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L4 - The Heart as a Pump & ECG Explain the mechanical events…

- - - - 2. Passive Ventricular Filling (Atria open, no contract.)
        
        Passage of Blood from A => V
        
        High pressure => Low Pressure (Because initially no blood in V)
        ~75% of blood volume enters through this means?
        
        3. Atrial Conctraction (Systole)
        
        Priming the Ventricle pump by increasing blood volume
        
        Ventricular Systole (Emptying)
        
        1. Isovolumetric Contraction
        
        Constant volume allows ventricular pressure to build up as the blood is compressed
        
        Once pressure inside V. exceeds aortic pressure, the ASL/PSL valves open
        
        Wigger's Diagram
        
        Corresponds with QRS on ECG
        
        Beginning of Ventricular contraction
        
        AV valves shut - isovolumetric
        
        Rapid increase in V pressure
        
        3. Ventricular Ejection
        
        Increase in V pressure prompts ASL valves to open
        
        Ejection fraction = fraction of blood remaining in heart after contract.
        
        1 more item...
        
        Wiggers Diagram
        
        Corresponds with P wave
        
        Ventricular volume increases, then equalises (Tricuspid valve stays open)
        
        Ventricular Pressure Increases
        
        Aortic Pressure reduces (BF drains to Systemic Cicruit)
        
        Wigger's Diagram
        
        Mitral and Tricsupid valves open
        
        Blood passively flows from high pressure (atria) into low pressure (ventricles)
        
        Aortic pressure falls (no longer recieving blood, and blood drains away)
      - Wigger's Diagram
        
        Aortic valves close after V ejection
        
        Aortic presure increases slightly before reducing
        
        Ventricular pressure plummets (no blood)
- - - - Pathology
        
        Stenotic (Stiff) valves = whistling sound
        
        Insufficient / incompetent valves (gurgle)
  - - - Comparison between Skeletal and Cardiac Muscle
        
        Wave summation and treppe in skeletal muscle is required to increase strength - tetanus = maximum power generated by muscle (multiple and frequent APs in quick succession)
        Cardiuac muscles does not seek to achiueve this - doing so would mean cardiac arrest - avoiding this necessitates a refectory period
        
        Plateau phase due to L-type (long-lasting) voltage-dependent Ca2+ channel - Dihydropyridine (DHPR)
        
        Important because these L-type channels cannot be reactivated until the cells has repolarised - provides a refectory period - allows myocardium to settle into a contractile rhythm.
        
        Depolarisation due to fast voltage gated Na+channels opening
        
        Stages leading to Contraction
        
        Early Repolarisation Phase - due to influence K+ channels - slower than Na+ and they reduce positive charge
        
        Calcium Influx - Comparison
        
        Cardiac Muscle
        Ryanodine receptors present on the sarcoplasmic reticulum are ligand gated in Cardiac Muscle, not mechanically gated as is the case in SkM - ligand being calcium
        
        Ca entering Muscle fibre due to action potential opening VG Ca+2 channels (DHPR)
        
        Increase in cytosolic calcium induces calicum release from Sarcoplasmic reticulum (Ca+2 binds to RyR2 and activates)
        
        To switch off contraption, must pump Ca+2 out of both SR and Cell - requires Ca channels to close, and the action SERCA + Calsequestrin, PMCA and NCX*
        
        Skeletal Muscle
        Ryandoine receptors in SkM are mechanically gated, and they are opened in synchronously to opening of VG DHPR on Sarcolemma/T-tubules
        Deactivating DHPRs also deactivates RyR2
- - - - Internodal Pathways
        
        Specialised conduction fibres (insulated and slow propogation ~1m/sec) conduct signal from SA node to Atrioventricular node
        
        Ensures Atrial contraction directs blood flow inferiorly/caudally into the Vs
        
        AV Node
        Total impulse delay between Atria and Ventricles thus far ~ 0.16s
        
        SA -> AV ~ 0.03s
        
        AV node ~ 0.09s
        
        Bundle of His (AV bundle) ~ 0.04
        
        Interventricular Septum & Purkinje Fibres
        
        L&R bundle branches conduct AP toward the Purkinje fibres very quickly so that the myocardium throughout the L&R ventricles virtually contracts simulateously and synchronously
        
        Superior
        
        Cardiac Action Potentials is dependant on Autorhythmicity of SA
        
        Base (superior posterior portion (pulmonary veins)) depolarises/contracts after apex, yet repolarises faster
        
        Electrocardiogram (ECG)
        
        1 more item...
- - - - 1. SA node = 100-110 bpm
      - 2. AV node = 40-60 bpm
      - 3. Purkinje fibres= 15-40 bpm
  - - - Parasympathtic NS - Vagus innervation (Nerve10)
        Only effects Chronotropy, not ionotropy => therefore only innervates SA node
      - Sympathetic NS -
        Controls both chronotropy and inotropy