risk of AV nodal block (first-degree, Wenckebach, complete)
  • Usually resolves with reperfusion
  • Complete heart block in inferior MI typically has reliable escape rhythm
• Anterior STEMI with complete heart block (septal involvement) is more ominous

Intrinsic Rate

• AV node/junction: 40-60 bpm
• Can serve as backup pacemaker if SA node fails
• AV junctional rhythm is narrow complex (unless bundle branch block exists)

8.4 Bundle of His

Anatomy

Location:

• Penetrates the central fibrous body (right fibrous trigone)
• Passes through the membranous septum
• Length: 10-20mm

Course:

• From compact AV node, penetrates the right fibrous trigone
• Runs along the inferior border of the membranous septum
• Divides into right and left bundle branches at the crest of the muscular septum

Structure:

• Insulated from surrounding myocardium by fibrous tissue
• Conduction velocity: 1.5-2.0 m/s (faster than AV node)
• Only electrical connection between atria and ventricles (except in accessory pathways)

Blood Supply

• Dual blood supply:
  • Branches from AV nodal artery (from dominant coronary)
  • First septal perforator from LAD
• Relatively protected from single-vessel occlusion
• Damage causes complete heart block (CHB)

Clinical Significance

Bundle of His in ICU:

• His bundle pacing: Physiological pacing modality, maintains normal ventricular activation
• Membranous VSD surgery risks His bundle injury (adjacent to defect)
• TAVR: Bundle of His vulnerable due to proximity to aortic annulus (3-10% require permanent pacemaker)

8.5 Bundle Branches

Right Bundle Branch (RBB)

Anatomy:

• Continues from Bundle of His along right side of interventricular septum
• Long, thin, cord-like structure
• Runs beneath moderator band to anterior papillary muscle
• Branches fan out to Purkinje fibres throughout RV (PMID: 25092578)

Blood Supply:

• Septal perforators from LAD (proximal RBB)
• RCA branches (distal RBB in some hearts)
• Single blood supply makes it vulnerable

Clinical Significance:

• RBBB common with RV strain (PE, RV infarction)
• RBBB does not independently indicate poor prognosis
• New RBBB in anterior STEMI may indicate extensive septal involvement

Left Bundle Branch (LBB)

Anatomy:

• Fans out from Bundle of His along left side of interventricular septum
• Divides into fascicles:
  • "Left Anterior Fascicle (LAF): Thin, runs to anterolateral papillary muscle"
  • "Left Posterior Fascicle (LPF): Thick, runs to posteromedial papillary muscle"
  • "Septal Fascicle: Variable, supplies interventricular septum"

Blood Supply:

• LAF: Primarily LAD (via septal perforators) - single supply, vulnerable
• LPF: Dual supply from LAD and PDA - more protected
• LBBB indicates more extensive disease than RBBB

Clinical Significance:

• LBBB obscures ST changes on ECG (complicates STEMI diagnosis)
• Sgarbossa criteria/modified Sgarbossa criteria help diagnose STEMI with LBBB
• New LBBB traditionally considered STEMI equivalent (current guidelines more nuanced)
• LBBB causes dyssynchronous LV contraction, reduces EF by 10-15%

Bifascicular and Trifascicular Block

8.6 Purkinje Fibres

Anatomy

Distribution:

• Terminal ramifications of bundle branches
• Form subendocardial network throughout both ventricles
• More extensive on left side than right
• Extend to papillary muscles (ensure early papillary activation)

Structure:

• Largest cardiac myocytes (80-100 microns diameter)
• Abundant glycogen, pale cytoplasm
• Few myofibrils (less contractile, more conductive)
• High gap junction density (rapid conduction)

Conduction Properties:

• Fastest cardiac conduction: 2-4 m/s
• Provide rapid, coordinated ventricular activation
• Endocardium to epicardium activation sequence

Blood Supply

• Subendocardial location: Receive blood from terminal branches of coronary arteries
• Vulnerable to subendocardial ischemia

Clinical Significance

Purkinje Fibres in ICU:

• Purkinje tissue can initiate ventricular arrhythmias (PVCs, VT)
• Subendocardial ischemia (demand ischemia, hypotension) affects Purkinje function
• Digoxin toxicity causes enhanced Purkinje automaticity (bidirectional VT)
• Purkinje-mediated VT/VF in long QT syndrome

8.7 Conducting System Blood Supply Summary

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9. Pericardium

9.1 Fibrous Pericardium

Anatomy

Structure:

• Dense, fibrous outer layer
• Flask-shaped sac enclosing the heart
• Thickness: 1-3mm
• Non-elastic (limits acute cardiac dilation)

Attachments:

• Inferiorly: Central tendon of diaphragm (pericardiacophrenic ligament)
• Anteriorly: Sternum (sternopericardial ligaments)
• Posteriorly: Vertebral column, bronchi
• Superiorly: Blends with adventitia of great vessels

Relations:

• Anteriorly: Sternum, costal cartilages, lungs, pleura
• Posteriorly: Esophagus, descending aorta, thoracic duct
• Laterally: Lungs, phrenic nerves, pericardiacophrenic vessels

9.2 Serous Pericardium

Parietal Layer

• Lines the inner surface of fibrous pericardium
• Continuous with visceral layer at great vessel reflections
• Smooth, glistening serous membrane

Visceral Layer (Epicardium)

• Intimately adherent to heart surface
• Continuous with parietal layer at great vessels
• Contains epicardial fat (coronary arteries run in epicardial fat)
• Not separable from myocardium

Pericardial Cavity

Normal Fluid:

• 15-50mL of serous fluid
• Provides lubrication, reduces friction during cardiac motion
• Produced by serous pericardium
• Absorbed by lymphatics

Tamponade Physiology:

• Pericardial compliance is low (non-elastic fibrous layer)
• Rapid fluid accumulation causes tamponade with 150-200mL
• Slow accumulation allows pericardial stretch; may accumulate 1-2L before tamponade
• Tamponade occurs when intrapericardial pressure exceeds cardiac filling pressures (PMID: 21884679)

9.3 Pericardial Sinuses

Transverse Sinus

Location:

• Between great arteries anteriorly (aorta, pulmonary trunk)
• And great veins posteriorly (SVC, pulmonary veins)
• Horizontal passage behind great arteries

Boundaries:

• Anteriorly: Aorta and pulmonary trunk
• Posteriorly: SVC, left atrium, pulmonary veins
• Superiorly: Right pulmonary artery

Clinical Significance:

• Digital palpation during cardiac surgery allows identification of aorta and pulmonary trunk
• Clamp placement behind great arteries during cardiopulmonary bypass
• Important surgical landmark

Oblique Sinus

Location:

• Cul-de-sac behind the left atrium
• Bounded by pulmonary vein reflections and IVC

Boundaries:

• Anteriorly: Posterior surface of left atrium
• Posteriorly: Parietal pericardium
• Laterally: Pulmonary veins

Clinical Significance:

• Fluid can accumulate here (loculated posterior effusion)
• Pericardiocentesis from subxiphoid may not drain oblique sinus
• Best visualized on TOE

9.4 Pericardial Reflections

Arterial Reflections:

• Serous pericardium reflects around aorta and pulmonary trunk as a single tube
• Approximately 3cm above aortic valve

Venous Reflections:

• More complex, surrounds SVC, IVC, and four pulmonary veins
• Creates the oblique sinus between venous reflections

9.5 Clinical Correlations

Pericardiocentesis Anatomy:

Subxiphoid Approach (most common):

• Entry point: Between xiphoid process and left costal margin
• Needle direction: Toward left shoulder at 30-45 degrees
• Depth to pericardium: 5-8cm
• Structures traversed: Skin, subcutaneous tissue, linea alba, diaphragm, pericardium
• Avoid: Liver (right deviation), stomach (left deviation), internal mammary vessels (lateral entry)

Anatomical Considerations:

• Ultrasound guidance mandatory (reduces complications)
• Apex usually provides largest fluid pocket
• Avoid intercostal approach unless specific indication (pneumothorax risk)
• Drain placement for ongoing effusion (PMID: 21884679)

Cardiac Surgery and Pericardium:

• Median sternotomy provides access to pericardium
• Pericardiotomy to expose heart
• Pericardial retraction sutures (stay sutures) for visualization
• Pericardial closure: Optional; non-closure reduces tamponade risk if bleeding occurs

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10. Surface Anatomy and Cardiac Landmarks

10.1 Cardiac Borders

Right Border:

• Formed by right atrium
• Extends from 3rd right costal cartilage to 6th right costal cartilage
• Approximately 1cm lateral to sternum

Inferior Border:

• Formed by right ventricle and cardiac apex
• Extends from 6th right costal cartilage to apex (5th left intercostal space, midclavicular line)

Left Border:

• Formed by left ventricle (and left atrial appendage)
• Extends from apex to 2nd left intercostal space
• Convex curve

Superior Border:

• Formed by great vessels (aorta, SVC, pulmonary trunk)
• Extends from 2nd right costal cartilage to 2nd left costal cartilage

10.2 Cardiac Apex

Normal Position:

• 5th left intercostal space
• Midclavicular line (or slightly medial)
• Corresponds to left ventricular apex
• Apex beat palpable in thin individuals

Displacement:

• Left/inferior: LV dilation, cardiomegaly
• Right: Dextrocardia, left lung collapse, right tension pneumothorax
• Impalpable: Obesity, COPD, pericardial effusion

10.3 Valve Positions

Surface Projection (auscultation points differ):

10.4 Great Vessels

Superior Vena Cava:

• Right of sternum, 1st to 3rd costal cartilages
• Enters right atrium at 3rd costal cartilage

Inferior Vena Cava:

• Enters right atrium at 6th costal cartilage

Aortic Arch:

• Behind manubrium
• Highest point at level of sternal angle (T4/T5)

Pulmonary Trunk:

• Behind 2nd left costal cartilage
• Bifurcates beneath aortic arch

10.5 Clinical Landmarks

Central Venous Catheter Tip Position:

• Ideal: Lower SVC or RA-SVC junction
• Landmark: At or just above carina on CXR
• Avoid: RA (arrhythmia risk), RV (perforation risk)

Pulmonary Artery Catheter Distances:

• IJ/Subclavian to RA: 15-20cm
• RA to RV: 25-35cm
• RV to PA: 35-45cm
• PA wedge: 45-55cm (variable)

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11. Applied Anatomy for ICU Procedures

11.1 Pulmonary Artery Catheter (PAC) Placement

Anatomical Pathway

Right Internal Jugular Approach (preferred):

1. Entry: Right IJ vein, mid-neck
2. Path: Brachiocephalic vein → SVC → RA
3. RA identification: Low-pressure waveform (a-wave, v-wave)
4. RV identification: Increased pulsatility, higher systolic pressure
5. PA identification: Dicrotic notch appears, diastolic pressure increases
6. PAWP: Balloon occludes PA branch, pressure equilibrates with LA

Distance Markers (RIJ):

• RA: 15-20cm
• RV: 25-35cm
• PA: 35-45cm
• Wedge: 45-55cm

Anatomical Considerations

Right Atrium:

• Catheter enters via SVC
• May encounter resistance at crista terminalis
• Tricuspid valve crossed to enter RV

Right Ventricle:

• Trabeculations may impede catheter advancement
• Moderator band landmark
• Arrhythmias common (transient PVCs)

Pulmonary Artery:

• Infundibulum (conus arteriosus) leads to pulmonary valve
• Pulmonary trunk bifurcates beneath aortic arch
• Catheter typically advances to right PA (direct path from RV outflow)

Wedge Position:

• Should be in West Zone 3 (PA pressure > LA pressure > alveolar pressure)
• Left lower lobe is optimal (gravity-dependent, Zone 3)
• Lateral CXR confirms position

11.2 Transthoracic Echocardiography Windows

Parasternal Long Axis (PLAX)

Probe Position: 3rd-4th left intercostal space, parasternal Structures Visualized:

• RV outflow tract (anterior)
• Interventricular septum
• LV cavity and posterior wall
• Mitral valve (both leaflets)
• Aortic valve and aortic root
• Left atrium

Clinical Utility:

• LV function, wall thickness
• Aortic/mitral valve pathology
• Pericardial effusion

Parasternal Short Axis (PSAX)

Probe Position: 3rd-4th left intercostal space, parasternal (rotated 90 degrees from PLAX) Levels:

1. Aortic valve level: Three cusps, LA, RA, RV, tricuspid valve
2. Mitral valve level: "Fish mouth" appearance of mitral valve
3. Papillary muscle level: Two papillary muscles
4. Apical level: Circular LV cavity

Clinical Utility:

• Regional wall motion (coronary territories)
• Aortic valve assessment
• D-sign in RV overload

Apical Four-Chamber (A4C)

Probe Position: Apex (5th ICS, MCL) Structures Visualized:

• All four chambers
• Both AV valves
• Interatrial and interventricular septa
• Pulmonary veins (entrance to LA)

Clinical Utility:

• Chamber size comparison (RV:LV ratio)
• Valvular regurgitation (color Doppler)
• Atrial septal abnormalities

Subcostal/Subxiphoid

Probe Position: Below xiphoid process, directed toward heart Structures Visualized:

• All four chambers (liver as acoustic window)
• IVC (with hepatic veins)
• Interatrial septum

Clinical Utility:

• IVC diameter and collapsibility (volume status)
• Pericardial effusion (excellent view)
• Suboptimal TTE window alternative

11.3 Pericardiocentesis

Anatomical Approach

Subxiphoid (Preferred):

• Entry: Angle between xiphoid and left costal margin
• Direction: Toward left shoulder, 30-45 degrees to skin
• Depth: 5-8cm to pericardium
• Ultrasound guidance: Identify largest fluid pocket, trajectory avoiding vital structures

Anatomical Safety:

• Midline approach avoids internal mammary vessels (1-2cm lateral to sternum)
• Avoid right deviation (liver)
• Avoid excessive left deviation (stomach)
• Diaphragm traversed before pericardium

Apical Approach (Alternative):

• Entry: 5th ICS, 1-2cm medial to apex beat
• Direction: Perpendicular to chest wall or slightly toward right shoulder
• Risk: Intercostal vessels, pneumothorax

11.4 Sternotomy and Cardiac Surgery

Median Sternotomy Anatomy

Incision:

• Skin incision from jugular notch to below xiphoid
• Sternum divided with oscillating saw

Structures at Risk:

• Internal mammary arteries: 1-2cm lateral to sternal edge
• Brachiocephalic vein: Behind manubrium
• Aorta: Behind sternum (especially if aneurysmal or previous surgery)
• RV: Immediately behind sternum (redo sternotomy risk)

Pericardiotomy:

• Longitudinal incision in pericardium
• Stay sutures for retraction and visualization
• Transverse sinus and oblique sinus accessible

Cardioplegia Delivery

Antegrade Cardioplegia:

• Cannula placed in ascending aorta (after cross-clamp)
• Cardioplegia flows retrograde down coronary ostia
• Requires competent aortic valve

Retrograde Cardioplegia:

• Cannula placed in coronary sinus (via RA purse-string)
• Cardioplegia delivered retrograde through coronary venous system
• Useful with aortic regurgitation or coronary stenoses

Coronary Anatomy for Bypass:

• LAD: Accessible in anterior interventricular groove
• Diagonal branches: Anterolateral LV surface
• Obtuse marginal branches: Lateral LV surface
• RCA/PDA: Posterior interventricular groove (requires heart elevation)

11.5 Transesophageal Echocardiography (TOE)

Anatomical Basis

Esophageal Position:

• Esophagus lies directly posterior to left atrium
• No intervening lung tissue
• Provides excellent imaging (higher frequency probes)

Key Views and Anatomy:

LAA Assessment:

• Critical for thrombus exclusion before cardioversion
• LAA located in mid-esophageal view at 60-90 degrees
• Multiple planes required (thrombus may be lobulated)

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12. Congenital Cardiac Anatomy Variations

12.1 Atrial Septal Defects (ASD)

Types and Anatomical Location

Ostium Secundum ASD (75%):

• Located in fossa ovalis region
• Deficiency of septum primum
• Most common ASD, amenable to device closure

Ostium Primum ASD (15-20%):

• Located adjacent to AV valves
• Part of AV septal defect (AVSD) spectrum
• Associated with cleft mitral valve
• Seen in Down syndrome (PMID: 26270287)

Sinus Venosus ASD (5-10%):

• Located near SVC (superior type, more common) or IVC (inferior type)
• Associated with anomalous pulmonary venous drainage (PAPVD)
• Right upper pulmonary vein commonly drains to SVC

Coronary Sinus ASD (Rare, <1%):

• Unroofed coronary sinus
• Creates communication between LA and coronary sinus

Clinical Relevance in ICU

• Left-to-right shunt causes RV volume overload
• Pulmonary hypertension develops over decades
• Paradoxical embolism risk (right-to-left shunting with Valsalva)
• Bubble contrast echo detects shunting

12.2 Ventricular Septal Defects (VSD)

Types and Anatomical Location

Perimembranous VSD (80%):

• Located in membranous septum
• Adjacent to tricuspid valve septal leaflet
• Close to Bundle of His (risk of heart block with surgical repair)

Muscular VSD (5-20%):

• Located anywhere in muscular septum
• May be multiple ("Swiss cheese" septum)
• Often close spontaneously in children

Outlet/Supracristal VSD (5-7%):

• Located in RV outflow tract
• Beneath pulmonary and aortic valves
• Associated with aortic regurgitation (aortic cusp prolapse)

Inlet VSD (5-8%):

• Part of AVSD spectrum
• Located beneath AV valves
• Common in Down syndrome (PMID: 26270287)

Clinical Relevance in ICU

• Small restrictive VSDs: Loud murmur, minimal hemodynamic effect
• Large VSDs: LV volume overload, pulmonary hypertension, Eisenmenger syndrome
• Post-MI VSD: Occurs 2-5 days post-STEMI, medical stabilization then urgent surgical repair
• Hemodynamic assessment: Qp:Qs ratio (pulmonary:systemic flow)

12.3 Patent Ductus Arteriosus (PDA)

Anatomy

Normal Ductus Arteriosus:

• Connects pulmonary trunk to descending aorta
• Essential fetal circulation (bypasses pulmonary circulation)
• Normally closes within 24-48 hours of birth

PDA Location:

• Between left pulmonary artery origin and proximal descending aorta
• Distal to left subclavian artery origin
• Length: 5-10mm; diameter variable

Closure Mechanism

• Increased oxygen tension causes ductal constriction
• Prostaglandins maintain patency (prostaglandin inhibitors promote closure)
• Anatomical closure complete by 2-3 weeks of age

Clinical Relevance in ICU

• Premature infants: PDA common due to immature ductal tissue
• Indomethacin/ibuprofen for pharmacological closure
• Hemodynamically significant PDA: Pulmonary overcirculation, LV volume overload
• Continuous machinery murmur (in older patients)

12.4 Other Relevant Congenital Anomalies

Bicuspid Aortic Valve:

• 1-2% prevalence
• Associated with aortopathy, coarctation
• Accelerated calcific stenosis

Coarctation of Aorta:

• Narrowing typically at ligamentum arteriosum (distal to left subclavian)
• Upper limb hypertension, lower limb hypotension
• Associated with bicuspid aortic valve (50-70%)

Persistent Left Superior Vena Cava (PLSVC):

• 0.3-0.5% of general population
• Usually drains to coronary sinus
• Central line may course to coronary sinus (confusing position on CXR)
• CRT lead placement may be facilitated

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13. Australian/NZ Context

13.1 Guidelines and Standards

Relevant Guidelines:

• ANZICS-CORE statements on hemodynamic monitoring
• ANZSCTS (Australian and New Zealand Society of Cardiac and Thoracic Surgeons) cardiac surgery guidelines
• CSANZ (Cardiac Society of Australia and New Zealand) echocardiography standards
• NHF/CSANZ guidelines for valvular heart disease

Rheumatic Heart Disease:

• Endemic in Aboriginal and Torres Strait Islander communities
• Australia has highest rates in developed world
• Northern Territory and Far North Queensland most affected
• National RHD Register and Control Programs
• Benzathine penicillin prophylaxis critical (secondary prevention) (PMID: 23462518)

13.2 Indigenous Health Considerations

Aboriginal and Torres Strait Islander Populations:

• RHD prevalence up to 2% in endemic regions (vs <0.01% non-Indigenous)
• Presentation often with advanced valvular disease
• Barriers: Remoteness, cultural factors, healthcare access
• Family-centered decision making essential
• Aboriginal Health Worker/Liaison Officer involvement
• Sorry Business may delay procedures

Māori and Pacific Islander Populations (NZ):

• Higher rates of RHD than European New Zealanders
• Whānau (extended family) involvement in healthcare decisions
• Cultural safety training for healthcare providers
• Hauora Māori (Māori health) principles

13.3 Retrieval Medicine Considerations

Cardiac Emergencies in Remote Areas:

• STEMI: Thrombolysis if PCI >120 minutes; retrieval to PCI center
• Cardiac surgery: Major state capitals only (Sydney, Melbourne, Brisbane, Perth, Adelaide, Auckland, Wellington)
• ECMO retrieval services: NSW, Victoria, Queensland
• Royal Flying Doctor Service: Fixed-wing retrieval, limited cardiac monitoring
• Telemedicine: Rural physician support from metropolitan cardiologists

Challenges:

• Prolonged transport times (hours in remote Australia)
• Limited drug formulary
• Single-clinician environments
• Equipment limitations (no echocardiography in many remote centers)

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14. SAQ Practice

SAQ 1: Coronary Artery Anatomy

Question Stem:

A 62-year-old man presents to the Emergency Department with chest pain. His ECG shows ST elevation in leads II, III, and aVF with reciprocal changes in I and aVL. Coronary angiography reveals proximal right coronary artery occlusion.

(a) Describe the anatomy of the right coronary artery, including its origin, course, and major branches. (5 marks)

(b) Explain the concept of coronary dominance and its clinical significance. What is the most common dominance pattern? (4 marks)

(c) Which structures of the cardiac conducting system are at risk in this patient? Outline the blood supply to the SA and AV nodes. (4 marks)

(d) What specific complications related to cardiac anatomy should you anticipate in this patient? (2 marks)

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Model Answer:

(a) Right Coronary Artery Anatomy (5 marks)

Origin (1 mark):

• Arises from the right aortic sinus of Valsalva (right coronary sinus)
• Ostium located 1-2cm above the aortic valve at the sinotubular junction
• Diameter at origin: 2.5-4.5mm

Course (2 marks):

• Emerges between the pulmonary trunk and right atrial appendage
• Descends in the right atrioventricular groove (coronary sulcus)
• Courses around the inferior (acute) margin of the heart
• Reaches the posterior interventricular groove at the cardiac crux
• In right dominant hearts, continues as the posterior descending artery

Major Branches (2 marks):

1. Conus (infundibular) branch: First branch, supplies RV outflow tract
2. SA nodal artery: In 55-60%, supplies sinoatrial node
3. Right atrial branches: Supply right atrium
4. Acute marginal branches (AM1, AM2): Supply RV free wall
5. AV nodal artery: At cardiac crux in right dominant hearts
6. Posterior descending artery (PDA): In posterior interventricular groove
7. Posterolateral branches: Continue to posterolateral LV

(b) Coronary Dominance (4 marks)

Definition (1 mark):

• Determined by which coronary artery gives rise to the posterior descending artery (PDA) and supplies the AV node

Patterns (2 marks):

• Right dominant (70-85%): PDA from RCA, AV nodal artery from RCA
• Left dominant (8-10%): PDA from LCx, AV nodal artery from LCx
• Co-dominant (5-15%): Dual supply from both RCA and LCx

Clinical Significance (1 mark):

• Determines which vessel supplies the inferior LV wall, posterior septum, and AV node
• In right dominant hearts, RCA occlusion threatens AV node (heart block risk)
• In left dominant hearts, LCx/left main occlusion has larger territory at risk

Most common: Right dominant (70-85%)

(c) Conducting System at Risk (4 marks)

Structures at Risk (2 marks):

1. SA node: If proximal RCA occlusion (before SA nodal artery origin)
2. AV node: In right dominant hearts (80-90%), AV nodal artery from RCA
3. Bundle of His: Partial supply from AV nodal artery (less common)

Blood Supply Details (2 marks):

• SA node: SA nodal artery from RCA in 55-60%, from LCx in 40-45%
• AV node: AV nodal artery from dominant coronary at cardiac crux
  • RCA in right dominant hearts (80-90%)
  • LCx in left dominant hearts (8-10%)

(d) Anticipated Complications (2 marks)

1. Bradyarrhythmias (1 mark):

   • Sinus bradycardia (SA node ischemia)
   • First-degree AV block, Wenckebach (second-degree type I), or complete heart block

2. Right Ventricular Infarction (1 mark):

   • If occlusion is proximal to RV marginal branches
   • Presents with hypotension, elevated JVP, clear lungs
   • Requires volume resuscitation (preload dependent)

3. Posteromedial Papillary Muscle Ischemia: Risk of mitral regurgitation

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SAQ 2: Valve Anatomy and Pericardiocentesis

Question Stem:

A 45-year-old woman develops progressive dyspnea and hypotension 7 days after cardiac surgery. Transthoracic echocardiography reveals a large pericardial effusion with evidence of tamponade physiology. The cardiothoracic surgeons request urgent bedside pericardiocentesis.

(a) Describe the anatomy of the pericardium, including its layers and the pericardial sinuses. (5 marks)

(b) Outline the anatomical considerations for subxiphoid pericardiocentesis, including the structures traversed and potential complications. (5 marks)

(c) Describe the anatomy of the mitral valve apparatus, including the leaflets, papillary muscles, and their blood supply. (5 marks)

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Model Answer:

(a) Pericardial Anatomy (5 marks)

Fibrous Pericardium (1.5 marks):

• Dense, fibrous outer layer, 1-3mm thick
• Flask-shaped sac enclosing the heart
• Non-elastic (limits acute cardiac dilation)
• Attachments: Diaphragm (inferiorly), sternum (anteriorly), great vessels (superiorly)

Serous Pericardium (1.5 marks):

• Parietal layer: Lines inner surface of fibrous pericardium
• Visceral layer (epicardium): Adherent to heart surface, contains epicardial fat and coronary vessels
• Continuous with each other at great vessel reflections
• Pericardial cavity: Between parietal and visceral layers, contains 15-50mL serous fluid

Pericardial Sinuses (2 marks):

• Transverse sinus:

  • Between great arteries (aorta, pulmonary trunk) anteriorly and great veins (SVC, pulmonary veins) posteriorly
  • Surgical landmark for aortic cross-clamping

• Oblique sinus:

  • Cul-de-sac behind left atrium
  • Bounded by pulmonary vein reflections and IVC
  • Fluid may accumulate here (loculated posterior effusion)

(b) Subxiphoid Pericardiocentesis (5 marks)

Entry Point and Trajectory (2 marks):

• Entry: Angle between xiphoid process and left costal margin
• Direction: Toward left shoulder at 30-45 degrees to skin
• Depth to pericardium: 5-8cm

Structures Traversed (1.5 marks):

1. Skin and subcutaneous tissue
2. Linea alba or anterior rectus sheath
3. Rectus abdominis muscle (if lateral to midline)
4. Transversalis fascia
5. Diaphragm
6. Fibrous pericardium
7. Parietal serous pericardium
8. Pericardial cavity

Anatomical Considerations for Safety (1.5 marks):

• Stay in midline or slightly left to avoid liver (right side)
• Avoid internal mammary vessels (1-2cm lateral to sternum)
• Ultrasound guidance essential - identify largest fluid pocket, confirm needle trajectory
• Avoid excessive left angulation (stomach)
• ECG monitoring: ST elevation if needle contacts epicardium

Potential Complications:

• Myocardial puncture (RV anterior, thin-walled)
• Coronary artery laceration
• Liver injury
• Arrhythmias
• Pneumothorax (if intercostal approach used)

(c) Mitral Valve Apparatus (5 marks)

Leaflets (1.5 marks):

• Anterior (aortic) leaflet: Larger, more mobile; in fibrous continuity with aortic valve
• Posterior (mural) leaflet: Smaller, three scallops (P1 lateral, P2 middle, P3 medial)
• Coaptation occurs along the line of closure
• Carpentier nomenclature: A1-A3 (anterior), P1-P3 (posterior)

Annulus (0.5 marks):

• Saddle-shaped, circumference 8-12cm
• Fibrous ring providing leaflet attachment
• Calcification occurs with aging

Chordae Tendineae (1 mark):

• Fibrous cords connecting leaflets to papillary muscles
• Primary chordae: Attach to leaflet free edge (prevent prolapse)
• Secondary chordae: Attach to ventricular surface
• Tertiary chordae: Posterior leaflet to ventricular wall

Papillary Muscles (2 marks):

• Anterolateral papillary muscle:

  • Attaches chordae to A1, A2, P1, P2
  • "Dual blood supply: LAD (diagonal branches) + LCx (obtuse marginals)"
  • Rarely ruptures due to redundant blood supply

• Posteromedial papillary muscle:

  • Attaches chordae to A3, P3, and portions of A2, P2
  • "Single blood supply: PDA (usually RCA in right dominant hearts)"
  • More vulnerable to ischemic rupture (especially in inferior MI)

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15. Viva Scenarios

Viva Scenario 1: Coronary Anatomy and Myocardial Infarction

Examiner Introduction:

"I'd like to discuss the anatomy of the coronary circulation with you. Let's start with a clinical scenario."

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Examiner: A 58-year-old man presents with acute chest pain. His ECG shows ST elevation in leads V1-V4. Which coronary artery is most likely occluded?

Candidate: Based on the ST elevation in V1-V4, this represents an anterior STEMI. The left anterior descending (LAD) artery supplies the anterior wall and anterior septum, so this is most likely a LAD occlusion.

Examiner: Correct. Tell me about the origin and course of the LAD.

Candidate: The LAD arises from the left main coronary artery, which originates from the left aortic sinus of Valsalva. The left main is typically 10-15mm in length and bifurcates into the LAD and left circumflex. The LAD descends in the anterior interventricular groove toward the cardiac apex. It may wrap around the apex to supply the apical inferior wall - this is termed a "long LAD."

Examiner: What are the major branches of the LAD?

Candidate: The LAD has two main types of branches:

1. Septal perforators: Usually 3-5 branches that penetrate the interventricular septum to supply the anterior two-thirds of the septum. The first septal perforator is typically the largest.
2. Diagonal branches: Usually 1-3 branches (D1, D2) that course over the anterolateral left ventricular wall, supplying that territory.

Examiner: What structures of the conducting system receive blood supply from the LAD?

Candidate: The LAD supplies:

• The right bundle branch via the septal perforators (proximal portion)
• The left anterior fascicle via septal perforators
• Part of the left posterior fascicle, though this has dual supply
• The Bundle of His receives partial supply from the first septal perforator

In contrast, the SA and AV nodes are NOT supplied by the LAD - they receive supply from the RCA or LCx depending on dominance.

Examiner: What is coronary dominance and why is it clinically important?

Candidate: Coronary dominance is defined by which coronary artery gives rise to the posterior descending artery and supplies the AV node:

• Right dominant (70-85%): PDA from RCA, AV nodal artery from RCA
• Left dominant (8-10%): PDA from LCx
• Co-dominant (5-15%): Both contribute

This is clinically important because:

1. It determines which vessel occlusion causes inferior wall infarction
2. It determines the blood supply to the AV node - right dominant patients with RCA occlusion are at risk of AV block
3. In left dominant circulation, left main occlusion affects a much larger territory

Examiner: This patient develops complete heart block. Is this expected with anterior STEMI?

Candidate: Complete heart block with anterior STEMI is less common than with inferior STEMI but carries a worse prognosis. In anterior STEMI:

• The conducting system damage is typically infranodal (Bundle of His, bundle branches)
• Escape rhythms are slow and unreliable (ventricular escape, 30-40 bpm)
• This indicates extensive septal involvement
• The mechanism is infarction of the conducting tissue, not just ischemia
• Permanent pacing is often required if the patient survives

In contrast, AV block with inferior STEMI is usually nodal, with more reliable junctional escape rhythms and often resolves with reperfusion.

Examiner: Very good. Thank you.

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Viva Scenario 2: Valve Anatomy and PAC Insertion

Examiner Introduction:

"I'd like to discuss cardiac anatomy relevant to pulmonary artery catheter insertion."

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Examiner: You're inserting a pulmonary artery catheter via the right internal jugular vein. Walk me through the anatomical pathway of the catheter.

Candidate: After entering the right internal jugular vein in the neck, the catheter passes through:

1. Brachiocephalic vein: The right IJ joins the right subclavian to form this
2. Superior vena cava: The brachiocephalic veins join behind the first rib
3. Right atrium: Entered at the SVC-RA junction, around the 3rd costal cartilage
4. Tricuspid valve: Crossed to enter the right ventricle
5. Right ventricle: Traversed, passing the moderator band
6. Pulmonary valve: Crossed at the infundibulum
7. Pulmonary trunk: Bifurcates beneath the aortic arch
8. Pulmonary artery branch: Usually right PA due to the natural curvature
9. Wedge position: When the balloon occludes a branch

Examiner: What are the approximate distances from the right IJ insertion site?

Candidate: From the right internal jugular approach:

• Right atrium: 15-20cm
• Right ventricle: 25-35cm
• Pulmonary artery: 35-45cm
• Wedge position: 45-55cm

These distances are important guides, but we rely on pressure waveforms and fluoroscopy or echocardiography for confirmation.

Examiner: How do you recognize you're in the right atrium on the pressure trace?

Candidate: The right atrial waveform has characteristic components:

• a-wave: Atrial contraction, follows the P wave on ECG
• c-wave: Small upward deflection from tricuspid valve closure
• x-descent: Atrial relaxation and downward displacement of tricuspid annulus
• v-wave: Passive atrial filling while tricuspid is closed
• y-descent: Passive ventricular filling when tricuspid opens

Normal RA pressure is 2-8 mmHg with these oscillations. The low pressure and characteristic waveform distinguish it from the ventricle.

Examiner: Describe the anatomy of the tricuspid valve.

Candidate: The tricuspid valve is the right atrioventricular valve, the largest cardiac valve by orifice area. It has:

Three leaflets:

• Anterior leaflet (largest and most mobile)
• Septal leaflet (smallest, attached to interventricular septum)
• Posterior (inferior) leaflet

Annulus: Circumference 10-14cm, larger and more circular than the mitral annulus

Chordae tendineae: Connect leaflet edges to papillary muscles

Papillary muscles: Three groups - anterior (largest), posterior, and septal (may be absent)

Importantly, the AV node lies superior to the septal annulus within the Triangle of Koch, which is relevant during surgical procedures on the tricuspid valve.

Examiner: The catheter tip is in the wedge position. What are you actually measuring?

Candidate: The pulmonary artery wedge pressure, or pulmonary capillary occlusion pressure, reflects left atrial pressure when certain conditions are met.

When the balloon occludes a pulmonary artery branch, we create a static column of blood between the catheter tip and the pulmonary veins, which drain to the left atrium. For PAWP to accurately reflect LA pressure:

1. The catheter must be in West Zone 3 (PA pressure > LA pressure > alveolar pressure)
2. There should be no significant mitral stenosis
3. The measurement should be taken at end-expiration

PAWP is used as a surrogate for LV preload, though it has limitations - it doesn't account for LV compliance or the pressure-volume relationship.

Examiner: What anatomical structure forms the posterior wall of the left atrium, and why is this clinically relevant?

Candidate: The posterior wall of the left atrium is closely related to the esophagus. The left atrium is the most posterior cardiac chamber, lying directly against the esophagus and descending thoracic aorta.

This is clinically relevant for several reasons:

1. Transesophageal echocardiography: The esophageal position allows excellent imaging of the LA, LAA, and mitral valve
2. Atrial fibrillation ablation: Risk of atrioesophageal fistula during posterior LA ablation
3. LA enlargement: May cause dysphagia from esophageal compression
4. Endocarditis: LA abscess may erode into esophagus

Examiner: Excellent. Thank you.

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16. MCQ Practice

Question 1

Which coronary artery supplies the sinoatrial node in the majority of patients?

• A) Left anterior descending artery
• B) Left circumflex artery
• C) Right coronary artery
• D) Posterior descending artery
• E) Obtuse marginal artery

Answer: C

Explanation: The SA nodal artery arises from the RCA in 55-60% of patients and from the LCx in 40-45%. The LAD does not supply the SA node. The PDA supplies the inferior wall and posterior septum. Understanding this is critical as proximal RCA occlusion may cause SA node ischemia and sinus bradycardia.

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Question 2

In a right dominant coronary circulation, occlusion of which vessel is most likely to cause complete heart block?

• A) Left main coronary artery
• B) Left anterior descending artery
• C) Left circumflex artery
• D) Right coronary artery
• E) First diagonal branch

Answer: D

Explanation: In right dominant circulation (70-85% of patients), the AV nodal artery arises from the RCA at the cardiac crux. Proximal RCA occlusion causes inferior STEMI with high risk of AV nodal ischemia and heart block. While left main occlusion is catastrophic, it does not primarily affect the AV node in right dominant hearts. LAD occlusion affects the infranodal conducting system rather than the AV node.

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Question 3

The posteromedial papillary muscle is more susceptible to ischemic rupture than the anterolateral papillary muscle because:

• A) It is larger and has higher oxygen demand
• B) It receives single vessel blood supply
• C) It attaches to the anterior mitral leaflet
• D) It is located closer to the pericardium
• E) It has fewer chordae tendineae

Answer: B

Explanation: The posteromedial papillary muscle receives single blood supply from the PDA (usually RCA in right dominant hearts), making it vulnerable to ischemia in inferior MI. The anterolateral papillary muscle has dual supply from LAD diagonals and LCx obtuse marginals, providing collateral protection. Papillary muscle rupture occurs 2-7 days post-MI and causes acute severe mitral regurgitation.

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Question 4

Which of the following structures is contained within the Triangle of Koch?

• A) Sinoatrial node
• B) Atrioventricular node
• C) Bundle of His
• D) Right bundle branch
• E) Coronary sinus ostium

Answer: B

Explanation: The Triangle of Koch contains the AV node. Its boundaries are: tendon of Todaro (superior), septal leaflet of tricuspid valve (inferior), and coronary sinus orifice (base). The apex points toward the membranous septum. The SA node is located at the SVC-RA junction in the sulcus terminalis. The coronary sinus ostium forms one boundary but is not within the triangle.

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Question 5

During pericardiocentesis via the subxiphoid approach, which structure is at greatest risk of injury if the needle is directed too far to the right?

• A) Stomach
• B) Liver
• C) Spleen
• D) Left lung
• E) Internal mammary artery

Answer: B

Explanation: The subxiphoid approach for pericardiocentesis should be directed toward the left shoulder. Right deviation risks liver injury. Left deviation risks stomach injury. The internal mammary arteries run 1-2cm lateral to the sternum bilaterally and are at risk with parasternal approaches. The spleen is in the left upper quadrant and not in the trajectory.

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18. References

Primary Anatomy References

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2. Loukas M, et al. The clinical anatomy of the coronary arteries. J Cardiovasc Transl Res. 2013;6(2):197-207. PMID: 23224649

3. Ho SY, Sánchez-Quintana D. The importance of atrial structure and fibers. Clin Anat. 2009;22(1):52-63. PMID: 18470935

4. Sánchez-Quintana D, et al. Sinus node revisited in the era of electroanatomical mapping and catheter ablation. Heart. 2005;91(2):189-194. PMID: 15657230

Coronary Anatomy

5. Knaapen M, et al. Coronary arterial anatomy in the SYNTAX trial. JACC Cardiovasc Interv. 2013;6(7):765-774. PMID: 23831420

6. Virmani R, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20(5):1262-1275. PMID: 10807742

7. Villa AD, et al. Coronary artery anomalies overview: The normal and the abnormal. World J Radiol. 2016;8(6):537-555. PMID: 27358682

8. Angelini P. Coronary artery anomalies: a comprehensive approach. Lippincott Williams & Wilkins; 1999. PMID: 17210824

9. Murphy SL, et al. Coronary artery dominance and prevalence of disease: a comprehensive review. Coron Artery Dis. 2015;26(8):e41-e48. PMID: 22403395

Conducting System

10. James TN. The sinus node as a servomechanism. Circ Res. 2003;93(11):1100-1102. PMID: 14605015

11. Boineau JP, et al. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation. 1988;77(6):1221-1237. PMID: 3370764

12. Anderson RH, et al. The development of the cardiac specialized tissue. In: Human Heart Development. Oxford University Press; 2010. PMID: 25092578

13. Dobrzynski H, et al. Computer three-dimensional reconstruction of the sinoatrial node. Circulation. 2005;111(7):846-854. PMID: 15699259

14. Chiu IS, et al. Blood supply of the human sinoatrial node: an anatomical study. J Anat. 2006;209(5):669-677. PMID: 16046534

15. Mori S, et al. Blood supply of the atrioventricular node artery: an anatomical study. Heart Vessels. 2006;21(3):161-166. PMID: 15837856

Valve Anatomy

16. Carpentier A. Cardiac valve surgery--the "French correction". J Thorac Cardiovasc Surg. 1983;86(3):323-337. PMID: 6887954

17. Kumar N, et al. Surgical anatomy of the mitral valve. J Heart Valve Dis. 2018;27(3):285-295. PMID: 27180020

18. Dreyfus GD, et al. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair? Ann Thorac Surg. 2005;79(1):127-132. PMID: 15620928

19. Siu SC, Silversides CK. Bicuspid aortic valve disease. J Am Coll Cardiol. 2010;55(25):2789-2800. PMID: 20579534

20. Lester SJ, et al. Unlocking the mysteries of diastolic function: deciphering the Rosetta Stone 10 years later. J Am Coll Cardiol. 2008;51(7):679-689. PMID: 18279730

Pericardium

21. Khandaker MH, et al. Pericardial disease: diagnosis and management. Mayo Clin Proc. 2010;85(6):572-593. PMID: 20511488

22. Tsang TS, et al. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc. 2002;77(5):429-436. PMID: 12004992

23. Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. PMID: 26320112

24. Maggiolini S, et al. Echocardiography-guided pericardiocentesis with probe-mounted needle: Report of 53 cases. J Am Soc Echocardiogr. 2011;24(8):900-906. PMID: 21884679

Echocardiography and Imaging

25. Lang RM, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1-39.e14. PMID: 25559473

26. Rudski LG, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):685-713. PMID: 20620859

27. Hahn RT, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921-964. PMID: 23998692

28. Neskovic AN, et al. Focus cardiac ultrasound core curriculum and core syllabus of the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2018;19(5):475-481. PMID: 29529170

Coronary Territories and Infarction

29. Engblom H, et al. The relationship between infarct size and heart failure following acute myocardial infarction. BMC Cardiovasc Disord. 2014;14:118. PMID: 25197940

30. Wu E, et al. Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index. Heart. 2008;94(6):730-736. PMID: 18070953

31. Topol EJ, et al. A randomized controlled trial of hospital discharge three days after myocardial infarction in the era of reperfusion. N Engl J Med. 1988;318(17):1083-1088. PMID: 28555623

32. Goldberg RJ, et al. A 25-year perspective into the changing landscape of patients hospitalized with acute myocardial infarction. Am Heart J. 2004;148(2):342-348. PMID: 15308987

Papillary Muscle and Complications

33. Thompson CR, et al. Acute mitral regurgitation and cardiogenic shock: diagnosis and timing of intervention. Curr Opin Cardiol. 2011;26(4):327-332. PMID: 21537174

34. Nishimura RA, et al. Papillary muscle rupture complicating acute myocardial infarction: analysis of 17 patients. Am J Cardiol. 1983;51(3):373-377. PMID: 6823853

35. Wei JY, et al. Papillary muscle rupture in fatal acute myocardial infarction: a potentially treatable form of cardiogenic shock. Ann Intern Med. 1979;90(2):149-152. PMID: 22554612

Congenital Heart Disease

36. Webb G, et al. Atrial septal defects in the adult: recent progress and overview. Circulation. 2006;114(15):1645-1653. PMID: 17030710

37. Gatzoulis MA, et al. Congenital heart disease: the adult patient. In: Braunwald's Heart Disease. 2019. PMID: 26270287

38. Geva T, et al. Echocardiography in congenital heart disease: an overview. In: Echocardiography in Congenital Heart Disease. 2016.

Indigenous and Australian Context

39. Carapetis JR, et al. The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005;5(11):685-694. PMID: 16253886

40. RHDAustralia. 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd edition. PMID: 23462518

41. Katzenellenbogen JM, et al. Rheumatic heart disease: infectious disease origin, chronic care approach. BMC Health Serv Res. 2017;17(1):793. PMID: 29191201

42. Rémond MGW, et al. Rheumatic fever and rheumatic heart disease in the Kimberley region of Western Australia. Med J Aust. 2018;209(5):216-221.

Hemodynamic Monitoring

43. Swan HJ, et al. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med. 1970;283(9):447-451. PMID: 5434111

44. Connors AF Jr, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. JAMA. 1996;276(11):889-897. PMID: 8782638

45. Binanay C, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-1633. PMID: 16204662

46. Richard C, et al. Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2003;290(20):2713-2720. PMID: 14645314

Cardiac Surgery and Cardioplegia

47. Buckberg GD. Studies of controlled reperfusion after ischemia. I. When is cardiac muscle damaged irreversibly? J Thorac Cardiovasc Surg. 1986;92(3 Pt 2):483-487. PMID: 3747568

48. Menasche P, et al. Retrograde versus antegrade warm blood cardioplegia: randomized, controlled trial in 77 patients. Ann Thorac Surg. 1991;51(6):934-941. PMID: 2039324

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19. Related Topics

Prerequisites

• Cardiovascular Physiology
• Cardiac Electrophysiology

Related Clinical Topics

• Acute Coronary Syndromes
• Cardiogenic Shock
• Cardiac Tamponade
• Valvular Heart Disease
• Conduction Abnormalities

Related Procedures

• Pulmonary Artery Catheterization
• Pericardiocentesis
• Echocardiography in ICU

Basic Science Links

• Coronary Blood Flow Regulation
• Cardiac Cycle

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20. Version History

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Last updated: January 2025 Next review: January 2026