Step Up - Diseases Of The Cardiovascular System Flashcards
1
Q
In a patient with CAD, goal of LDL is:
A
Less than 100mg/dL
2
Q
Ischemic pain - What should be noted especially?
A
- Does NOT change with breathing nor with body position.
2. Patients do NOT have chest wall tenderness.
3
Q
Two conditions termed syndrome X:
A
- Metabolic syndrome X
2. Syndrome X
4
Q
Syndrome X?
A
- Exertional angina with NORMAL coronary arteriogram - Patients present with chest pain after exertion but have no coronary stenoses at cardiac catheterization.
- Exercise testing and nuclear imaging show evidence of myocardial ischemia.
- Prognosis is excellent.
5
Q
Diagnosis of CAD - Physical exam?
A
Most of the times –> normal.
6
Q
Best initial test for all forms of chest pain?
A
ECG
7
Q
Diagnosis of CAD - Resting ECG:
A
- Usually normal in patients with stable angina.
- Q waves are consistent with a prior myocardial infarction.
- If ST segment or T wave abnormalities are present during an episode of chest pain, then treat as for unstable angina.
8
Q
Diagnosis of CAD - Stress test - Features?
A
- Useful for patients with an intermediate pretest probability of CAD based upon age, gender, symptoms.
- For patients with normal resting ECG, determine whether the patient is capable of performing treadmill exercise.
- If so, proceed to an exercise stress test.
9
Q
Stress ECG - Use where?
A
- To confirm diagnosis of angina
- To evaluate response of therapy in patients with documented CAD.
- To identify patients with CAD who may have a high risk of acute coronary events.
10
Q
Stress ECG - Features?
A
- Recording ECG before, during, and after exercise on a treadmill.
- 75% sensitive if patients are able to exercise sufficiently to increase HR to 85% of max predicted value for age.
11
Q
How do we calculate a person’s max HR?
A
By substracting age from 220 (220-age).
12
Q
Stress ECG - Detection of ischemia is based on?
A
ST depression –> Exercise-induced ischemia results in subendocardial ischemia, producing ST segment depression.
13
Q
Stress ECG - Other findings besides ST depression?
A
- Onset of HF
- Ventricular arrhythmia during exercise
- Hypotension
14
Q
Patients with a positive stress test should undergo what?
A
Cardiac catheterization
15
Q
To sum up - A stress test is considered positive, if the patient develops any of the following during exercise:
A
- ST depression
- Chest pain
- Hypotension
- Significant arrhythmias
16
Q
Stress Echocardiography - When to perform?
A
Performed before and immediately after exercise.
–> Exercise-induced ischemia is evidenced by wall motion abnormalities (eg akinesis, dyskinesis) not present at rest.
17
Q
Stress Echo - Better than stress ECG?
A
- Favored by many cardiologists over stress ECG.
- More sensitive in detecting ischemia.
- Can assess LV size and function.
- Can diagnose valvular disease.
- Can be used to identify CAD.
18
Q
Patients with a positive stress Echo should undergo?
A
Cardiac catheterization.
19
Q
To sum up - Types of stress tests:
A
- Exercise tolerance test –> ST-segment depression.
- Exercise or dobutamine echo –> Wall motion abnormalities
- Exercise or dipyridamole thallium –> Decr. uptake of the isotope during exercise.
20
Q
Thallium - What happens with viable myocardial cells?
A
Viable myocardial cells extract the isotope from the blood - No isotope uptake means no blood flow to an area of the myocardium.
–> Important for… REPERFUSION!
21
Q
Thallium perfusion imaging - Pros and cons?
A
- Incr. the sensitivity/specificity of exercise stress test.
- More expensive.
- Subjects patient to radiation.
- It is not helpful in the presence of a LBBB.
22
Q
If the patient cannot exercise - Perform what?
A
A pharmacologic stress test.
23
Q
Pharmacologic stress test - How to perform?
A
- IV adenosine
- Dipyridamole
- Dobutamine
are used.
Combined with: ECG, echo, nuclear perfusion imaging.
24
Q
IV adenosine and dipyridamole lead to GENERALIZED coronary vasodilation. What is the importance of this?
A
Since diseased coronary arteries are already MAXIMALLY DILATED at rest to increase blood flow, they receive relatively less blood flow when the entire coronary system is pharmacologically vasodilated.
25
Holter monitoring (ambulatory ECG) - useful in what?
1. Detecting silent ischemia.
2. Arrhythmias
3. HR variability
4. Assess pacemaker and implantable cardioverter-defibrillator (ICD) function.
5. Useful in evaluating unexplained syncope and dizziness as well.
26
What is the definitive test for CAD?
Coronary angiography
27
Coronary angiography is often performed together with?
PCI or for patients being considered for revascularization with CABG.
28
What happens if coronary angiography is severe?
CABG - for Left main or 3-vessel disease.
29
Cardiac catheterization - Features?
1. Most accurate method of determining a specific cardiac diagnosis.
2. Provides info on hemodynamics, intracranial pressure measurements, CO, SaO2.
30
Indications for cardiac catheterization?
Generally performed when revascularization or other surgical interventions are considered.
1. Positive stress test
2. Angina + Non invasive tests are nondiagnostic/angina despite medical therapy/Angina post MI/Angina that is diagnostic dilemma.
3. Severely symptomatic patient and urgent diagnosis/management are necessary.
4. Evaluation of valvular disease, and to determine the need for surgical intervention.
31
Coronary angiography - Features?
1. Most accurate method of identifying presence and severity of CAD.
2. Standard test for delineating coronary anatomy.
32
Coronary angiography - Purpose?
Main purpose is to identify patients with severe coronary disease to determine whether revascularization is needed. Revascularization with PCI involving a balloon and/or a stent can be performed at the same time as the diagnostic procedure.
33
Standard of care for stable angina?
Aspirin + Beta blocker (only ones to lower mortality).
| + Nitrates for chest pain.
34
Side effects of nitrates?
1. Headache
2. Orthostatic hypotension
3. Tolerance
4. Syncope
35
First line beta blockers?
Atenolol and metoprolol.
36
Routes for nitrates?
1. Oral
2. Sublingual
3. Transdermal
4. IV
5. In paste form
For chronic angina, oral or transdermal patches are used.
37
CCB - Mechanism of action?
Cause coronary vasodilation + AFTERLOAD reduction, in addition to reducing contractility.
38
If CHF is also present - Give what?
ACEIs + Diuretics.
39
Revascularization - Where is it preferred?
1. May be preferred for high risk patients.
2. Some controversy whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%.
40
Revascularization - Methods?
1. PCI
| 2. CABG
41
Revascularization - does it reduce the incidence of MI?
NO - But does result in significant improvement of symptoms.
42
General guidelines - Management of all patients?
Risk factor modification + Aspirin.
43
General guidelines - Mild disease (normal EF, mild angina, single vessel disease):
1. Nitrates
2. Beta blocker
3. Consider CCBs if symptoms continue.
44
General guidelines - Moderate disease (normal EF, moderate angina, two-vessel disease):
If the above regimen does not control symptoms --> Coronary angiography to assess suitability for revascularization (either PCI or CABG).
45
General guidelines - Severe disease (Decreased EF, severe angina, 3 vessel/left main or LAD disease):
Coronary angiography and consider for CABG.
46
PCI - What is it?
Consists of both coronary angioplasty with a balloon and stenting.
47
PCI - Should be considered in?
1. Patients with one-, two-, three-vessel disease.
| 2. Best used if proximal lesions.
48
PCI - Significant problem?
Restenosis --> Up to 40% within the first 6 months.
49
Main indications of CABG:
1. 3-vessel disease with >70% stenosis in each vessel.
2. Left main coronary disease with >50% stenosis.
3. LV dysfunction
50
Acute coronary syndrome:
The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion.
USA, NSTEMI, STEMI
51
USA - Pathophysiology?
O2 demand is unchanged - Supply is decreased secondary to reduced resting coronary flow.
This is in contrast to stable angina - which is due to increased demand.
52
Why is USA significant?
Because it indicates stenosis that has enlarged via thrombosis/hemorrhage/or plaque rupture.
--> May lead to total occlusion of a coronary vessel.
53
Which patients may be said to have USA?
1. Chronic angina + Incr. frequency + duration + intensity of chest pain.
2. New-onset angina that is severe + worsening.
3. Angina at rest.
54
How do we distinguish USA from NSTEMI?
Only with cardiac enzymes.
55
What ECG finding is common in BOTH NSTEMI + USA?
ST elevation + Q waves.
56
Is there a problem with USA and stress testing?
YES - Patients with USA have a higher risk of adverse events during stress testing - Should be stabilized first.
57
Treatment of USA - First things to do?
1. Hospital admission on a floor with continuous cardiac monitoring.
2. Establish IV access and give supplemental O2.
3. Provide pain control with nitrates + morphine.
58
Medical management of USA?
AGGRESSIVE --> Treat as MI except fibrinolysis.
59
What drugs to give in USA?
1. Aspirin/Clopidogrel
2. Beta blockers
3. LMWH - Enoxaparin (DoC)
4. Nitrates are 1st line therapy
5. O2 if patient is hypoxic.
6. Abciximab/Tirofiban
7. Morphine is CONTROVERSIAL (may mask symptoms).
60
Clopidogrel and CURE trial?
Shown to reduce the incidence of MI in patients with USA compared with aspirin alone in the CURE trial.
This benefit persists whether the patient undergoes revascularization with PCI or not.
61
What has NOT been proven to be beneficial in USA?
1. Thrombolytics
| 2. CCBs
62
Many patients with USA that is controlled with medical therapy eventually require:
Revasculatization.
63
The CARE trial show what?
1. Patients with prior history of MI were randomized to treatment with statins and placebo.
2. The statin group had:
a. A reduced risk of death (by 24%)
b. A reduced risk of stroke (by 31%)
c. A reduction in need for CABG or coronary angioplasty (by 27%)
64
Variant Prinzmetal's angina - Mechanism?
Transient coronary vasospasm that usually is accompanied by a fixed atherosclerotic lesion - 75% of cases.
Can also occur in normal coronary arteries.
65
Variant Prinzmetal's angina - Classic presentation?
Episodes of angina occur at rest and are associated with ventricular dysrhythmias some of which may be life threatening.
--> Classically occurs at night.
66
Prinzmetal's angina - Definitive test?
Coronary angiography - Displays coronary vasospasm when the patient is given IV ergonovine (to provoke chest pain).
67
MI mortality rate?
30% - Half of the deaths are prehospital.
| Most patients have a history of angina, risk factors for CAD, or history of arrhythmias.
68
Up to how many patients may MI be asymptomatic?
```
Up to 1/3 of patients:
Painless infarcts or atypical presentations more likely in:
1. Post-op patients
2. Elderly
3. Diabetics
4. Women
```
69
ECG - Markers of ischemia/infarction?
1. Peaked T waves - Occur very early and may be missed.
2. ST segment elevation --> indicates transmural infarcts.
3. Q waves --> Evidence for necrosis (specific) - usually seen late.
70
ECG changes based on the location of infarct - Anterior?
1. ST segment elevation in V1-V4 (acute/active)
| 2. Q waves in V1-V4 (late changes)
71
ECG findings - Posterior MI?
1. Large R wave in V1-V2.
2. ST depression in V1-V2.
3. Upright and prominent T waves in V1 and V2.
72
ECG findings - Lateral infarction?
Q waves in leads I and aVL (late change).
73
ECG findings - Inferior MI?
Q waves in leads II, III, aVF (late change).
74
Cardiac monitoring for a patient with an acute MI:
1. BP and HR: HTN increases afterload and thus O2 demand, whereas hypotension reduces coronary and tissue perfusion.
2. Both nitrates + morphine can cause hypotension.
3. Rhythm strip with continuous cardiac monitor.
4. Auscultations.
5. Hemodynamic monitoring (CVP etc.)
75
Diagnostic gold standard of MI?
Cardiac enzymes
76
How must cardiac enzymes be drawn?
Serially --> Once on admission and every 8 hrs until three samples are obtained.
77
Have cardiac enzymes also a prognostic factor?
The higher the peak and the longer enzyme levels remain elevated, the more severe the MI + the worse the prognosis.
78
Agents shown to reduce mortality in MI?
1. Aspirin
2. Beta blockers
3. ACEIs
the ONLY ones.
79
What has the CAPRICORN trial showed?
Carvedilol reduces risk of death in patients with post-MI LV dysfunction
80
First thing in the treatment of MI?
Admit patient to a cardiac monitored floor (CCU) and establish IV access.
Give supplemental O2 + analgesics (nitrates, morphine).
81
What has the HOPE trial shown?
```
Ramipril reduces:
1. Mortality
2. MI
3. Stroke
4. Renal disease
in a broad range of patients with high risk cardiovascular disease.
```
82
Medical therapy of MI - What is indicated?
1. O2
2. Nitroglycerin
3. Beta blocker
4. Aspirin
5. Morphine
6. ACEIs
7. IV heparin
83
Which statin is superior in treatment of MI?
Atorvastatin
84
What is the main role of morphine in MI treatment?
Causes venodilation --> decreases PRELOAD.
| + Analgesia.
85
Why to give heparin in ALL patients with MI?
Prevents progression of thrombus; however, has NOT been shown to decrease mortality.
86
Is heparin used for stable angina?
NO - Only for USA, NSTEMI, STEMI.
87
Treatment of MI - Revascularization?
1. Benefit highest when performed early.
| 2. Should be considered in ALL patients.
88
Revascularization options?
1. Thrombolysis
2. PCI
3. CABG
89
Fibrinolysis or PCI is a better option?
PCI --> If performed by skilled personnel and rapidly (within 90min of arrival at the hospital.
Otherwise, fibrinolysis may be a better option.
90
Urgent/emergent CABG is performed when?
ONLY in the setting of mechanical complications (shock, v-arrhythmias, faiure of PCI).
It is almost NEVER performed in the acute setting on a stable patient.
91
Role of clopidogrel in MI treatment?
1. Additive to the effects of aspirin.
2. In ALL patients who undergo PCI and receive a stent.
3. Dual antiplatelet (aspirin + clopidogrel) should continue for at least 30 days in patients who receive a bare metal stent, and at least 12months in patients who receive a drug-eluting stent.
92
MCC of in-hospital mortality in an AMI patient?
Pump failure - CHF.
93
After MI, what should ALL patients have before leaving the hospital?
A stress test - To determine the need for angiography --> which in turns determine the need for angioplasty or CABG.
94
Complications of MI - MCC of in-hospital mortality?
Pump failure (CHF).
95
Mild CHF after MI - What to give?
Treat medically - ACEI + diuretic..
96
Severe CHF after MI - What to give?
May lead to cardiogenic shock - Invasive hemodynamic monitoring may be indicated.
97
MI and risk for stroke?
After MI --> High risk of stroke for the next 5 years.
| --> The lower the EF and the older the patient, the higher the risk of stroke.
98
PCI - When to prefer?
1. STEMI as long as it can be performed expeditiously (door to ballon time less than 90 min) and by skilled personnel.
2. Also preferred in patients with contraindications for thrombolytic therapy; no risk of intracranial hemorrhage.
99
Thrombolytic therapy for MI - Can replace PCI?
1. Remains an important treatment modality since PCI is still available only at specialized centers.
2. Useful for patients who present later, and for those in whom PCI is contraindicated.
100
Thrombolytic therapy for MI - Time frame?
1. Early treatment is crucial to salvage as much of the myocardium as possible.
2. Administer as soon as possible up to 24h after the onset of chest pain.
101
Thrombolytic therapy for MI - Best time?
Outcome is best if given within the first 6 hours.
102
Thrombolytic therapy for MI - Indications?
ST elevation in two contiguous leads in patients with pain onset within 6hrs who have been refractory to nitroglycerin.
103
Thrombolytic therapy for MI - Best choice?
Alteplase has been shown to have the best outcomes amongst thrombolytic medications, and is the first choice in many centers, despite its high cost.
Alternatives: streptokinase, tenecteplase, reteplase, lanoteplase, urokinase.
104
In ED setting, what is the main reason to initiate therapy with thrombolytics/angioplasty?
ST elevation.
105
Absolute contraindications to thrombolytic therapy:
1. Trauma - Recent head trauma or traumatic CRP.
2. Previous stroke
3. Recent invasive procedure or surgery
4. Aortic dissection
5. Active bleeding or bleeding diathesis.
106
CABG - When to use?
1. Less often used than the other two in the acute setting.
| 2. Benefits of CABG include low rates of event free survival and reintervention free survival.
107
CABG - When is the procedure of choice?
In patients with severe multivessel disease and complex coronary anatomy.
108
What arrhythmias may occur after MI?
1. Premature ventricular contractions (PVCs).
2. A-fib
3. Ventricular tachy
4. V-fib
5. Accelerated idioventricular rhythm
6. Paroxysmal SVT
7. Sinus tachy
8. Sinus brady
9. Asystole
10. AV block
109
V-tachy after MI - What to do?
Sustained VT requires treatment:
A. If the patient is hemodynamically UNSTABLE, electrical cardioversion is indicated.
B. If the patient is hemodynamically STABLE, start IV amiodarone.
110
V-fib after MI - What to do?
Immediate unsynchronized defibrillation and CRP are indicated.
111
Accelerated idioventricular rhythm after MI - What to do?
Does NOT affect prognosis - No treatment needed in most cases.
112
Sinus tachycardia after MI - May be caused by?
1. Pain
2. Anxiety
3. Fever
4. Pericarditis
5. Medications
113
Sinus tachy after MI - Effect on ischemia?
Worsens ischemia - Incr. myocardial O2 consumption.
114
Sinus tachy after MI - What to do?
Treat underlying cause - Analgesics for pain, aspirin for fever etc.
115
Sinus brady after MI - When happens?
A common occurrence in early stages of acute MI.
116
Sinus brady after MI - Why happens?
May be a protective mechanism - reduces myocardial O2 demand.
117
Sinus brady after MI - What to do?
No treatment is required other than observation.
| If brady is severe or symptomatic (hemodynamic compromise), atropine may be helpful in increasing HR.
118
Asystole after MI - Problem?
Yes - Very high mortality.
119
Asystole after MI - What to do?
Treatment should begin with electrical defibrillation for V-fib, which is more common in cardiac arrest and may be difficult clearly differentiate from asystole.
120
Asystole after MI - If asystole is clearly the cause of arrest, what to do?
Transcutaneous pacing is the appropriate treatment.
121
AV block after MI:
1. Associated with ischemia involving the conduction tracts.
2. 1st and 2nd degree (type I) blocks do NOT require therapy.
3. 2nd degree (type II) and 3rd degree blocks: Pacemaker.
122
CAD can have the following presentations:
1. Asymptomatic
2. Stable angina
3. Unstable angina
4. AMI - either STEMI or non STEMI
5. Sudden cardiac death
