UNCONTROLLED WHEN PRINTED

Important for circulation (pulmonary & systematic) of fluids, nutrients and blood around the body to keep tissues alive. Heart’s action can change based on the situation change impacting circulation, volume and pressure.

The heart is one-way valved that operates systematically:

  • Fist size
  • Located more towards left side of chest
  • Responds to homeostatic changes
Cardiac anatomy
Chambers of the Heart:
  1. Right Atrium (from body)
  2. Left Atrium (from lungs)
  3. Right Ventricle (from right atrium – move blood to pulmonary trunk [artery])
  4. Left Ventricle (from left atrium – move blood to aortic arch then to body)
Major Heart Vessels:

Contains Trabeculae (Ventricles) & Pectinate (Atria) ridges which allow continuous bloodflow without clots

  1. Vena Cava Deoxygenated blood to Right Atrium
  2. Pulmonary Vein Oxygenated blood to Left Atrium
  3. Pulmonary Trunk Deoxygenated blood to Lungs for gas exchange from right ventricle
  4. Aorta Oxygenated blood from left ventricle
Valves of the Heart:

Atrioventricular Valves (AV)

  • Tricuspid Between right atrium & ventricle
  • Bicuspid Between left atrium & ventricle

Semilunar Valve (SL)

  • Right SL Valve (Pulmonary) Right atrium & ventricle junction
  • Left SL Valve (Aortic) Left atrium & ventricle junction
Coronary Artery Supply

Vary from person-to-person, heart has a large muscle mass and needs bloodflow to deliver oxygen and remove CO2

  1. Blood supply comes from aortic root (the ostia)
  2. Artery travel on heart surface (sulci)
  3. Smaller branches penetrate myocardium
  4. Ostia has two (2) artery openings; Right & Left Coronary Artery
  5. Cardiac veins return to coronary sinus (posterior heart)
  6. Deoxygenated blood from coronary sinus empty into right atrium

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https://en.wikipedia.org/wiki/Heart#/media/File:CG_Heart.gif

Right Coronary Artery (RAD): Inferior Region

  • Supplies to inferior section of the heart – inferior wall of left & right ventricles and SA & AV nodes.
  • Branches half-way along right ventricle then split distally into posterior descending & posterolateral artery

Left Main Artery (LM / LCA): Anterior Region

  • Branches into left anterior descending (LAD) and circumflex (Cx) artery – Supplies to anterior wall of left ventricle and anterior portion of interventricular septum and bundle branches
  • LAD is diagonal branch
  • Cx branch is obtuse marginal and supplies

Circumflex (Cx): Lateral Region

  • Branched off the LCA with arteries supplying to lateral and posterior walls of the left ventricles
Nodes & Conductors of the Heart

Sinoatrial Nodes (SA Node): 60-100bpm

Oval-shaped near superior vena cava – Generates automatic depolarisation impulses modified by the Autonomic Nervous System (ANS). Primary pacemaker has the most intrinsic rate of depolarisation

The impulse is sent to atria through the internodal pathways where atrial will send impulse to AV node.

Atrioventricular Nodes (AV Node): 40-60bpm

Serves as a bridge between atria & ventricles (located in atrial septum) – receives impulse and delays It before conducting the ventricles; this delay is so the atria can fill up adequately before ventricular contraction.

Secondary (Latent) Pacemakers:

Additional structures (to the SA node) that can serve as pacemakers – Term ‘latent’ refer to its role when the SA node fails. These nodes can assume the role of pacemaker as (normal autonomy) to prevent cardiac arrest

  1. Atrial myocardium (primary): Atrial myocardial cluster cells at the coronary sinus and inferior vena cava that serve as contractile cells (not conduction cells)
  2. Myocardium surrounding the AV Node (secondary): Cell clusters around the AV node that can be autonomic
  3. His-Purkinje Network (tertiary latent): Bundle of His & entire Purkinje network can possess automaticity if all other latent pacemakers fail.

Bundle of His (AV Bundle): 40-60bpm

From AV node impulse – Splits impulse into left & right bundle branches – Subsequently branching into smaller bundles into Purkinje fibres.

Purkinje Fibres (PKF): 20-40bpm

From AV Bundle – Fast impulse (4m/sec) which runs through endocardium where impulse is sent to myocardial contractile cells (some extend into myocardium). Ventricular contraction therefore begins in endocardium and spread to epicardium

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Cardiac Cycle & Action Potential

Cardiac Cycle:

  1. SA node activity begins, atrial activation begins (t = 0ms)
  2. Stimulus spreads across atrial surface, impulse reaches AV node (t = 50ms)
  3. AV node delays impulse from spreading by ~100ms as atrial contraction begins (t = 150ms)
  4. Impulse reaches AV bundle & PKF then papillary muscle (t = 175ms)
  5. PKF distribute impulse to ventricles (atrial contraction completed); then ventricle contracts (t = 225ms)

Cardiac Electrophysiology:

Cardiac cycle begins at cell-level where particle movement between cell membrane creates action potential which is transmitted along the conduction pathway – Done in five (5) stages. Any changes in electrolyte values (Na+ / Ca+ / K+) can affect cell’s action potential.

  • Resting Membrane Potential (Phase 4): -85 to -95mV Heart chamber diastole
    • Resting, isoelectric awaiting external stimulus (ie. Adjacent cell) or spontaneous depolarisation without influences (cardiac muscle automaticity). Resting mV is determined by membrane permeability to ions. Outside more charged than inside (more Na+ & K+)
  • Depolarisation (Phase 0): Charged to +30mV (~65mV) Ventricular myocardium depolarisation
    • Comes from SA node creating sudden voltage change on cell surface resulting rapid Na+ influx into cell as sodium channel opens shifting resting mV. Ca+ ions enter cell at the threshold voltage (~65mV).
  • Early Rapid Repolarisation (Phase 1): +20 to 0mV
    • The sodium channel closes, and brief partial repolarisation occurs as result of K+ moving outwards reducing the cell voltage.
  • Plateau (Phase 2): +20 to 0mV Refractory phase
    • Longest phase of action potential due to slow Ca+ movement into cell and K+ out of cell to maintain voltage.
  • Repolarisation (Phase 3): -90mV
    • Simultaneous Ca+ & K+ movement out of cell reduces voltage until resting membrane potential is reached.

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References

College of Pre-Hospital Care. (2015). 12-Lead ECG Analysis: Self-Directed Learning Package. Version 3. St John Ambulance Ltd.  

Curtis, K., & Ramsden, C. (2016). Emergency and trauma care for Nurses and Paramedics (2nd ed.). Elsevier Australia.

DeLaune, S. C., Ladner, P. K., McTier, L., Tollefson, J., & Lawrence, J. (2016). Australian and New Zealand fundamentals of nursing (1st ed.). Cengage Learning Australia Pty Limited.

ECG & ECHO Learning. (2020). Clinical ECG Interpretation. https://ecgwaves.com/topic/ecg-normal-p-wave-qrs-complex-st-segment-t-wave-j-point/

Life in the Fast Lane. (2020). ECG Library. https://litfl.com/ecg-library/

St John WA Ltd. (2017). Electrocardiography (ECG). Clinical Resources. https://clinical.stjohnwa.com.au/clinical-skills/assessment/vital-signs/electrocardiography-(ecg)

WikiEM. 2020. The Global Emergency Medicine Wiki. https://www.wikem.org


Page contributors:

60825Thanh Bui, AP60825
Event Medic, Emergency Medical Technician &
Volunteer Development Officer

 

16790

Andrew Moffat, AP16790
Volunteer Training Manager & Volunteer Development Officer

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