Cardiac Flashcards
Normal troponin levels after bypass:
When do troponins peak?
Do serum troponins provide predictive and prognostic value for short and long term outcomes?
BELOW 1ng/mL
Trop peaks at 24 hours following injury to the myocardium
Yes
What is pulsus paradoxus? Explain pathophys of cardiac tamponade. Explain collapse-what collapses first?
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.
Milrinone leads to increased ____ and ___.
Inotropy and vasodilation
Why does CVP INrease with aortic cross clamping?
Because with increased catecholamine levels there is increased venoconstriction distal to the clamp driving CVP higher.
Why is there an increase in ABP after aortic cross clamping?
Because same amount of blood occupying smaller space-ABOVE the level of the clamp
Pulmonary artery wedge pressure after aortic clamping
Pulmonary artery wedge pressure increases as blood redistributes in smaller container.
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
Increased everything except pressure below and cardiac output and renal blood flow
NPO Guidelines are based on what?
Gastric residual volumes
What does hypocapnia do to the uterus?
If severe enough, it can cause vasoconstriction
UBF is proportional to what pressure??
It’s inversely proportional to which resistance and pressure?
Uterine arterial pressure (prop)
Inversely to uterine venous pressure and uterine vascular resistance.
ST segment depression means what? How does it differ from acute coronary occlusion? why do you see this more often than transmural injury?
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.
ST segmebt elevation is seen with what?
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
What is needed to make a dx of STEMI?
ST elevation in 2 or more contiguous leads is required to make an ECG diagnosis of STEMI.
What do T wave inversions mean?
T wave inversions (D) are a sign of acute myocardial ischemia but do not specifically pertain to a subendocardial or transmural injury
T/F:V5 is the best lead for monitoring intraoperative ischemia.
TRUE
What are the most sensitive and earliest signs of myocardial ischemia?
Echocardiographic wall motion abnormalities
Elective repair of an aneurysm is indicated if
if the size is > 5.5 cm or the rate of growth is > 1.0 cm per year.
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.
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
Whats the deal with adenosine and asthma?
Adenosine should be cautiously used in patients with asthma or upper respiratory disease because adenosine can cause bronchoconstriction.
T/F: femoral dissection presents with hypotension and peritoneal extravasation.
FALSE:Femoral dissection generally will not present with severe hypotension or peritoneal extravasation
Most common complication of TAVR: Other complications:
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
What are the 3 types of protamine reactions:
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.
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?
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
Common systolic murmurs and common diastolic murmurs:
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
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.
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
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
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.
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.
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)
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.
with transcutaneous-After the RV is paced, then what is paced?
After RV, then LV
t/F:
The most common reason for not obtaining capture with transcutaneous pacing is not adequately increasing the current.
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.
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
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.
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.
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.
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
What happens to preload during laparoscopic surgery?
It is decreased-keep in mind that CVP is increased.
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.
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.
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.
Typical joule dose for cardioversion is what?
100 Joules
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.
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).
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.
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
Centrifugal pump flow varies with what?
Centrifugal pump blood flow varies depending on pump preload and afterload.
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.
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.
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
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.
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.
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.
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.
Contraindications to IABP:
Contraindications to IABP placement include moderate to severe AI, aortic disease, and severe peripheral vascular disease
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
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.
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).
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.
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
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.
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
