TEST 3 Flashcards
1
Q
Epidemiology of Hyperlipidemia
A
In the US by far, the leading cause of death is coronary artery disease. It accounts for over 500,000 deaths per year.
2
Q
Why do we have Cholesterol?
A
Physiological cholesterol is:
- A component of our cell membranes.
- Important in the synthesis of hormones.
- It also makes up the majority of our Bile Acids which are squirted out by the gall bladder to help digest food.
- It is also part of the biophospholipid layer of the skin. This helps to protect the body from stuff that is trying to get in, but also keeps stuff in that could otherwise get out.
This is why we cannot lower cholesterol to zero. It has important roles within the body.
3
Q
** Production of Cholesterol
A
we do get some of our cholesterol from nutritional intake, however the vast majority of cholesterol is endogenously produced by the liver.
4
Q
Is TLC as effective in Hyperlipidemia as it is in Hypertention?
A
No
Unlike HTN, where we have TLC that is just as effective as Pharmacotherapy, this is not the case with Hyperlipidemia. Especially as it pertains to bad cholesterol.
TLC is not nearly as effective for patients who have had an MI and think that they can eat their way to an exceptable cholesterol level. It cannot be done because it is part of your genertic make-up.
5
Q
There are 6 major classes of plasma lipoproteins. Out of the 6, which 3 have the most CLINICAL relevance?
A
- VLDL
- LDL
- HDL
6
Q
What does VLDL stand for?
A
Very Low Density Lipoproteins (VLDL)
7
Q
What does LDL stand for?
A
Low Density Lipoprotiens (LDL)
8
Q
What does HDL stand for?
A
High Density Lipoproteins (HDL)
9
Q
What are Very Low Density Lipoproteins (VLDL)?
A
**The majority of Very Low Density Lipoproteins (VLDL) is Triglycerides.
Back in the day, they thought that Triglycerides were way to big to have a DIRECT effect on your risk for coronary artery disease ect…But, we have found out more recently that they do have a direct effect on your risk.
Therefore, we are starting to pay more attention to Triglycerides.
**Triglycerides ARE considered a INDEPENDENT risk factor for Coronary Artery Disease,
10
Q
What are Low Density Lipoprotiens (LDL)?
A
**Low Density Lipoprotiens (LDL) are the most important BY FAR.
The role of LDL is to DELIVER cholesterol away from the liver to NON-Hepatic Tissues.
So essentially it is a deliverer of Cholesterol.
This is notoriously called the “BAD” cholesterol.
The Higher your LDL, there is a DIRECT correlation with risks of diseases caused by cholesterol.
For every 1% REDUCTION in LDL, there is a 1% reduction of risk for cardiovascular disease. (Direct Correlation)
11
Q
What are High Density Lipoproteins (HDL)?
A
High Density Lipoproteins (HDL) are kind-of like a vacuum cleaner. It runs around and picks up cholesterol remnants, and takes them back to the liver to be metabolized.
HDL instead of delivering cholesterol, it grabs it and RETURNS it to the liver.
This is the good stuff. We call this the “GOOD” cholesterol.
The HIGHER your HDL, the better off you are going to be. For instance, probably the best reason that women typically live longer than men because they naturally have a higher HDL level.
** The HIGHER your HDL level, the LOWER your risk is of having Cardiovascular Disease.
12
Q
What is the role of LDL in Atherosclerosis?
A
LDL can pass freely from the arterial lumen into the sub-endothelial space,
In the sub-endothelial space, LDL can become Oxidized.
Oxidation attracts macrophages, which go into the sub-endothelial space and engulf the oxidized LDL and eventually become to fat to come back into the lumen. They then are white foam cells.
An accumulation of these foam cells causes a fatty streak within the artery which eventually herniates inward (stenoses). This makes a rough fibrous cap.
Which causes a supply and demand mismatch because not enough blood can flow through. (Angina).
If sheer forces occur, such as from sexual activity, elevated Blood Pressure, constipation,sudden stress, the fibrous cap can tear off (like a scab) and lipid contents can spill out causing a thrombus formation that can lead to a complete bloackage.
This causes an infarct of the area that the artery supplied.
13
Q
What does NCEP stand for?
A
National Cholesterol Education Program (NCEP)
14
Q
What does the National Cholesterol Education Program (NCEP) do?
A
They make the guidelines (bible) that Doctors follow in order to properly manage a patients cholesterol.
15
Q
What is the first step that the NCEP recommends that patients follow?
A
Screening:
The first step is educating patients to get their initial screening at 20 years of age or older.
This should be a FASTING lipid panel .
Once they have their initial screening, they need to repeat it every 5 years or so.
16
Q
Who is at greatest risk for hyperlipidemia?
A
Patients who already have established CHD (coronary heart disease)
Always ask the patient if they have any kind of heart disease or previous MI. (including people the had by-pass, stents ect)
17
Q
What is secondary prevention?
A
This refers to a person who already has Established CHD (coronary heart disease)
18
Q
What is primary prevention?
A
People that have RISK EQUIVALENTS for CHD but to NOT have CHD yet.
19
Q
What are the 5 risk equivalent categories?
A
Patients with:
- Peripheral Vascular Disease
- Carotid Artery Disease
- Type 2 Diabetes
- AAA
- Framingham of <20% risk
These patients, along with pre-existing CHD are at greatest risk for an MI
20
Q
According to NCEP, first we identify patients according to PMHx, then risk equivalents such as AAA, PVD, T2DM, and CAD. At this stage, if we have not found anything, what do we look for next?
A
screen for Major Risk factors.
The order of screening is:
- Past history of CHD
- Risk Equivalents
- Risk Factors
The higher on the list you are, the more likely you are to have problems.
21
Q
What are the Major Risk Factors that NCEP has you screen for?
A
- Cigarette Smoking- 1 cig within the last month would count.
- HTN- 140/90 - even if on BP meds and well controlled.
- LOW HDL- if less than 40
- Positive Family History for CHD
- Age- male 55, female 65
This is the one negative risk factor. (meaning it is a good thing)
- If HDL >= 60
22
Q
If your patient already has existing CHD, do you need to screen them for risk equivalents or risk factors?
A
No, if they have existing CHD, they go straight to the top of the list.
(Secondary Prevention)
23
Q
If your patient does not have existing CHD but they do have a risk equivalent, do you need to screen them for risk factors?
A
No, even though they do not have existing CHD, if they have a risk equivalent it takes them to the top of the list
(Primary Prevention)
24
Q
If you have evaluated your patent and they do not have existing CHD, they do not have any risk equivalents, but they do have 2 or more major risk factors, what would you complete next?
A
If 2 or more risk factors are present, calculate Framingham 10 year risk assessment and place the patient in the correct category of risk.
25
What is FRAMINGHAM?
it is an estimation of 10 Year risk for CHD for men and women.
26
What are the major factors in FRAMINGHAM? (5 of them)
1. Age
2. Smoking
3. Systolic BP
4. Total Cholesterol
5. HDL
These are the things that you need to know in order to evaluate the patients risk. There is a different sheet to use for men and women. What you do is plug these variables in and it comes out with some sort of risk. This is used to categorize the patient. This is important in determining how aggressive you will treat the patient as well as what medication and dose they should be on.
27
What are the categories of risk in Framingham?
Patient Populations are:
1. High Risk
2. Moderate Risk
3. Low Risk
28
Who falls into the High Risk Population in a Framingham assessment and what is their treatment goal?
High Risk Patient Population includes:
Patients with CHD and CHD risk equivalents.
(10 year risk of MI of >20%)
Their LDL goal is <100
29
Who falls into the Moderate Risk Population in a Framingham assessment and what is their treatment goal?
Moderate Risk Patient Population includes:
Multiple 2+ risk factors
(10 year risk of MI of 10-20%)
Their LDL goal is < 130
30
Who falls into the Low Risk Population in a Framingham assessment and what is their treatment goal?
Low Risk Patient Population includes:
0-1 Risk Factor
(10 Year risk of <160
31
Patients with:
1. Peripheral Vascular Disease
2. Carotid Artery Disease
3. Type 2 Diabetes
4. AAA
5. Framingham of
32
Once we establish the risk establishment goals from the framingham assessment, What is the next thing that we do?
We look for secondary causes of dyslipidemia BEFORE initiation of various therapies.
Just like in HTN, we learned that diseases such as Pheocromocytoma can be a secondary cause of HTN and if you fix it, it can resolve the patients HTN.
Patients can also have secondary causes to their dyslipidemia that if fixed could resolve it.
33
What are the secondary causes of Dyslipidemia?
1. Uncontrolled Diabetes
2. Hypothyroid Disease
3. Protein Wasting Syndromes
4. Certain Medications such as anabolic steroids and certain progesterone types of medications.
If you identify a secondary cause, you MUST try and control it first.
In most cases it is not caused by secondary issues.
34
TRUE OR FALSE
TLC in patients with Dyslipidemia is just as effective as Pharmacotherapy, like TLC in HTN was
False
TLC may only lower the Patients LDL about 10% even if they ate like a bird.
It is generally not enough to keep the patient from having to utilize pharmacotherapy.
Any reduction is better than nothing so we do teach the patient about TLC.
35
Therapeutic Lifestyle Changes (TLC) are non-drug measures used to positively impact the lipid panel.
What do they consist of?
1. Diet- reduce saturated fat and cholesterol in the diet by drinking low fat milk, trimming the fat off of meat ect.. and also increasing your fiber.
2. Weight Reduction
3. Increasing Physical Activity.
36
Metabolic syndrome is a secondary target of therapy. What is it defined by?
Metabolic Syndrome is defined when 3 or more of the following are present within the same patient:
1. Abdominal Obesity - < 35 in for women. Central Adiposity is the worst fat to have because it surrounds the vital organs.
2. Triglycerides- >= 150
3. HDL < 40 in men and 130/85 (just know elevated)
5. FBG >100
(normal FBS is 70-99. takes FBS of 126 to diagnose diabetes.)
37
Patients that have Metabolic Syndrome need to be educated about what?
They need to be educated about their extreme risk for a major event.
Their treatment is aggressive and you have to treat the underlying causes such as pre-diabetes.
TLC is PARAMOUNT
38
Is a diabetics LDL the same as a normal Persons LDL?
No, Normal peoples LDL is big and Fluffy.
Diabetics have an LDL that is more small and dense.
The reason for this is because high triglycerides can have a impact on LDL which makes it small and dense. This means that even though a diabetics LDL is the same number as a normal person, it is a worse form of LDL because it is smaller and more likely to get oxidized.
39
TRUE OR FALSE
Triglycerides a risk factor for CHD
TRUE
BUT, they are an INDEPENDENT risk factor for CHD and important as a SECONDARY cause
The theory is that when triglycerides are gobbled up and metabolized, they leave remnants behind that are small enough to get oxidized and to form plaques just like LDL.
THUS- VLDL can be a secondary target of therapy.
40
What are the factors for Hypertriglyceridemia?
```
obesity
physical inactivity
smoking
excess ETOH
high carb diets
diabetes
chronic renal failure
nephrotic syndrome
genetics
drugs- corticosteroids, estrogens, retinoids, high dose beta blockers
```
41
What are the normal triglyceride levels
< 150
42
What are borderline triglyceride levels
150 - 199
43
What are high triglyceride levels?
200 - 499
44
What are Very high triglyceride levels?
<= 500
45
When triglycerides are over 500 what are you at risk for?
Pancreatitis.
When over 500, VLDL becomes your primary target because if pancreatitis is not treated it can cause a septic like syndrome and the patient can die.
Once the triglycerides are back below 500, the primary target goes back to LDL.
46
When a patients LDL has been treated and is at goal, what do you perform next?
You re-evaluate the patients triglycerides.
If they are greater than 200, you need to calculate a NON-HDL calculation.
This is done by taking the patients Total Cholesterol and subtracting the HDL.
That number should be less than 30 points higher than the patients LDL goal.
47
If the patient has an LDL goal of < 100, what is their NON-HDL goal?
130
48
What are the secondary targets of therapy for CHD?
Metabolic Syndrome
Hypertriglyceridemia if <200
Low HDL
49
TRUE OR FALSE
Triglycerides respond great to TLC
TRUE
If you eat right, your triglycerides go down
if you exercise, your triglycerides go down
If you control your diabetes, your triglycerides typically improve.
If you drink excessive alcohol, your triglycerides will improve.
50
What is Low HDL defined as
< 40.
Patients that have high triglycerides have low HDL.
51
TRUE OR FALSE
Through randomized controlled trials, we actually found that using pharmacotherapy to manipulate a persons HDL makes a huge impact in CHD
FALSE
It actually showed no evidence that it even makes a difference.
HDL also responds to TLC so better to use that instead of Pharmacotherapy
52
What is Pressor?
The most powerful statin
53
True or False
The lower you get someones LDL, the better off they will be
True
Studies proved that significantly lowering a patients LDL especially after the patient has already had By-pass or stents placed, the better off they are
we have yet to figure out how low is too low.
patients are now being kept below 70 even though they are at their LDL of less than 100.
Some people have decreased all the way to 30 and are fine.
This only pertains to secondary prevention patients.
54
65 year old male
PMH- PCI, type 2 diabetes
Drinks excessively
Smokes 2 packs PD
TOT CH- 324
HDL- 37
VLDL- 675
LDL- 193
What do you ask yourself first?
Is it primary or secondary prevention.
This is secondary prevention because of PCI
This already puts him at the very top risk of getting a MI
55
65 year old male
PMH- PCI, type 2 diabetes
Drinks excessively
Smokes 2 packs PD
TOT CH- 324
HDL- 37
VLDL- 675
LDL- 193
What is his LDL goal?
since it is secondary prevention his LDL goal is < 100 or less than 70
56
65 year old male
PMH- PCI, type 2 diabetes
Drinks excessively
Smokes 2 packs PD
TOT CH- 324
HDL- 37
VLDL- 675
LDL- 193
What is his VLDL goal?
< 150
57
65 year old male
PMH- PCI, type 2 diabetes
Drinks excessively
Smokes 2 packs PD
TOT CH- 324
HDL- 37
VLDL- 675
LDL- 193
What is his Non- HDL goal
< 130 or <100
58
65 year old male
PMH- PCI, type 2 diabetes
Drinks excessively
Smokes 2 packs PD
TOT CH- 324
HDL- 37
VLDL- 675
LDL- 193
Which of these would you address first?
VLDL- because over 500 puts him at risk for pancreatitis
Need to address drinking and triglycerides
59
What is The most effective and widely used cholesterol medication that we have?
Statins:
The most potent LDL reducers that we have that is what makes them the most effective.
They can reduce events by up to 30-35%
It is prolonging how long we live.
60
What is the MOA of Statins?
hydroxymethylglutaryl coenzyme A (HMG-CoA) Reductase Inhibitor.
This is an enzyme that is critical in the synthesis of cholesterol. So if we wipe this enzyme out, out body cannot make an adequate amount of cholesterol.
61
If you wipe out (HMG-CoA) Reductase and the body needs more cholesterol, what does the liver do?
it sucks it out of the blood stream because it cannot make it,
This is how it lowers LDL
62
Are statins linear or non linear drugs?
Non- Linear
This means that you get a big bang for your buck at the lowest doses.
This means that if you double your dose, it will not lower your LDL any more than like 6%.
63
What are the net results of Statin therapy?
It can lower your LDL up to 60%
can lower VLDL by like 3%
64
What are the Kinetics of Statin therapy
SAL
Simvastatin
Atorvastain
Lovastatin
are metabolized by CYP3A4
These have significant drug interactions
65
What is the category for pregnancy for statins?
x
Not safe during pregancy
66
What are the side effects of Statin therapy?
1. Myalgia (1-5%)- myalgia simply means that something is going on with the muscles.
2. Myositis- (Moderate elevation in CPK) Inflammation of the muscles.
- Large muscles like thighs and butt, back.
- Is terrible, like being beaten with a bat.
- It is BILATERAL, usually associated with a fever.
- Older people show signs of weakness and less pain
3. Rhabdomyolysis- this is where muscles start to break down. It can lead to kidney failure. (Very rare)
4. Transaminase Elevation- Approx 0.5-2%.- which is AST/ALT. When these are elevated it means that the liver is inflamed or irritated. Not indicative of function. Very Rare.
- For Liver function we test- Albumin is low, Billirubin is high, PT/INR is high. Those are indicative of liver function.
67
What is the MOA of Niacin?
Decreases production of VLDL.
****Increases HDL
Decreases LDL
This is the one drug that does everything correctly.
***It is THE BEST HDL increaser.
It is the 2nd Best LDL reducer (2nd to statins)
It is the 2nd best VLDL reducer
68
If a patient cannot take a Statin due to true Myosytis, than which drug are you going to put them on to lower their LDL?
Niacin
Reduces LDL by about 35%
69
To what percent does Niacin lower VLDL?
up to 40%
70
To what percent does Niacin increase HDL?
up to 35%
71
What are the adverse effects of Niacin?
Flushing (More common with IR)
GI Toxicity
Hepatoxicity (more common with SR)
Hyperglycemia - only 1/3 of diabetics will require any adjustment in dose
Hyperuricemia- (can cause gout)
72
What is your counseling for Niacin?
**1. Start low and go slow
**2. Take it with food.
**3. Take an NSAID or Aspirn 30 min before Niacin
**4. Avoid taking with alcohol and hot or spicy foods or beverages.
**5.After a week or 2, you will become tolerant to that dose. Teach them to take IR at night.
**6. Avoid Interruption of therapy. If you run out of it, you have to start over with your tolerance level. (flushing, burning, itching)
7. 2 grams per day cap on SR niacin. Not a cap on IR Niacin
73
What are the fibrates?
Gemfibrozil and Fenofibrate (Tricor)
74
What is the MOA of fibrates?
| Gemfibrozil and Fenofibrate (Tricor)
interacts with peroxisome proliferator-activated receptor alpha (PPAR Alpha) witch increases synthesis of Lipoprotein Liapase. This accelerates the clearance of VLDL.
This is the most effective VLDL reducer.
Typically in a case where you have to address Triglycerides first, this is what you would give them.
They are the 2nd most effective HDL increaser (2nd to Niacin)
They do not do diddly for LDL
75
What are the effects of Fibrates? Gemfibrozil and Fenofibrate (Tricor)
can reduce VLDL up to 90% so these are the best triglyceride reducers.
Can increase HDL by about 20% (2nd best)
No effect on LDL
76
What are the side effects of Fibrates? Gemfibrozil and Fenofibrate (Tricor)
**It can cause irritation of the liver. So need to check baseline transaminase levels.
-If the patient complains of flu like symptoms or abdominal pain, you would want to repeat the transaminase levels and compare to the baseline.
**It can also produce myopathies similar to statins. You can use fibrates in combination with statins so that can double the risk of myalgias.
-need to council the patient on the symptoms.
77
What are the drug interactions of Fibrates? Gemfibrozil and Fenofibrate (Tricor)
Can increase Warfarin concentrations. Will Elevate the INR. Will need to reduce Warfarin,
When Combined with statins can increase the chances of Myopathies.
78
What drugs are Bile Acid Sequestrants (BAS)?
**Cholestyramine
Colestipol
Colesevelam
79
What is the MOA of Bile Acid Sequestrants (BAS)? **Cholestyramine
form insouluable complex in the small intestine with bile acids that are RICH in cholesterol, reducing the reabsorption of the bile acids (Enterohepatic recirculation). Through the loss of Bile Acids, causes a demand for increased bile acid synthesis which requires cholesterol. Thus LDL receptors are increased on the liver to allow additional uptake. The Net Result is reduction in plasma LDL concentration.
80
What are the effects of Bile Acid Sequestrants (BAS)? **Cholestyramine
Can reduce LDL by about 20%. So not as effective as Statins or Niacin.
Has no effect on HDL
**Can Increase Triglycerides.
This is typically an add on therapy to Niacin, or Statins.
81
What are the Kinetics of Bile Acid Sequestrants (BAS)? **Cholestyramine
It is not absorbed, it just passes on through
comes in a powder form that you have to mix with water and drink it. It is like drinking Sand, its nasty.
It also comes in tablets but they are HUGE. 8-12 of them at a time.
82
What are the side effects of Bile Acid Sequestrants (BAS)? **Cholestyramine
GI side effects-
devoid of systemic side effects.
This stuff looks like sand going in and a brick coming out.
Constipation
Bloating
Indigestion
Reduces absorption of fat-soluable vitamins (A,D,E,K)
Welchol- has less of these side effects but is more expensive.
83
What are the drug interactions of Bile Acid Sequestrants (BAS)? **Cholestyramine
Just like it can grab bile acids and make you poop them out, it can also grab medications and make you poop them out as well.
Warfarin
Thyroid Replacement
Recommendation is to take your other drugs 1 hour before the BAS so that they get a 1 hour head start or take the BAS first and the medications 4 hours later.
84
What is the MOA of Etetimibe (Zetia)
Inhibits the passage of dietary and biliary cholesterol absorption across the brush border of the small intestine.
Actually blocks the absorption of cholesterol in the small intestine.
85
What are the effects of Etetimibe (Zetia)?
Very similar to BAS
lowers LDL by about 20%
Will be an add on therapy to either Niacin or Statins for additional LDL reduction.
Neutral for VLDL
HDL Neutral
86
When you take up to 6-8 grams a day, it is a pretty significant _______ reducer.
Triglyceride
87
What is the problem with taking that much fish oil?
You get fish burps
Acid Reflux Disease
GI Things
smelling it through your skin
88
What is Omacor, now called Lovaza.
Very concentrated fish oil tablets.
2 caps BID is equivalent to taking about 16 over the counter fish oil tablets.
Through very high concentrations of EPA and DHA, it can reduce Triglycerides by 20-50%
we have zero data that tells us that it changes the outcome of CHD,
89
What is PPAR Alpha?
Fibrates Gemfibrozil and Fenofibrate (Tricor)
90
What is HMG-CoA?
Statins
91
What is Lipa-protein Lipase?
Niacin
92
What is Angina?
A Supply and demand Mismatch in the heart
Anginal pain is precipitated when oxygen demand exceeds the supply.
Remember Dead meat don't hurt
93
What is demand?
Demand is determined by heart rate, contractility, wall tension,
The greater the preload, the further the stretch, the greater the contraction, the greater the afterload.
This makes it harder for the heart to pump
94
What is afterload?
The force that the heart has to overcome to pump blood.
95
What is supply?
This is determined by blood myocardial blood flow.
This happens during diastole when the coronary arteries fill with blood. Your ventricles and atriums stretch which in a sucking motion kind of pulls the blood towards it.
When demand is increase such as in fight or flight, supply is supposed to increase as well.
Increasing supply primarily happens through coronary artery dilation.
96
How does the heart keep supply and demand in check?
Through coronary artery dilation
97
What is stable angina?
Exertional Angina
This is what happens when you start to exert your self like running or in more severe cases just walking to the mailbox. causes chest pain
98
What is the pathophysiology of stable angina?
CAD via atherosclerosis.
Macrophages oxidize LDL, turns into foam cell, fatty streak, starts to herniate, causes mature lesion that starts to herniate and causes a stenosed vessel.
It causes less blood to get to the heart. Even in a resting state. The heart compensates by dilating the vessels distally from the stenosed area, due to supply and demand mismatch.
99
What is the treatment for Stable (exertional) Angina?
decrease demand
Pharmacotherapy is based on fixing demand issues. not supply. That is fixed with bypass or stents.
100
What are the drugs that decrease demand?
Nitrates- work through preload by dilating the veins.
Beta Blockers- decrease HR, Contractility
Calcium Channel Blockers-
- Non-DHP= Deltiazem and Verapamil- decrease HR and contractility and dilate arteries which decrease afterload.
- DHP CCB- Nifedipine- All of the PINES, work purely on dilating arteries which is afterload reducers.
Antilipemics- Statin therapy- stabilizes the lesion and prevents it from progressing. Also can cause regression of the lesion.
ASA- Aspirin
101
What happens if a lesion is unstable and pops open?
It causes a thrombus.
A thrombus causes an occlusion which causes MI
1/3 of all heart attacks die of sudden cardiac death and die right on the spot. Another 1/3 die within a year.
102
What is variant angina?
or Vasospastic angina
This is an artery that spasms. (coronary) This causes it to not deliver blood effectively.
103
What is the treatment for variant or vasospastic angina?
You do not typically use beta blockers.
Calcium Channel blockers because they relax arteries.
Nitrates- reduce spasms as well
104
What is Unstable Angina?
This is a Medical Emergency.
New onset of symptoms.
New chest pain, Angina at rest, any change in angina symptoms.
Could be reflux, pleurisy…you just don't know so it is considered unstable until you do know.
105
What is the pathophysiology of Unstable Angina?
medical emergency, severe CAD complicated by vasospasm, platelet aggregation, and thrombus formation.
Probably almost completely occluded.
106
What is the treatment for Unstable Angina?
1. To increase Oxygen Supply by anti-ischemic therapy.
- Nitroglycerin Sublingual or IV
- Beta Blockers
- CHB if cant take BB
- Oxygen
- Morphine
- ACE I
2. Anti-platelet therapy
- Aspirin
- Clopidogrel
- Abcixamab
- Eptifibitide or Tirofiban
3. Anticoagulants
- Heparin
107
What is the MOA of Nitroglycerin?
Venodilator- preload reducer
Reduces oxygen demand due to the "stretch"
****Nitrate is taken into your smooth vascular muscles. There is a presence of sulfhydyl group there. The sulfhydyl is necessary to convert nitroglycerin to nitric oxide which is the bodies natural venodilator. So it has to have sulfhydyl in order to work without them nitrates are useless.
108
What are the kinetics of Nitrates?
many routes
It is lipid soluble- (penetrates membranes)
huge first pass effect
has a short 1/2 life of 5-7 min
109
What are the adverse effects of Nitroglycerin?
causes profound headache
Orthostasis
Reflex Tacycardia through baroreceptors
110
What are the drug interactions of Nitroglycerin?
Anything that can lower blood pressure.
PDE5 Inhibitors such as viagra, cialis (sildenafil, tadalafil, vardenafil)
These are absolute contraindications
111
Tolerance and Nitrates
When you start using nitrates, you have to have sulfhydyl in order for them to work.
You only have limited amount of sulfhydyl. In the first 24 hours you will run yourself out of sulfhydyl which is why you cannot use it as BP medication.
This is why you cannot list Nitrates as an Antihypertensive in someones chart.
To avoid tolerance, you have to have a nitrate free period of at least 8 hours per day.
Typically at night
do not abruptly discontinue the med. can cause vasospasm.
112
Beta Blockers-
Propranolol (Non selective)
Metroprolol (Specific Beta 1)
Carvedilol / Labetalol (Alpha 1 Beta 1 Blockade)
Decrease oxygen Demand.
try and titrate BB to get a HR between 50-60 BPM.
Side effects of BB are- bradycardia,
decreased AV Conduction, Decreased contractility,
113
What two beta blockers have Alpha 1 and Beta 1 blockade capabilities?
Carvedilol and Labetalol
114
beta 1 receptors-
heart rate increases
contractility increases,
sympathetic nervous system
115
Name 2 NON-DHP Calcium channel blockers-
Verapamil and Diltiazem
116
What is the MOA of NON-DHP Calcium channel blockers-
block calcuim channels on arterioles and on the heart (works similar to a Beta Blocker)
117
What are the effects of Verapamil?
dilation of peripheral arteries
dilation of coronary arteries (increases perfusion)
Blockade of CA+ channels at SA Node (reduces HR)
Bockade of CA+ channels at the AV node
Blockade of CA+ channels in the myocardial tissue (decreases contractility)
118
What is a couple of differences between Nondihydropyridine Calcium Channel Blockers
and
Dihydropyridine Calcium Channel Blockers
NON-DHP=
- blocks calcium channels on arteries and heart
- Causes constipation
- bradycardia
- Prophylaxis of migranes
DHP-
- No constipation
- Reflex tachycardia
- Immediate release causes MI
119
What are the drug interactions for NON-DHP Verapamil and Diltiazem
Digoxin- is a narrow therapeutic index drug that if added to verapamil NON-DHP can exacerbate bradycardia and lower HR way to much. Digoxin might need to be reduced by as much as 50% while taking Verapamil
Beta Blockers- causes profound supressant effects on the heart because NON-DHP verapamil has the same effects as a beta blocker (lowers HR and Contractility
120
Dihydropyridine Calcium Channel Blockers (DHP)
anything that ends in PINE
most common antihypertensive peripheral artery dilating class, not as much effect on the heart as NON-DHP
121
What is the DHP prototype?
Nifedipine
122
What are the indirect hemodynamic effects of Nifedipine?
by lowering BP significantly, they can trigger the Barrowreceptor reflex
Barroreceptors are little monitors in our blood vessels that protect us from shock, when BP drops significantly they kick in.
This is a sympathetic response (Norepi) Beta 1 ->alpha 1...stimulated HR and Vasoconstriction.
Primarily occurs with Immediate Relsease DHP only
Immediate relsease calcium channel blockers are now banned due to causes MI
123
We use pharmacotherapy to manipulate demand, how can we manipulate supply?
Through Invasive therapy
CABG- Coronary artery by-pass graft.
PCI- Percutaneous Coronary Intervention can cause fatty streak to burst and form clot, must put on blood thinners and antiplatelets
PTCA- Percutaneous Transluminal Coronary Angioplasty
Coronary stent
124
What is the treatment for chronic Stable Angina?
Antiplatelet Drugs
Cholesterol Lowering Drugs
ACE Inhibitors
Beta Blockers
Calcium Channel Blockers
Pecking order is : once angina is stable, use Beta Blockers first because most ppl die of V-Fib
second choice is Calcium Channel Blockers
third choice is Nitrates because not 24 hours of coverage and side effects.
125
What are the risk factors for CAD that you would want to reduce if you were diagnosed with stable angina?
Quit Smoking
lose weight
Exercise-
Cholesterol Reduction
Treatment of hypertension
Diabetes Control
Coexisting conditions- BP and Angina= Beta Blocker and Calcium Channel Blockers.
Heart Failure and BP= Beta Blockers and ACE Inhibitors
126
TRUE or FALSE
The most dangerous lesions in the body are the largest lesions
False
Why? Because the more dangerous lesions are the smallest lesions due to collateral flow. The large lesions did not get there over night. It took years for them to develop. When they develop slowly, you have these little hairlike projections that come off of your arteries that do not do anything, but due to chronic hypoxia as the lesions get bigger, your body stimulates those projections to turn into arteries which will bypass the lesion totally. This is called collateral blood flow.
Little lesions do not have time to do this.
127
So if a patient has HTN and Angina what medications would they be on?
Beta Blockers- Propranolol
Metroprolol
Carvedilol / Labetalol
Calcium Channel Blockers- Verapamil and Diltiazem or PINES (Nifedipine)
128
If a patient has heart failure and HTN what medications would they be on?
Beta Blockers - Propranolol
Metroprolol
Carvedilol / Labetalol
Ace Inhibitors- PRILS- Lisinopril, Captropril
129
What class are PRIL's?
Ace Inhibitors
MOA- Reduces levels of Angiotension 2, Dilates arteries and veins. Preload and afterload reducer.
Lisinopril, Captropril
```
ADR-
Hypotension
HYPERKALEMIA
cough
angioedema
```
DRUG OF Choice for diabetic nephropathy and heart failure.
CONTRAINDICATED- Renal Artery Stenosis
CATEGORY X
130
What is hemostasis?
Process by which bleeding is stopped.
It happens within two phases
131
What is stage 1 of hemostasis
The formation of a platelet plug.
Platelets are like little tire patches that float around in our blood stream and they eventually adhere to areas of injury.
132
What is the initial phase of the formation of a platelet plug? (stage 1 of hemostasis)
platelet aggregation- initiated when platelets come in contact with collagen exposed on the surface of damaged blood vessels.
Collagen is something that is within the vessel, and it is never exposed unless there is injury.
133
What is the second phase the formation of a platelet plug? (stage 1 of hemostasis)
Platelet Adhesion- platelets adhere to the site of the injury. Adhesion leads to the platelets releasing substances that recruit other platelets (substantial aggregation).
This is kind of like the tire patch.
134
What is the third phase of the formation of a platelet plug?
| stage 1 of hemostasis
Activation of Glycoprotein II b/ III a receptors.
After adhesion, GPIIb/IIIa receptors on the platelets (50 to 80 thousand per platelet) undergo activation via stimulation of one or more receptors:
a. Thromboxane A2
b. Thrombin
c. Collagen
d. Platelet Activation Factor
e. ADP
135
After GPIIb/IIIa is activated, what does it cause?
Fibrinogen Bridging.
This occurs between activated GPIIb/IIIa receptors on adjacent platelets. (holding hands from spiderman webs) … Completed aggregation and fibrinogen bridging forms an UNSTABLE PLATELET PLUG.
When the "tire patch" or unstable platelet plug is unstable, sheer forces, such as blood rushing by, can tear it off.
136
What is stage 2 of hemostasis?
Coagulation Cascade-
unstable platelet plug may stop the bleeding but it is still unstable to hold the fort. Further reinforcement is necessary with Fibrin. (protein that reinforces the platelet plug, like glue)
Fibrin production is produced via the convergence of 2 pathways.
137
The convergence of 2 pathways (Intrinsic and extrinsic) to produce ________.
Thrombin,
Which leads to the production of Fibrin.
Fibrin is the glue that really stabilizes the scab or clot.
138
What is the intrinsic pathway?
All of the necessary clotting factors are present WITHIN the vasculature system.
They are all within the blood stream, but still need to converge with the extrinsic pathway in order to produce thrombin.
139
What is the extrinsic pathway?
tissue thromboplastin is necessary and is found OUTSIDE of the vasculature system.
This means inside your vessel walls or tissue. So you get this when there is injury and it is exposed.
So intrinsic and extrinsic pathways cross -> thrombin -> fibrin = stabilization
140
There are some clotting factors within this pathway that are called vitamin K clotting factors. These are clotting factors that are made by your ______.
Liver
And they are dependent upon vitamin k in order for this to work.
This is important because-
Warfarin will actually work here by targeting the vitamin k clotting factors.
141
What are the vitamin K clotting factors?
2, 7, 9, 10 and prothrombin
Remember, Warfarin works here.
142
***Where do the intrinsic and extrinsic pathways merge?
at factor 10 A.
Both Pathways are necessary for the optimal production of fibrin.
Once this cascade is initiated, it becomes self sustaining. One step leads to another kind of like a slinky.
143
When we do start to clot, how do we keep it from clotting through our whole body?
Antithrombin
This is a way that we keep the clot local. (Keeps Hemostasis local)
This protects against widespread total body coagulation, the body must inactivate clotting factors that stray from the site of injury.
Antithrombin is a protein that will bind to clotting factors and render them inactive. (This is where Heparin works)
144
Once the "Tire Patch" is formed locally, what makes it go away after it heals?
Lysis of the clot:
As healing ensues, it is important to remove the clot.
1. Plasminogen: precursor to plasmin. When activated produces plasmin?
2. Plasmin is the enzyme that digests the fibrin meshwork of the clot.
This is where thrombolitics work such as TPA. It actually dissolves the clots.
145
What causesSt an arterial thrombosis?
An arterial Thrombosis is kind of classic.
Where you have this stenotic lesion that pops open and the goo comes out, this releases platelet aggregating factors, which causes platelets to stick to it. Too much of a good thing ensues and it can cause total obstruction of the vessel leading to lack of bleed flow to whatever that vessel was feeding.
a. adhesion of platelets to arterial wall injury of ruptured atherosclerotic plaque
b. after adhesion, release of ADP and TXA2 (recruits buddies)
c. with continued aggregation, occlusion of an artery could take place
d. with stasis of the blood, coagulation cascade ensues to reinforce platelet plug with fibrin
e. can lead to tissue injury or tissue death due to lack of perfusion.
Arterial thrombus is neatly packed platelet clot
146
The arterial side of the body is a very much a _____ driven process.
Platelet
If you start having heart attacks, antiplatelet therapy is extremely important. Because it all starts with platelets first.
147
What causes venous thrombosis?
a. stagnation: blood flow much slower with high concentrations of clotting factors present, could lead to initiation of the coagulation cascade.
b. fibrin meshes together platelets AND red blood cells for the thrombus formation.
c. More unstable. Typically has a long tail.
d. Embolization potential if the tail breaks off (pulmonary embolus potential.
*** therefore, greatest damage occurs distally via embolization whereas arterial thrombosis is more local
Venous causes fibrin first then it grabs red blood cells, white blood cells anything it can grab…. this is not neatly packed like arterial thrombus. Very unstable
the bigger the vessel, the bigger the clot, and the most dangerous.
148
What are most effective to treat venous thrombosis?
Anticoagulants- such as warfarin
Antiplatelet drugs are relatively ineffective for venous thrombosis.
149
Where does Heparin (unfractionated) come from?
secured from the lungs of cattle and intestines of pigs.
need to make sure that this does not contraindicate peoples religions ect.
150
What are the pharmacokinetics of Unfractionated Heparin?
a. highly polar. cannot cross membranes (including placenta or breastmilk) cannot take it orally. Must be IM, IV ect.
b. 1/2 life of 1.5 hours (short). If significant hepatic or renal disease, this should be more prolonged. This is usually given IV via continuous infusion because of its short 1/2 life.
c. variable levels- unpredictable due to variable plasma protein and tissue binding. Necessitates intensive monitoring of degree of anticoagulation.
151
What is the MOA of Heparin?
it activates ANTITHROMBIN
antithrombin is capable of acting on all coagulation serine proteases, but does so most notably on thrombin and factors Xa and IXa
greatly reduces fibrin production and suppresses clotting.
keeps clotting local
At sufficient doses, this can happen quickly.
152
What are the therapeutic uses of Heparin?
preferred when situations require rapid onset of anticoagulation
a. Developing stroke
b. PE
c. DVT
d. lower doses for DVT prevention- can be used SQ
e. others-
153
What are the adverse effects of Heparin?
A. Hemorrhage
B. Heparin Induced Thrombocytopenia: HIT development of antibodies against heparin-platelet complexes. Activates platelets, which leads to thrombosis. Also leads to rapid destruction of platelets. Treatment is discontinuation of heparin and substitution of non-heparin anticoagulant.
- Incidence is 1-3% if treated with heparin for greater than 4 days.
- Need to Monitor CBC frequently. If Hematocrit drops a little each day that is indicative of bleeding.
C. Allergic reactions because comes from animal source.
154
What would you give someone if they overdosed on heparin?
Protamine Sulfate
protein that binds with heparin and neutralizes heparins anticoagulant properties.
occurs quickly and lasts for about 2 hours.
may need to administer repeat doses
155
What is the test that you use to monitor Heparin?
A. aPTT: want to thin blood enough to suppress coagulation, but not so much that you excessively risk hemorrhage.
- To do this, we measure the activated partial thromboplastin time (aPTT).
- Normal is 40 seconds.
- Therapeutic heparin is 1.5-2 times the normal (approx 60-80 seconds). Most hospitals have an algorithm for heparin dosing based on the body weight (bolus dose) and aPTT level.
- Initially, frequent monitoring is necessary (Q4-6 hours), but afterwords, can reduce to Q-day.
B. CBC- to check for drop in hematocrit and platelets
156
How is heparin administered?
can be SQ but typically administered IV avoid IM due to hematoma formation.
157
Name the low molecular weight heparins?
***enoxaparin , dalteparin, tinzaparin
158
What makes low molecular weight heparin different from heparin?
simply heparin, but shorter molecular structure. As effective as unfractionated heparin, but more predictable. Preferential inactivation of factor Xa (10a) (less activity on thrombin). Longer 1/2 life. Can dose on a fixed dosing schedule and does NOT require aPTT monitoring (weight based dosing).
159
What are the advantages of low molecular weight heparin? enoxaparin (Lovanox)
a. can be used at home since monitoring is unnecessary.
b. much less likely to cause thrombocytopenia (10x lower incidence)
c. First line therapy for prevention and treatment of DVT (s/p hip/ knee surgeries)
d. Used to bridge anticoagulation until coumadin therapy is therapeutic. If you have a mitral valve replacement you would have to hold Warfarin 5 days before procedure and 10 days after. You dont have to do this with lovanox. but they can take lovanox while they are getting warfarin back up.
e. overdose my also be treated with protamine
160
What are the disadvantages of low molecular weight heparin? enoxaparin (Lovanox)
a. expensive- $14 a day as opposed to $3 a day. but it keeps people out of the hospital
b. SQ route only
161
What monitoring do you need to complete for low molecular weight heparin? enoxaparin (Lovanox)
CBC- if they are on it for a long time. to look at platelets and HH to check for bleeding. Do not check aPTT with lovanox
162
Name the Direct Thrombin Inhibitors
Bivalirudin, Lepirudin, **Argatrobin, Desirudin
163
What is the MOA of the Direct Thrombin Inhibitors? Argatrobin
direct inhibitors of thrombin (does not work through antithrombin activity)
used when people can not take heparin due to religious issues or allergies
164
What are the the advantages of Direct Thrombin Inhibitors?
A. Just as effective as heparin.
B. Causes less bleeding when compared to Heparin.
C. Does not cause thrombocytopenia. If a patient had heparin induced thrombocytopenia you would switch them to this drug.
165
What are the disadvantages of Direct Thrombin Inhibitors?
A. Less data to support its use (providers are hesitant)
B. About 42 times as expensive when compared to Heparin.
C. IV constant infusions only (except for desirudin which is SQ)
166
Warfarin-
"rat poison" like heparin, is used to prevent thrombosis. Has delayed onset of action. Since PO therapy, is well suited for long term treatment and prophylaxis.
167
What is the MOA of Warfarin?
blocks the biosynthesis of vitamin k dependent clotting factors: VII, IX, X, and pro-thombin. (2,7,9,10) (2 is prothrombin)
168
What are the kinetics of Warfarin?
A. Highly Protein Bound (99%)- potential for displacement drug interactions. Free/Unbound warfarin is the ACTIVE warfarin. (1%)
B. Long 1/2 life (Approximate 24 Hours) once a day dosing
C. Delayed onset of activity (due to having no effect on circulating clotting factors--- half lives range from 6 hours to 2.5 days. (Steady state 10 days)
D. Metabolism via the CYP450 system. means lots of drug interactions ,very narrow therapeutic index.
169
What is the dosing of Warfarin?
1,2,3,4,5,6, 7, 7.5, 10 mg tabs available because the dose is so varied
highly individualized.
Very Unpredictable
170
What are the uses of Warfarin?
Long term prophylaxis of thrombosis.
**number one indication for warfarin is a-fib and a-flutter. to avoid stroke
second biggest use is DVT to avoid PE
third use--- mechanical valves to prevent stroke
171
What should you monitor while one Warfarin?
a. Prothrombin Time (PT)- coagulation test highly sensitive to the activity of vitamin K dependent clotting factors. Was unstandardized.
B. International Normalized Ratio (INR)- standardized INR. An INR at one hospital or clinic is the same as at another.
C. Frequent INR monitoring is necessary at first. Provider experience is important with the ability to PREDICT what the levels will do (is an art that must be developed)
d. Once stabilized, may reduce frequency to Q4 weeks
e. Point of care devices- widely used now. do not use venus draw, actually just pricks finger.
f. CBC- periodic checks to evaluate H/H, can also help find cancer if it keeps going down slowly.
172
What are the adverse effects of warfarin?
a. hemorrhage potential- questions to ask?- Are you having dark stools (melanic), nose bleeds, bleeding while brushing teeth, abnormal bruising that takes up large amounts of their body. Pouring bright red blood out of their rear-end. Eyes hemorrhage .
b. category x (fetal hemorrhage as well as malformation) would have to be on heparin
c. Avoid while breast feeding because it does enter breastmilk
173
What are the drug interactions of Warfarin?
There are a ton
Assume that every drug they take interacts with warfarin until proven otherwise.
Have to look up everything
You can dose warfarin around certain meds as long as they TAKE IT EVERYDAY
Cant take Bactrim (Sulfa) Flagyl, Amliodarone
dont take NSAIDS
174
What are the food interactions of Warfarin?
vitamin k clotting factors
very rich in dark green leafy veggies
Have to treat vitamin k veggies like a drug. Do not tell them that they cannot eat it. They can as long as they eat it every day in the same amounts it is ok.
175
What do you give for a Warfarin overdose?
Vitamin K- orally, IV, or Sub Q
FFP- If there is a serious bleed (fresh frozen plasma)
176
What is the MOA of Aspirin? ASA-
Irreversible inhibition of cyclooxygenase (an enzyme required by platelets to synthesize thromboxane A2 (TXA2) (one of the stimulants that turn on GPIIb/IIIa which is the spidy-webs)
Thromboxane A2 is one of the factors that can promote platelet activation. Effects persist for the life of the platelet (Approximately 7-10 days) so stop for procedure 7-10 days prior
177
What are the therapeutic uses for Aspirin?
Primary prevention of MI
Secondary Prevention of MI
Prevention of stroke in patients with history of TIA's
Secondary Prevention of stroke
178
What are the side effects of Aspirin?
GI bleeding and Hemorrhagic Stroke
179
What is the dosing for Aspirin?
81mg QDay is adequate in most cases (especially in cardiac cases)
180
What are the ADP receptor Blockers
Ticlopodine and Clopidogrel
181
What is the MOA of ADP receptor Blockers?
| Ticlopodine and Clopidogrel
irreversibly blocks the ADP receptors (adenosine diphosphate) on the platelet surface. Prevents ADP stimulated platelet aggregation.
182
Ticlopodine
largely replaced by Clopidogrel due to side effect profile
A. Neutropenia
B. Thrombotic Thrombocytopenic Purpura (TTP) Highest risk within the first 12 weeks. Necessary to check CBC with DIFF every 2 weeks for the first 12 weeks of therapy.
C. GI disterbance- diarrhea, abdominal pain, ect
D. Dermatologic Reactions
183
Clopidogrel
much better tolerated.
No Neutropenia
Much less incidence of TTP
Uses include an ASA replacement for s/p MI, Stroke Prevention, and also for use after stent placement (in combo with ASA)
184
What are the Glycoprotein IIB/IIIA Inhibitors?
Super aspirins. Abciximab, Tirofiban, Eptifibatide
185
What is the MOA of Glycoprotein IIB/IIIA Inhibitors?
reversible blockade of platelet GP IIB/IIIA receptors (Thus inhibit the final step of aggregation)
186
What are the therapeutic uses of Glycoprotein IIB/IIIA Inhibitors?
short term to prevent ischemic events in patients with ACS and those undergoing PCI (Typically used in combo with aspirin and heparin)
187
What are the disadvantages of Glycoprotein IIB/IIIA Inhibitors?
Very Expensive and does increase the risk of bleeding but does not increase the risk of fatal bleeding.
188
Thrombolytic Agents:
also known as fibrinolytics and clot busters. Focus on Streptokinase, Alteplase, and Tenecteplase.
189
What is the MOA of Thrombolytic Agents?
directly or indirectly catalyzes the conversion of plasminogen into plasmin (Enzyme that digests the fibrin network of clots) all are IV.
190
What are the contraindications for Thrombolytic Agents?
.
191
Streptokinase
1. Uses: Acute MI, DVT, PE
Side Effects: Bleeding- ICH is biggest concern
2. Antibody Production- Produced from protein extraction of streptocci.. Some may develop an allergic reaction and this can also neutralize thrombolyic effects. Because of risk of antibody production, if repeat thrombolytic treatment is indicated, use alternative thrombolytic angent.
3 Hypotension
192
Alteplase
(TPA) Genetically pioneered and identical to our own tissue plasminogen activator. Cleaner than streptolianase but much more expensive. Void of allergic reactions and hypotension. Also has an indication of acute ischemic stroke. Possibly better outcomes when compared with streptokinase for MI, but higher bleeding rates. People still argue over this today. Requires 90 min to infuse.
193
Tenecteplase
very similar in structure to tpa, however, may give in bolus dose as opposed to slow infusion. Thus, anti thrombotic effects occurs much sooner (time is everything)
194
what is DABIGATRAIN- (Prodaxia)-
NEW direct thrombin inhibitor.
THIS IS ORAL!! The first one ever in pill form
Very predictable
Compared to Warfarin
There are no food or drug interactions
no monitoring
VERY EXPENSIVE.
Potential Warfarin Replacement
195
What is Rivaroxaban
Factor Xa inhibitor
So if you block 10a you never turn prothrombin to thrombin
Oral Therapy
Very similar to Dabigatrain (a-fib) or Apixaban
No monitoring or drug interactions''
First non-Warfarin agent that is approved for DVT
196
What is the patho behind an MI
Atheroscleriosis, pops open, platelets flood, thrombus forms, occlusion happens
197
Myocardial ischemia
thrombus causes complete occlusion and ischemia.
Once ischemia occurs, if blood flow is not restored, tissue death can occur.
198
necrosis and remodeling
we mentioned this when we talked about ace inhibitors, and a little bit with heart failure.
The remodeling process occurs within minutes. When you start having cell damage, your dead myocardial cells turn to non viable tissue or scar tissue.
Dead cells are immediately moved out and scar tissue forms
This can weaken that particular area of the heart.
If you have a high pressure balloon, and a weak area, it will pop, or as the heart does…ruptures.
The heart changes shape. Which leads to heart failure
199
What are three things that drive the remodeling process?
Aldosterone
Angiotension 2
Sympathetic Nervous system
200
What are the drugs of choice for heart failure?
Ace and arbs
| Beta Blockers
201
If you have NY Heart Failure class 3 or 4 you are given what drug?
Aldosterone Antagonists
Spironolactone and Eplerenone
202
Once you get to end stage heart failure, When you begin to have structural damage, need to have what medications right away
ACE or ARB
203
Diagnosis of MI
A. Chest pain
(dead meat don't hurt, chest pain is a good sign)
described as severe, crushing, constricting, horse sitting on my chest, radiation to shoulder blades, radiate to left arm, radiates to the jaw.
Not from exertion and not relieved by nitro,
Pain can be absent in Diabetics. Silent MI
SOB
Nausea
B. Electrocardiographic changes- conduction of electricity is altered through ischemic or injured areas of the heart.
ST elevation- first thing you see if classic MI, you don't have a STEMI.
Q wave- represents dead tissue
T Wave Inversion- eventually this happens…T wave comes after the RST segment and insead of popping up, it goes downward. This indicates a completed MI.
204
Biochemical Markers-
These indicate cell injury.
-CK-MB- rises 4-8 hours, peaks 24 hours, baseline 36-72 hours. Used to be preferred marker but not anymore.
LDH- Serial determinations if patient presents after 24 from the onset of chest pain, peaks 24-48 h, elevated 10-14. DAYS. (Indicator for injury after 24 hours)
Troponin- The best indicator of MI, very specific to cardiac cells. detected within 2 hours peak in 10 -12 and return to normal within 1-2 weeks.
205
What is the goal for someone who had a STEMI?
Limit the degree of damage and re-perfuse ASAP.
Protect against arrhythmias
206
What drug would you give to re-perfuse the heart in a person with STEMI?
Thrombolytics
Streptokinase
Alteplase
Tenecteplase
Could also re-perfuse with PCI procedure.
207
What are the immediate interventions for MI
oxygen
Aspirin
Morphine- controls pain and hemodynamics
decreases preload and afterload
Beta Blockade
1. ) Decreases pain
2. )Decreases demand which can decrease the size of injury
3. ) short term mortality
4. ) indicated for 2-3 years after the event
208
What is the MOA of Beta Blockers?
decreases sympathetic simulation thus stimulation (Decreasing Demand). (negative inotrope and chronotrope), may increase supply by prolonging diastole and prolonging filling time, and also ***anti-arrhythmic properties...
209
Nitroglycerin -
Action- decreases preload, may assist with BP
Mortality- it has no effect
Administration- typically given SL initially then IV if indicated. Avoid if hypotensive (systolic pressure less than 90) severe bradycardia, or suspected rt.
Avoid id PDE5 inhibitors within the last 24 hours
210
What are the two classes that effect mortality rate in MI
Antiplatelet and Beta blockers
211
Reperfusion therapy goal
to re-perfuse as soon as possible. Hopefully within the first 1-2 hours of symptom onset.
Thrombolytics- Always use heparin and antiplatelet as well. The faster you present, the better candidate you are for a thrombolytic (within4 hours) works about 80% of the time.
PCI
212
contraindications for thrombolytics
any kind of recent bleed or surgery
Severe HTN
213
PCI
Always give Heparin,
duel anti-platelet drugs (plavix and aspirin)
and GPIIb/IIIa inhibitor (Super aspirin)
Procedure can start in 90 min of presentation
later presentation is later than 3 hours ofter presentation
214
Adjunctive Drug Therapy
Heparin
Thrombolytics
PCI
to reduce the risk of re-thrombosis
215
Adjunctive Drug Therapy
Clopidogrel (PLavix) ADP platelet receptor blocker
Aspirn
216
Adjunctive Drug Therapy
GPIIb/IIIa inhibitor used with ABCiximab for PCI
217
Adjunctive Drug Therapy
ACEI after STEMI reduces short and long term mortality because of remodeling
218
complications
ventricular dysrhythmias- the major cause of death following MI treated with lidocaine IV. 60% of Deaths
Cardiogenic Shock- total body hypoperfusion secondary to compromised cardiac function
CHF-
Cardiac rupture
219
Risk Reduction
```
smoking
cholesterol
diabetes
HTN
Exercise
Weight loss
```
220
Secondary Prevention
```
Beta Blockers
Antiplatelet drugs
ACEI
Anticoagulants- ASPIRIN
STATIN
```
ASA contraindicated- AFib, LV, Trombus wall motion abnormalities, severe Systolic Dysfunction
