Cardiac Flashcards
1
Q
Normal troponin levels after bypass:
When do troponins peak?
Do serum troponins provide predictive and prognostic value for short and long term outcomes?
A
BELOW 1ng/mL
Trop peaks at 24 hours following injury to the myocardium
Yes
2
Q
What is pulsus paradoxus? Explain pathophys of cardiac tamponade. Explain collapse-what collapses first?
A
A decrease of >10 mmHg during INSPIRATION
So, normally when we inspire, the RV fills and the RV bulges (ventricular interdependence), lessening the space that the LV has, decreasing systolic pressure NO MORE than 10. BUT, when there is tamponade, the RV can’t distend out the way it used to, and bulges even more into the left side of the heart. This makes preload drop even more->10 mmHg. As the fluid filling the sac gets bigger, it will become unable to distend, and so in order to prevent total collapse of the heart, the body increases systemic venous and pulmonary pressures. This causes an increase in PCWP, and all distokics
If the heart becomes compressed, atrial compression happens first, then ventricular. If it happens, RV collapse is during diastole.
3
Q
Milrinone leads to increased ____ and ___.
A
Inotropy and vasodilation
4
Q
Why does CVP INrease with aortic cross clamping?
A
Because with increased catecholamine levels there is increased venoconstriction distal to the clamp driving CVP higher.
5
Q
Why is there an increase in ABP after aortic cross clamping?
A
Because same amount of blood occupying smaller space-ABOVE the level of the clamp
6
Q
Pulmonary artery wedge pressure after aortic clamping
A
Pulmonary artery wedge pressure increases as blood redistributes in smaller container.
7
Q
Hemodynamics effects of the clamp: Arterial blood pressure above Coronary artery perfusion Ventricular wall stress CVP Pulmonary artery wedge pressure Arterial blood pressure below Cardiac output Renal blood flow
A
Increased everything except pressure below and cardiac output and renal blood flow
8
Q
NPO Guidelines are based on what?
A
Gastric residual volumes
9
Q
What does hypocapnia do to the uterus?
A
If severe enough, it can cause vasoconstriction
10
Q
UBF is proportional to what pressure??
It’s inversely proportional to which resistance and pressure?
A
Uterine arterial pressure (prop)
Inversely to uterine venous pressure and uterine vascular resistance.
11
Q
ST segment depression means what? How does it differ from acute coronary occlusion? why do you see this more often than transmural injury?
A
ST segment depression is an indicator of acute subendocardial myocardial ischemia.Subendocardial ischemia is caused by an imbalance of myocardial oxygen supply and demand as opposed to acute coronary occlusion.Subendocardial ischemia is more commonly seen than transmural injury because the small capillaries and arterioles at the subendocardial level are subject to occlusive high intraventricular pressure.
12
Q
ST segmebt elevation is seen with what?
A
ST segment elevation (C) is seen with acute transmural myocardial injury in a patient with the appropriate clinical symptoms (angina, dyspnea, fatigue, diaphoresis, etc) and is a medical emergency requiring immediate management (e.g. revascularization). STEMI suggests injury or infarction, not just ischemia
13
Q
What is needed to make a dx of STEMI?
A
ST elevation in 2 or more contiguous leads is required to make an ECG diagnosis of STEMI.
14
Q
What do T wave inversions mean?
A
T wave inversions (D) are a sign of acute myocardial ischemia but do not specifically pertain to a subendocardial or transmural injury
15
Q
T/F:V5 is the best lead for monitoring intraoperative ischemia.
A
TRUE
16
Q
What are the most sensitive and earliest signs of myocardial ischemia?
A
Echocardiographic wall motion abnormalities
17
Q
Elective repair of an aneurysm is indicated if
A
if the size is > 5.5 cm or the rate of growth is > 1.0 cm per year.
18
Q
Once the stent-graft is deployed, it cannot be repositioned. This makes the time of deployment very crucial. Windsock effect? and what does this mean for you? and explain the 3 things that will help with that.
A
As the stent-graft begins to open, the ejection force of the heart can push the stent-graft, and cause it to migrate distally. This is referred to as the “windsock effect”. This is especially a concern with thoracic aortic aneurysm stenting. To prevent the stent-graft from migrating, maneuvers that will reduce the shear force felt by the graft while it is opening are employed. These include: 1) induced-hypotension, 2) transient cardiac asystole, and 3) rapid ventricular pacing. 1) Inducing hypotension pharmacologically will reduce the shear force on the stent-graft and decrease the likelihood of migration. Systolic blood pressure between 70-80 mmHg is used to avoid the windsock effect.
2) Transient asystole during deployment of the stent-graft is also an option. Adenosine is used to provide a short period of asystole (this reduces shear force on the graft). Half-life of adenosine is about 10 seconds because red blood cells and vascular endothelial cells rapidly inactivate it.
3) Rapid ventricular pacing (> 180 beats per minute) will cease left ventricular ejection. Transvenous pacing wires are placed and during deployment of the stent-graft the ventricular rate is increased to >180. After the graft is fully opened the heart is returned to its normal rhythm
19
Q
Whats the deal with adenosine and asthma?
A
Adenosine should be cautiously used in patients with asthma or upper respiratory disease because adenosine can cause bronchoconstriction.
20
Q
T/F: femoral dissection presents with hypotension and peritoneal extravasation.
A
FALSE:Femoral dissection generally will not present with severe hypotension or peritoneal extravasation
21
Q
Most common complication of TAVR: Other complications:
A
Vascular injurySudden and unexplained hypotension is often the earliest indication of a major complication and can be due to: severe aortic regurgitation, cardiac tamponade secondary to ventricular wall perforation, aortic arch or annulus rupture, perforation of the ilio-femoral axis leading to retroperitoneal hemorrhage, or coronary ostium obstruction resulting in myocardial ischemia.Hypotension combined with retroperitoneal extravasation of contrast should clue the provider to perforation of the ilio-femoral axis
22
Q
What are the 3 types of protamine reactions:
A
I Systemic hypotension from mast cell degranulation and histamine release caused by rapid administration. It is the polycationic structure of protamine that triggers this reaction.
II Anaphylaxis from IgE-mediated dose-independent reaction. Previous exposure to protamine or a similar protein (such as neutral protamine Hagedorn found in NPH insulin) is required for anaphylaxis to occur.
III Pulmonary hypertensive crisis causing pulmonary hypertension, vasoconstriction, and possible right heart failure. The mechanism for this reaction is thromboxane A2 released from platelets and macrophages stimulated by protamine-heparin complexes.
23
Q
Mitral stenosis-what kind of murmur is it? when is it best heard? which part of the stethescope needs to be used? does it increase after exercise? can it be silent?
A
diastolic. The murmur is best heard during exhalation and with the patient in the left lateral recumbent position. The bell of the stethoscope should be used (since the murmur is low frequency) and held lightly over the point of maximum impulse (typically in the left fifth intercostal space at the midclavicular line). Murmur intensity may be increased after brief exercise. can be silent
24
Q
Common systolic murmurs and common diastolic murmurs:
A
Common systolic murmurs are MR AS (“Mr. Ass”), Mitral Regurgitation and Aortic Stenosis. Diastolic murmurs at the valves will therefore be mitral stenosis and aortic regurgitation.
sys-your mr is an ass
25
What metabolic abnormalities are associated with Torsades? how do you treat Torsaddes?
hyhpokalemia and hypomagmesemiaTreatment includes recognizing TDP from normal VT and removal or correction of the offending agent. can treat with unsynchronixed cardioversion. Correcting electrolytes with the early use of magnesium is recommended. Magnesium can be given as an initial 1-2 gram IV bolus over 30-60 seconds, which can then be repeated in 5-15 minutes. Alternatively, a continuous infusion can be started at a rate of 3-10 mg/min. Magnesium is effective even in patients with normal magnesium levels.
26
Torsaddes can be induced by which drug class?
Torsades can be induced by many antiarrhythmic drugs including class Ia (sodium channel blockade) and class III (inhibit potassium channels) by prolonging the QT interva
27
what can you do to reduce bradycardia whn stents are being placed in the carotid?
Administering intravenous glycopyrrolate or atropine prior to deploying the stent can reduce the incidence of bradycardia
28
Explain how hypotension and bradycardia can occur during stent placement?
Hypotension and bradycardia can occur during or after carotid angioplasty with stenting. The carotid sinus, which contains baroreceptors, is stimulated by the placement of the stent. This signal is sent through the glossopharyngeal nerve to the medulla and inhibits the sympathetic neurons. This inhibition produces hypotension due to reduced peripheral sympathetic tone. Furthermore, the nucleus ambiguous and the vagal nucleus are stimulated, leading to bradycardia. This physiologic response is normally seen when the baroreceptors in the carotid sinus detect elevated blood pressure. However, direct manipulation of the carotid sinus (e.g. carotid stent placement) can produce the effects independently of the blood pressure.
29
Can hypotension and bradycardia occur during CEA? if so, explain how/why?
A similar situation occurs with carotid endarterectomy (C). Patients with carotid stenosis have an atheromatous plaque located near the baroreceptors. As a result, the pressure waves detected by the baroreceptors become dampened. To compensate for this decreased signal, the baroreceptors increase their sensitivity. However, once the plaque is removed (after carotid endarterectomy), the baroreceptors can be over-stimulated by small changes in the blood pressure. This can cause hypotension and bradycardia.
30
What improves defibrillation success?
Defibrillation success decreases with arrhythmia time. Factors that improve defibrillation include electrode gel, applying force if paddles are used, biphasic defibrillation, and larger electrodes. (at least 8-12 cm)
31
What part of the heart is activated first during transcutaneous pacing? why? what pacemaking mode is it similar to? Typical capture threshold?
Right ventricle.
The anatomy of the heart and its relation to the chest are the reason the right ventricle is activated first (it is the closest to the anterior chest)imilar to VOO mode for implantable pacemakers. ypical capture thresholds are between 20 to 120 mA however pacing may require up to 200 mA. Most resources suggest starting at 10 mA and increasing the settings by 10 mA until capture. Once capture has occurred, the device should be set 5 to 10 mA above that threshold (some say 25% more). The rate should be set 10 to 20 beats per minute higher than the spontaneous heart rate to capture 100% of the beats and avoid R-on-T phenomenon.
32
with transcutaneous-After the RV is paced, then what is paced?
After RV, then LV
33
t/F:
The most common reason for not obtaining capture with transcutaneous pacing is not adequately increasing the current.
34
How do Milrinone and inamrinone work?
| Benefits of PDE III inhibitors:
specific phosphodiesterase III (PDE III) inhibitors that function by interfering with the breakdown of cAMP. As cAMP levels increase in myocardial cells, intracellular calcium stores increase which improves contractility. Increased cAMP in vascular smooth muscle cells promotes vasodilation, and results in a reduction in systemic vascular resistance (SVR) and PVR. Overall, the net effect is improved cardiac output.
The added benefit of PDE III inhibitors is the improved ionotropic effects WITHOUT β receptor stimulation. They are therefore less likely to induce tachycardia.Also, PDE III inhibitors do not increase myocardial oxygen demand. Consequently, if added inotropy is required, synergism exists with β-agonists.
35
Why would you not use imanrinone in a patient with ITP?
Inamrinone is known to cause a dose-dependent reduction in platelet count if the drug is used for longer than 24 hours, and therefore would not be ideal in a patient with idiopathic thrombocytopenic purpura
36
Why is inamrinone not great in patients with sepsis?
Inamrinone would not be an ideal drug for a patient with sepsis (B) because of sepsis-associated reduced vascular tone and since, in general, most septic patients have high cardiac output. they need drugs that improve vascular tone.
37
Tell me whats going on with the ICP in laparoscopic surgery:
who has a relative containdication for laparoscopic surgery?
The pneumoperitoneum created by gas insufflation causes an increased intra-abdominal pressure which translates to increased intra-thoracic pressure. The increased intra-thoracic pressure increases CVP and decreases cerebral venous drainage. Cerebral perfusion pressure is maintained with laparoscopic surgery and the increase in ICP (D) is often negligible in otherwise healthy patients. However, patients with intracranial pathology may not have the reserve to compensate for even small elevations in ICP. The prolonged Trendelenburg position required for certain procedures, such as robotic radical prostatectomy, is a relative contraindication for patients with a history of stroke or cerebral aneurysm.
38
What happens with afterload in laparoscopic surgery?
Afterload is increased with laparoscopic surgery. The increased intra-abdominal pressure is transmitted to the great vessels causing a mechanical increase in afterload. This increase in afterload creates an increase in SVR that can be seen with elevations in blood pressure during insufflation of the abdomen. The increase in afterload will cause a decrease in end organ perfusion. Renal blood flow can be reduced with a 25% drop in GFR for an insufflation pressure of 20 mmHg.
39
What happens with pulmonary compliance in laparoscopic surgery?
Pulmonary compliance is decreased with laparoscopic surgery. Pulmonary compliance is the ability of the lungs to expand and fill with air. The increased intra-abdominal pressure prevents motion of the diaphragm and moves it cephalad which also decreases tidal volumes and increases inspiratory pressures. This increases atelectasis and decreases pulmonary compliance. Atelectatic lung takes a greater force to reopen and leads to V/Q mismatch
40
What happens to preload during laparoscopic surgery?
It is decreased-keep in mind that CVP is increased.
41
WPW EKG what does it look like, and how does that determine how you'll treat it?
Patients with WPW are at increased risk of developing paroxysmal tachycardia. The ECG in a patient with WPW is characterized by a short PR interval and a widened QRS with delta wave. When these patients develop tachycardia the ECG can demonstrate a narrow or wide complex on ECG. Widened complexes develop when antidromic conduction occurs in a retrograde manner up the bundles of His. The treatment for orthodromic and antidromic tachycardia is somewhat different, as antidromic rhythms are potentially more unstable because of retrograde conduction.
42
What is the drug of choice in anti-dromic conduction seen in WPW? How does it work?
Procainamide. Procainamide is a sodium channel blocker in class 1a. Procainamide prolongs slow conduction in both the atrium and the ventricles. Procainamide increases the refractory period of the myocardium without increasing the refractory period of the AV node. The sparing of the AV node helps break antidromic rhythms and prevents orthodromic rhythms from becoming antidromic.
43
How does adenosine work? what is it recommended for? why must it be flushed? why is iy undesirable to use in WPW?
Adenosine is a purine nucleoside. Adenosine causes vasodilatation and acts on adenosine receptors, which causes a block of the AV node. Adenosine is recommended for narrow complex arrhythmias and has been used in wide complex arrhythmias, but should be used with caution. The dose of adenosine is typically 6mg rapid push. Adenosine has a very short half-life and must be flushed, to prevent peripheral degradation prior to therapeutic action. Blocking AV node conduction may result in conduction only through the bundle of Kent, which may not be desired.
44
Typical joule dose for cardioversion is what?
100 Joules
45
How does verapamil work? which myocytes does it work better in? do you use it in WPW?
what other AV nodal blocking drugs should you NOT use in WPW?
Verapamil is an L-type calcium channel blocker in the anti-arrhythmic class IV. Verapamil blocks voltage-gated calcium channels with a higher affinity for cardiac tissue than vascular cells. Verapamil is contraindicated in antidromic WPW as it is associated with worsening the rhythm and cardiovascular collapse. Verapamil works well to convert AV nodal reentry tachycardia (AVNRT), but not AVRT like WPW. Other medications that block the AV node are not recommended in WPW with tachycardia, such as beta-blockers (e.g. metoprolol, esmolol) and diltiazem.
46
The main goal of medical treatment in patients with aortic insufficiency is to
decrease afterload, augment contractility if needed and to avoid bradycardia. Metoprolol would increase the time in diastole, allowing more time for more regurgitant flowA mnemonic for both aortic insufficiency and mitral insufficiency is: fast, full, forward which means fast heart rate (or avoiding bradycardia), full preload, and forward flow (avoiding afterload).
47
Cardiac tumors-what are the most common kinds, and why are they there?
The most common primary tumor of the heart is a cardiac myxoma, which is typically located in the left atrium. However, metastatic disease to the heart is not uncommon from adjacent lung or renal cancer. Cardiac tumors have the potential to cause arrhythmias, ventricular obstruction, heart failure, pulmonary edema, pulmonary hypertension, arterial hypoxemia, dyspnea, positional hemodynamic compromise and embolism.
48
If youre fixing a PDA, which nerve can you encounter and possibly mess up?
Due to its anatomical location, recurrent laryngeal nerve injury can occur during surgical repair of a patent ductus arteriosus
49
Centrifugal pump flow varies with what?
Centrifugal pump blood flow varies depending on pump preload and afterload.
50
Both roller and centrifugal pumps can deliver adequate systemic pressure during CPB periods via ____ flow.
Non-pulsatile-however, there are commercil pumps that can make both of them deliver blood in a pulsatile fashion.
51
Major difference between roller and centrifugal pumps
A major difference between the two types of pumps is that centrifugal pumps require flowmeters on the arterial portion of the CPB circuit since flow can vary from alterations in pump preload and afterload. Assuming the inflow and outflow are not occluded, roller pump flow is essentially only dependent on the speed of the rollers.
52
Compressive force between the rollers can cause what in roller pumps?
Due to compressive forces between the rollers, tubing, and blood, roller pumps have a higher incidence of blood element destruction, creation of plastic microemboli (spallation), and inflow/outflow obstructions
53
Why are centrifugal pumps preferred?
Centrifugal pumps are preferred to roller pumps in CPB circuits due to less blood element destruction, lower line pressures, lower risk of air emboli, and elimination of tubing wear and spallation.
54
How do IABPs work? How does it increase coronary perfusion pressure? What does it do to afterload and when?
The IABP augments coronary perfusion by inflating during early diastole which improves aortic diastolic pressure.
Coronary perfusion pressure (CPP) increases since CPP is the difference between aortic diastolic pressure (AoDP) and left ventricular end diastolic pressure (LVEDP): CPP = AoDP - LVEDP. An IABP also aids in unloading the left ventricle by reducing afterload with deflation at end diastole. Assisted aortic EDP is therefore less than unassisted aortic EDP. The combined effect increases myocardial O2 supply and reduces myocardial O2 demand.
55
Indications for IABP:
cardiogenic shock (due to ischemia or nonischemic cardiomyopathy), failure to wean from cardiopulmonary bypass (CPB), severe mitral regurgitation, augmentation during percutaneous coronary interventions, and bridge to transplantation or ventricular assist device (VAD) placement. It is not considered a long-term therapy for cardiogenic shock. Placement is also indicated in right ventricular dysfunction which may acutely appear after CPB.
56
Complications of IABP:
Complications of IABP use include failed triggering of device, early inflation (during end-systole) or late deflation (during early systole) leading to increased afterload, late inflation or early deflation leading to poor augmentation of coronary circulation, aortic dissection, arterial injury, ischemia (lower extremity, intestinal, renal, or spinal), thromboembolism or plaque rupture, left upper extremity ischemia due to occlusion of the left subclavian artery, hemolysis, and infection.
57
Contraindications to IABP:
Contraindications to IABP placement include moderate to severe AI, aortic disease, and severe peripheral vascular disease
58
Why is ephedrine bad in AR?
Ephedrine (A) is sympathomimetic amine which causes natural catecholamine release. Ephedrine increases heart rate and afterload. The increase in afterload is unfavorable for a patient with aortic regurgitation, as the increase in afterload will increase the regurgitant fraction
59
Why is nitroprusside good in AR?
Nitroprusside (D) is an inorganic molecule that contains nitric oxide (NO). The release of NO causes arteriole and vasodilatation. The arteriole dilatation decreases afterload and promotes forward flow, decreasing the amount of regurgitation. Additionally, the decrease in afterload causes a compensatory increase in heart rate. Increasing heart rate is favorable for patients with aortic regurgitation because it decreases the amount of time regurgitation can occur. Regurgitation during aortic insufficiency occurs during diastole.
60
Can esmolol help with hypotension in pts with IHSS aka HOCM?
YesEsmolol is a cardioselective beta-blocker which would slow heart rate and promote ventricular filling. Esmolol has a short duration of action because it is metabolized by plasma esterases. This makes esmolol an ideal drug to prevent brief periods of sympathetic stimulation (e.g. laryngoscopy).
61
Hemodynamics goals in IHSS/HOCM are:
Hemodynamics goals in IHSS/HOCM are:
- Preload should be kept up.
- Afterload should be kept up.
- Heart rate should be kept down.
- Myocardial contractility should be kept down.
- Sinus rhythm should be maintained.
62
Pacemaker placement is indicated for:
second-degree (type II) AV block (D), third-degree AV block, any symptomatic bradyarrhythmia, and refractory supraventricular tachyarrhythmias.
Symptomatic sinus node disease
- Symptomatic atrioventricular node disease, particularly high grade AV block
- Long QT syndrome
- Hypertrophic obstructive cardiomyopathy
- Dilated cardiomyopathy
63
Types of heart block:
Atrioventricular (AV) block is when conduction from the atria to the ventricles is either delayed or interrupted. First degree AV block is slowed conduction without missed beats, and shows up as a prolonged PR interval on ECG. Second degree AV block type I (Mobitz type I) is progressive prolonging of the PR interval and then a dropped beat. In second degree AV block type II (Mobitz type II) the PR interval remains unchanged, and the atria suddenly fail to conduct a beat across the node to the ventricle. In third degree heart block, no impulses are conducted from the atria to the ventricles. Permanent pacemakers are indicated in patients with Mobitz type II and third degree heart block.
64
Go through CVP tracing:
A normal CVP tracing is seen here. (look at photo)
a – atrial contraction
c – tricuspid valve bulging into right atrium during right ventricle isovolemic contraction
x – tricuspid valve descends into right ventricle with ventricular ejection
v – venous return to the right atrium
y – atrial emptying into right ventricle through open tricuspid valve
65
Cannon A wave means what?
A “cannon a wave” is a sign of atrioventricular (AV) dissociation (tall a wave lacking c component).atrium is contracting against a closed tricuspid valve.
66
Cardiac pathology and corresponding CVP waveform changes: A fib
Atrial fibrillation: loss of a wave
67
CVP waveform changes: AV dissociation
cannon a wave
68
CVP Tricuspid regurgitation
tall c and v waves, loss of x descent
69
CVP Tricuspid stenosis:
tall a and v waves, minimal y descent
70
CVP RV ischemia:
tall a and v waves, steep x and y descent, M or W configuration
71
CVP Pericardial constriction
tall a and v waves, steep x and y descent, M or W configuration
72
dominant x descent, minimal y descent (CVP)
Cardiac tamponade
73
how do you deal with HOCM refractory to medical treatment? common red herring?
Septal myectomy is the treatment of choice for HOCM refractory to medical treatment. Dual chamber pacing is a common red-herring. Treatment goals of HOCM and SAM are adequate preload, reduced contractility, avoidance of tachycardia, and adequate SVR
74
Thermodilution in a nutshell:
| Bottom line on thermistor:
When cardiac output is low, a standard volume of cold saline will cause a greater decrease in blood temperature and will take longer for baseline temperature to recover
Any technical error during CO measurement using the thermodilution technique that results in less of a temperature change detected at the thermistor (e.g. smaller volume of injectate than calibrated volume or warmer injectate than calibrated temperature), will cause an overestimation of CO. Any technical error that increases the temperature change (e.g. room temperature fluid bolus prior to injectate administration, larger volume or colder temperature of injectate than calibrated) will lead to an underestimation of CO.
75
Reducing volume of injectate will cause overestimation of injectate by how much?
Reducing the volume of injectate (whether iced or room temperature) will cause a false OVERestimation of CO by 5-10% for every 0.5 mL. This occurs since there is less fluid (which is cooler than the blood temperature) being injected so the temperature change detected at the thermistor will be decreased, which results in a greater calculated cardiac output.
76
What does a right to left shunt do to the thermistor?
he presence of a right-to-left intracardiac shunt will divert injectate away from the thermistor. Since the temperature change will, therefore, be less, this leads to a false overestimation of CO.
77
Patients with long QT syndrome (LQTS) and a history of cardiac arrest warrant
warrant automatic cardioverter-defibrillator placement
78
Long QT syndrome with and without deafness:
Congenital LQTS may occur with deafness (Jervell, Lange-Nielsen syndrome) or without deafness (Romano-Ward syndrome).
79
Anesthesia and surgery for patients with LQTS should proceed after appropriate workup and management. Explain what that means:
Taking the patient to the OR with an esmolol drip is not ideal. The patient will need treatment with beta-blockers, which are the mainstay of therapy in long QT therapy, however starting short acting beta-blocker immediately prior to surgery is not recommended. The initiation of a beta-blocker should occur under the supervision of a cardiologist and it should be titrated appropriately via an exercise treadmill test.
80
Risk factolrs for sudden death in LQTS:
| acute vs long term mgmt of LQTS
Risk factors for sudden death:
- Female gender
- Males with QT3
- Deafness
- QT > 500 ms
- Widened T waves
Acute management:
- Intravenous magnesium
- Replacement of potassium
- Replacement of calcium
- Avoidance of amiodarone
- kim beta blocked patients dont do well with hypovoemia
Long term management:
- Beta blockade
- Permanent pacing (especially LQT3)
- Cardioverter defibrillator placement
- Left stellate sympathectomy if refractory
81
Managing mitral regurg:
fast, full, forward
82
Ao cross clamp changes-issa lot
Aortic Cross Clamp Hemodynamic Changes:
- Increased arterial blood pressure above the clamp
- Decreased arterial blood pressure below the clamp
- Segmental wall motion abnormalities
- Increased left ventricular wall tension
- Decreased ejection fraction
- Decreased cardiac output
- Decreased renal blood flow
- Increased pulmonary occlusion pressure
- Increased central venous pressure
- Increased coronary blood flow
Aortic Cross Clamp Metabolic Changes:
- Decreased total-body oxygen consumption
- Decreased total-body carbon dioxide production
- Increased mixed venous oxygen saturation
- Decreased total-body oxygen extraction
- Increased epinephrine and norepinephrine
- Respiratory alkalosis
- Metabolic acidosis
83
Native coronary artery dz in cross clamping
Native coronary artery disease (E) will have a significant impact on coronary blood flow. Areas distal to a stenotic lesion will receive less blood flow even when coronary perfusion is increased. If the area distal to the stenosis has increased oxygen requirements and cannot compensate, then ischemia will result.
84
Normally SVO2 is what?
Normally, SvO2 is approximately 75%
85
In what conditions is svO2 increased?
SvO2 is increased in the setting of decreased VO2 (e.g. methemoglobinemia, sepsis, carbon monoxide poisoning, cyanide toxicity, hypothermia) or increased CO (e.g. sepsis, hyperdynamic circulation, left-to-right intracardiac shunting, arteriovenous fistulas).
86
When is sVO2 decreased?
SvO2 is decreased in the setting of reduced Hgb, SaO2, and CO, as well as increased VO2 (e.g. fever, shivering, stress response)
87
Pericardial effusion and hematoma are characteristically identified as
echo-free spaces between the epicardium and the pericardium.
88
Echocardiographic signs of pericardial tamponade
Moderate to large pericardial effusion (shown in image)
Right and/or left ventricular collapse during diastole
Right and/or left atrial collapse during systole
Decreased left ventricular filling with inspiration
Increased right atrial and ventricular filling with inspiration
89
Complications from lead extraction:
| Predictors of complications from lead extraction
Major complications that can be seen with ICD lead extraction include death, cardiac avulsion or tear, stroke, pulmonary embolism, arrhythmia, and infection. Other complications include pericardial effusion, hemothorax, hematoma at extraction site, arm swelling or thrombosis, vascular injury at site of extraction, migrated lead fragment, and pneumothorax. Predictors of complications include longer implant duration, physician inexperience, large number of leads needing extraction, use of laser techniques, and female gender
90
Adverse outcomes with machines are most likely due to:
Adverse outcomes secondary to equipment related malfunction or misuse occur, with misuse being the primary issue. Proper training and upkeep of the equipment can help decrease the risk. However, it is most likely secondary to human error which cannot be completely eliminated.
91
When considering flow through a narrow orifice (valvular or airway stenosis), what formula/principle is helpful? Which masks use this principle? Explain
Bernoulli. Pressure Gradient = 4 * (Velocity)^2
Venturi masks:Venturi masks (or venti-masks) use the Bernoulli principle to deliver a specific concentration of oxygen to the patient. The mask uses 100% oxygen flowing into a wider point via a narrow orifice. Because of the narrowing, the oxygen speeds up and the pressure drop at that point is below atmospheric pressure. This causes room air to be drawn to this low pressure point, hence diluting the 100% oxygen to the calibrated value set by nozzle. This is known as the Venturi effect and is a consequence of the Bernoulli principle.
92
Transplanted heart: when it comes to bradycardia,
During cardiac transplantation, the heart is denervated and can only respond to direct-acting agents.
93
Which drugs can you give for bradycardia in the denervated heart?
Isoproterenol, a nonselective β-adrenergic agonist, is the drug of choice for this patient population due to its direct chronotropic and inotropic effects.
Epinephrine and norepinephrine should be reserved for refractory bradycardia because beta effects will be exaggerated as a result of the lack of the baroreceptor reflex.
94
Transplanted heart and muscle relaxants, cardiac drug and antichoinesterases (igmines)
The transplanted heart shows no response to pancuronium or digoxin. The response to anticholinesterases is unpredictable and may lead to profound bradycardia.
95
What would you possibly see on the EKG in a patient with a transplanted heart?
lectrocardiographic analysis of a patient with a transplanted heart may demonstrate two P waves, especially during the first few weeks, since one technique involves the native right atrium being sutured to the transplanted right atrium. The appearance of two P waves should not be confused with complete heart block. Newer techniques, such as complete bicaval, would not show two P waves.
96
Maintenance in cardiac tamponade:
| Best diagnostic tool for detecting pericardial fluid collection:
Keep it fast, full, and tight!
Cardiac output is heart rate dependent (“fast”), stroke volume is fixed and dependent on adequate preload (“full”), and the vascular tone should be (“tight”). Transesophageal echocardiography is the best diagnostic tool for detecting a pericardial fluid collection.
97
What is Beck's triad and when would you see it?
Acute cardiac tamponade presents with falling arterial pressure, increasing venous pressure, and muffled heart sounds (Beck triad)
98
What could happen if you reduced afterload in cardiac tamponade? Agents of choice for induction? Would you intubate these patients?
Reducing afterload could prove to be extremely detrimental and lead to cardiovascular collapse. Etomidate or ketamine are the induction agents of choice since maintaining SVR is imperative.
Intubating is tricky, as you want to avoid PPV. there was a question where they wanted the Wrong answer, and it was either intubation (awake) or afterload reduction, and afterload reduction is always a no.
99
What pressures are equillibrated in Cardiac tamponade?
nitially, the hemodynamic consequences begin as pressure is exerted upon the right atrium and continues until there is equilibration of right atrial pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure.
100
What does fenoldopam do-what does it dilate? What does it do to PVR? What does it to do natriuresis and diuresis? When is it indicated?
Fenoldopam has been shown to preferentially dilate renal and splanchnic vascular beds, leading to an increase in renal blood flow and an overall decrease in peripheral vascular resistance (A). It also has been shown to increase natriuresis (C) and diuresis. It is indicated for use during cardiac surgery and aortic aneurysm repair because of its anti-hypertensive and renal protective effects
101
Fenoldopam should be avoided in which type of patients?
Fenoldopam will lead to increases in intraocular pressure and should be administered with caution or avoided all together in patients with glaucoma or intraocular hypertension.
102
So with Furosemide, What does it do to those Frank Starling curves?
It still is on the same line as heart failure, but the EDV decreases. The cardiac output doesn't increase.
103
Know all of the points on that Starling curve photo
Okay
104
Loop diuretics and pulmonary:
Loop diuretics also have mild pulmonary vasodilatory properties and are useful in the setting of right ventricular failure to reduce right ventricular preload and afterload.
105
T/F:Patients with left or right ventricular dysfunction may have especially large reductions in ventricular work with increased afterload (systemic or pulmonary vascular resistance).
TRUE
106
could increase in PCWP be a sign of an MI?
Yes.
107
Lead II is the lead that best characterizes
Lead II is the lead that best characterizes P waves and detects arrhythmias
108
Lead V5 is the single lead that is the most sensitive for detection of:
Lead V5 is the single lead that is the most sensitive for detection of MI.
109
Where do you place lead V5?
Lead V5 is placed at the anterior axillary line of the 5th intercostal space and has a sensitivity for myocardial ischemia of 75%.
110
What can V5 tell you? What part of the heart is it monitoring? Elevations vs depressions?
Lead V5 detects changes in conduction over the left ventricle, which is the thickest portion of the myocardium and the most sensitive to subendocardial ischemia as a result of oxygen supply-demand imbalance. With ischemia, conduction slows, and ST depression and T wave inversions may be seen. ST segment elevations suggest full thickness myocardial ischemia, whereas ST depressions suggest subendocardial ischemia.
111
When do troponin levels begin to elevate?
Troponin levels begin to elevate within a few (2-3) hours of ischemia and cellular damage.
112
he only cardiac biomarker that elevates earlier than troponin and CK-MB is ____. Why don't we use this more often?
myoglobin. Myoglobin is very sensitive to cardiac ischemia. However, it is not specific and cardiac myoglobin is indistinguishable from skeletal myoglobin which can be elevated with surgical damage.
113
CKMB may begin to elevate ___ hours after ischemia, but doesn't peak until ____.
2-3 hours after, but doesn't peak for several hours after ischemia
114
The most common cause of an intraoperative MI:
| What causes this type of MI?
The most common cause of an intraoperative MI is an oxygen supply-demand mismatch, also known as a type 2 MI.
A type 2 MI can occur when a patient becomes tachycardic from any cause. Tachycardia increases myocardial oxygen demand while decreasing the time of supply (the left heart receives blood during diastole). Other factors that make a type 2 MI more likely intraoperatively are hypoxia, anemia, and hypotension.
115
What's more sensitive for myocardial injury? Troponin or CKMB?
Troponins are more sensitive than CK-MB for myocardial injury.
116
What does tamponade look like on TEE?
Tamponade results in primarily diastolic dysfunction and compression of the atria or ventricles by the fluid in the surrounding pericardium.
117
Can patients with sepsis have myocardial depression?
Yes, even though they can still have a normal EF-Myocardial depression often occurs early and can be present despite a normal or increased cardiac output. So you can still have some amount of hypokinesis.
118
What would you see on TEE in sepsis?
echocardiography typically shows dilation of both ventricles with global systolic dysfunction and a depressed ejection fraction.
119
Spinal cord injury at T6 or higher-can that affect the heart?
Yes.
120
What does tricuspid regurg do to thermistor measurements?
Tricuspid regurgitation usually, but not always, causes lower cardiac output measurements.
121
What is the typical dose of ATIII, and explain the deal with this deficiency and needing to give it in the OR sometimes.
Typical dose is 2-3 units. Patients can get an iatrogenic ATIII deficiency from being in the hospital and continuously receiving heparin.
122
ACT prior to going on bypass:
480 seconds
123
inheritance for prolonged QT, and caused by which type of mutations?
Prolonged or long QT syndrome (LQTS) can be an inherited disorder (autosomal dominant or recessive) caused by mutations in genes encoding cardiac sodium and potassium channels that cause abnormalities in ventricular repolarization.
124
What can volatile anesthetics do to the QT interval?
| In pts with QT syndrome refractory to Beta blockers, what can they get?
Volatile anesthetics can prolong it
| Refractory? They can get a beta blocker
125
Look at list of drugs that can prolong the QT interval
okay
126
Absolute contraindications to TEE:
perforated viscus, esophageal stricture, esophageal tumor, esophageal tear, esophageal diverticulum, and active upper GI bleed.
127
Look at chart for ways to treat pulmonary hypertension:
Okay
128
Rationale and mechanism-Inhaled Nitric oxide:
Pulmonary vasodilator (minimal systemic effects)
129
R&M-Nitroprusside
Pulmonary vasodilator, decreases preload and afterload
130
R&M-Nitroglycerin
Pulmonary vasodilator, decreases preload
131
R&M-Alprostadil
Prostaglandin E1, direct pulmonary vasodilator
132
R&M-Inhaled epoprostenol
Inhaled epoprostenol-Prostacyclin (PGI2), pulmonary vasodilator (also available IV)
133
R&M-Isoproterenol
Improves ventricular function, β1 and β2 agonist with cardiac inotropy, decreases systemic blood pressure via vasodilation
134
R&M-Epinephrine
Improves ventricular function via β agonism, but may increase PVR via α1 agonism
135
R&M-Norepinephrine
α and β agonist, good cardiac inotrope, combine with inodilators like milrinone, may worsen pulmonary hypertension via α1 agonism if used alone
136
R&M-Dobutamine
β1 agonist, treatment of low cardiac output and right heart failure
137
R&M-Sildenafil
PDE-5 inhibitor, increases cGMP → pulmonary vasodilation
138
R&M-Milrinone
PDE-3 inhibitor, increases cAMP → increased cardiac inotropy, systemic and pulmonary vasodilation; improves right heart failure
139
R&M-Furosemide
Loop diuretic and pulmonary vasodilator
140
What are the factors that contribute to cardiac collapse in VAE?
Factors that contribute to the sudden and catastrophic cardiovascular collapse due to massive VAE include RVOT air lock phenomenon, failing RV due to sudden increased right ventricular afterload, and coronary artery occlusion.
141
Is PEEP good in the prevention of VAE?
There is no proven role for PEEP in the prevention of VAE. It may impair surgical visualization by impairing venous return. It may also increase RA pressures thereby reversing flow through a PFO and introducing air to left-sided circulation.
142
VAE pathophysiology
Look at photo, but basically, air fills up right side of heart, making it difficult to push blood through, and also resulting in collapse of the right side of the heart, air can get into the left side also and even go into the coronaries.
143
After CPB, it is most common to have air in which coronary?
The RCA, but it doesn't mean that it can't happen to other coronaries.
144
Treatment for coronary embolism in a patient after coronary artery bypass:
Support the patient’s hemodynamics and re-heparinize in preparation for return to CPB.
145
Major principle of Starling curve:
Heart will increase pumping with distention up to a certain point. Increasing preload will increase CO until the plateau of the Starling curve is reached
146
What is vasoplegic syndrome? When is it seen? what is it associated with? How can you treat vasoplegic syndrome?
Vasoplegic syndrome can be seen as resistant hypotension following CPB. Vasoplegic syndrome is often seen in patients taking ACE-I and with long CPB times. Vasoplegic syndrome is associated with decreased SVR and relative vasopressor resistance. It is defined as low systemic vascular resistance (SVR index < 1,600 dyn*seg/cm^5/m^2 ) and high cardiac output (cardiac index > 2.5 L/min/m^2) within the first 4 postoperative hours.
Methylene blue and vasopressin are treatment options for vasoplegic syndrome.
KIM vasoplegic people would have a hyperdynamic left ventricle.
147
Would hypovolemia cause wall motion abnormalities?
Not really
148
How do VADs work?
A VAD drains blood returning to the heart and then pumps it downstream of the failed ventricle.
149
New LVADs-will those patients have a pulse? why or why not?
The later generation LVADs are non-pulsatile and the setup is similar to the first generations however they eject blood in a non-pulsatile manner potentially leaving a patient with no pulse. It’s important to note that some patients who have a non-pulsatile device may still have a pulse due to some sustained left ventricular function and ejection through the aortic valve.
150
Can you place an A line in a patient with an LVAD?
You can, but it probably won't read. You could use it to gain access to ABGs though.
151
In LVADS, hypotension results from which two things? Explain?
In patients with LVADs, hypotension results from either inadequate preload or decreased systemic vascular resistance. Right ventricular failure or hypovolemia are the two most common causes of inadequate preload and should be assessed rapidly if hypotension occurs.
152
Look at types of shock photo
Okay
153
Normal cardiac output:
4-8 L
154
Normal cardiac index:
2.5-4 L
155
Normal stroke volume:
60-100 mL/beat
156
Normal stroke volume index:
33 - 47 mL/m^2/beat
157
What is neurogenic shock (aka ____)? What would be seen in it?
Neurogenic shock (distributive shock) may be seen following cervical or high thoracic spinal cord trauma or transection. It is characterized by a loss of sensation and motor function below the level of injury. Autonomic dysfunction results from loss of sympathetic activity and unopposed vagal tone. This leads to hypotension, vasodilation, decreased CVP and PAWP, and usually a reduction in HR and CO.
158
What is septic shock (aka ____) and what parameters would you see?
Sepsis, or vasodilatory shock, leads to a reduction in CVP, PAWP, MAP, and SVR. This is accompanied by an increase in CO and HR. The SvO2 may increase during early sepsis and then fall during late sepsis.
159
Cardiogenic shock parameters:
Cardiogenic shock (either systolic or diastolic associated) will lead to an increase in CVP and PAWP. There will be a decrease in cardiac index, blood pressure, and mixed venous oxygen saturation. Systemic vascular resistance and heart rate may be unchanged or increased.
160
Why can't we ever use the RIJ for central lines?
The right external jugular vein has the least success of central line placement due to its tortuosity and angulation with the clavicle making catheter advancement into the SVC difficult.
161
Subclavian central lines-lowest rate of ___, highest rate of ___. Avoid subclavian lines in:
Subclavian vein central catheterization carries the lowest risk of infection but the highest risk of pneumothorax. Subclavian vein catheterization should be avoided in patients with bleeding diathesis as its location under the clavicle precludes application of pressure for hemostasis.
162
Femoral central line-highest rate of infection T/F:
TRUE
