| Term 
 | Definition 
 
        | the amount of blood pumped by each of the ventricles in one minute. 
 CO = HR x SV
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | Stroke volume is the amount of blood ejected by the left ventricle in one contraction. 
 SV = EDV - ESV
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | EDV = volume of blood in ventricle before contraction ESV = volume of blood in ventricle after contraction
 |  | 
        |  | 
        
        | Term 
 
        | Typical resting values: HR
 EDV
 ESV
 SV
 CO
 |  | Definition 
 
        | Typical resting values: HR = 75bpm
 EDV = 135ml
 ESV = 65ml
 SV = 70ml
 CO = 5250ml.min-1
 |  | 
        |  | 
        
        | Term 
 
        | What is the ejection fraction at rest? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | How do these values change in severe exercise? HR
 EDV
 ESV
 SV
 CO
 |  | Definition 
 
        | HR = 180bpm EDV = 145ml
 ESV= 25ml
 SV= 120ml
 CO= 21.6L.min-1
 Ejection fraction = 0.83
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | EDV (preload) ESV (afterload)
 strength of ventricular contraction
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | - filling pressure (venous return) - filling time (note: as HR increases, less time is spent in diastole and therefore filling time increases)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | the preload on the heart ie the volume load on the ventricles before ventricular contraction begins |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | - the pressure on the artery against which the ventricle is pumping (the afterload) - the strength of ventricular contraction as this determines the pressure that can be achieved in the ventricle.
 |  | 
        |  | 
        
        | Term 
 
        | Describe afterload for the left ventricle |  | Definition 
 
        | the afterload represents diastolic pressure in the aorta (about 80mmHg). For blood to be ejected from the LV, this afterload has to be exceeded for the aortic semilunar valve to open |  | 
        |  | 
        
        | Term 
 
        | How do cardiac and skeletal muscle differ in regards to sarcomere length? |  | Definition 
 
        | SM = 2-2.2micrometers CM = 1.8micrometers
 |  | 
        |  | 
        
        | Term 
 
        | What are the benefits of stretching cardiac muscle? |  | Definition 
 
        | increases the number of cross-bridges that can be formed between actin and myosin filaments and increases the strength of contraction. |  | 
        |  | 
        
        | Term 
 
        | How can cardiac muscle be stretched? |  | Definition 
 
        | an increase in preload/EDV (ie increasing the volume of blood in the ventricles) stretches the muscle cells of the myocardium before they contract. |  | 
        |  | 
        
        | Term 
 
        | State the Frank-Starling law of the heart |  | Definition 
 
        | as the degree of stretch on the heart increases so does the force of contraction. |  | 
        |  | 
        
        | Term 
 
        | What are the consequences of increased venous return? |  | Definition 
 
        | - more blood returns to the heart, this increases EDV - larger EDV stretches the ventricular muscle and more force is developed to pump out the larger volume of blood.
 
 It is important to balance inflow and outflow so that each ventricle pumps the same amount of blood.
 |  | 
        |  | 
        
        | Term 
 
        | What would be the consequence of RV pumping 0.1ml more blood than the LV with each cardiac cycle? |  | Definition 
 
        | in one hour the difference in blood volume pumped would be 420ml this blood would accumulate in the lungs, impair gas exchange (fatal in 2 hours)
 |  | 
        |  | 
        
        | Term 
 
        | In a healthy heart, this does not happen, why? |  | Definition 
 
        | Fluid build up in the lungs would increase pulmonary venous pressure and therefore LV filling and then by FS law increase the strength of contraction of the LV to clear the extra blood volume. |  | 
        |  | 
        
        | Term 
 
        | What occurs in left ventricular heart failure? |  | Definition 
 
        | Fluid builds up in the lungs, making breathing more difficult and reducing exercise tolerance CONGESTIVE HEART FAILURE
 |  | 
        |  | 
        
        | Term 
 
        | What occurs in right ventricular heart failure? |  | Definition 
 
        | build up of fluid in the extremities (ie peripheral oedema) |  | 
        |  | 
        
        | Term 
 
        | How do I remember which failure causes which build up? |  | Definition 
 
        | Think about where the blood is coming from before it flows into each ventricle/atrium. The ventricles failed so are not clearing the extra blood volume. |  | 
        |  | 
        
        | Term 
 
        | What is afterload/ESV on the left ventricle? |  | Definition 
 
        | diastolic aortic pressure left ventricular pressure has to exceed the afterload before any blood can be ejected from the ventricle
 |  | 
        |  | 
        
        | Term 
 
        | When would afterload increase? |  | Definition 
 
        | patients with high blood pressure |  | 
        |  | 
        
        | Term 
 
        | What are the consequences of increased afterload? |  | Definition 
 
        | 1. less blood will be ejected from the ventricle, increasing ESV 2. SV and CO fall at a constant rate
 3. the heart has to work harder to oppose higher afterload
 4. the heart muscle hypertrophies and LV wall of the heart becomes thicker
 |  | 
        |  | 
        
        | Term 
 
        | Which fibres terminate throughout the heart? |  | Definition 
 
        | sympathetic fibres which release noradrenaline (aka norepinephrine) |  | 
        |  | 
        
        | Term 
 
        | How does sympathetic stimulation increase the force of contraction? |  | Definition 
 
        | 1. NA binds to beta-1 receptors and in turn activates Gs 2. alpha subunit dissociates from beta and gamma and binds to adenylate cyclase
 3. adenylate cyclase converts ATP to cAMP
 4. cAMP activates PKA which then phosphorylates a number of protein targets.
 |  | 
        |  | 
        
        | Term 
 
        | List the 4 proteins PKA targets |  | Definition 
 
        | 1. L-type calcium channel 2. Ryanodine receptor
 3. Phospholamban
 4. Troponin
 |  | 
        |  | 
        
        | Term 
 
        | What is the effect of phosphorylating L-type calcium channels? |  | Definition 
 
        | larger channel conductance increasing the flux of ca2+ across the sarcolemma |  | 
        |  | 
        
        | Term 
 
        | What is the effect of phosphorylating ryanodine receptors? |  | Definition 
 
        | increase ca2+ release from SR |  | 
        |  | 
        
        | Term 
 
        | What is the effect of phosphorylating phospolamban? |  | Definition 
 
        | Phospholamban normally acts to slow the rate of SR ca2+ uptake, however when phosphorylated, this inhibition of SR ca2+ uptake is diminished allowing SR ca2+ uptake to speed up. This causes an increase in the amount of ca2+ stored ni the SR and so more can be released every heartbeat. |  | 
        |  | 
        
        | Term 
 
        | What is the effect of phosphorylating Tn-1? |  | Definition 
 
        | This leads to a decrease in the sensitivity of the myofilaments to ca2+. This accelerates the phase of relaxation so contractions are over more quickly. Any reduction in force developed is compensated by the 3 mechanisms that increase ca2+ |  | 
        |  | 
        
        | Term 
 
        | What are the two mechanisms to increase SV? |  | Definition 
 
        | Intrinsic : due to FS mechanism, stretching heart muscle increases the force of contraction. Extrinsic : due to sympathetic stimulation of the heart which increases the force of contraction.
 |  | 
        |  | 
        
        | Term 
 
        | What is the heart innervated by? |  | Definition 
 
        | - the parasympathetic arm (the vagus nerve) innervates atrial muscle and the SA and AV nodes. - the sympathetic arm innervates all parts of the heart
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | increased activity in sympathetic nervous system leads to a faster heart rate |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | increased activity in the parasympathetic nervous system leads to a slower heart rate |  | 
        |  | 
        
        | Term 
 
        | What happens when autonomic nerves are severed and what does this suggest? |  | Definition 
 
        | Increased heart rate (110bpm - the intrinsic rate of SAN) Suggests intrinsic activity in the ANS which slows down HR
 PNS is dominant (bradycardiac influence).
 |  | 
        |  | 
        
        | Term 
 
        | What happens to the heart when you begin exercising? |  | Definition 
 
        | the sympathetic arm of the ANS is stimulated and NA is released into the vicinity of the heart cells: 1) increases the strength of cardiac contractions
 2) SAN generates APs at higher frequency so HR increases
 |  | 
        |  | 
        
        | Term 
 
        | What are the direct effects inside a cell after sympathetic stimulation? |  | Definition 
 
        | 1) rise in cAMP increases If, so pacemaker potential rate is accelerated. 2) reduction in K+ permeability so MDP more positive
 3) Increased L-type ca2+ current, so upstroke is faster - more AP per unit of time
 4) increases the speed of conduction of the AP through AVN
 5) shortens the duration of the ventricular AP so that the duration of systole is reduced.
 |  | 
        |  | 
        
        | Term 
 
        | How does cAMP enhance funny current? |  | Definition 
 
        | cAMP is an activator of funny current and speeds up depolarisation rate of the pacemaker potential |  | 
        |  | 
        
        | Term 
 
        | A summary of sympathetic stimulation on the heart... |  | Definition 
 
        | 1. APs generated more frequently and propagated through the heart more rapidly 2. AP are shorter in duration
 3. strength of contraction is greater
 4. duration of each contraction is reduced
 |  | 
        |  | 
        
        | Term 
 
        | What does parasympathetic stimulation release? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What are the effects of ACh? |  | Definition 
 
        | - decreases If (inhibits adenylate cyclase and reduces cAMP) so the pacemaker potential is slowed and takes longer to reach threshold - increases K+ permeability of the SAN (via IK=ACh), which hyperpolarises the MDP
 |  | 
        |  | 
        
        | Term 
 
        | How is blood supplied to the heart? |  | Definition 
 
        | coronary circulation the coronary arteries branch off from the aorta just above the aortic semilunar valve
 |  | 
        |  | 
        
        | Term 
 
        | When does most of the blood flow in the coronary arteries occur? |  | Definition 
 
        | 70% occurs during diastole because during systole, the arteries are compressed as the ventricular muscle contracts |  | 
        |  | 
        
        | Term 
 
        | How much does blood flow to the heart increase by during exercise? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | How is this accomplished? |  | Definition 
 
        | dilating the coronary vessels to allow greater blood flow to increase the delivery of nutrients to the working heart muscle |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 1. Metabolic activity increases 2. Increased breakdown of ATP
 4. Increase in adenosine
 5. vasodilation of the coronary vessels
 6. increases blood flow to heart muscle
 7. increases delivery of oxygen metabolic fuel
 |  | 
        |  |