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For Acute Coronary Syndrome: _____ people in U.S. admitted each year to the hospital and ___% will die
1.4 million; 38
What is the continuum of ACS?
The pathogenesis for ACS is the same, more than __% are from disruption of plaque
Tell me the pathogenesis of ACS
disruption of plaque → platelet aggregation → coronary thrombus will form. Result is the imbalance of myocardial oxygen supply & demand.
The actual type of ACS that will develop depends on what?
- The degree of coronary occlusion
- The associated ischemia w/that coronary occlusion.
- Usually a thrombosis that’s only partially occluded responsible for unstable angina and NSTEMI. (these being fairly closely related)
What is really the only difference between NSTEMI and unstable angina?
NSTEMI results in necrosis of myocardium whereas unstable angina does not
When would we see a STEMI? (the cause)
the thrombus completely obstructs the coronary arteries
Explain the evolution of myocardial infarction (the short version from Sue's slide)
- Acute coronary artery occlusion w/ insufficient collateral flow
- Dilation of local vessels filled with stagnant blood
- Oxygen consumed & hgb deoxygenated→ Tissue edema
- Death of heart muscle
When the acute occlusion in coronary artery happens, coronary blood flow stops, and if not enough collateral flow, infarction results. What happens next?
Shortly after the onset of the infarct a small amount of blood will begin to works its way into the infarcted area. Local vessels dilate and filled w/stagnant blood. Because the muscle fibers are continuing to use up whatever O2 avail. The HgB becomes deoxygenated. The color that the infarcted area takes on is bluish/brownish hue because of deoxygenated HgB. Blood vessels engorged blue/brown color. As progression, vessel walls becomes highly permeable and fluid leaks out, local tissue around area of infarct becomes edematous. Decrease cell metabolism, no blood supply effectively so at this point the muscle dies
For heart to remain alive, requires ___mlof O2 /100g of muscle tissue/min as a minimum.
That’s substantially less than usual supply of ___ml/100g/min that goes to the LV.
If ______% of normal coronary flow remains, the muscle won’t die
What part of the ischemic area is most at risk of dying?
- central to infarct, not getting collateral blood flow.
- Also the subendocardial muscle, is at risk, because during contraction (systole) the perfusion to subendocardial area is decreased and those vessels are compressed during systole. The damage spreading out towards the epicardium.
What are the three clinical classifications of ACS?
- 1.Unstable angina (doesn’t result in necrosis as long as ischemic episode is terminated before necrosis occurs)
*2&3: when ischemia is enough to cause myocardial cell death
How do we describe the extent of necrosis? (classification)
1.Transmural (Will span entire thickness of the myocardium. Result from total prolonged occlusion of one of those epicardial coronary arteries)
2.Subendocardial (involves the innermost layers of myocardium, particularly susceptible to ischemia, the zone subjected to highest pressure of ventricular chamber (right next to it) & few collateral supply it. The vessels that perfuse it get squeezed during systole)
What dies first is the area of myocardium that’s supplied by whatever vessel is occluded. What happens to the adjacent tissues?
Adjacent tissue may not immediately die. Won’t necrose as long as blood vessel supply that tissue are still patent. The problem comes when O2 supply continues to be reduced. Consequently, the region of infarction will spread outward.
5 factors that really relate/predict the amount of tissue that will ultimately die.
- 1. Mass of myocardium perfused by occluded vessel
- 2. Magnitude and duration of impaired flow
- 3. Oxygen demand in that particular area that’s affected
- 4. Collateral flow, how good is that in perfusing the area
- 5. Degree of the response of the tissue that might modify the ischemic process.
All the pathological changes that occur happen in two stages. What are the two stages and their (Basic) definitions
Early: occur during the time of the infarctionLate: those that happen during period of healing and remodeling.
Why happens at the cellular level during an MI?
- Shift from aerobic to anaerobic metabolism. Mitochondria can’t break down fat or oxidize the products of glycolysis, so ATP production fails. Lactic acid builds causing acidosis.
- No ATP which is needed for Na/K ATPase pump, so K+ out of and Na+ (& H2O) into the the cell = intracellular edema. Too much ECF K+ + leaky cell membranes = altered electrical potentials across the membrane so arrhythmias are likely to occur. Calcium also will accumulate inside the cell. Contribute to the whole pathway of cell destruction. Which happens because lipases (breakdown lipids) proteases (break down protein) get activated and membrane is protein lipid bilayer.
After there is an occlusive thrombosis. Within ____ min the myocardial function is compromised. Unless there is some sort of intervention to revascularize tissue, cell injury becomes irreversible in ____ min.
With occlusive thrombosis, the myocardium becomes really edematous in ________hr. Why does this happen?
4-12hr because of increase permeability, defective membranes.
With occlusive thrombosis, an acute inflammatory response happens and the ________ begin to infiltrate so the damage continues for ________________
neutrophils (WBC); another 18-24hrs
Early changes, minute by minute & hour by hour (from a table she put on the slide)
- 1-2min: ATP levels fall; cessation of contractilty
- 10min: 50% depletion of ATP, cellular edema, ↓membrane potential & susceptibility to arrhythmias
- 20-24min: irreversible cell injury
- 1-3hr: wavy myofibers (WTF?)
- 4-12hr: hemorrhage, edema, PMN (aka neutrophils) infiltration begins
- 18-24hr: coagulation necrosis & edema
- 2-4days: total coagulation necrosis, monocytes appear, PMN infiltration peaks
Late changes: (per the table on sue's slide)
- 5-7 days: yellow softening from resorption of dead tissue by macrophages
- 7+ days: ventricular remodeling
- 7 weeks: fibrosis and scarring complete
Late changes (long version)
- Clearing of necrotic myocardium.
- Then there's deposition of collagen which forms scar tissue
- Neutrophils go in w/macrophages they will invade the inflamed myocardium and that’s what takes away the necrotic tissue.
- That clearing by neutrophils and macrophages, gets combined w/both thinning and dilation of infarcted area so the ventricular wall becomes weakened structurally.
- d/t that possibility of rupture of the myocardial wall.
- Finally, fibrosis and scarring. Fibrosis occurs and scarring gets complete about 7weeks post infarct
One of the functional alterations of an MI is impaired contractility & compliance. Describe this.
- Systolic dysfunction: Destruction of myocardial cells, naturally ventricular contraction is impaired & results in systolic dysfunction. Loss of synchrony of contraction of myocardial cells, so CO gets further compromised.
- Diastolic dysfunction:ventricular relaxation is also dependent on ATP, ventricular compliance is impaired
Part of the systolic dysfunction in impaired contractility and compliance can be described by three different types of wall motion abnormalities. Name and describe them.
- 1. Hypokinesis: localized region of reduced contraction.
- 2. Akinesis: there is segment of myocardium not contracting at all.
- 3. Dyskinesis: region that bulges outward during contraction (normal part of ventricle is contracting inward) this is working in opposite direction, going outward.
Stunned myocardium is a functional alteration from an MI. What is this?
- refers to tissue that will demonstrate a prolonged systolic dysfunction after a period of sever ischemia.
- Isolated period ischemia, even though blood flow is restored, myocardium is stunned, not function properly from a systolic perspective.
- Over period of days to weeks, gradually, the heart is able to pump normally.Initially could appear as infarct in this area, because of the contractile systolic dysfunction but overtime function will return, as long as just stunned and not necrotic
Ischemic preconditioning is a functional alteration from an MI. What is this?
- Actually a phenomenon where brief periods of ischemia to particular region of myocardium makes area more resistant to subsequent episode of ischemia.
- Clinically relevance: if pt sustains an MI in the context (angina episodes leading up to it) will have less morbidity and mortality perhaps because of this ischemic preconditioning as opposed to pt. who didn’t have periods of ischemia, major coronary thrombosis, they are more likely to have higher morbidity and mortality
Ventricular Remodeling is a functional alteration from an MI. What is this?
- Changes in geometry of infarcted areas and non infarcted areas of ventricular muscle.
- Will effect the long term prognosis and how well the heart will function long term.
- The infarct can expand where the effected part of the ventricle enlarges.
- There can be an increase in wall stress, a decrease in systolic contractile function, and an increase in likelihood of an aneurysm can form (A ventricular aneurysm).
- There can also be dilatation, of the non infarcted segments that are really now working harder, subjected to increased wall stress.
- This gets back to frank starling, initially dilation is somewhat compensatory, to maintain CO the chamber dilates but ultimately results in heart failure and ventricular arrhythmias
What are a few things that can modify ventricular remodeling?
- Reperfusion therapy, something that will limit the size of the infarct and limited the expansion of the infarct.
- Drugs, ACE-I, shown to attenuate progress remodeling and decrease both short and long term post infarct mortality.
What is the clinical presentation of unstable angina?
- Acceleration of ischemic symptoms.
- Can happen in 1 of 3 ways:
- 1.Crescendo pattern- Pt.. had chronic stable angina, used to have angina only w/exertion but now has angina at rest, without any provocation.
- 2. Can have sudden increase in frequently,
- duration, and intensity of episodes.
- 3. New onset of anginal symptoms that are
- described as severe, in a patient w/no previous symptoms of coronary disease.
Any of these presentations is unstable angina & unless the ischemia is corrected, they’ll continue on continuum. (STEMI or NSTEMI) unless things get quickly treated.
Characteristic pain is a symptom of an acute MI, describe this.
- Severe persistent typically substernal
- Resembles angina qualitatively but usually much more severe, lasts longer, and it often radiates more widely.
- Lactate or adenosine might be responsible as mediator for the sensation.
- Dermatome level being C7-T4, but if talking MI it may radiate more widely.
- Symptoms crescendo fast and pt.has feeling of doom. Pain not relieved by rest, not usually relieved by Nitro
What are the SNS effects during an acute MI?
Diaphoresis and cool, clammy skin
What are the PNS effects during an acute MI?
What are the inflammatory s/s during an acute MI
What are the cardiac findings during an acute MI?
- catecholamine release: ↑HR, systolic dysfunction, ↓SV & ↑ EDVP depending on how much muscle is involved
- Stiff LV diastolic dysfunction →pulmonary congestion→ stimulate juxtacapillary receptors (rapid shallow breathing & dyspnea) Transudation of fluid into alveoli if there is pulmonary congestion.
- S4- indicative of atrial contraction into a non compliant LV. S3 may be heard if there is systolic dysfunction
- Volume overload
- LV failure
When would you hear a systolic murmur during an acute MI?
papillary muscle rupture, mitral insufficiency VSD cause by infarct that ruptures the intraventricular septum
Describe the typical symptoms, serum biomarkers, and EKG findings of unstable angina
- Crescendo, rest, or new onset angina
- No serum biomarkers
- ST depression and/or T wave inversion
Describe the typical symptoms, serum biomarkers, and EKG findings of NSTEMI
- Prolonged "crushing" chest pain more severe and wider radiation than usual angina
- Serum biomarkers
- ST Depression and/or T wave inversion
Describe the typical symptoms, serum biomarkers, and EKG findings of STEMI
- Prolonged "crushing" chest pain more severe and wider radiation than usual angina
- Serum biomarkers
- ST elevation (and later Q waves)
When tissue are damaged, cell membranes break down consequently intracellular contents leak into interstitial space and then into circulation.
The fact we can use troponins and the CK-MB these are helpful because ????
they rise above a normal threshold and do so in a defined sequence over time
What exactly is troponin?
a protein in muscle cells, helps actin and myosin filaments come together
There are 3 subtypes or subunits of troponin found in both skeletal and cardiac muscle but the cardiac forms of ______and ______ are structurally unique and there are specific assays to detect them.
TRUE or FALSE. Any elevation in troponin I or T likely means myocardial damage.
- TRUE! A healthy individual has essentially non of these, even minor elevation in troponin I or T sensitive and powerful biomarker of myocardial issue (not necessarily an MI)
- HOWEVER, both troponins are highly specific and highly sensitive so they are really the preferred biomarkers for necrosis.
How can we tell if the elevated troponin is an MI vs something like myocarditis?
Troponin can also be detected in certain other cardiac situations (Strain, inflammation, myocarditis, HF, pulmonary embolism, RV strain) but what helps in dx an MI is that if the level is fairly predicable when it rises.
With an MI the cardiac troponin levels rise ____hr after onset of discomfort. Then peak at
_____hrs. Decline slowly so you could still detect troponin levels up to _____days following a large MI.
- onset: 3-4hr
- peak: 18-36hr
- Duration: up to 10-14 days
CK is a biomarker. Where is CK found?
- heart, skeletal muscle, brain, and a # of other organs.
- Gets released w/damage to any of those tissues.
There are three isoenzymes of CK, helps determine what organs involved, heart is CK- MB isoenzyme but where else is this found?
- small amounts in uterus, prostate, gut, diaphragm, tongue.
- Makes up 1-3% of CK in skeletal muscle as well.
- So part of it would be determining no damage or trauma to these other organs in which case if there is increase CKMB is suggestive of MI
We use a ratio of CKMB to total CK in order to facilitate dx of MI. what is the % that suggests an MI?
- Ratio is greater than 2.5% (MI)
- Less when the increase is from other source.
** we can also use the time pattern of increase, peak and normal to see if MI or another source**
What is the time pattern of increase in CK-MB post-MI?
- Time to increase 3-8 hrs post MI
- Peaks in 24 hrs
- Returns to normal within 48-72 hrs
Which is more specific and sensitive to an MI, troponin or CK-MB?
Biomarkers are important but sometimes we need to figure out if it's an MI without them, why?
because there is delay in being able to detect these biomarkers, not useful the acute period, where we rely on s/s and EKG
What is the myocardial infarction triad?
- --Transient T wave inversion 2° altered repolarization of ischemic cells
- --ST segment deviates from baseline
- ****Subendocardial = ST depression
- ****Transmural = ST elevation
- Infarction (Necrosis)
- --Q waves (significant)
- ***1 mm wide (1 small square)
- ***1/3 the height of the QRS
- **Avoid lead AVR (Q’s unreliable)
TRUE or FALSE. In order for a Q wave to be significant, it must be 1/3 height of the QRS and 1mm wide
FALSE can be either or
On the EKG, the only difference between NSTEMI and unstable angina is...
whether the changes or transient or persistant
What changes will you see on an EKG w/unstable angina or NSTEMI?
ST depression and/or T wave inversion
Explain the changes on an EKG overtime with a STEMI
- Acute: ST elevation
- Hours: ST elevation, ↓ R wave, Q wave
- Day 1-2: T wave inversion, Q wave deepens
- Days later: ST normalizes, T wave inverted
- Weeks later: ST & T normal, Q wave persists
which coronary is involved w/an anterior infarct? Where would you see changes on the EKG?
- Q’s & ST elevation in leads V1, V2, V3, V4
Which coronary is involved in a lateral infarction? Where would you see changes on the EKG?
- Q’s & ST elevation in leads I & AVL
Which coronary is involved in an inferior infarction? Where would you see changes on the EKG?
= RCA dominant in most individuals supplying the posterior descending artery
Q’s & ST elevation in leads II, III, & AVF
Which coronary is involved with a posterior infarct? Where would you see changes on the EKG?
RCA dominant in most (85%) individuals, in 8% the supply is from the circumflex & the rest are “codominant”
Large R’s & ST depression in leads V1 – V3, possible Q in V6
Always check V1 and V2 for
- ST elevation & Q waves (anterior infarct)
- ST depression & large R waves (posterior infarct)
- Due to LAD occlusion
- Results in Q’s in V1-V4
- ST elevation if acute
- Anterolateral (V3 & V4)
- Anteroseptal (V1 & V2)
Left circumflex occlusion
Q’s in I, AVL, V5 & V6
Lateral changes: I and aVL
Anterolateral :I, aVL, V5 and V6
- Caused by an occlusion of either the R or L coronary depending on which is dominant
- (the R is dominant in most individuals) Dominant in terms of supplying the diaphragmatic surface of the heart
- Inferior MI: leads II, III, and aVF
What causes an acute posterior infarct?
- Occlusion of RCA.
- Odd w/posterior infarct changes you see are opposite
- ST depression as opposed to ST elevation.
- ST depression in V1-V3
- Similarly there is a large R wave instead of a large Q wave in V1-V3 (reciprocal finding)
Both inferior and posterior infarcts are due to?
Acute Inferior MI (II, III, aVF) no q waves so pretty early on.
V1 and V2, ST depression so possible there is a posterior extension. (ST depression in those leads, represents posterior infarct)
V2, V3, V4, V5 and V6, ST elevation anterolateral
What are the anti-ischemic therapies for MI?
- Maybe a Ca+ channel blocker
What are some general measures for an MI
- Admit to ICU
- Continuous EKG monitoring
- Bed Rest
- Pain control (Morphine)
- Supplemental O2
Who benefits from immediate reperfusion therapy? (pharmacological or mechanical)
STEMI (total occlusion of coronary artery)
What are the anti-thrombotic therapies for a STEMI or NSTEMI/unstable angina?
- Antiplatelet agents:
- ASA, clopidogrel, GIIb/IIIa inhibitor (potent anti-platelet agents-for select high risk patients)
- LMWH, Unfractionated IV Heparin,
What is used as an adjunct for ACS?
When would a patient be placed on GIIb/IIIa inhibitor?
- Particularly helpful in decreasing the incidence of recurrent coronary event for pt. that’s undergoing a PCI, often given then Biggest benefit is seen w/pt. w/greatest risk for complications.
- Elevated troponin levels and recurrent chest pain.
If a patient has a STEMI, what are the two immediate options for management?
If emergent PCI available in 90min then Primary PCI
If not, then fibrinolytic therapy (TPA)
If a patient has a NTSEMI/unstable angina, what is the treatment (based on risk assessment = TIMI score)
Low Risk: Conservative Therapy (proceed to cardiac cath only if recurrent angina or predischarge stress test is markedly positive)
High Risk: Invasive strategy (cardiac cath leading to PCI or CABG)--TIMI score 3+
Thrombolysis in Myocardial Infarction Risk Score (TIMI)
- Age > 65>
- 3 risk factors for CAD
- Known coronary stenosis of > 50% by prior angiography
- ST segment deviations on the EKG at presentation
- At least 2 anginal episodes in prior 24 hours
- Use of ASA in prior 7 days (implies a resistance to the effect of aspirin)
- Elevated serum troponin or CK-MB
***score greater than or equal to 3, an early invasive approach is recommended. If an early invasive approach is decided upon, that should mean angiography within 24hrs.
Should you chew ASA?
YES! Chewing an ASA facilitates absorption, therapy continued daily after that
What is the goal HR of Beta Blockade?
Goal HR is 50-60
Why should we use Betablockade w/caution?
reserve those for pt. who is HTN, because increase risk of cardiogenic shock w/pt. w/STEMI.
When is Nitro helpful?
- help w/ischemia pain
- vasodilator in pt. w/HF or severe HTN.
Do patients w/NSTEMI/unstable MI benefit from fibrinolytic therapy?
Fibrinlytic therapy will accelerate the lysis of thrombus, restore blood flow. Limiting myocardial damage--for STEMI pt. only!!!
What is the advantage of new drugs in fibrinolytic therapy?
preferentially bind to fibrin in formed thrombus, not in general circulation so bleeding is less of a problem.
- TPA and RPA new
- Streptokinase is old
Fibrinolytic therapy will restore circulation in ______% of patient w/coronary occlusion
Rapid initiation of fribinrolytic therapy is imporant, why?
if pt. receive therapy within 2hrs of onset of symptoms they have ½ the mortality of the patient who receives after 6hrs
How do we know if reperfusion is successful?
relief of pain, ST segments return to baseline, earlier than usual peaking of the biomarkers
During reperfusion the patient may have arrhythmias, do we treat them?
transient arrhythmias but don’t usually require tx
Do we need antithrombotic agents after reperfusion?
Antithrombotic agents given after reperfusion to prevent reocclusion.
What are some complications of reperfusion? What % of patients aren't suitable for reperfusion therapy?
Complications d/t bleeding risk, up to 30% of pt. may not be suitable candidates for this type of tx.
Primary PCI is an alternative to fibrinolytic therapy, what is this?
immediate cardiac cath and angioplasty w/stenting
How effective is primary PCI?
- Effective in more than 95% of pt greater survival w/lower rates of reinfarction & lower rates of bleeding of fibrinolytic therapy.
- Because of this, preferred tx, but performed by experienced individual w/in 90min of pt. getting to hospital.
When is primary PCI preferred over fibrinolytic therapy? (besides if experienced person can do it within 90min)
- Preferred w/contradincation to fibrinolysis
- In the case of a late presentation (more than 3hrs from symptom onset to hospital arrival)
- Preferred it pt. is in cardiogenic shock, rescue for pt. who don’t’ get adequate response for fibrinolysis
**the antithrombotic therapy has to be used as an essential adjunct.
What are ACE-I good for?
- limit ventricular remodeling.
- Decrease incidence of HF, recurrent ischemia, mortality.
- Benefit becomes additive to BB and ASA.
- Particularly useful for high risk pt. (those w/anterior wall infarct or LV dysfunction)
Acute Management of a STEMI: If pt. at risk for thromboembolism, anticoagulation w/_______ is appropriate.
For unstable angina potential complications
death 5-10% progression to infarction 10-20%.
Once STEMI has occurred the complications are from
the inflammatory and mechanical electrical abnormalities associated w/tissue necrosis. Any early complication from necrosis itself and later complications from inflammation and healing of necrotic tissue
A complication of STEMi is recurrent ischemia, in what % of patients?
- 20-30% of patients
- ischemia = risk of reinfarction
- Urgent cardiac cath & revascularization
Who is at lower risk of recurrent ischemia?
- Not reduced in pt. w/antithrombotic therapy
- Lower in those w/angioplasty and stent placement as part of their early management.
Acute ischemia results in LV not working properly...what happens?
- Systolic dysfunction and stiffness (diastolic dysfunction).
- Both will lead to s/s of HF.
- S/S may include dyspnea, rales, S3.
- Tx involves: diuretics, ACEI, BB, Sometimes an aldosterone inhibitor if EF is less than 40% but if it gets added to ACE (Think about hyperkalemia, watch for it!).
What is cardiogenic shock (complication of MI)
- Severely decrease CO
- Hypotension w/systolic less than 90
- Peripheral tissues aren't adequately perfused.
Cardiogenic shock develops if more than ___% of LV mass has become infarcted.
What is the progression of cardiogenic shock?
Hypotension leads to decrease coronary perfusion, making ischemic work, decrease SV, increase LV size, gets larger, increase O2 demand
Cardiogenic shock occurs in up to ___% of patients following an MI and has a mortality rate of up to ___%.
What is the major source of mortality prior to hospital arrival during an acute MI?
When would you see sinus bradycardia during an acute MI?
- ↑Vagal tone
- ↓SA node perfusion
When would you see Sinus Tachycardia during an acute MI?
- Pain and anxiety
- Volume depletion
- Chronotropic durgs (Dopamine)
When would you see APBs and Afib during an acute MI?
When would you see VPBs, VT and VF?
When would you see AV block (1°, 2°, & 3°)
- IMI (inferior myocardial infarction): ↑vagal tone & ↓AV nodal artery flow
- AM (anterior myocardial infarction)I: extensive destruction of conductive tissue
SA node (~60% of people) and the AV node (80% of people) is supplied by the?
Bundle of HIS is suppied by the LAD
Right BB is supplied by
- Proximal portion: LAD
- Distal portion: RCA
Left BB is supplied by
- left anterior fascicle: LAD
- left posterior fascicle: LAD & PDA
What types of arrthymias would we see during an acute MI?
- Conduction Blocks
What are the different causes of arrhythmias?
- Anatomic interruption to conduction system.
- Accumulation of waste byproducts(acidosis)
- Ion concentrations from leaking membranes. ANS stimulation can cause S. Brady w/increased Vagal tone or S.tach w/SNS stimulation.
- Also frequently give arrhythmogenic drugs like Dopamine that could also contribute.
Vfib is largely responsible for sudden cardiac death in acute MI. What is the importance of the 48hr mark and Vfib?
First 48hrs: transient electrical instability, long term prognosis for survivors of it is not effected.
After 48hrs: Usually from severe LV dysfunction so higher mortality rate from late occurring
Why is S.Tach imporant to tx in the acute MI patient?
↑Myocardial O2 consumption
RV will infarct in about ____ of patients who also have infarct of inferior wall of LV. This again is because the same CA perfuses both, usually the RCA
Mechanical complications of an acute MI
- Papillary muscle rupture
- Ventricular wall rupture
- Ventricular septum rupture
- Ventricular aneurysm
papillary muscle rupture leads to ___
- Mitral regurg
- Could be rapidly fatal
- If only partial rupture might not be fatal but lead to HF and pulmonary edema
If tear in the necrotic myocardium, can lead to rupture of the free wall of the LV. This can occur in _____ weeks, not very common but deadly.
first TWO weeks
Wall ruptures, bleeds into pericardium, tamponade, survival unlikely.
Incomplete rupture of the ventricular wall can result in what?
- Pseudoaneurysm can result = time bomb.
- There might be rupture of the ventricular septum, blood can go into the RV from LV precipitating congestive HF.
True ventricular aneurysm is a ____ complication.
late; occurs in weeks to months
The ventricular wall gets weakened by phagocytosis of that necrotic tissue, there is a local bulge, and there is dyskinesis.
For a true ventricular aneursym, there isn’t any communication of LV cavity and pericardium, so rupture and tamponade don’t develop. What can happen ?
But can get thrombosis w/possible embolization, arrhythmias and HF.
Why can pericarditis happen acutely post MI?
- The inflammation that goes on during infarct can spread to adjacent pericardium.
- Sharp pain, fever, friction rub, usually responds to ASA.
What is Dressler syndrome?
- uncommon form of pericarditis
- can occur in weeks following MI
- Believed to be an immune process, unclear cause.
- Responds to ASA or NSAIDs
Thromboembolism is a complication of an MI. What causes this?
LV not pumping properly, esp. occurs if area of infarct is LV apex or true aneurysm, embolism could lead to CVA or any other similar scenario.
Causes of Patient Death from Acute Coronary Occlusion
- Decreased cardiac output
- Damming of blood in venous system
- Ventricular fibrillation
- Infarct rupture
During an acute infarction, the _____ is the area of nonfunctional tissue
central; If area of ischemia is small, there is little to no death to cardiac muscle cell but even then if its still ischemic, the muscle is temporarily not function, not getting enough nutrition to support contraction.
When area of ischemia is large, what happens is the muscle cells in center of are will die rapidly in _______hrs from total absence of blood supply to that area.
In infarction, the central area is dead, what is the area surrounding that like?
- surrounding that dead are is a non functional area. Here there is both a failure of contraction and failure of impulse conduction
- Further out there is an area that is still contracting weakly
Over time, what happens to the areas injured during an MI?
- The dead cells in middle die, in few days following (the MI) the area gets large.
- The non functional cells are still at risk, some get lost from prolonged ischemia but much of non functional area will recover mostly because of the collaterals.
- After a few days to about 3 weeks most of that non functional becomes functional again or dies (depending on how good the collateral flow is).
- At the same time, fibrous tissue develops among the dead fibers so eventually normal areas hypertrophy to compensate for lost muscle. In this way the heart can partially or totally recover within a few months
Why is the role of rest important durying recovery from an acute infarction?
- Because again the degree of cell death is dependent on degree of severity and workload of heart.
- Anything increased workload will increase O2 consumption (physical or emotional)
- Also coronary steal (on another card)
What is the coronary steal that can occur during recovery of an MI?
- The normal vessels will respond to exercise or stress and vasodilate, w/this steals blood from area of ischemia.
- For that reason we want to limit (eliminate) coronary steal. Another factor in role of rest in recovery of MI (don’t want vasodilation and steal)
Usually post infarct the heart does not retain it pre-infarct pumping ability. Certain normal cardiac reserve built in so usually resting Cardiac function is preserved. What does get effected?
decreased ability to respond to stress, the ability to increase CO during strenuous exercise.
Most periop MI occur in 1st ______hr post-op
Surgery can cause an MI through the inflammatory response and the neuroendocrine response. Describe the basics of this.
- Preceded by tachycardia, and an episode of ST depression (ischemia).
- They are often silent (pt. under GA can’t describe Chest pain) present as NSTEMI.
- Setting of increased demand and decreased supply.
- Can be d/t thrombotic process w/plaque rupture.
- 2 things at work: not mutually exclusive, decreased in coronary perfusion (thrombosis) and increased oxygen demand.
What are the causes of decreased oxygen supply during surgery (cause of an MI)
- Thromboemboli (hypercoaguable state and plaque rupture)
- Decreased Hct
- Decreased Blood Pressure
What are the causes of increased oxygen demand during surgery (cause of MI)?
- HR and BP increase
- Metabolic changes
- Post op shivering
Hx of prior MI is very significant,
surgery is delayed for __ weeks
Highest risk of recurrent MI occurs within the 1st ___days. So in general elective non cardiac surgery delayed________ weeks following angioplasty & __ weeks following stent placement,(up to ___M if a drug eluding stent (allows complete endothelialization and completion of anti-platelet therapy)
30; 4-6; (12M if drug eluding stent)
Risk of MI is increased in known vascular disease, in pt. w/peripheral vascular aortic surgery the combined risk of death from cardiac cause is ______
1:3 (everytime someone appears w/peripheral vascular disease we should assume it’s probably wide spread, not just in coronaries)
Pt. who are stable and going elective major non cardiac surgery, there are 6 independent predictors of major cardiac complications including:
- 3rd degree HB
- Pulmonary edema
There are six cardiac risk factors in patients undergoing elective major noncardiac surgery, what does it NOT include?
- Prior CABB
- Pre-op ST or T wave changes
- Tx w/BB
- Critical AS
- Abnormal cardiac rhythms
- Advanced age.
There are six cardiac risk factors in patients undergoing elective major noncardiac surgery
- High risk surgery (AAA, periph vasc., thoractomy, major abdominal surgery)
- Ischemic heart disease (hx MI, + exercise test, angina, current nitrate therapy, Q waves)
- Congestive heart failure
- Cerebral vascular disease
- Insulin dependent diabetes mellitus
- Pre-op Serum Creatinine >2mg/dL
If the patient is having elective surgery and is stable, what should you do?
Statisfy risk further
If the patient is having elective surgery and has unstable CAD (major clinical risk factors) &/or change in cardiac condition, what should you do?
If pt. has undergone revascularization or not to determine whether and when the pt. has had invasive or non invasive testing. So if revascularization has occurred within __ years or coronary evaluation is within __years and the pt. status has not deteriorated from that time than further cardiac evaluation isn’t indicated.
3 categories of clinical risk factors
Major: unstable coronary syndrome. Decompensated HF, significant arrhythmias or severe valvular disease
Intermediate: the patient with stable angina or previous MI by hx or by q waves on the EKG. Either compensated or prior hx of HF. Insulin dependent diabetes and renal insufficiency.
Minor: those w/thing like HTN, L. BBB, non specific ST /T wave changes. Or a hx of CVA. Not proven to be independent risk factors. The risk is increased in patients w/poor MET capacity.
There are surgery specific factors as well. Non cardiac procedures. Graded as high (emergency major surgery, aortic and another major vascular, peripheral vascular, longer surgeries w/large fluid shifts and/or blood loss) the cardiac risk for those surgeries is greater than __%
The surgeries w/intermediate risk include carotid endocarectomy, head and neck surgery, intraperitoneal surgery, intrathoracic surgery, orthopedic surgery and prostate surgery. Here the risk is _________
less than 5%
Low risk surgery include endoscopic, superficial, cataract and breast surgery with risk of _______________
less than 1%
According to guidelines if 2/3 risk factors present pt. should be considered for further cardiac evaluation:
- high risk surgery, low exercise tolerance and moderate clinical risk factors.
- Whole point is try to determine pts risk assessment first and manage appropriately and get further evaluation.
Most don’t need revascularization. Before surgery, they are managed medically. How?
- Anti-ischemic meds
(Meds helpful may be nitrates or BB)
BB are indicated during periop when?
- Already receiving Beta Blockers (including high or intermediate risk surgery)
- Major clinical risk factors or positive ischemia on preoperative stress testing
When is there insufficient evidence for beta blockers?
- Minor Clinical Risk Factors
- Low risk surgery (despite clinical risk factors)
For beta blockers periop, titrate to a goal HR of ____________
~60 is reasonable.
How are alpha 2 agonist helpful periop to decrease risk of MI
have both sedative and sympatholytic properties that also may help to decrease periop cardiac injury
Are Ca+ channel blockers useful peri-op?
Ca+ channel blockers are controversial perioperatively
Part of Pre-op prep is anxiety reduction, how can we do this?
- Preop visit = 10 mg Diazepam
Intraoperative monitoring (EKG) includes what?
- Know what area of the myocardium is at risk
- Use 5-lead cable whenever available
- Place electrodes in proper location
- Select location for chest lead according to your assessment of “at risk” areas.
- If possible print a pre-induction tracing for later comparison
Intraoperative management includes maintaining stable HD, how?
- HR < 110 bpm
- BP within 20% of baseline
Up to ____% of patients have myocardial ischemia by thallium scans during tracheal intubation
45; But….most episodes of intraop ischemia occur without hemodynamic changes
Tracheal intubation is very stimulating (MACBAR)-ANS stimulation w/incision and intubation
Why is increased HR so bad?
Increase in HR is more likely than HTN to produce ischemia esp. if HR is more than 110. Problem w/HR, not only are we increasing our demand but we’re decresing our supply, shortening filling time, decreased time for coronary blood flow during diastole
TRUE or FALSE. Maintain oxygen supply balance is MOST important than any particular technique or any particular drug.
What meds can we use during induction?
- Propofol, Thiopental, Etomidate all OK
- (As long as you can maintain adequate HD nothing wrong w/the rest of the meds)
- Avoid Ketamine
Which should you use for intubation, succs or NDMR?
- Succs ok if needed for RSI.
- Often will use NDMR because you can titrate NDMR and induction drug more carefully and essentially dial a BP by maintaining just the right depth of anesthesia so you don’t have sympathetic discharge during laryngoscopy
What could you use to attenuate the response during laryngoscopy?
- Lidocaine 1.5 mg/kg IV 90 seconds before
- Fentanyl (slows HR-good, more time for coronaries to fill, less work on heart, etc.)
For intraop. management, how would we maintain the patient?
- Volatiles = vasodilation. (can be good or bad, as long as you maintain adequate HD, it’s ok)
- But also can get coronary steal w/Isoflurane (if steal prone anatomy)
- Also decreases myocardial oxygen consumption.
For Intraop management, opioids can be used for maintenance, which one is especially useful?
Fentanyl (decreases HR)
Muscle Relaxation is used intraoperatively for maintenance. What should we know about this?
- Consider side effects:
- Histamine release (give slow)
- Ganglionic blockade (can ↑ HR)
- Anticholinesterase side effects (↓HR)
- Antimuscarinic side effects (↑HR)
- (for pt. that has risk factors, this the pt that we tailor glycopyrrolate dose, don’t automatically give standard dose)
What would be our tx for intraop ischemia?
- Tachycardia → Beta blockade (Esmolol)
- HTN → NTG vs Labetolol
- Hypotension → Ephedrine vs Phenylephrine vs IV fluids
Intraop, what could be some causes of SNS stimulation
- Pain → Adequate analgesia
- Hypothermia → Avoid &/or treat shivering
- Hypercarbia & hypoxemia→ Insure adequate ventilation & MR reversal
What is a bundle brach block?
- Non-simultaneous ventricular depolarization
- Widened QRS
- 2 “R” waves--R & R1
In Right BBB, the impulse goes where first (right or left)?
impulse to L first, then delayed to R BB
Why can't we diagnose an MI for an EKG w/ L. BBB
any Q WAVES get buried in middle of QRS. Distortion of bundle makes EKG interpretation more difficult.
If RIGHT ventricular hypertrophy, we look at which leads and see LARGE r waves?
- V1 & V2
- LARGE r wave as opposed to small that we'd expect to see in V1 and V2.
- Also cause of R axis deviation.
If there is LV hypertrophy (fairly common from HTN and AS), which leads are we looking for a large R wave? What else might we see?
- V5 & V6 (really large R wave)
- Also see a very large S wave in V1.
- Reflects large muscle mass that’s developed.
If the QRS is + (above line) in both aVF and Lead I, what is the axis?
If the QRS is + in lead I, and - in aVF, what is the axis?
Left axis deviation
If the QRS is - in lead I and + in aVF, what is the axis?
Right Axis Deviation
If the QRS is - in both lead I and aVF, what is the axis?
Extreme Right Axis Deviation
RV hypertrophy causes R. axis deviation, what could be the causes of this?
- Pulmonic stenosis
- Tricuspid insufficiency
- Tetrology of Fallot
- Posterior infarction
- Hypertrophic cardiomyopathy
- Right BBB
- “normal variant”
LV hypertrophy causes L. axis deviation, what could be the cause of this?
- Aortic stenosis
- Aortic regurg
- Congenital heart disease
- Left BBB
What would you like to do?
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