Flashcards in Chapter 4 - Heart As A Pump Deck (26):
Factors affecting strength of contraction. (There are 2 main ones)
i. EXCITATION-CONTRACTION COUPLING
Contraction of the heart is triggered by the spread of electrical excitation throughout the syncytium of muscle cells. Ultimately, the strength of contraction of each cardiac cell is determined by the chemical proc-esses linking or “coupling” this excitation to actin-myosin cross-bridge cycling, a process known as “excitation-contraction coupling”. For normal excitation-contraction coupling, the heart requires optimal concen-trations of Na + , K + , and Ca ++ .
Effects of hyperkalemia on the heart
Modest increases cause increased excitability. Large increases in extracellular K + produce dysrhythmias, depolarization, loss of excitability of the myocardial cells due to the sodium channels being trapped in the inactivated state which is accommodation, and cardiac arrest in diastole.
Effects of hypernatremia on the heart
the resting membrane potential is independent of the Na + gradient across the membrane, so hypernatremia does not really do much
Effects of hypokalemia on the heart
Under normal conditions, the extracellular K + concentration is about 4 mM. A moderate reduction in extracellular K + has little effect on myocardial excitation and contraction, but it flattens the T wave of the electrocardiogram. A severe reduction in extracellular K + produces weakness, paralysis, and cardiac arrest.
Effects of Hyponatremia on the heart
In the absence of Na + , the heart is not excitable and will not beat because the action potential depends on extracellular Na + .
Effects of hypocalcemia
Ca ++ is essential for cardiac contraction; removal of Ca ++ from the extracellular fluid results in decreased contractile force and eventual arrest in diastole.
Effects of hypercalcemia on the heart
n increase in extracellular Ca ++ enhances contractile force, and very high Ca ++ concentrations induce cardiac arrest in systole (rigor).
During the plateau (phase 2) of the action potential, Ca ++ permeability of the sarcolemma increases. Ca ++ enters the cell through voltage-dependent L-type Ca ++ channels in the sarcolemma and in the T-tubules. The Ca ++ channel protein is called the dihydropyridine receptor because it has high affinity for this group of Ca ++ chan-nel antagonists.
The amount of Ca ++ that enters the cell from the extracellular space is not sufficient to induce contraction of the myofibrils, but it serves as a trigger (trigger Ca ++ ) to release Ca ++ from the intracellular Ca ++ stores in the SR. The Ca ++ leaves the SR through calcium release channels, which are called ryanodine receptors because the channel protein, also called foot protein or junctional processes of the SR, binds ryanodine avidly.
Effects of catecholamines
Cardiac contraction and relaxation are both accelerated by catecholamines and adenylyl cyclase activation. The resulting increase in cAMP activates cAMP-dependent protein kinase, which phosphorylates the Ca ++ channel in the sarcolemma. This allows a greater influx of Ca ++ into the cell and thereby increases contraction. However, it also accelerates relaxation by phosphorylating phospholamban, which enhances Ca ++ uptake by the SR and by phosphorylating troponin I, which inhibits the Ca ++ binding of troponin C. iiii
Volume of blood in ventricle before contraction begins. Exerts a preload on the ventricle. Mechanism is explained by the Frank-Starling Law Of The Heart
Frank-Starling Law Of The Heart
Postulates that the increased ventricular wall tension associated with increased EDV stretches ventricular myocytes and results in a greater overlap of actin and myosin filaments.
This greater overlap causes more forceful contractions and increases the SV.
Volume of blood ejected from ventricle during systole.
Cardiac Output = Heart Rate X Stroke Volume
CO = HR X SV
Measured using Fick's method.
Normal value ~ 5L
Number of heart beats per minute.
Measured in bpm.
Normal is ~ 72bpm
Volume of blood ejected with each heart beat.
Measured in ml.
Normal is ~ 70ml.
Can be calculated from EDV - ESV
Fick's Principle, method
Is simply an application of the law of conservation of mass. It is derived from the fact that the quantity of O2 delivered to the pulmonary capillaries via the pulmonary artery plus the quantity of O2 that enters the pulmonary capillaries from the alveoli must equal the quantity of O2 that is carried away by the pulmonary veins.
An example of calculation of cardiac output in a normal, resting adult. With an O2 consumption of 250 mL/min, an arterial (pulmonary venous) O2 content of 0.20 mL O2 /mL blood, and a mixed venous (pulmonary arterial) O2 content of 0.15 mL O2 /mL blood, the cardiac output would equal 250 ÷ (0.20 −0.15) = 5000 mL/min.
The sequence of electrical changes, pressures, and mechanical events within the heart and great vessels leading to and away from the heart during each beat is known as the cardiac cycle.
i. Rapid Ventricular Filling
iii. Atrial Systole
i. Isovolumetric Contraction
ii. Rapid Ejection
iii. Reduced Ejection
The heart produces four distinct heart sounds whose timings and frequency are diagnostically relevant of several heart disorders including valvular diseases and chamber dilation.
Detected using a phono radiogram
First heart sound
Described as a lub
initiated at the onset of ventricular systole and consists of a series of vibrations of mixed, unrelated, low frequencies (a noise). It is the loudest and longest of the heart sounds, has a crescendo-decrescendo quality, and is heard best over the apical region of the heart.
Second heart sound
The second heart sound, which occurs with closure of the semilunar valves, is composed of higher-frequency vibrations (higher pitch), is of shorter duration and lower intensity, and has a more snapping quality than the first heart sound.
Described as a dub.
Contractility represents the performance of the heart at a given preload and afterload, and it depends on the state of the excitation-contraction coupling processes within the cells.
Estimated from - i. dP/dt
ii. Ejection fraction
ii. Velocity of ventricular ejection
An increase in systolic Ca ++ is also achieved by increasing extracellular Ca ++ or decreasing the Na + gradient across the sarcolemma.
The sodium gradient can be reduced by increasing intracellular Na + or decreasing extracellular Na + . Cardiac glycosides increase intracellular Na + by inhibiting the Na-K pump, which results in an accumulation of Na + in the cells. The elevated cytosolic Na + reverses the Na+/Ca ++ exchanger(3Na+ in, 1Ca++ out normally) so that less Ca ++ is removed from the cell. This Ca ++ is stored in the SR. A lowered extracellular Na + results in a reduction in Na + entry into the cell and hence less exchange of Na + for Ca ++.
Developed tension is diminished by a reduction in extracellular Ca ++ , by an increase in the Na + gradient across the sarcolemma, or by administration of Ca ++ blockers that prevent Ca ++ from entering the myocardial cell.