Cardiac Physiology Flashcards
Parasympathetic fibers to the heart arise from the… and … and are carried by …
Parasympathetic fibers to the heart arise from the dorsal vagal nucleus and nucleus ambiguous and are carried by the vagus nerve.
This gives rise to two plexuses: dorsal and ventral cardiopulmonary plexuses, which are located between the aortic arch and tracheal bifurcation. From there the cardiac nerves carry the signal to the heart itself.
Muscarinic acetylcholine receptors are found in the greatest concentration at the SA node, followed by the AV node, followed by the various heart chambers.
Parasympathetic stimulations result in … chronotropy (heart rate) and dromotropy (conduction speed).
Decreases both.
Its effects on decreasing inotropy are relatively small and it can mildly decrease lusitropy as well (relaxation).
Sympathetic stimulation to heart arises from … and is carried to …
T2, 3, & 4,
the stellate ganglion first and then down to the heart as the cardiac nerves which often join together and course with the left main coronary artery.
Sympathetic stimulation increases chronotropy, dromotropy, inotropy, and lusitropy.
S3 heart sounds indicates ?
Has a strong association with Major Adverse Cardiac Event (MACE)
S3 is an abnormal heart sound occurring in early diastole and often explained as the atrial blood reverberating against poorly functioning ventricular walls that relax slowly, leading to a knocking sound just after S2. Another way to think of S3 is diastolic flow that is poorly compensated for (noncompliant ventricle or increased atrial blood with MR). Both of these are gross oversimplifications, but you don’t need to develop a complete differential diagnosis for abnormal heart sounds for the boards, what you need is realize what it means. When the stem mentions an S3, think heart failure (in most cases) and realize that it occurs during diastole. Preoperative evaluation will likely be a big subject on the basic exam, and heart sounds and murmurs have always been fair game.
Would you offer perioperative echo if you hear S3 heart sound?
According to guidelines, a patient with heart failure would qualify for a preop echo if they have worsening clinical status or other signs (such as NEW onset S3, etc).
A lower degree of recommendation is made for patients with stable heart failure that have not had an LV evaluation of some sort over the last year (basically if you want to get one its ok, but you do not have to get one routinely).
What effect on below with spontaneous inspiration:
Preload Afterload Blood pressure S2 heart sound HR
During (spontaneous) inspiration, intrathoracic and plueral pressures are negative leading to increased venous return and therefore more blood volume to right ventricle, hence increasing RV preload.
At the same time pulmonary venous capacitance increases with spontaneous inspiration, and LV preload is decreased. Furthermore, since the LV has to overcome negative intrathoracic pressures to contract, afterload is actually increased (very slightly in normal cases).
The result of the decrease in LV preload and increase in LV afterload is a slight decrease in BP (about 6 mm Hg).
As discussed below, with increased RV volumes, the pulmonic valve closes later than the aortic valve, causing a split S2 (physiologically split).
The slight increase in heart rate seen with inspiration is due to inhibition of vagal tone (respiratory sinus arrhythmia).
When is non-invasive stress test indicated perioperative
1) the patient will be having an intermediate or high risk elective surgery.
2) they have a functional status that is poor (<4 METS) or is unknown,
3) the patient would agree to angiography and possibly even revascularization if the stress test were positive,
4) and finally if the patient and members of the perioperative care team agreed that it would change the patient’s overall care and outcome.
A lot of loosey-goosey rubbish, really, but those are the guidelines, which become increasingly more amorphous each year. At the same time the guidelines state that even if you have CAD, routine coronary revascularization for the sole purpose of reducing perioperative cardiac events is NOT recommended. So why get the bloody stress test in the first place! Basically, the primary indications for revascularization (either by angioplasty, stents, or CABG) are medical (“that bothersome, annoying chest pain that just seems to come every time I walk”). The European Guidelines are a little more clear and concise, but are essentially identical.
ST depressions are seen in ECG leads I, aVL, V5, and V6 at very high heart rates. Which of the following coronary arteries would most likely be affected by stenosis
LCx will affect the lateral left ventricle and ischaemia will be seen in the V5 and V6 leads because they are the most lateral.
Look at Einthoven’s triangle and note that aVL would be perpendicular to the left lateral wall and therefore also be a sensitive lead to pick up ischaemia.
Lead I can classically help identify lateral LV ischaemia as well
ST depressions are seen in ECG leads V1-6.Which of the following coronary arteries would most likely be affected by stenosis
LAD disease can manifest with septal and or anterior LV ischaemia. Therefore leads V1-4 are classically always involved and V5-6 often as well.
Left main disease would involve the territory of the LAD and LCx.
ST depressions are seen in ECG leas II, III, aVF, Which of the following coronary arteries would most likely be affected by stenosis
Right coronary disease classically presents as inferior MI involving II, III, aVF.
S1 heart sounds occur … p wave and … c wave
After p wave
Before c wave
The S1 heart sound occurs at the beginning of systole when ventricular pressure is greater than atrial pressure and the mitral and tricuspid valves close.
This occurs just before the c wave on the cvp waveform and just after the QRS complex on ECG.
S2 heart sound occur … T wave and …. v wave on CVP.
After T wave
Before v wave
Normally S2 will be heard just after the T wave, and during or just before the ‘v’ wave on cvp.
The S2 heart sound occurs at the end of systole when the ventricles have begun isovolumetric relaxation and aortic pressure is greater than ventricular pressure thus snapping the aortic valve closed (or when pulmonary artery pressure is greater than RV pressure for the pulmonic valve).
S2 splitting caused commonly by …
S2 is broke into two components: A2 and P2 for the aortic and pulmonic valve, respectively. A2 normally closes before P2, and this splitting is greater with inspiration (due to increased preload in the RV and decreased preload in the LV).
Pathological splitting has many causes, but on the boards this will most likely be due to increased RV volume such as a left to right ASD or pulmonary stenosis. I can’t imagine they would expect you to know about less classic etiologies such as bundle branch bocks and widened S2’s, much less the rare etiologies.
S3 commonly caused by
The S3 heart sound is classically indicative of heart failure with a noncompliant heart that cannot relax quick enough for the degree of filling and in some cases a distinct heart sound can be heard. This will also occur with some valvular diseases
S4 commonly caused by
The S4 heart sound is due to atrial contraction ejecting blood into a noncompliant ventricle and is also called a gallop. It is associated with LV concentric hypertrophy such as seen in chronic hypertension and aortic stenosis. Since it is due to atrial contraction it has to occur just after the p wave and obviously during the ‘a’ wave on cvp.
Why does mixed venous oxygen saturation of haemoglobin (MVsat) tend to be lower than superior vena cava Hb saturation (ScvO2):
Right atrial mixing with blood from the coronary sinus
Unlike other tissues, the heart is always living on the edge of disaster because it nearly maximally extracts as much oxygen from Hb as possible. Under most circumstances the coronary sinus Hb sat is about 30-40%. Therefore the blood from the superior vena cava with HB sats around, lets say 75% mix with inferior vena cava HB sats which are usually not much different than the superior vena cava (typically a bit higher actually) and mix with blood from the coronary sinus. This means that when you sample blood from the SVC it will be higher than the downstream blood in the pulmonary artery that has mixed with the coronary sinus. Normally MVsat is about 2-5 points lower than ScvO2 on exams.
As an aside, the terminology can be confusing, the MVsat is more often referred to as an SvO2, which is confusing when your trying to learn because ScvO2 is replacing this measurement in clinical practice as the use of PA catheters have declined. With rare exception, the ScvO2 and MVsat will correlate with each other nicely. As a second aside, you will come across sources that seem to say that MVsat is higher than ScvO2, and while this can be true in some cases, I think the safest bet is to assume that MVsat will be lower than ScvO2. In periods of extreme myocardial stress coronary sinus saturation can fall to 10%, which increases the difference between ScvO2 and MVsat.
Coronary blood flow best described by which physics law?
Ohm’s law where flow is dependent on the ratio of perfusion pressure to resistance
Perfusion pressure for the left ventricle (LV) is defined as aortic diastolic pressure minus LV end diastolic pressure (LVEDP) and only occurs during diastole. Resistance can be manipulated by coronary dilation. Coronary dilation occurs when the myocardium is not receiving enough oxygen, often from inadequate flow.
What’s the potential downside from increasing aortic diastolic pressure to increase coronary blood flow?
Increase aortic diastolic pressure that will increase coronary perfusion pressure.
Potential downside:
1) it will increase LV afterload and (depending on degree of increase in BP and the patient’s LV function) can decrease cardiac output and therefore coronary flow.
2) Also increased afterload means increased LV wall tension, which means more O2 consumption.
4 way to increase coronary blood flow by …
When myocardial oxygen consumption outpaces delivery one can either:
1) Increase aortic diastolic pressure that will increase coronary perfusion pressure.
2) Decrease LVEDP, which will result in a greater proportion of time that aortic diastolic blood pressure is greater than LVEDP and therefore have perfusion (depending on coronary resistance).
3) Slowing heart rate, which will increase the time in diastole and lead to more time for perfusion. Also myocardial oxygen consumption will decrease (O2 consumption will fall greater by decreasing HR than decreasing afterload or contractility).
3) Decreasing contractility, which will decrease LV wall tension and therefore myocardial oxygen consumption.
4) Dilating coronary arteries can shift blood away from stenotic coronary distributions (LCx in this case) that are absolutely dependent on high perfusion pressures to overcome the resistance to normal areas. This is called coronary steal.
What’s the downside of decreasing LVEDP to improve coronary perfusion?
Decreasing LVEDV which will result in a greater proportion of time that aortic diastolic blood pressure is greater than LVEDP and therefore have perfusion (depending on coronary resistance)
Downside: if associated with too great a reduction of LVED blood volume (and therefore pressure) it can also decrease cardiac output (by decreasing preload).
What’s the downside of decreasing HR to improve coronary perfusion?
Slowing heart rate, which will increase the time in diastole and lead to more time for perfusion. Also myocardial oxygen consumption will decrease (O2 consumption will fall greater by decreasing HR than decreasing afterload or contractility).
Downside: hardly any assuming the HR is not so low cardiac output falls too far.
What’s the downside decreasing Contractility to improve coronary perfusion?
Decreasing contractility, which will decrease LV wall tension and therefore myocardial oxygen consumption.
Downside: can decrease cardiac output especially at its extremes. (Notice that beta blockers do a nice job of decreasing heart rate and LV wall tension!)
