Week 2 Flashcards
- List the general processes that use ATP in the working heart.
Cellular processes (25%) and cross-bridging to produce contractions (75%, 50% of which is due to isovolumetric contraction)
- State the phase of the cardiac cycle in which the most energy is expended, and which cardiac variable the amount of that energy use is most dependent upon.
Most energy is spent in the isovolumetric phase of contraction, cardiac afterload being a major determinant of myocardial oxygen consumption
- Explain what feature of the ventricular pressure-volume loop represents “stroke work,” list the two general ways that stroke work can be increased, and note which of those two mechanisms are more costly in terms of myocardial oxygen consumption.
Stroke work is equal to the area enclosed by the left ventricle pressure- volume loop. Stroke work is increased wither by an increase in stroke volume or by an increase in afterload, an increase in afterload being the most costly parameter to change
- Describe the effects of increasing heart rate and increasing myocardial contractility on the oxygen requirements of the heart, and explain which of these changes is the most efficient way to increase cardiac output.
Increasing heart rate and myocardial contractility increase the oxygen requirements of the heart. The most efficient way to increase cardiac output is with a low heart rate and high stroke volume.
- List three noninvasive techniques that are used to evaluate electrical function, valve function, and mechanical pumping action of the heart.
Electrocardiographic record, auscultation of the chest, echocardiography
- Draw a stereotypical electrocardiogram trace showing one beat of the heart, label the three major wave features, and explain what electrical events are indicated by those waves and the intervals/segments that interconnect them.
P wave is depolarization of the atria, the QRS complex is ventricular depolarization and T wave the ventricular repolarization; PR segment/ interval indicates the time takes for an action potential to spread through the atria and the AV node; ST segment follows the QRS complex is a phase of no rapid changes in membrane potential; the QT interval roughly approximates the duration of the ventricular myocyte depolarization and thus the period of ventricular systole
- Explain the electrical conventions that create Lead’s I, II, and III of Einthoven’s triangle, specifying which end of each lead is negative (reference electrode) and which end is positive (recording electrode) for each lead.
Lead II between right arm (-) and left leg(+); Lead I between right arm (-) and left arm (+); lead III between left arm (-) and left leg (+). When a lead registers, if charge is flowing from (-) to (+) then the lead read up will deflect upward, whereas the converse is also true
- Explain how a moving wave of depolarization can be represented by a net electrical dipole that can be detected by electrodes on the surface of the body, and list the two factors that determine the magnitude of the dipole.
A net electrical dipole describes the net direction of the charge separation on the AP wavefront, each dipole being oriented in the direction the local wave is traveling. Extracellular fluid conducts these net dipoles to be detected on the surface of the skin. The magnitude of the dipole is determined by how many cells are depolarizing at the same time as well as the consistency of the orientation between individual dipoles.
- Demonstrate how a net dipole simultaneously is recorded as electrical voltage in different ECG Leads, using an example where one lead shows a negative voltage difference and the other two leads show a positive voltage difference. Explain how the voltage in a given lead is affected when the dipole is oriented perpendicular or parallel to that lead.
the more parallel the dipole is to the lead poles, the greater the magnitude of the voltage on the trace, if the dipole is in the same orientation as – to + then it will appear positive voltage.
- Describe the nature of the cardiac dipole while an action potential is traveling through the AV node, and how that event appears on the ECG.
The P wave terminates when the depolarization reaches the non-muscular border between the atria and the ventricles and the number of individual dipoles becomes very small. The number of cells in the AV node is so small that it does not register on the EKG
- Draw a figure showing how the net cardiac dipole changes during the spread of depolarization through the ventricle, and show how that spread would appear when viewed by Leads I, II, and III.
just do it.
- List the components of an idealized ECG recording that are typically isoelectric.
PR and ST intervals are typically isoelectric, the PR being when depolarization is traveling through the AV node and the ST interval when all the ventricular cells are in their plateau
- Explain why the T-wave is typically broader than, and in the same direction as, the R wave in a Lead II recording.
Typically the ventricular depolarization occurs in a less unified way where the dipoles created are not in a similar direction. It is in the same direction because the cells that depolarized first are the first to repolarize and therefore demonstrate a repolarization in the opposite direction (opposite direction and opposite charge mean same dipole) and same positive deflection
- From a sample recording of a QRS complex, be able to determine the mean electrical axis of ventricular depolarization by the method you learn in our ECG workshop.
Mean electrical axis: the orientation of the cardiac dipole during the most intense phase of ventricular depolarization, used to determine whether the ventricular depolarization is proceeding over normal pathways
- Draw a figure that shows the convention by which the angle (in degrees) of electrical axis is reported, and define left axis deviation and right axis deviation. (Note: use the ranges taught in the workshop rather than in the textbook).
The downward direction is designated 90+, and anywhere in the patients left hand quadrant is considered normal
- Describe how the augmented unipolar limb leads (aVR, aVL, and aVF) are measured, and state their orientation (in degrees) on the standard axes.
Between right arm and aVR, left arm and aVL and left leg and aVF, these leads describe additional “perspectives” defined by drawing a line from the center to vertices of Einthoven’s triangle with (-) in the center and (+) at the vertices the leads together can be considered a hexaxial reference system for observing the cardiac vectors in the frontal
- Describe how the precordial limb leads (V1-V6) are measured, and describe the electrical orientation (“view”) of each of those leads.
12 unipolar leads that look at the electrical system in the transverse plane, the indifferent leads are formed by electrically connecting the limb electrodes, the electrical orientation the this view is of the transverse plane with the first 6 leads forming a central point of reference
- List the criteria that are used to define an ECG trace as being a normal sinus rhythm with respect to the following variable: Frequency, QRS duration, PR interval duration, QT interval duration and P-wave occurrence.
Frequency of QRS complex is 1/s, the shape of the QRS is normal for lead II and duration is less than 120 milliseconds, each QRS complex is preceded by a P wave of proper configuration , indicating SA node origin of excitation, PR interval Is less than 200 milliseconds, indicating proper delay through AV node, the QT interval is less than half the P-T interval, indicating normal ventricular repolarization and there are no extra P waves, indicating that no AV nodal conduction block is present; deviation of ST segment from isopotential baseline is indicative of cardiac ischemia
- Define tachycardia and bradycardia.
Tachycardia, excessively fast HR limiting the time for cardiac filling between beats and bradycardia, excessively slow HR, which is inadequate to support sufficient cardiac output or decreases the coordination of myocyte contraction, which will reduce stroke volume
Normal sinus rhythm
typical EKG discussed earlier
Supraventricular tachycardia
occurs when the atria are abnormally excited and drive the ventricles at a very fast pace
First degree heart block
the only electrical abnormality is unusually slow conduction through the AV node
Second-degree heart block
some but not all atrial impulses are transmitted through the AV node to the ventricle, impulses are blocked in the AV node if the cells of the region are still in a refractory period form a previous excitation
Third degree block
no impulses are transmitted through the AV node, atrial and ventricular rate are completely independent, and ventricle output can be slowed significantly
Atrial fibrillation
complete loss of normally close synchrony of the excitation and resting phases between individual atrial cells, cells in different areas of the atria depolarize, repolarize and are excited again randomly ** no P wave is present, can lead to blood clots
Right and Left bundle branch blocks
leads to reentrant conduction pathway, less synchronous ventricle depolarization and wider QRS complex
Premature ventricular contraction
ectopic focus starts an independent ventricular contraction, often followed by a compensatory beat which can affect the filling volume of the ventricles
Ventricular tachycardia
ventricles are beating at a high rate, often by an ectopic center (very serious condition, can lead to inefficient filling of ventricles)
Long QT syndrome with torsades des pointes
a result of delayed ventricular myocyte repolarization which maybe due to inappropriate opening of sodium channels or prolonged closure of K channels during the AP plateau phase, when QT interval is greater than 50% of cycle length which can occur with ventricular electrical complexes cyclically varying in amplitude around the baseline and can deteriorate rapidly into ventricular fibrillation
Ventricular fibrillation
various areas of the ventricle are excited and contract asynchronoysly
- Write the Fick equation and, given appropriate data, use it to calculate cardiac output.
tissue substance rate/ substance consumed = flow; requires invase methods to obtain measurements (venous blood requires mixing by heart to get adequate measurement
- Describe the echocardiography imaging technique, and explain how it can be used to determine the ejection fraction.
Eco uses sound waves which come in contact with substances of varying densities and the reflection of the waves off those substances are reflected back to a computer and interpreted by that computer to make an image of the heart and its vessels. Eco can be used to find the end diastolic volume, which is used to calculate ejection fraction (EF = SV/EDV)
- Write the equation for ejection fraction, and state the range and mean value observed in people with normal cardiac contractility.
EF= SV/ EDV, range 55-87% with the mean at 67%; ejection fraction is useful in estimating contractility
- Describe how the end-systolic pressure-volume relationship can be used to determine myocardial contractility.
use one of the imaging techniques to measure ESV (measured based on the insicura or rebound on the aortic valve) and measure ESP via the arterial pressure next to the aortic valve - that gives you a data point. you can draw a line from point to origin and the slope of that will give you contractility. Higher contractility = a leftward shift of the curve (like the hand on a clock going in reverse), lower c = rightward shift
- Draw pressure volume loops comparing the function of a normal heart, a failing heart with depressed contractility (untreated), and the failing heart after a treatment that reduces arterial blood pressure.
in an untreated heart, there is reduced contractility and less ability to fight the atrial pressure so that leads to reduces EF and SV(taller/skinnier curve), if you treat by decreasing arterial pressure, you will increase the pumping abilities of the heart and increase EF and SV
- With regard to valve function, define “stenosis” and “insufficiency,” and explain how the different effect these two abnormalities have on ventricular chamber remodeling.
Stenosis is narrowing (or does not open fully) of the valves and since this narrowing leads to extra force required to move fluid through the valve, it can lead to ventricular hypertrophy insufficiency relates to valves that do not close completely and leads to regurgitation of the valves, leading to a greater volume load on the ventricle. Stenoic SL valves cause increased thickness of walls of the upstream chamber; insufficient valves tend to cause an increase in “volume work” and dilation of chambers
Aortic stenosis
a much greater pressure is required by the ventricular contraction to overcome the extra obstruction of the stenoic valve and would lead to a whistling sound between the lub and the dup (systolic murmur)
Mitral stenosis
a much greater left atrial pressure (leading to pulmonary edema and SOB) leading to a whistling between the dup and the lub (diastolic murmur)
Aortic insufficiency (aka regurgitation, incompetence)
aortic pressure falls much faster and farther than normal so it is normally low and EDV and pressure are also elevated, leads to a gurgling diastolic murmur
Mitral insufficiency (aka regurgitation, incompetence)
causes an increase in left atrial pressure as excess fluid re-enters the atria from the ventricle and results in a gurgling systolic murmur (common to hear both an insufficiency and stenosis)