Basic Cardiac physiology Flashcards
So, how do BB decrease aldosterone?
Beta 1 agonism within the macula densa leads to renin production, which leads to angiotensin, then angiotensin II formation, and finally aldosterone release. BBs decrease the production of renin and therefore aldosterone release.
PS and Symp innervation to the heart:
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 decreased chronotropy (heart rate) and dromotropy (conduction speed). Its effects on decreasing inotropy are relatively small and it can mildly decrease lusitropy as well (relaxation).
Sympathetic stimulation arises from T2, 3, & 4, and is carried to 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.
When is S3 heard, and what should you think of if you hear it?
A: 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). Can think of S3 as heart failure
Explain how: A. The S2 heart sound is split to a greater extent B. Arterial blood pressure decreases C. Left ventricular afterload increases D. Right ventricular preload increases During inspiration
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).
Guideline indications for a stress test:
outlined indications for a non-invasive stress test. The indications are in general: the patient will be having an intermediate or high risk elective surgery, they have a functional status that is poor (<4 METS) or is unknown, the patient would agree to angiography and possibly even revascularization if the stress test were positive, and finally if the patient and members of the perioperative care team agreed that it would change the patient’s overall care and outcome.
S1 heart sound:
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.
S2heart sound:
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 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. Normally S2 will be heard just after the T wave, and during or just before the ‘v’ wave on cvp.
S3 heart sound
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 heart sound
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.
MV Sat vs SCVO2 sat:
MV sat-technically plum artery sat, will be lower than SCVO2 Superior vena cava sat because the SVC has not yet mixed with the coronary sinus (which is about 30-40% compared to the 75%).
You’ve got a patient with ST depressions on LCX area, they have left circumflex coronary artery stenosis. What could you do?
Coronary perfusion is a complex subject, but to simplify it can be thought of in terms of 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. When myocardial oxygen consumption outpaces delivery one can either:
Increase aortic diastolic pressure that will increase coronary perfusion pressure. Potential downside: 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. Also increased afterload means increased LV wall tension, which means more O2 consumption.
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). Downside: if associated with too great a reduction of LVED blood volume (and therefore pressure) it can also decrease cardiac output (by decreasing preload).
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.
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!)
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 (you need to know this term) and it is a real thing…on the boards. In reality, in most cases there is plenty of pressure and blood for everyone (all coronary distributions), but this is the boards and that is why this choice would be the second best and not the best answer to the ambiguous question.
ATP binding to myosin results in:
Release of myosin from actin.
Amiodarone-what type of anti arrhythmic, and then how does it work? Amiodarone and half life and what happens after single bolus? Key side effects of amiodarone?
It is a class III antiarrhythmic agent which means it is classified as a potassium-blocking agent which therefore would delay phase 3 repolarization of the cardiac action potential. Altogether, it slows conduction, acts as an AV nodal blocker (like a beta-blocker), and is generally effective for both atrial and ventricular arrhythmias. For atrial fibrillation is it is often used for “chemical” cardioversion and should be used with caution if you think your patient with a-fib might have an atrial clot. In general, bolusing amiodarone has less depressant effects on blood pressure than beta-blockers or calcium channel blockers.
Amiodarone has a long half-life and is very fat soluble, giving it a high volume of distribution. Loading doses require up to 10 g over the course of days, especially when given oral. You’ll be using it IV, and realize that a single bolus of amiodarone will redistribute and be ineffective after a couple hours, and a drip needs to be started afterwards in most cases.
Amiodarone is most known for its side effects. The major ones you need to know for not only the written boards but also the orals are pulmonary fibrosis, leading to significant restrictive lung disease and decreased gas exchange (decreased DLCO on PFTs). Amiodarone also can lead to hypothyroidism as well as (less often) hyperthyroidism. It can lead to a transaminitis and jaundice, and if not discontinued can lead to cirrhosis. Also chronic use can lead to peripheral neuropathies.
Do you remember the equation to SVR….because you need to know it:
SVR = [(MAP-CVP)/CO] X 80.
Which vessels contribute to SVR?
The arterioles, AKA precapillary resistance vessels, contribute about 60% of SVR and have distal sphincters that can regulate blood flow into the capillaries. The Windkessel vessels are the aorta and other large arteries.
