Res & cardiac physiology > M5 > Flashcards
M5 Flashcards
Muscles involved in expiration vs inspiration?
Internal intercostal, expiration
External intercostal, inspiration
Muscles involved in Inspiration
Diaphragm
Strap muscles
External intercostal
Back muscles, shoulder and pecs
Muscles involved in expiration
Internal intercostal
Abdominal muscle
But with normal expiration it’s passive
Airway resistance is primarily due to?
Conducting system 90%
Factors increases airway resistance
Turbulent flow > laminar High density gas Faster flow Increase gas viscosity Increasing length of airway
Smaller airway radius
When is the risk of barotrauma? (Which platueau pressure number)
> 30 cm H2O
Specifically when transpulmonary pressure (alveolar pressure - pleural pressure) is high
the plateau pressure in obese is high but their transpulmonary pressure is not high? why
because the pressure in alveolar are not high.
therefore, to measure accurate transpulmonary pressure, need esophageal pressure to subtracted from plural pressure.
plateau pressure?
pressure in alveolar
“plateau has e a u a which all trying to be alveolar”
Peak pressure?
pressure in airway
Static compliance?
= TV/(plateau - PEEP)
it is the pressure needed to keep the lung inflated at a given TV
Dynamic compliance?
= TV/(peak-PEEP)
it is the pressure needed to overcome the airway resistance
transpulmonary pressure?
= plateau - plural/esophageal pressure
it represents the actual pressure across the lungs
anatomical point of craina?
sternal angle
Airway resistance directly related to …. + …. +…. and inversely too …
Density, velocity, and diameter
Viscosity
Which lung volume or capacity would pleural pressure be most negative?
Most to let atmospheric air get in
TLC
When PaO2 drops, O2 sensing receptors in … + … and send signals back to …. to increase ventilation
As ventilation increases, the drop in PaCO2 will cause a movement of H in CSF out to plasma, … pH of CSF. This will stimulate medullary chemoreceptors to offset the increased ventilation
Carotid and aortic bodies
Brain stem
Increased
Maximal benefit is stopping smoking before surgery is
8 weeks
If stoped the day of surgery, sputum and secretions increases
Ciliary function returns after 2-4 weeks of stopping
Causes that decreases EtCO2 and increases PaCO2?
Which means increase in dead space.
Decreased CO
PE
Asthma
COPd
Calculate the dead space %
(PaCO2 - ETCO2)/PaCO2
The binding of ATP to myosin result into ?
Release of myosin from actin
AP > influx of Ca > binding to ryanodine rec > release of Ca intracellular from SE > binds to troponin
Now the myosin-ADP can bing to actin > Myosin let’s ADP go free and produce “power stroke” > contraction
ATP has to come and bind myosin to let go of actin.
Cycle continue if Ca continues to bind to troponin
MoA of Amiodarone?
AV nodal blocker (like B blocker) and effective for both atrial + ventricular arrhythmias.
Long 1/2 t because of very fat soluble and high volume of distribution (single bolus will be ineffective after hours and needs gtt).
Which law implies on wall tension on ventricular as well as alveoli?
LaPlace’s law
T= PR/2h
Tension
Pressure
Radius
H: wall thickness
The law implies on laminar fluid flow through a tube ?
Poiseuille’s law
Q= (PR) / (nL)
Pressure + radius is directly related
Viscosity (n) + length (L) inversely
The primary contributor to vascular resistance is …
Arterioles (precapillary resistance vessels)
SVR =
[(MAP-CVP) / CO] x 80
Antidote of Beta blocker overdose? And it’s MoA?
Glucagon (increases cAMP and therefore protein kinase A
At which HR the CI would be maximized and at what HR the SV would be greatest?
HR of 120 would have the maximum CI ~ 5.5 L/min/m2 (CI= CO/BSA)
Where the stroke volume would be the greatest at HR of 60 (CO = SV x HR)
Organs that receive most of CO?
Liver, heart, lung, and muscles (19% each)
Kidney (16%)
Medium are brain and GI ~10% each
Lowest are skin and everything els.
Von Bezold-Jarisch reflex (Jarishch-Bezold reflex) is
Is a reflex fired from ventricular I’m setting of very low pressure and causes the BRADYcardia and further hypotension but also leads to coronary vasodilation (which might be the reason why it’s exist)
Brainbridge atrial reflex is
+ SA from atrial stretch and causes tachycardia after a bolus of IVF or acute hypervolemia
Phenylephrine leads to activation of … within vascular SM
Alpha 1 -> PLC -> IP3 -> Ca release from SR ->increased contraction
Beta 2 receptors stimulation of which molculular level and how about alpha 1
Beta 2 -> cAMP -> uptake of Ca back into SR -> decrease contraction
Alpha 1 -> PLC -> IP3 -> Ca release -> increases contraction
NO -> cGMP -> decrease contraction
Pulmonary artery pressure =
Flow x PVR
So increase flow will increase PA if PVR stays the same
When can elective case go the earliest timing after a patient have DES ??
Either 12 months or after a year
If the stent placed for asymptomatic CAD (found on stress test) then 12 months
If Stent places after UA or MI then after a year.
Venous system that bypass the right heart and empty directly to left atrium are ….? And counted as shunt.
Thebesian, bronchiolar, and pleural veins.
(Contribute less 5% of CO and it’s one of the reasons that there always be A-a gradient).
Calculation of V/Q ratio (VQI)
(1-SaO2)/(1-SmvO2)
SaO2 arterial sat
SmvO2 venous sat
At what % of shunt that the increasing FiO2 will have no effect on increasing arterial pO2 ?
If the shunt is 40% and more.
DLCO tests ….
Measures of how well gas exchange btw the alveolar and capillary blood.
Any disease that effect the alveolar will decrease DLCO, so all the restrictive disease and pulse COPD. (Asthma: normal or increase)
What factors causes non-cardiogenic acute pulmonary vasoconstriction
Non-cardiogenic causes of acute pulmonary hypertension include hypoxia, hypercarbia, acidosis, and the autonomic system. Of these, hypoxia is the most important, and in fact, it is hypoxic pulmonary vasoconstriction (HPV) that limits shunt fraction. That is to say, for poorly oxygenated alveoli, HPV will decrease blood flow to those regions. Hypercarbia and acidosis are less powerful pulmonary vasoconstrictors, but can still lead to pulmonary hypertension.
It’s important to note that the opposite is opposite in the systemic vascular beds where hypoxia, acidosis, and hypercarbia would be expected to vasodilate.
What can inhibits HPV?
Nitrous oxide and high doses of other volatile agents (2 MAC sevoflurane) can have clinically appreciable inhibition of HPV. Other vasodilators such as nitrates and inhaled nitric oxide also can significantly interfere with HPV.
Would increasing CO widens or tights A-a gradient?
There are two reasons that increasing cardiac output may decrease the A-a gradient: First, as cardiac output rises, mixed venous PO2 (MVO2) also rises (because more oxygen is delivered to tissues yet the tissues are consuming the same amount; hence more oxygen is ‘left over’, returning to the heart). By increasing MVO2, additional oxygen uptake by the lungs will increase the PaO2 more than if the MVO2 were lower in situations where blood leaving the lungs (post capillary) is not completely saturated (low PaO2). Secondly, as cardiac output increases intrapulmonary shunting also tends to decrease*. These two things combined lead to a tightening, or reduction, of the A-a gradient. Do not get caught up in the fact that it would take a boat load of dobutamine to increase the CO by 50% or how you (in clinical practice) rarely see even the slightest difference in oxygenation with dobutamine drips…this is the boards….figure out what they are asking and answer the question.
*Although there are plenty of data to say the exact opposite -that increased CO will worsen intrapulmonary shunting and even data to say that increasing the mixed venous sat will worsen shunt! That being said, I believe that the classic teaching of A-a gradients tightening with increased CO would be the correct answer.
Why never give a CO2 retainer (severe COPD) too much oxygen since they are completely dependent on hypoxic drive?
The thought was that chronically elevated CO2 has rendered the patient unable to respond to further increases in hypercarbia, and therefore since saturations will fall quickly on room air with apnea, it is the peripheral oxygen chemoreceptors in the carotid and aortic bodies solely responsible for the respiratory drive. Oxygen supplementation will interrupt the drive to breath, leading to CO2 narcosis and respiratory failure. If true at all, this is only a small component of commonly seen phenomenon. The more modern explanation is that high oxygen levels interrupt badly needed HPV in patients with significant V/Q mismatches. In this theory, previously unoxygenated alveoli are now barely oxygenated enough to interrupt HPV, but not enough to participate in meaningful gas exchange (CO2 release/ O2 uptake of the blood); leading to hypercarbia (worsening deadspace) and hypoxia (worsening V/Q mismatch). There is no evidence for pneumonia or CHF in this patient. ARDS from oxygen toxicity is a phenomenon which occurs in some patients (not all) due to high levels of oxygen free radicals. It is most likely to occur in patients ventilated with FiO2’s over 60% for long periods of time (> 24 hours at least).
How long do you wait to preform a second CEA in same patient?
Ok, this is a piece of academic dogma for which there appears not to be enough evidence to confirm or refute.
The classic teaching is that following CEA the patient’s carotid bodies are dysfunctional (denervated, etc). It is assumed that if they are to return to function, it could take up to a year. Therefore, the safest thing (as far as respiratory function – perhaps not neurologic outcome!) is to delay the second CEA up to a year. Increases in PaCO2 are in fact seen after CEA; however they are traditionally small (< 6 mm Hg) and loss of peripheral chemoreceptors are unlikely to result in large increases of CO2 retention.
How much % of shunt that is the minimum to be unresponsive to high FiO2?
Significant shunts (>25%) are poorly responsive to increased inspired oxygen and a shunt of 35% is almost completely unresponsive due to the large amount of deoxygenated venous admixture. Therefore if the shunt were as high as 50%, the patient would have dramatically low sats unresponsive to increased FiO2.
Why brain injury patients hyperventilate?
There are likely a variety of reasons that head injured patients may hyperventilate. The thought that it was a compensatory (protective) mechanism to decrease ICP (by decreasing blood flow to the brain secondary to hypocarbia) is probably not true. Intracerebral haemorrhage leading to blood exposure in the CSF is a likely culprit. H+ ions from blood disassociate in the CSF (from its conjugate base) and stimulate chemoreceptors on the anterolateral surface of medulla exposed to the 4th ventricle (see question 16), stimulating an increase in minute ventilation, thus lowering the paCO2. Since it is blood that is providing the acid load and not systemic hypercarbia, the patient continues to hyperventilate in the setting of hypocarbia. This may also help explain why hyperventilation is a more common finding during the first week and a poor prognostic finding. With a spontaneously breathing patient without weakness or other ventilatory impairments, increasing pressure support tends to increase tidal volume with a concurrent decrease in respiratory rate and more or less preserved minute volume. If the patient had been on a ventilatory rate with increased pressure support, then the increased tidal volumes would lead to increased minute volume in that case.
Epi dose to break bronchospasm?
The patient is having a profound bronchospasm and has absent breath sounds because there is no airflow. Therefore, breaking the asthma flare through inhaled medications would be impossible, leaving iv, im, and direct to the trachea as the available options. Of the listed options 20 mcg of epinephrine is likely to relieve the bronchospasm while having fewer unintended systemic effects as the 1 mg dose. Also note that the patient’s sats are still 100%, and if she was preoxygenated, it will likely not drop precipitously initially allowing for careful dose titration of epinephrine. Lidocaine can be used both iv and to the trachea, but will likely be less effective. Albuterol and volatile agents require air movement to be effective. Removing the stimulus (ETT) with extubation in this situation may help break the flare, but may be unwise even after easy intubations. Cisatricurium binds to nicotinic acetycholine receptors on the muscle junction, therefore will not affect smooth muscle (responsible for bronchoconstriction). Ketamine, a useful induction agent in asthma, is less effective as a rescue agent. Steroids and methylxanthines (theophyline, aminophyline) are ineffective in acute situations such as this.
High peak pressure differential
High peak pressures can result from problems within the circuit and ETT (kinking, clot), the lungs (endobronchial intubation, mucous plug, pneumothorax, bronchospasm, pleural disease, pulmonary oedema), or outside the lungs (obesity, patient bucking/ breathing, trendelenburg position).
What dose sever COPD translates to clinical use?
In GOLD criteria, COPD is categorized as mild, moderate, severe, and very severe. All COPD is categorized with a reduced FEV1/FVC ratio as the reduction in FEV1 is greater than FVC, which is essentially the definition of obstructive disease. In other words, with increased airway obstruction and resistance, the flow of air from the alveoli to the trachea takes longer. Therefore, when looking at the volume of air that can be forced out of the lungs in one second (FEV1), it will be a smaller and smaller volume as the disease progresses.
Very severe disease has either an FEV1 < 30% predicted or FEV1 < 50% predicted and right heart failure. Not part of the definition, but very predictive of severe disease, is a paCO2 > 45
Mgmt of small pneumothorax after interscalne block? Would u send home or put a CT?
Extrapolating from the American College of Chest Physicians guidelines for spontaneous small pneumothorax in a stable patient in the ED, a repeat CXR after 3-6 hours and discharge is appropriate. Large pneumothoraxes >50% of lung volume on CXR or CT should be treated with a chest tube. Answer C may also be reasonable, but is more conservative than the guidelines quoted above. Pneumothoracies can be graded by CXR or CT; although CT can define the actual volume better.
How to decrease work of breath due to breath stacking in COPDers?
note, that with breath stacking (auto-PEEP, increases intrinsic PEEP), the patients ability to decrease transpulmonary pressures is more difficult and represents an increased respiratory load (additional boards pearl). Think of it this way, if your iPEEP is +3 cm H20 and you generate a breath at -3 cm H20, you had to change your pleural (transpulmonary) pressure by -6. If you’re autoPEEPing at +8 cm H20, you now have to generate -11 cm H20 to take the same breath. This becomes an issue with both spontaneous and mechanical ventilation (triggering breaths). Therefore for patients triggering their own breaths (pressure support in the OR, all modern modes of ventilation in the ICU) the PEEP should be increased to meet the patient’s intrinsic PEEP. In the above example if the PEEP were placed at 8 cm H2O, then the patient would only have to generate -3 cm H2O to take a breath. This is, of course, called decreasing work of breathing, which is exactly what needs to be done for patients with a COPD exacerbation.
When to chose small Vt vs large with either low/high RR on ventilation? Vent setting for RLD vs OLD?
The best strategy for patients with noncompliant, restrictive lungs tends to be small tidal volumes to minimize plateau pressures and increased respiratory rate to maintain ventilation. Prolonged inspiratory times may be helpful with high resistance airways. Prolonged expiratory times is helpful for obstructive disease. PEEP is often needed for effective oxygenation in severe patients.
The acute decrease in ETCO2 implies a dead space lesion which could be due to PE/ VAE or hypotension from MI, how to differentiate between them?
VAE is characterized (at least on board questions) as an increase in ETN2 (end tidal nitrogen), which was not seen here. Furthermore since the patient was in the supine position (not reverse trendelenburg or sitting) VAE is even less likely. Regarding MI, the patient does not have pre-existing coronary artery disease (CAD) but has risk factors for PE (prior orthopaedic surgery, DVT, reversal of coumadin), making PE the most likely answer. PE large enough to drop BP to a significant degree probably indicates that a large portion of pulmonary blood flow has been occluded. This significantly increases pulmonary artery (PA) pressures leading to right heart failure. Acute right heart failure presents with hypotension, low cardiac output, high CVP, distended jugular veins, and right heart strain on ECG. Right heart strain on ECG appears as ischaemic changes in the anterior precordial leads, especially V1 and V2, such as T wave inversion or st segment depression. In fact, the most common ECG change seen with massive PE, other than tachycardia, is right heart strain. Right bundle branch block with V1-2 RR’ complexes are also a common finding with PE as well, from ischaemic changes to the strained heart. The classic finding of S1Q3T3 (answer A) is very specific for PE, but rarely seen.
Lateral decubitus in anesthesia vs no anesthetic affect on lung compliance and V/Q
The lateral decubitus patient when anesthetized, and especially muscle relaxed, has a decrease in FRC putting the nondependent lung in the more compliant area of the curve. Airflow will preferentially direct towards the area of greater compliance (since the pressure will rise slower for the given volume) whereas perfusion continues to be gravity dependent and is directed preferentially towards the dependent lung. Muscle relaxation allows abdominal contents to rise up in the thorax which will affect the dependent thorax more than the nondependent portion due to gravity. Positive pressure ventilation will favor areas of improved compliance as described above.
Which has the plateau phase of Action Potential, ventricular myocardial Potential or SA node ?
Myocardial action potentials include phases 0 -3. Phase 0 is the upstroke caused by activation of fast Na+ channels. Phase 1 is early rapid repolarization, characterized by fast Na+ channel inactivation and an increase in K+ permeability. Phase 2, or the plateau phase is caused by Ca2+ channels opening, prolonging the action potential. Phase 3, represents the closing of the Ca2+ channels and increased K+ permeability. SA nodal cells have a phase 0, followed by 3, then 4 (not present in ventricular cells) characterized by a slow leak of Ca2+and Na+ into the cell that sets of a subsequent action potential. SA nodal activation and impulse towards the AV node is responsible for the P wave.
Volatiles effect on automaticity of the SA node?
Volatile agents depress the SA node to a greater extent than the AV node. This is one of the explanations for the (relatively) increased occurrence of junctional rhythms under inhaled anesthesia. Opioids, especially potent opioids, increase AV nodal conduction times, but have a lesser effect on the SA node. Local anesthetics bind to fast Na+ channels (phase 0 of normal myocardial cells), and can depress the SA node at high concentrations (phase 4, as the Phase 0 in pacemaker cells are due to the “funny” current).
Volatiles depress ventricular Contractility through …
Volatile agents likely depress contractility by indirectly decreasing the release of calcium from the sarcoplasmic reticulum.
Right carotid massage or left sided that has more likely to slow AV node in SVT?
Cardiac autonomic innervation tends to have the SA node supplied from the right vagus and sympathetic chain, and the AV node from the left. Parasympathetic innervation comes by way of the vagus nerve, whereas sympathetic innervation arises from T1-4 and innervates the heart by way of stellate ganglion to cardiac nerves.
Also note that this means that during SVT treatment, right carotid massage is more likely to inhibit sinus discharge and left carotid massage slows the AV node.
SVR measurable factor?
Afterload is essentially the arterial impedance to ejection, which is a function of the vaso-elastic properties of the aorta, arteriolar tone, the density and viscosity of the blood, and returning pulse waves in the blood. SVR is only a measure of arteriolar tone. Because aortic elastic properties are fixed within a patient, and density and viscosity are dependent on haemoglobin levels; SVR is usually a surrogate for afterload clinically.
What’s the effect of Aortic Stenosis on preload?
Left ventricular end-diastolic volume (LVEDV) represents preload and is increased by increasing venous return, venous tone, intravascular volume, atrial contraction, and recumbent posture (compared to standing). Likewise, increased intrathoracic pressure and increased heart rates can decrease ventricular filling by decreasing venous return and decreasing filling time, respectively. Mitral stenosis represents an obstruction to blood leaving the atrium to the ventricle, causing high atrial volumes and pressures and an underfilled ventricle. Aortic stenosis represents a high afterload state, necessitating an increase in preload to maintain cardiac output (Starlings Law of the Heart, see above). Furthermore, concentric hypertrophy associated with aortic stenosis requires increased pressures for a given volume (less compliant, diastolic dysfunction).
Why wedge pressure gives only accurate LVEDP but not LVED volume?
Wedge pressure equals pulmonary venous pressure, which very nearly equals left atrial pressures, which very nearly equals left ventricular end diastolic pressure (LVEDP).
In normal hearts, wedge pressure is an accurate measure of LVEDP, but not necessarily volume because the pressure volume relationship is non-linear. That is to say that as volume increases, pressure may proportionately rise more (or less). There is normally no significant gradient between wedge and LVEDP. The PA catheter normally causes clinically insignificant tricuspid regurgitation, but does not transverse the mitral valve.
Acidemia will affect the most of cardiac Contractility or PVR?
Acidaemia will cause an increase in PVR, not a decrease. The right ventricle is comparatively more compliant than the left, and acidaemia would have less of an effect, if any. Preload would be less affected by the acidaemia itself, compared to contractility. Contractility is predictably depressed by acidaemia, anoxia, decreased sympathetic tone, and hypocalcaemia. An ABG can identify three of the aforementioned causes. Depending on what you read, contractility is not usually affected until the pH drops below 7.0-7.2. Overall, humans are designed to tolerate acidemic states surprisingly well.
ECG finding of PDA occlusion In leg dominance patients?
PDA supplies the inferior surface of the heart and can be evaluated by analysis of ECG leads II, III, and AVF.
ST elevations and Q waves would be characteristic of a 100% occlusion of the proximal PDA.
RCA occlusion can also presents this way, unless the PDA is derived from the left main coronary (left dominant circulation) as is this case.
Supply to mitral papillary muscle vs anterior papillary muscle?
The posterior mitral papillary muscle is typically solely supplied by the PDA; whereas the anterior papillary muscle has dual supply from left circumflex and LAD. This would present with flash pulmonary oedema, low cardiac output, and large bizarre V waves on wedged PA catheter tracing
The effect of aortic clamp on venous return is .,.
The cardiovascular response to aortic cross-clamp is a bit complex and essentially depends whether its above or below the splanchnic circulation.
In a supraceliac clamp of the aorta, blood ejected by the LV will be redistributed above the clamp (heart, lungs, brain). That means that the heart will have increased venous return, increased after load, and variable changes in cardiac output (usually decreased). Also there is a surge of catecholamine release which will affect venous capacitance. Since venous tone will increase with high catecholamine levels, there will be additional venous return.
With aortic cross-clamp both systolic and diastolic blood pressure will increase. Left end-diastolic ventricular pressures (LVEDPs) and wall motion abnormalities increase, and ejection fraction decreases. The reduction in EF is likely from reduced subendocardial perfusion exacerbated by a very elevated LVEDP (remember perfusion is Aortic diastolic pressure - LVEDP). So in this case the increase in preload (venous return) is exacerbating the reduction in CO. Its also worth saying that the reduction in CO is far less predictable than the increase in venous return.
If the clamp is placed below the splanchnic circulation things get more complex. Now blood ejected by the LV will also be circulating in the gut. The haemodynamic response to this depends on the venous capacitance of the splanchnic circulation. If, at the time of the clamp, the splanchnic venous tone is high (low capacitance), the cross-clamp will result in a situation similar to that of a supra-celiac clamp, with increased venous return to the heart. If the splanchnic venous tone is low (high capacitance) venous return decreases as blood volume distributes to the highly compliant splanchnic vasculature.
Changes in left end-diastolic ventricular pressures, wall motion abnormalities increase, and decreases in ejection fraction are less pronounced than with supraceliac. Perfusion distal to the clamp is pressure dependent and relies, of course, on collateral circulation. Increasing cardiac output does not increase perfusion distal to the cross clamp and is dependent on the pre-clamp aortic pressures (because physically only so much collateral flow is possible). One would assume that at some point if there was enough collateral circulation present, then increased CO alone could increase blood flow distal to the clamp.
Obtaining a Perioperative ECG guidelines?
Recommendations for ECG testing are essentially as follows:
Patients with one clinical risk factor should get an ECG if undergoing vascular surgery and in most cases its “reasonable” in intermediate surgery.
It’s also “reasonable” (a nebulous term used by the ACC/ AHA) to get an ECG on a person who is undergoing vascular surgery without any clinical risk factors.
Low risk surgery does not require an ECG in asymptomatic individuals.
Perioperative Beta Blocker recommendation
For intermediate risk surgery with only one clinical risk factor the usefulness of beta-blockers is “uncertain,”
If the patient had 2 or more clinical risk factors undergoing intermediate risk surgery, then beta-blockers are “probably recommended.” Whatever the case, the ACC/AHA preoperative guidelines are something you should absolutely read in preparation for your boards and are very high yield.
Risk factors for cardiovascular risk are category
High risk (active cardiac conditions)
- acute/ recent MI;
- unstable or severe angina;
- high grade AV block (mobitz 2 or complete);
- Sx ventricular arrhythmias
- SVTs with uncontrolled ventricular rate;
- severe valvular disease
- decompensated or new heart failure.
Intermediate risk (clinical risk factors) - ischemic heart disease - compensated CHF - mild angina - diabetes (especially IDDM) - CVA - renal insufficiency. minor risk (which aren't used in the algorithm for preoperative cardiac evaluation any more).
Minor risk factors (which are no longer recognized but helpful to know what they were so you do not get confused with them being clinical risk factors) are
- abnormal ECG (not including specific signs of ischaemia);
- low functional capacity,
- uncontrolled hypertension,
- arrhythmias with controlled ventricular rate,
- advanced age.
Why ask this question? Its important that you understand what patient characteristics traditionally represent an increased risk. As ACC/AHA guidelines evolve to essentially become completely ambiguous, I feel you need to have a reference point to deal with the ambiguity.
When to chose pressors vs NTG for intraoperative MI?
Is the primary problem aortic diastolic pressures or LVEDP?
Since myocardial perfusion is the difference between aortic diastolic pressure and LVEDP, the significant reduction in perfusion pressure was likely to blame.
Pressors?? If primary problem is aortic diastolic pressure low (hypotension)
NTG potently decreases LVEDP and can dilate coronary arteries (although they are often already presumed to be maximally dilated in these cases), but a small change in LVEDP will not make up for a dramatic change in aortic pressures.
BBs?? Although slowing the heart may lead to increased diastolic perfusion time, it is unlikely that the 10 point increase in HR was responsible for the ST depressions. Furthermore, labetalol has alpha antagonistic (not agonistic) properties that can further decrease blood pressure.
What’s the goal of MR management?
The patient has mitral regurgitation, which is accentuated with increased SVR (handgrip). Severe MR is diagnosed by echocardiography where the regurgitant jet is > 2/3 the length of the left atrium, a regurgitant stroke volume of > 65 ml, or evidence of pulmonary vein flow reversal during systole. MR results in an eccentric hypertrophy due to volume overload. As the ventricle dilates, the mitral valve annulus is further deformed causing worsening MR.
The goal of MR management is to decrease the regurgitant stroke volume and favor forward flow. Therefore afterload reduction is central to management. Low HR increases diastolic time and volume, which further distorts the annulus, causing increased regurgitant flow. Therefore moderately high HR (80-100) are suggested.
What is the normal mitral valve area? And what is sever MS area? What factors affect the transvalvalver gradient in MS?
MS is characterized by a reduced valve area (normal 5 cm, severe 1 cm). To maintain cardiac output, blood must flow quicker through the stenotic valve as compared to a normal one, causing a pressure gradient (< 2 mm Hg normal, >12 mm Hg severe).
Therefore, the greater the cardiac output (more blood), or higher the heart rate (shorter filling time), the higher the gradient. Atrial kick can account for 30% of ventricular filling; so therefore, loss of atrial kick (common in MS) would, if anything, increase the gradient needed to maintain cardiac output (assuming the same cardiac output). Slowing the HR with a beta blocker would probably not increase the gradient. The higher the gradient, the higher left atrial pressures (by definition) must be. High atrial pressures require elevated pulmonary vasculature pressures and pulmonary oedema is common. Fluid management is difficult as the patient cannot tolerate significant increases or decreases in intravascular volumes.
As a side note, choosing the choice stating that the transvalvular gradient would decrease with a change from sinus to a-fib would not be incorrect IF you assumed that this would lead to a decreased cardiac output (and therefore less flow through the valve and hense no increase in pressure). However, this assumption is something that you, the test taker, brought into the exam with you and not stated by the question. It is not clear in this situation whether the question’s author assumed an unchanged cardiac output (in which case an increased mean left atrial pressure would be needed). This is an example of the ambiguity of the boards and a very common cause for test takers to get questions wrong even though they understand the concept! It is very frustrating and the ABA board exam is filled with these (subjectively speaking). Unfortunately there is no good way to deal with this situation other than to say to (in general) try to minimize the assumptions that you bring into a question and try to answer it the best you can with only the information supplied.
Which induction agent could lead to cardiovascular collapse in CHF? Propofol Vs ketamine Vs fentanyl
Propofol
Patients with CHF, especially severe CHF, often have high LVEDPs in an effort to maintain cardiac output, which leads to pulmonary oedema. BNP levels are typically elevated, especially during times of decompensation. Patients with severe CHF rely on high levels of circulating catecholamines, and interruption of this can lead to cardiovascular collapse, such as with induction of anesthesia. Although opioids can decrease sympathetic outflow, a 2 mcg/kg bolus of fentanyl would be unlikely to lead to cardiovascular collapse as it does not possess significant direct depressant effects to the myocardium. Ketamine, a myocardial depressant, can often be safely used when titrated carefully due to its ability to maintain or even increase sympathetic outflow. Propofol in usual induction doses can lead to decreases in cardiac contractility and profoundly decreased afterload precipitating low coronary perfusion pressures leading to cardiovascular collapse.
Dysfunction of pacemaker during the case (previously working pacer) think of ddx ….
A functioning pacemaker cannot excite the myocardium in some circumstances such as (extreme) hypokalaemia, hypocarbia, hypothermia, myocardial infarction, antidysrythmic drugs (possible), and fibrotic buildup around the electrodes. Bipolar electrocautery for sure is a possibility
Describe CPB circuit?
Patient’s venous return flows from venous cannulas in the right atrium to the venous reservoir. From there blood is sent to the oxygenator and heat exchanger.
(The oxygenator oxygenates the blood as well as adds or removes CO2. Older oxygenators used small O2 bubbles for oxygen exchange but modern day CPB uses membrane oxygenators, as it is less traumatic to the blood. The heat exchanger can heat or cool blood. )
Next blood enters the main pump, which can be a roller pump or centrifugal. (Roller pumps are generally more traumatic to RBCs, and have a hand crank in case power is interrupted. Centrifugal pumps are pressure dependent and require a flow meter to monitor output.)
Before returning to the patient, blood passes through the arterial filter removing thrombi, calcium, debris, and fat. The blood returns to the patient through the aortic cannula.
pH stat va alpha stat ABG during CPB?
(1) pH-stat, is where the pH is kept static, which means that if the patient is 27 C, the temperature corrected blood gas should have a pH of 7.4.
- Since hypothermia increases CO2 solubility; at 27 C, the PaCO2 will be low (since it has dissolved into solution) leading to an elevated pH (looks like a respiratory alkalosis). Therefore CO2 has to be added to the patient’s blood to replace the amount that is dissolved, keeping the pH static. Furthermore, when the blood is warmed up in the blood gas analyzer to 37 C, the added CO2 causes a respiratory acidosis picture.
(2) With alpha stat, no CO2 is added to the circuit and at 37 C the pH is 7.40. When the patient is cooled and CO2 solubility increases, there is an apparent respiratory alkalosis.
It is suggested that the probable increase in neurologic sequelae associated with pH stat is a result of cerebral vasodilatation and therefore small emboli are more likely to be directed to the brain.
More clarification:
All ABGs are run at 37 degrees, and so temperature uncorrected means what the ABG looks like at 37 degrees.
pH stat means that CO2 is added to the blood gas. So, when you cool someone, the CO2 dissolves (becomes soluble) and the pCO2 decreases. When you take a sample of blood and warm it up, the CO2 comes out of solution and the pCO2 goes back to normal. That means with the patient’s blood with nothing done to it has a respiratory alkalosis (low CO2) when temperature corrected and a normal CO2 when temperature uncorrected.
Now lets add CO2 when the patient’s cold. With additional CO2 added to the cold blood, the ABG shows a normal pCO2 when temperature corrected (cold) and a reparatory acidosis (high CO2) when the ABG is temperature uncorrected (warm).
So, keeping this in mind lets go through the answer choices:
A. A temperature uncorrected (warm) ABG will show a respiratory acidosis (high pCO2). TRUE.
B. CO2 is added to the patient’s blood - TRUE (that is what pH stat is).
C. Neurologic outcomes - you either knew that or not, the secret to answering the question is knowing the next one is false.
D. A temperature corrected (cold) ABG will show a respiratory alkalosis (low pCO2)- FALSE, it would show a normal pCO2, because you added the CO2 when the patient was cold to achieve this goal.
Contraindications for aortic balloon pump
Balloon pumps should be avoided in patients with aortic insufficiency, mobile aortic plaques, and aortic dissection as it can worsen the underlying diseases.
Net effect of balloon aortic pump is …
Ballon pumps decrease afterload (as the balloon deflates a vacuum effect is created) and increases coronary perfusion (balloon inflation during diastole). The net effect of ballon pumps are increased stroke volume, improved coronary perfusion, but no real change in survival.
What is the most common complication of cross clamp of aorta during descending aortic aneurysm repair?
Lower extremity paralysis complicates up to 10% of thoracic aneurysm repairs and remains permanent in about half the cases. The typical presentation is anterior spinal artery syndrome where arteries feeding the anterior spinal artery off the aorta are interrupted or hypoperfused, especially the artery of Adamkiewicz. The artery of Adamkiewicz often is the primary source of blood flow for the lumbar and low thoracic anterior spinal cord. The anterior spinal cord includes tracks for motor, light touch, pain, and temperature; therefore, interruption of blood supply results in loss of these functions in the lower extremities. Proprioception, deep touch, and vibratory sense are often spared (supplied by paired posterior spinal cord arteries). Pressure monitoring distal to the cross clamp and neurological monitors (SSEPs) are used to identify when spinal cord ischaemia may be occurring. The primary treatment is deep hypothermia (decreasing cellular oxygen consumption), but intercostal reimplantation and shunts can be used to increase blood flow to the anterior spinal artery (increasing oxygen delivery). Since perfusion of the spinal cord is dependent on a pressure gradient between anterior spinal artery pressure and CSF pressure, a spinal drain can also be placed to decrease CSF pressures. Other common complications of aortic surgery (other than the usual suspects of bleeding, infection, etc) include myocardial ischaemia, renal failure, ARDS, and gut ischaemia.
What’s the drug of choice to treat hypertension in aortic dissection?
Aortic dissection is exacerbated by shear forces, resulting from the shear force of blood ejected by the left ventricle. Shear forces are increased with increased heart rates and cardiac output. Beta blockers reduce heart rate and contractility and are an ideal first line therapy. Nicardipine or nitroprusside can be added later, but when used alone can increase both heart rate and cardiac output. Traumatic aortic dissection typically occurs at the aortic isthmus in blunt trauma, presenting with hypotension and widened mediastinum.
Risk factors for cardiovascular risk are categorized as …
high risk (active cardiac conditions) intermediate risk (clinical risk factors) minor risk (which aren't used in the algorithm for preoperative cardiac evaluation any more).
Active risk factors are: acute/ recent MI; unstable or severe angina; high grade AV block (mobitz 2 or complete); symptomatic ventricular arrhythmias; SVTs with uncontrolled ventricular rate; & severe valvular disease; and decompensated or new heart failure. (and now these aren’t used anymore either!)
Multiple clinical risk factors in the absence of exercise capacity may warrant stress testing or coronary catheterization in some cases and include: ischaemic heart disease; compensated CHF; mild angina; diabetes (especially IDDM); CVA; and renal insufficiency.
Minor risk factors (which are no longer recognized but helpful to know what they were so you do not get confused with them being clinical risk factors) are abnormal ECG (not including specific signs of ischaemia); low functional capacity, uncontrolled hypertension, arrhythmias with controlled ventricular rate, and advanced age.
Why ask this question? Its important that you understand what patient characteristics traditionally represent an increased risk. As ACC/AHA guidelines evolve to essentially become completely ambiguous, I feel you need to have a reference point to deal with the ambiguity.
A patient has a a supraceliac aortic clamp placed. Which of the following would most likely be expected:
Decreased venous capacitance
The cardiovascular response to aortic cross-clamp is a bit complex and essentially depends whether its above or below the splanchnic circulation. In a t clamp of the aorta, blood ejected by the LV will be redistributed above the clamp (heart, lungs, brain). That means that the heart will have increased venous return, increased after load, and variable changes in cardiac output (usually decreased). Also there is a surge of catecholamine release which will affect venous capacitance. Since venous tone will increase with high catecholamine levels, there will be additional venous return. With aortic cross-clamp both systolic and diastolic blood pressure will increase. Left end-diastolic ventricular pressures (LVEDPs) and wall motion abnormalities increase, and ejection fraction decreases. The reduction in EF is likely from reduced subendocardial perfusion exacerbated by a very elevated LVEDP (remember perfusion is Aortic diastolic pressure - LVEDP). So in this case the increase in preload (venous return) is exacerbating the reduction in CO. Its also worth saying that the reduction in CO is far less predictable than the increase in venous return. If the clamp is placed below the splanchnic circulation things get more complex. Now blood ejected by the LV will also be circulating in the gut. The haemodynamic response to this depends on the venous capacitance of the splanchnic circulation. If, at the time of the clamp, the splanchnic venous tone is high (low capacitance), the cross-clamp will result in a situation similar to that of a supra-celiac clamp, with increased venous return to the heart. If the splanchnic venous tone is low (high capacitance) venous return decreases as blood volume distributes to the highly compliant splanchnic vasculature. Changes in left end-diastolic ventricular pressures, wall motion abnormalities increase, and decreases in ejection fraction are less pronounced than with supraceliac. Perfusion distal to the clamp is pressure dependent and relies, of course, on collateral circulation. Increasing cardiac output does not increase perfusion distal to the cross clamp and is dependent on the pre-clamp aortic pressures (because physically only so much collateral flow is possible). One would assume that at some point if there was enough collateral circulation present, then increased CO alone could increase blood flow distal to the clamp.
