#08 Heart III Flashcards
Cardiac Cycle
• A cardiac cycle is the time from the start of one heartbeat to the initiation of the next.
Systole vs. Diastole
- Systole is contraction of a heart chamber.
- Diastole is relaxation of a heart chamber.
How Is Cardiac Cycle Driven?
• Cardiac cycle is driven by pressure, traveling from area of high pressure to low pressure.
Step 1 of Cardiac Cycle: Atrial Systole
○ A brief contraction of atrial myocardium initiated by SA node. Before this, ventricles were being passively filled with blood to 70% of full volume. Atrial contraction “tops off” ventricles and fills it up to EDV.
End Dialostic Value
§ EDV means end diastolic volume, 130 mL. It is the total volume of the ventricle.
Importance Of Ventricles Being Able To Be Passively Filled
§ The passive filling of the ventricle makes it possible for the heart to be able to function without contraction of the atria, though not as much blood would be pumped.
Step 2 of Cardiac Cycle: Early Ventricular Systole
○ As you push blood into ventricle, pressure inside ventricle climbs up. Increased pressure will cause it to start contracting. But the semilunar valve remains close, so these are isolvolumic contractions. Ventricles contract, but volume isn’t changing.
○ Atria are in diastole and are passively filling with blood.
• Step 3 of Cardiac Cycle: Late Ventricular Systole
○ When pressure in ventricle surpasses pressure in atrium, that is the signal to open up the semilunar valves. Now ventricle produces isotonic contraction, contracting AND pushing out blood.
Stroke Volume
○ The blood being ejected by the ventricle during step 3 of cardiac cycle is called the stroke volume.
End Systolic Volume
○ Not all the blood is pushed out of ventricle during late ventricular systole and the volume of blood remaining in the ventricle is called the end systolic volume.
How To Calculate Stroke Volume
• Stroke Volume is calculated by the difference between End Diastolic Volume (EDV, amount of blood in ventricle following atrial systole) and End Systolic Volume (ESV, blood remaining in ventricle following isotonic contraction).
Step 4 of Cardiac Cycle: Early Ventricular Diastole
○ Still have ESV inside blood. We now have isolvolumic relaxation, which is going to lower the pressure. When pressure in ventricle is lower than pressure in artery, the semilunar valves will close. Atria are still filling.
Step 5 of Cardiac Cycle: Late Ventricular Diastole
○ Pressure has fallen very low in ventricle, while atria continuously fills with blood and increases pressure. Ventricle fills passively back to 70% EDV when the AV valves open.
Cardiac Output
• Cardiac Output is the Stroke Volume (mL/beat) multiplied by Heart Rate (beats/min), numerical representation of amount of blood pumped a minute. Normal number is 6L per min in humans.
How Is Cardiac Output Controlled?
It is regulated by the autonomic innervation, although the conductive cells are autorhythmic so they produce electrical signals automatically. The RATE is what is being controlled.
Regulating Cardiac Output: SNS
○ Sympathetic Nervous System: From the cervical and thoracic ganglia we have the cardiac nerve coming off. The signals themselves are coming from the brain, in the medulla there is a cardioacceleratory center. The catecholamines like epinephrine and norepinephrine are from fight or flight response of sympathetic nervous system, and they generally serve to increase rate of heart beat.
Regulating Cardiac Output: PNS
○ Parasympathetic Nervous System: Acetylcholine is the main neurotransmitter. They have a cardioinhibitory center, and use the vagus nerve as pathway from it to the heart. Innervates heart and releases acetylcholine onto the myocytes.
Cardioacceleration: Cateholamines
○ Catecholamines: Epinephrine and norepinephrine. They bind to beta-adrenergic receptors G-protein coupled receptors.
Cardioacceleration Process
○ So catecholamines bind to beta-adrenergic receptors, increasing catalayse cyclase activity, bringing up levels of cyclic AMP. The increased cAMP brings about activation of protiein Kinase A, PKA. It modulates every step in pathway of this process. Can increase amount of calcium coming in from L-type calcium channel, increase amount coming out through RyR, can change sensitivity of myofilaments altering interaction between calcium and troponin, and change how quickly calcium can travel back into the SR. Getting calcium back into SR is just as important as increasing calcium at the beginning so another contraction can occur.
○ All types of myocytes have these beta-adrenergic receptors and they will respond to the catecholamines.
Cardioacceleration: Targets
○ Targets
§ LTCC –> More Calcium Entry
§ Ryanodine Receptor –> More Calcium Release
§ Phospholamban –> Increases SERCA (SR) Activity
Cardioinhibitory Process
○ The parasympathetic nervous system lowers levels of cAMP, or open up potassium channels, making potassium come out of cell. So when trying to fire action potentials, need to depolarize, but the open potassium channels makes it harder to depolarize. Both contractile and conductive cells.
