Figure 12.1:  Location of the Heart

Fig 12.2: The Heart
• Figure 12.3: VentricularMusculature
Figure 12.4:  A-V Valves
Figure 12.5. Aortic & Pulmonary Valves
Figure 12.6:

Blood Flow

Systemic Capillaries --> Veins-->Vena Cava --> Right Atrium --> Right Ventricle
Pulmonary Artery --> Pulmonary Capillaries --> Pulmonary Vein
Left Atrium --> Left Ventricle --> Aorta --> Arteries --->Systemic Capillaries

Cardiac cell structure
• Small discrete cells
• Intercalated disks with desmosomes
• Gap junctions = syncytium
• Many mitochondria
• Sr and t tubules
• Striated
Figure 12.7: Cardiac Muscle Cells

Fig 12.8: Cardiac Conduction System

Electrical Activity of the Heart

Fig 12.10: Pacemaker Cell

Ion channels in pacemaker cells: see page 381
• Slow initial depolarization caused by closing of K+ channels
• Next funny channels open
        – Allow Na+ to enter causing depolarization
        – Only open briefly
• This depolarization opens two types of Ca++ channels
        -T - type channels open briefly before inactivating
        - L - type channels then open finishing depolarization

Note Differences in Conduction Velocity Due to Rates of Depolarization!

RECTIFICATION
Minimized efflux of K+ during AP plateau because of decreased K+ conductance at this positive Vm

See Fig 12.10 !!!!

 
 

• Duration for complete contraction of the ‘pump’
• Long AP with long refractory period to prevent fibrillation

Fig 12.12: Einthoven’s Triangle and the ECG:  Figure 12.13



 

Terminology
• End Systolic Volume   (ESV in ml)
• End Diastolic Volume  (EDV in ml))
• Stroke Volume  (SV in ml/beat)
• SV = EDV - ESV
• Heart Rate (in beats/min)
• SV (ml/beat)
• Cardiac Output (CO in ml/min)
• CO = HR x SV

Starling’s Law of the Heart
Increased EDV or myocardial fiber length results in increased SV or increased strength of contraction.
Basis for Starling’s Law:
P = 2T/r
where
P = pressure in ventricle or aorta at ejection
T = myocardial tension required to generate that tension
r = radius of ventricle at beginning of systole
P = 2T/r

Which ventricle must develop more tension or contractile force, a fuller, larger EDV or a smaller EDV?

Sympathetic response
•  receptors on nodes and atrial and ventricular muscle cells
• Increases rate
• Increases ca⁺⁺ released per beat via cyclic amp

receptor activation
• G protein --> adenylate cyclase --> cyclic AMP
• Activates cAMP-dependent protein kinase
• Phosphorylates an SR protein, phospholamban
• myocardial SR takes up and releases more Ca⁺⁺ per beat
result = more cross bridges = more tension
As heart rate increases,
filling time decreases
DIGITALIS
DECREASE HR
           BUT
INCREASE STRENGTH
 

Vagus nerve
• Parasympathetic fibers
• Baroreceptors from aortic arch
• Stretch receptors from lungs

Parasympathetic nerves
Right vagus to SA node
Left vagus to AV node and bundle
Decreases rate
No DIRECT  influence on strength