CAD, ACS & Cardiac Conduction Problems Chapter 23 Flashcards
Atherosclerosis
Disease of the large and medium-sized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and the build up of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall.
**Plaque formation
**Vascular remolding (fiber after inflmmation/injury)
**Acute and chronic luminal obstruction
**Abnormalities of blood flow
**Diminished O2 supply
IT ALL STATRS WITH THE FATTY STREAK (A fatty streak is the first grossly visible (visible to the naked eye) lesion in the development of atherosclerosis)
Total cholesterol?
< 200 low risk
200-239 borderline
>239 high risk
High Density Lipoprotein (HDL)
> 35
< 35
Low Density Lipoprotein (LDL)
<129 low
130-159 medium
>159 high
Triglycerides
<200
201-399
400-1000
>1000
Cholesterol Medications : Six types of lipid-lowering agents: affect the lipid components somewhat differently
- 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) (or statins)
- Nicotinic acids
- Fibric acids (or fibrates)
- Bile acid sequestrants (or resins)
- Cholesterol absorption inhibitors
- Omega-3 acid-ethyl esters
Atherosclerosis. Risk Factors
- Modifiable: Smoking (causes vasoconstriction), obesity, lack of exercise, stress (because it affects our vessels), diet
- Controllable: HTN, hyperlipidemia, DM (the large glucose molecules damage the tunica intima pf the BV and they block the circulation of tiny BV)
- Non-modifiable: Gender, age, heredity, ethnicity (can be modified when r/t systemic racism, poverty, etc.)
Atherosclerosis. Signs & Symptoms
- Hyperlipidemia
- CAD
**4th heart sound, tachycardia, hypotension, HTN, angina - CV disease (includes CAD meaning coronary vessels and other vessels in the body in general )
**Diminished carotid pulses, carotid artery bruits, focal neurological deficits, headaches - PVD
**Decreased peripheral pulses, peripheral artery bruits, pallor, peripheral cyanosis, gangrene, ulceration, difficulty ambulating, pain with ambulation - AAA
**Pulsatile abnormal mass, peripheral embolism, circulatory collapse, pre/syncope, weakness
-Atheroembolism
**Gangrene, cyanosis, ulceration
Atherosclerosis. Diagnostics
- History and physical
- ECG
- Risk factor assessment (diabetes, HLPD, gender, LV function, provocation of angina, genetics, stress)
- Echocardiography (assess LV function, EF, predicts survival)
- Echo or ECG cardiac stress test
- CXR
- Labs
Coronary Artery Disease(CAD)Coronary arteriesRCA, L main, LAD, circumflex
What causes CAD
- Caused by an imbalance between myocardial (heart muscle) O2 demand and supply leads to ischemia
- CAD causes of supply-demand imbalance, It can be due to:
*Obstruction (thrombus or embolus)
*Spasm (Involuntary muscle contraction)
*Hypovolemia (Because if there is not enough volume of blood to prime the left ventricle there won’t be enough blood to feed the coronary arteries, {starling’s law} )
*Anemia (why? Because if a person’s blood doesn’t have enough hemoglobin to carry oxygen to cardiac arteries ) This can lead to ischemia and this is why we check the CBC.
*HR up/down arrows (If the HR is too low we don’t have enough cardiac output and when the heart rate is too high we don’t have time to fill and on top of this the O2 demand of the heart goes up as well )
*BP up/down arrows (If the blood pressure is too high there is too much afterload and there is too much pressure in the left ventricle and it has to push too hard. If it’s too low we go back to starlings law because there is not enough stretch or stroke volume, so we don’t have enough to prime the pump)
Prevention of CAD
- Control cholesterol
- Dietary measures
- Physical activity
- Medications
- Cessation of tobacco use
- Manage HTN
- Control diabetes
Angiography Risk Stratification. Meaning categorization
- High - Disease of left main or left anterior descending coronary artery, 3-vessel disease with proximal stenosis
- Medium - Significant lesion in large or proximal artery, but no high-risk features
- Low - Normal coronary arteries or nonobstructive plaques, they can have some plaque but nothing major or that can cause us to worry.
Angina Pectoris? ( It’s cardiac chest pain in a nutshell )
- A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow
The things that trigger it are :
- Physical exertion or emotional stress increases myocardial oxygen demand, and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand
Types of Angina. Chronic Stable Angina
- Decreased blood flow to myocardium usually caused by CAD
- Temporary pain/pressure. That is relieved with rest, O2 or it can be resolved with nitroglycerin and it’s deemed temporary.
- Usually, it follows a predictable pattern (Every time someone is about to have sex they take nitroglycerin and if they forget that they have angina, everytime someone walks a hill and they forget to rest they get angina till the rest or they use oxygen) long-term, a familiar pattern
- Resolves with NTG or rest
- Lasts 5 to 10 min. The exertional one lasts a little bit more but both go away.
Types of Angina. Exertional
- It’s kinda similar to Chronic Stable Angina but it’s only caused by exertion.
-Anything that increases the O2 demand of the myocardium is deemed exercise : Exercise, stress anxiety, large meals, tachycardia, anemia, hypoglycemia, hyperthyroidism (these are increased metabolic demands) - Resolves with rest or NTG
- Lasts < 15 minutes
- May radiate to arm, shoulder, back, jaw, neck, wrists
- Both for stable and exercise angina; if they don’t go away we say that they are unstable.
Types of Angina. Variant or atypical or Prinzmetal
- Not caused by exertion, it’s caused by coronary artery spasms (calcium channel blockers work very well for these)
- Often there is no coronary artery blockage or atherosclerosis
- Check slide of different types of angina.
Assessment and Findings (angina)
- May be described as tightness, choking (pressure around neck or chest), or a heavy sensation
- Frequently retrosternal (Retro; behind sternal ; sternum )and may radiate to neck, jaw, shoulders, back, or arms (usually left)
- Anxiety frequently accompanies the pain
- Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting
- The pain of typical angina subsides with rest or NTG after about 15 min and that unstable angina doesn’t go away. Let’s say that we have a pt with stable angina and somebody takes one nitroglycerin and sits down and rests the pain usually goes away. If they have to take a second nitroglycerin we usually have them call EMS just in case that chest pain won’t go away. If they have 2 nitros or 3 for the pain to go away we go ahead and have them take a 12 lead ECG to see what’s going on.
- Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention!
Assessing Patients and their Chest Pain Angina
Language of Chest Pain is its own.
Patient Assessment
Assessment of Chest pain
On the scale of 1-10
OPQRST:
Quality
Severity
Frequency
Location and radiation
Duration
Precipitating factors ( with angina ex: exercise )
Relieving factors (rest)
Gerontologic Considerations angina
- Diminished pain transition that occurs with aging may affect presentation of symptoms
- “Silent” CAD
- Teach older adults to recognize their “chest pain–like” symptoms (i.e., weakness)
- Pharmacologic stress testing; cardiac catheterization
- Medications should be used cautiously!
Gerontologic Considerations angina
- Diminished pain transition that occurs with aging may affect presentation of symptoms
- “Silent” CAD. There is no pain involved at all.
- Teach older adults to recognize their “chest pain–like” symptoms (i.e., weakness)
- Pharmacologic stress testing; cardiac catheterization to diagnose
- Medications should be used cautiously because they respond differently!
Angina Management
3 Goals:
1-Identify and respond ASAP. The first thing is to rest the patient and give them O2 and aspirin.
2-Establish prophylactic drug regimen
3-Widen or circumvent narrowed arteries
Treatment of angina.
- All treatment evolves around time; decreasing the amount of time that the heart is without oxygen.
- Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply. put the head of the pt bed at 30 degrees and give them oxygen and rest.
- Medications
- Oxygen
- Reduce and control risk factors
- Reperfusion therapy may also be done (NGT)
Medications angina
- Nitroglycerin
- Beta-adrenergic blocking agents
- Calcium channel-blocking agents
Anti-platelet and anticoagulant medications:
**Aspirin
**Clopidogrel and ticlopidine
**Heparin
**Glycoprotein IIb/IIIa agents
(abciximab, eptifibatide, and tirofiban)
ASA (aspirin). For angina. The most bank for your buck and it does a really good job.
- Acetylsalicylic Acid
**Antiplatelet effect
**we can give: 81 to 325 mg
**Chewable when we want them to be absorbed quickly in the event of angina (eureka) if it’s prophylactically you can just take it orally and it will be absorbed slowly.
NTG. Nitroglycerin for angina
- Causes venous and arterial dilation. Also dilation of coronary arteries, resulting in decreased preload, afterload, and increased blood flow to the myocardium
- Take 1 every 5 minutes X 3 doses sublingually. It also comes in a spray, paste(do not touch) or IV.
**Don’t swallow
**Take out the cotton ball in the container as it absorbs the drug (make sure you have gloves on)
**Keep in a dark (because it destabilizes with light), glass bottle, dry, cool (don’t keep it in your pocket) & renew every 6 months.
**Usually burns/fizzes under tongue and it usually always causes a headache - Check BP before and after administration
- AHA recommends contacting EMS (911) after the client takes the first dose of NTG. Don’t wait more than 5 minutes to call 911
MSO4. Morphine. Angina.
Morphine –decreases cardiac workload. Because it slows down everything.
- Analgesic effects decrease the sympathetic response thereby decreasing diaphoresis lightheadedness, & Decreases HR, BP and venous return
- Stimulates local histamine-mediated responses (vasodilatation)
- Might inhibit or delay of antiplatelet absorption (it literally means that it delays or inhibits the effects of aspirin )
O2Beta BlockersCalcium Channel Blockers. Angina
-Oxygen
- Beta Blockers (beta1 selective
*Decrease BP, P and myocardial contractility
*Improve LV function - Calcium Channel Blockers (Decrease BP and dilate coronary arteries)
Check 28
Patient Education
- Avoid isometric exercise (bacause it adds work to the heart )
- Avoid overeating (small meals about 6 a day)
- Rest frequently
- Avoid excess caffeine or any drugs the increase HR
- Wait 2 hours after eating to exercise
- Dress warmly in cold weather (because we don’t want to vasoconstriction)
- Adhere to medication regimen profalactically
- Take NTG prophylactically
- Stop smoking
- Manage diabetes
- Lose weight if overweight
- Diet modifications/changes
Unstable Angina
- it is defined as a change in pattern and increased in severity or > time to subside
- Not relieved by NTG or rest or O2
- It usually occurs at rest or awakens the patient at night
- It’s an angina that is not predictable anymore and it lasts more than 15 min. This is when we call for help and get the pt to the ED ASAP
Acute Coronary Syndromes
Decreased blood flow to the myocardium resulting in ischemia, necrosis or both usually unrelated to predisposing factor and unrelieved by NTG
MI (non ST segment elevation)
Unstable Angina
Signs and symptoms:
Pain
Cold (no blood circulating) and clammy (Clammy skin is cool, moist, and usually pale .)
Increased WBC and increased temp from the inflammation in their body due to damage
ECG changes
N & V
Check slide 32
You MUSTTTTTTTTTTTTTTTTTTT
Serial Cardiac Enzymes. CPK
CK-MM, CK-BB, CK-MB
**CK-MB elevate at 3-8 hours after the onset of chest pain
***Peak in 12-24 hours and return to baseline within 3 days
Serial Cardiac Enzymes. LDH ( lactate dehydrogenase ) an acid
*Helps determine the location of the tissue damage
*Normal: 5-150 U/L
*LDH 1 found primarily in heart and RBC & LDH 2 is concentrated in WBC
Serial Cardiac Enzymes. Troponin
*Highly specific for myocardial cell injury
Detected 3-4 hours after onset of chest pain
*Peak in 4-24 hours and returns to normal in 1-3 weeks
*Normal : 0.0-0.1 ng/mL
**Always normal in non-cardiac muscle diseases
