CV-3
LVEDP is about 10 and DBP is about 80, so DBP is major determinant of CPP.
- Epicardium is the outer most layer that supplies myocardium. Flow to the epicardium area is not affected during cardiac cycle.
- Subendocardium is beneath the endocardium and most vulnerable to ischemia.
- The LV subendocardium has the highest metabolic requirements and is compressed during systole due to pumping power of LV (increased resistance).
RV subendocardium is perfused during both systole and diastole.
Adenosine is released from endothelium when 02 is low/ increased metabolism.
Low 02 causes ATP degradation into adenosine monophosphate.
Once Adenosine is used for dilation it is taken back up into cell for ATP production.
Adenosine has the greatest vasodilatory capacity.
Adenosine controls coronary vascular tone.
The most potent vasodilator substance released by cardiac cells is adenosine .
The greater the rate of metabolism or the lower the availability of oxygen, the greater the accumulation of adenosine.
There is also an accumulation of carbon dioxide, lactic acid, histamine, potassium ions and hydrogen ions with higher metabolism or low oxygen availability.
Vasodilation increases blood flow to meet the metabolic demands of the myocardium.
Sympathetic stimulation (norepi) dilates coronary vessels.
Parasymp stimulation (Ach) vasoconstricts coronary vessels.
Epicardial coronary vessels have more alpha receptors and cause vasoconstriction.
Intramuscular arteries have more beta receptors and cause vasodilation.
Histamine, bradykinin, CO2, prostaglandin, lactic acid, K and H all cause vasodilation.
SNS directly causes coronary dilation by causing Epi and NE to increase HR and contractility. That in turn increases myocardial oxygen demand and causes coronaries to vasodilate.
The PNS acts indirectly to cause coronary constriction with the release Ach from vagus nerve which decreases HR. The decreased HR causes a decreased 02 demand and coronaries constrict.
Distribution of nerve fibers of PNS is not great.
The striations in cardiac muscle are the actin and myosin filaments within the myofibrils.
Intercalated discs are the cell membranes that separate individual cardiac muscle cells from one another.
Intercalated discs fuse with one another to form communicating junctions which allow action potentials to travel easily between cells.
Myofibrils contain the contractile element of the cardiac fiber.
Cardiac muscle fibers are made up of thousands and thousands of myofibrils.
The myofibril is composed of repeating units called the sarcomere.
Each sarcomere is bound by two Z lines and contains thin and thick filaments.
The thick filaments create the M line which is within the H zone.
The sarcolemma is the cell membrane of the muscle fiber.
The sarcolemma invaginates through the cell at regular intervals.
Sarcoplasmic reticulum surrounds the contractile elements of the myofibrils and is a source of calcium. Sarcoplasm is the intracellular fluid where electrolytes and mitochondria.
The thick filaments are myosin.
The myosin molecule is composed of two alpha strands combined into a super coil.
Each myosin strand terminates with a globular head which contain ATPase.
They myosin molecules are arranged in a tail to tail fashion.
The thin filament is a G actin polymerized double helix.
The thin filaments contain tropomyosin and troponin.
When calcium is bound to troponin it frees tropomyosin binding site which allows interaction between thick and thin filaments to allow contraction.
The resting membrane potential in a cardiac cell is negative 90.