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
when does ACS occur ? (meaning unstable angina and MI)
- Common Precipitating - Factors
- Exercise 13%
- Unusual exertion 18%
- Surgery 6%
- Rest 51%
- Sleep 8%
Signs & Symptoms
ACS
CP > 30 min severe. Not relieved by NTG and/or rest
Dyspnea
Orthopnea
N & V
Diaphoresis
Weakness and/or fatigue
Anxiety, apprehension, denial
Palpitations
Dizziness
Dysrhythmias
ACS Diagnosis
Patient history
Signs & Symptoms
Type of pain OPQRST
ECG changes especially inverted T-wave
Inverted T waves
ST elevation or depression
Q waves if the MI is already developed
Other tests
Cardiac enzymes and markers
Look if they are anemic or not.
ECG evolution with MI
Phases:
Hyper acute phase
Early acute phase
Later acute Phase
Fully Evolved
Healed
Locating MI by ECG changes:
V1, V2, V3, V4/LAD/Anterior wall
II, III, aVF/RCA/Inferior wall
V1, V2, V3, V4/RCA or left circumflex/posterior wall
I, aVL, V5, V6/left circumflex/Lateral wall
Time is MuscleDoor to Balloon Initiative < 90 minutes
Treatment. We want to be as fast as possible. We want to save heart muscle. If we can perform a PCI intervention before 90 min it’s great. (Remember once we have a necrotic area that’s never going to come back)
- Medications
ASA, O2, NTG, morphine = vasodilation and decrease workload of heart
- AONMT
- Positioning
Head up decreases workload on heart and increases CO
- Medical Interventions
**PCI
****PTCA, stents
**CABG
**Fibrinolytics
Fibrinolytics
- These days they are not the initial thing that we go for.
-The goal with them is to dissolve the clot that is blocking the blood flow to the heart and thereby decreasing the size of the infarction
**Medications
Nursing considerations
**Detailed H & P are critical (bleeding and time of onset)
**Initiate bleeding precautions, assess ECG, and minimize anything that causes bleeding
***Must be given in a compressible site
**F/U therapy
***Antiplatelet
**ASA, clopidogrel (Plavix), abciximad (ReoPro IV), eclientifibatide (Integrilin)
Check slide 41
Check slide 41
Fibrinolytic Therapy Nursing Considerations
Check slide 42
Nursing Management: ACS/MI
- Oxygen and medication therapy
- Frequent VS assessment
- Physical rest in bed with head of bed elevated
- Relief of pain helps decrease workload of heart
- Monitor I&O and tissue perfusion
- Frequent position changes to prevent respiratory complications
- Report changes in patient’s condition
- Evaluate interventions!
Invasive Coronary Artery Procedures
- Percutaneous transluminal coronary angioplasty (PTCA)
- Coronary artery stent
- Coronary artery bypass graft (CABG)
- Cardiac surgery
Check slide 45
PCI
- Known as balloon angioplasty or percutaneous transluminal angioplasty
- Minimally invasive
- Used to treat CAD, angina, acute MI in order to re-perfuse and save cardiac muscle
- Often combined with stent placement
Bare-metal stent
Drug eluting stent
Coronary Artery Bypass Graft (CABG) Check slide 47 and organize
- Thoracic surgery
- The choice of bypass graft depends on
Location and extent of blockage
Size of coronary arteries
Availability of arteries and veins
Patient condition/conditions
Graft choices
Left Internal thoracic artery ITA (internal mamary) and right ITA
Radial artery, gastropiploic artery and saphenous vein
Advanced Support
Pulmonary artery catheter (PA) used to measure intra-cardiac pressures , volume status
Intra aortic balloon pump( IABP)used for counter pulsation to improved perfusion while LV heals
Left ventricular assist device (LVAD) is a pump
Patients will only have a MAP, no pulse
Check 48 onward on ppt
hi
A bruit ?
A bruit is the sound of blood flowing through a narrowed portion of an artery.
Atheroembolism?
Cholesterol embolism or atheroembolism is a phenomenon where cholesterol crystals and atheroma debris such as cholesterol, platelets, and fibrins embolizes from proximal large arteries such as the aorta and its major branches to distal small arteries.
Spasm
A coronary artery spasm is a sudden contraction of the muscles within the arteries of your heart. They are taking matters to their own hands because they are thirsty for O2
Why does eating a large meal cause angina ? AKA as heart attack
Eating and digesting food releases many hormones into the bloodstream. Those substances increase the heart rate and blood pressure, and may increase the substances that help form clots. The temporary rise in blood pressure increases the oxygen requirements and creates an extra burden on the heart.
Why can hypoglycemia cause angina?
low blood glucose also encourages a hypercoagulant state resulting from an increase in plasma concentrations of coagulation factors and by promoting platelet aggregation
It can because if the heart doesn’t get enough glucose to make ATP it can’t make energy to live
Both for stable and exercise angina; if they don’t go away we say that ?
they are unstable.
What is Prinzmetal angina aka as vasospastic disease?
It’s is when there is a vasconstriction of a coronary vessel for unclear reasons which leads to ischemia and therfore angina
Unstable angina and myocardial infarction are collectively called ?
acute coronary syndrome.
Aspirin and MI
All patients with suspected myocardial ischemia should be given 325 mg of aspirin, unless there’s a contraindication, like a history of an anaphylactic reaction or if they’ve already received it.
Palpitation meaning ?
Heart pounding
women vs men angina? Google
Also, women, older adults, and patients with diabetes often have atypical presentations like just dyspnea, epigastric pain or discomfort, syncope, or sudden death from cardiac arrest.
stable angina ?
Patients with stable angina don’t feel pain at rest, but they do feel chest pain during intense physical exercise, because that’s when the myocardium has increased oxygen demand, which leads to transient or demand ischemia.
Unstable angina ?
Now, angina is considered unstable if it presents at rest, or if it becomes more frequent, lasts longer, or occurs with less exertion than previous episodes of angina.
In unstable angina there’s prolonged myocardial ischemia, but there’s no myocardial cell death yet, so it’s not a myocardial infarction.
But if it’s not taken care of promptly, the ischemia can get prolonged and can lead to myocardial infarction, which is life-threatening.
Syncope? No O2
Syncope is used to describe a loss of consciousness for a short period of time. It can happen when there is a sudden change in the blood flow to the brain. Syncope is usually called fainting or “passing out.”
Angina symptoms in women ?
Men ?
Dizziness,
backpain,
neck pain
anxiety
SOB
nausea and vomiting
MEN:
SOB
lightheadedness
perspiration
chest pain and pressure
stomach pain
Why does angina cause vomiting ?
Firstly, the necrotic, ischemic, and injured cardiomyocytes from infarcted regions release lactic acid, this ends up in the stomach and causes nausea and vomiting.
If a pt with a history of stable angina has to take a second NTG for the pain to go away?
Regardless…
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.
why does nitroglycerin decrease preload and afterload ?
Because not only it dilates the arteries but also the veins. When it dilates the veins there is less pressure in them. if there is less pressure in them less blood makes it back to the heart and if less blood makes it back to the heart the LV gets filled with less blood which decreases the preload.
Why does NTG cause a headache ?
because it’s a vasodilator and a lot of blood makes it to the head increasing cranial pressure.
when do we call EMS with nitroglycerin?
If chest discomfort/pain is unimproved or worsening 5 minutes after taking ONE NTG dose sublingually, it is recommended that the patient call 911 immediately to gain access to EMS.
The same shit as if we have to take the second dose.
What are calcium channel blockers ?
Calcium Channel Blockers (Decrease BP and dilate coronary arteries)
Acute Coronary syndrome or disease ?
It just means unstable angina or an MI
MI and ST ?
No St elevation
increased WBC wuith Acute coronary syndrome (Mi and angina)?
Because cell death causes inflammation and inflammation causes bleeding and the heart thinks that there is a chance of infection.
CK-MB:
Creatine kinase myocardial band (MB) increases with injury
Troponin is highly ?
specific for myocardial cell injury
When is troponin detected and when should you repeat test if negative the first time ?
Detected 3-4 hours after onset of chest pain
repeat after 6h
troponin peak ?
Peak in 4-24 hours
when do troponin levels return to normal ?
1-3 weeks
Why do we call MI ACS?
Because myocardium the M in MI is the heart muscle that pumps blood to the rest of tissues and if it can’t pump blood to the coronary arteries that feed it because ellas mismas si las coronary arteries no le estan de comer implemente se muere
PCI aka PTCA ?
Percutaneous coronary intervention (PCI) refers to a family of minimally invasive procedures used to open clogged coronary arteries (
Fibrinolytic kill fibrin (causes a clot ) aka Thrombolytic
Fibrinolytic Fink
Fibrinolytic therapy — or thrombolytic therapy — is an emergency treatment used to dissolve blood clots before they become fatal.
Active thrombin then converts the fibrinogen into fibrin, eventually forming a fibrin matrix (weblike structure/clot). So when we kill it with a fibrinolytic to dissolve clot
heparin? thrombolitic, antiplatlet or anticuagulant
No, heparin isn’t a thrombolytic drug. It’s an anticoagulant that helps your body make clots more slowly
A femoral PCI ?
it’s for atherosclerosis in an artery not a heart problem ACS
femoral sheath? google pic
The femoral sheath is a fascial tube encapsulating the key vascular structures passing through the retro-inguinal space,
PTCa heart
Percutaneous transluminal (lumen to get rid of blockage) coronary angioplasty
