Exam One Flashcards
Acute Coronary Syndrome (general)
Reduction/occlusion in the coronary arteries and degree of damage to the myocardium (heart muscle). This includes NSTEMI, STEMI, and unstable angina. All three types start with some sort of damage to the endothelium
STEMI
ST elevation myocardial infarction… the most dangerous of myocardial infarctions because it indicated complete occlusion of the artery!!!! Heart muscle is blocked off from oxygen = necrotic cardiomyocytes
Transmural infarction (across the whole myocardium)
Can lead to rupture of papillary muscles which can lead to further complication of mitral regurgitation or mitral prolapse
Non STEMI (NSTEMI)
Does not involve the presence of ST elevation on a 12 lead EKG… rather you see an ST segment depression
Characteristic finding = subendocardial infarction/ST segment depression
There is no elevation in cardiac markers/enzymes
Non modifiable risk factors for plaque build up
Aging, male sex, family history, caucasian
unstable angina vs stable angina
Unstable angina - you have chest pain even when you’re resting (a lot more serious). Pain usually lasts longer than 20 min and is unrelieved by nitroglycerin.
Stable angina - chest pain that goes away when resting - usually lasts 3-5 minutes
Modifiable risk factors for NSTEMI/myocardial infarction
Smoking, hypertension, dyslipidemia, obesity, poor diet, diabetes, sedentary lifestyle
Is acute coronary syndrome a medical emergency?
Yes
Acute Coronary Syndrome Clinical Presentation
Central chest pain (“crushing” “heaviness” “tightness”)
Pain radiates to neck, jaw, left arm
Diaphoresis (bc sympathetic activation)
Feeling of impending doom (anxiety)
N/V
Troponin and CK-MB during STEMI/NSTEMI
Elevated
They get released into the blood stream when the heart muscle becomes necrotic.. so we measure to see if heart muscle has died :-)
Troponin is released very fast, hits high peak at day 2 after chest pain and then decreases
CK-MB is also released fast (but not as high as troponin) and then decreases
Which heart marker (enzyme) is most important to measure for STEMI/NSTEMI?
Troponin
How do heart enzyme levels change during stable/unstable angina?
They don’t. They stay the same. Troponin and CK-MB only rise during STEMI/NSTEMI
Patient shows up to ER with major chest pain radiating to left arm. What do you do first?
Investigate! Start 12 lead EKG, get full blood count, EUC, check glucose and lipid profiles, cardiac enzymes (TROPONIN !!, CK-MB)
X-ray to rule out other differentials if suspected
DO NOT DELAY TREATMENT
ECG Changes in ACS - unstable angina
20% may be normal initially
Usually don’t see any ECG changes
Normal or sometimes T wave inversion (depression)
Unstable angina physiology
1st hits the left anterior descending artery (which supplies anterior wall and septum)
2nd hits the right coronary artery (supplies right wall and posterior wall)
3rd hits the left circumflex artery (which supplies lateral wall of heart)
Which artery is most affected during myocardial infarction/”heart attack” ?
The left anterior descending artery
STEMI ECG Changes
ST elevation
Also need to look for new left bundle branch block (WILLIAM)
Widened QRS
V1 = W shape
V6 = M shape
New left bundle branch block may suggest infarction of hear
Initial management of all ACS - MOAN
Morphine (IV Opioids)
Oxygen (if < 93%)
Aspirin (+ lopiridil)
Nitrates (to reduce <3 workload and increase O2)
STEMI Definitive Managment
Emergency Reperfusion
1st choice = PCI = primary percutaneous coronary intervention. Angiogram is performed. Dilated balloon/stent inserted to clear blockage.
2nd choice = fibrinolytic therapy = thrombolysis. Use streptokinase, alteplase.
Unstable Angina/NSTEMI Definitive Management
High Risk Patient = start on anti platelets, anticoagulants, beta blockers. Consider glycoprotein inhibitors and revascularisation.
Low Risk/Intermedate Patients = continuous monitoring of cardiac enzymes (TROPONIN) and ECG
Ongoing Management of all ACS
Lifestyle modification!!!
Quit smoking Reduce alcohol intake Eating healthy Exercise Lose weight
Pharm (BAAAS) Beta Blockers - BP, HR Aspirin - Prevent clots from forming ACE Inhibitors/Angiotensin Receptor Antagonist - help reduce BP/workload Statins - help reduce cholesterol
Myocardial Infarction Definition
limited blood supply to the myocardial tissue that causes it to die/become necrotic
Myocardial Infarction Causes
Blockage in coronary artery due to CAD (most common)
Coronary spasm/constriction from drug usage (cocaine)
HTN
Damage to artery due to coronary artery dissection (tear in inner layer of artery “tunica intima” which causes it to leak into “tunica media”)
Cardiac output is the amount of
blood ejected by the heart in 1 minute and is measured in liters.
What determines cardiac output?
Hr and stroke volume and is controlled by both
Stroke volume is the volume of
blood ejected during systole per minute.
Filling pressure of the right ventricle is based on
the right atrial pressure
Filling of the left ventricle is based on
the left atrial pressure
How to calculate Cardiac Output
SV x HR
Decreased HR and increased SV cause
an increase in CO
Increased HR and increased SV cause
an increase in CO
Normal CO for an adult is
4 - 7 L/min
3 factors affect SV
preload, after load, contractility
Preload
amount of blood returning to the heart from the pulmonary vessels (left side) and the venous return (right side).
Afterload
the resistance that the heart must overcome to pump blood through the valves and aorta to the peripheral circulation
Contractility
the amount of force generated by the myocardium to eject blood into circulation.
Increasing cardiac output
increased preload - blood returns to the right atrium
Increased contractility occurs
Decreased afterload - decreases pressure that the heart must pump against.
Factors affecting HR
HR affects the cardiac output by causing a decrease or increase in SV
HR is controlled by baroreceptors in the aortic arch, which are sensitive to changes in the BP
Stimulation of the parasympathetic nervous system (vagus nerve) decreases the HR
Stimulation of the sympathetic nervous system increases the HR
Atherosclerois is
A type of arteriosclerosis. It is a soft intraarterial build up of fat and fibrin that eventually thickens and hardens the arterial walls through several ways.
Atherosclerosis is NOT a single disease or problem. It is a process that affects the entire arterial vascular system and is the leading cause of coronary artery and cerebrovascular disease.
Causes of atherosclerosis
Consumption of high fat and LDL foods
HTN, smoking, + obesity (inhibits the oxidation of LDL)
Diabetes, hyperlipidemia
Increased C-reactive protein, insulin resistance, infection and periodontal disease (have been found to damage endothelium)
Atherosclerosis nursing teachings
Encourage intake of enriched fortified cereals that contain folic acid, vitamin B, + fresh veggies
Discourage meals high in LDL (red meats, eggs, food fried in saturated fats)
Exercise + weight management
Diabetes - control glucose
Cardiac ischemia is
Partial or temporary loss of blood flow/tissue oxygenation
Ischemia in the heart is called
Angina - chest pain that occurs when the myocardium does not get enough blood.
In a severe ischemic environment cardiac cells remain viable for
approx. 20 minutes
Can myocardial ischemia be asymptomatic?
Yes, it can be “silent” with no chest pain
Q Wave
0.04 seconds wide OR 1/3 height of the R wave
May take 8-48 hours to show up on the ECG
Never goes away.
Transmural injury on ECG
Marked ST elevation with hyper acute T wave changes
Necrosis on ECG
Pathologic Q waves, less ST elevation, terminal T wave inversion
Ischemia ECG
ST depression
Northwest Deviation ECG
Emphysema
Hyperkalemia
Ventricular Tachycardia
Verticle Axis ECG
1 small square = 1mm
1 large square = 5mm
2 large squares = 1mV
Horizontal Axis ECG
1 small square = 0.04s
1 large square = 0.2s
5 large squares = 1s
