Basic Cardiac physiology Flashcards
(34 cards)
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.
Other things that Beta Bkockers do:
BBs have antinociceptive properties and can be used to reduce opioid doses, especially for outpatient surgery (typically high dose esmolol gtts). It is questionable whether BBs have anxiolytic properties, but they do effectively treat many of the manifestations of anxiety (shaking, sweating, etc).
BBs can decrease glycogenolysis and glucagon secretion and can lower glucose levels (although the greater risk of BBs are masking the symptoms of hypoglycaemia, not directly affecting the glucose levels). BBs can be used to treat glaucoma because they decrease aqueous humor secretion from the ciliary epithelium (beta 2 agonism increases production of aqueous humor). 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.
Other board-worthy properties of BBs are decreasing peripheral conversion on T4 to T3 as well as blunt the physiological effects of hyperthyroidism. BB overdose with resultant bradycardia can be treated with glucagon by increasing cAMP and therefore protein kinase A.
Phenylephrine, nitroglycerin, nitro prissier, aortic stenosis and what they all do to preload
Phenylephrine and aortic stenosis represent states of increased afterload. With increased afterload there is typically a compensatory increase in preload in normal individuals as measured in both volume and pressure. In the case of aortic stenosis compensatory left ventricular hypertrophy leads to decreased ventricular compliance and LVEDP increases out of proportion to the increases in LVEDV. With phenylephrine, not only will there be a compensatory increase in preload in normal individuals, but decreased HR will also facilitate this process (of increasing stroke volume).
Nitroglycerin will increase venous capacitance and decrease preload. Nitroprusside, in addition to its effects on venodilation, will also decrease afterload, leading to reductions in LVEDV.
SV and CI-which HR will give you max CI? Which HR will give you max stroke volume?
In otherwise healthy adults, cardiac index (CI) increases up to a HR of about 120 and then falls precipitously afterwards. For children CI is maximal at far higher heart rates (~150 for toddlers and even higher for infants). Remember as HR increases, stroke volume decreases, and around a rate above 120 the decreases in stroke volume outweigh the increases in HR. A nice number to remember for a resting cardiac index is about 3.5 l/min/m2. At a rate of 120 this value raises to about 5.5 (lots of variation depending on reference source). At rates below 40, CI starts to drop precipitously as increases in stroke volume have a limit. If this question asked at which HR would stroke volume be the greatest, the answer of the above choices would have been 60 beats/min.
Decreased contractility and how the body compensates
Let’s return to contractility. Decreasing contractility leads to decreased stroke volume or compensation of maintaining stroke volume by increasing preload. Increasing afterload would worsen stroke volume. Decreasing afterload will improve stroke volume and is one of the few things you can do outside of inotropic support for a low contractile state (that’s why severe heart failure patients are on afterload reducers). Decreasing intracellular calcium will decrease contractility because troponin will block the actin-myosin binding site more often.
High, Med, and low organ systems and the CO they receive
High: Liver (19%), Muscle (19%), Heart & Lungs (19%), Kidneys (16%)
Medium: Brain (10%), Intestines (6%)
Low: Skin, other organs
Bezold-Jarisch reflex. What is it, and in which two situations would you see it?
Bezold-Jarisch reflex is long standing. It just so happens that in the left ventricle (LV) there are receptors (mechano- and chemo-) that will fire in the setting of very low pressures. The only problem is that they are wired to vagal afferents that lead to bradycardia and hypotension, but also leads to coronary vasodilation (which perhaps is the reason it exists). This highly tested reflex rears its head in two situations on the boards. First, a hypovolaemic patient has a sudden further decrease in preload (as the stem above) or spinal anesthesia. The second scenario that may appear on the boards is following a myocardial infarction or coronary reperfusion. There are other causes, but these are the two you should know.
Brainbridge reflex
The Brainbridge atrial reflex is paradoxical tachycardia in response to fluid bolus. Takes place in atria.
Vasovagal reflex:
The Vasovagal reflex is very commonly seen in people and has a million causes. The two that you will see is stimulus from mesenteric retraction or distention leading to a vagal afferents sending signal to the brainstem, and then the brainstem (nucleus tractus solitarii) sending out vagal efferents with resultant bradycardia, hypotension, and even apnea. The other stimulus you will see anxiety and noxious stimuli (especially regional anesthesia!) leading to a vasovagal episode. In many cases the reflex is strong enough to lead to syncope.
Baroreceptor reflex!!! Not to be confused with:
The baroreceptor reflex is described in detail elsewhere, but its worthy of another discussion here…you need to know this one backwards and forwards. Increased blood pressure will lead to increased firing of action potentials from the baroreceptors in the carotid sinus. It is board-worthy to remember afferent signal is carried by the Hering nerve (glossopharyngeal) to cardiovascular centers in the medulla. The net effect is inhibition of sympathetic activity and increased parasympathetic outflow, decreasing heart rate, contractility, and vascular tone. It is responsible for the second to second maintenance of blood pressure. Remember that anesthetics depress this reflex, depending on dose.
Don’t confuse it with:
Don’t confuse this with the very similar response chemoreceptors have in the carotid and aortic bodies. Chemoreceptors in the carotid body respond to low oxygen tension and acidaemia, and also have outflow through the Herring nerve. The big difference is that this response can increase ventilation and can have a secondary effect to increase blood pressure. These receptors are even more sensitive to anesthetics (especially volatiles).
