BIO 3324 1nd Edition Lecture 14Outline of Last LectureI. circulatory systemII. flow of bloodIII. heart of four chambersIV. heart valvesV. atrial executionOutline of Current LectureI. ventricular excitationII. eggIII. cardiac cycleIV. eventsV. ejectionVI. capillariesCurrent lecture:Ventricular excitation:• At the AV node, the AP is conducted relatively slowly• Causes a delay (called the AV nodal delay) which enables atria to completely depolarize & contract before ventricles do• Impulse travels rapidly down Bundles of His & purkinje fibers to the ventricular myocardium• Ensures that the ventricles contract as a unit• Does not travel to all cells – done by gap junctions from excited cells• More highly organizedThese notes represent a detailed interpretation of the professor’s lecture. Grade Buddy is best Used as a supplement to your own notes, not as a substitute.– Ventricular mass > atrial mass• Ensures a single, smooth, coordinated contraction that simultaneously ejects blood into the pulmonary & system circulationThe Electrocardiogram (ECG):• Recording of the electrical currents generated by cardiac muscles• Represents– A recording of the electrical activity induced in the body fluids by the cardiac muscles that reaches the surface… NOT a direct recording of electrical activity of the heart– An overall spread of activity throughout the heart during depolarization and hyperpolarization… NOT a recording of a single AP– Comparison in voltage detected by electrodes at two different pointsDifferent parts of the ECG are correlated to a specific cardiac event:• 3 distinct wave forms– P wave: atrial depolarization– QRS complex: ventricular depolarization– T wave: ventricular repolarization• Important notes:– Firing of the SA node is not detectable– No separate wave for atrial repolarization (masked by QRS complex)– P wave is smaller than QRS because atria have less mass & generate less electrical activity• No net current flow during 3 periods– PR segment: AV nodal delay– ST segment: plateau phase of ventricular contractile cells– TP interval: heart is at rest & ventricular filling is taking placeECG provides information about rate and rhythm:• Determining heart rate – counting the number of peaks of a specific wave form over a period of a minute (e.g. P wave or R peak in QRS complex). Is it between 60-100 beats/min, resting.• Looking for irregular rhythms – any interruptions in spacing of the P→QRS→T waves• Looking for the presence of the individual waves• Is each P wave followed by a QRS complex. Lack of QRS suggests a transmission problem in the AV nodeAbnormalities seen in the ECG:• Abnormalities of rate: can be determined by the distance between QRS complexes– Tachycardia – rapid heart rate– Brachycardia – slowed heart rate• Abnormalities in rhythm: variations from the norm in regards to ECG waves– Atrial fibrillation – no definitive P waves resulting from irregular uncoordinated depolarization– Ventricular fibrillation –no detectable pattern or rhythm resulting from irregular uncoordinated chaotic contractions– Atrial flutters – atria contract faster than ventricles and thus not all impulses are translated by to the ventricles (due to refractory period)– Heart blocks – ventricles fail to be stimulated & thus fail to contract• Cardiac myopathy: damage to the heart muscle– Abnormal QRS waveforms because the muscle is unable to contract properly as aresult of damaged or necrotic tissueMechanical events of the cardiac cycle:• The heart alternatively contracts to empty and relaxes to fill– Systole: contraction and emptying; spread of excitation– Diastole: relaxation and filling; subsequent repolarization• Both atria and ventricles have their own cycles of systole and diastole– Usually referring to ventricles unless otherwise statedMid-ventricular diastole:• TP interval• Atrial pressure > ventricular pressure (due to venous inflow)• AV valve is open• Ventricular volume increasesLate ventricular diastole:• Corresponds to the P wave• Atrial contraction• Atrial pressure increases and more blood is pushed into the ventricle• Rise in ventricular pressure• Atrial pressure > ventricular pressure (due to venous inflow)• AV valve is openEnd of ventricular diastole:• End-Diastolic Volume (EDV)– Volume of blood in the ventricle at the end of diastoleVentricular excitation:• Corresponds to the QRS complex• Beginning of ventricular systole• Impulse travels to AV node & beyond to excite the ventricle• Sharp increase in ventricular pressure• Closing of the AV valveIsometric ventricular contraction:• Ventricular pressure must be greater than aortic pressure to open aortic valve• No blood enters or leaves• Muscles don’t change lengthVentricular ejection:• Ventricular pressure > aortic pressure• Aortic valve opens• Ventricular volume decreases• Subsequent rise in aortic pressure (resulting from the blood volume increasing faster than it is leaving the aorta)• Blood volume ejected is called the stroke volumeEnd of ventricular systole:• Not all of the blood is ejected during the systole• End-Systolic Volume (ESV)– Volume of blood in the ventricle at the end of systole– EDV – ESV = SV (stroke volume) or the amount of blood pumped per contractionVentricular repolarization:• Corresponds to the T wave• Onset of diastole• Ventricular pressure < aortic pressure• Closing of the aortic valve – Results in slight disturbance in aortic pressure curve called dicrotic notchIsovolumetric ventricular relaxation:• Both the AV and aortic valves are closed• No blood enters or leavesVentricular filling:• Ventricular pressure < atrial pressure• AV valve opens• Blood accumulating in atria rushes into ventricle then slows down as atrial pressure falls• Most ventricular filling occurs early in diastole• If heart rate increases, diastole time decreases… BUT this doesn’t affect the fill volumeCardiac output:• Dependent on heart rate and stroke volume– CO = HR x SV– The amount of blood pumped per minute• Heart rate is determined by autonomic influence on the SA node– Parasympathetic innervation (via Vagus nerve) primarily supplies atrium (esp. SA & AV nodes) as well as the ventricles (sparsely innervated)– Sympathetic innervation supplies the atria and ventriclesControl of heart rate:• Antagonistic autonomic