Week 5 and 6 Acute Coronary Syndromes Flashcards
What is infarction?
necrosis or cell death, causes irreversible damage
What causes infarction?
Prolonged severe ischemia and decreased perfusion
How to differentiate unstable angina from an MI (lab)
Will have ST changes on ECK but no elevation in CK or triponin
3 categories of MI
ST elevation MY(STEMI)
Non-ST elevation (NSTEMI)- most common in women
Unstable angina
Primary factor in development of MI
atherosclerosis
Major risk factor for heart disease
Metabolic syndrome
Metabolic syndrome
3 of the following risk factors: HTN, triglycerides, fasting blood glucose >110, waist > 40 M > 35 F, increased C reactive protein, increased blood clotting factors
Use of thallium scan
identify “cold spots” that indicate ischemia or infarction
Priority main medication in MI
morphine
Medications post MI
Beta blocker within 2 hours
ACE or ARB within 48 hours
Possible Ca+ blocker
Function of ACE or ARB order
prevent ventricular remodeling and development of heart failure
Class I HF
pts often respond well to reduction in preload with IV nitrates and diuretics, no crackles or S3
Class II HF
may need diuretics, IV nitroglycerin, need beta blockers, ACE and ARBs, crackles in the lower half of the lungs and possible S3
Class III HF
may need diuretics, IV nitroglycerin, need beta blockers, ACE and ARBs, crackles more than halfway up the lungs and frequent pulmonary edema
Class IV HF
Necrosis of more than 40% of the L ventricle occurs, stuttering pattern of chest pain, monitor for cardiogenic shock
Sx of cardiogenic shock
Tachycardia, hypotension, BP less than 90 or 30 from baseline, urine output less than 30!!, cold clammy skin and poor peripheral pulses, agitation restlessness confusion, pulmonary congestion, tachypnea, continuing chest discomfort
Myocardial O2 requirements during an MI
Increased O2 demand and tissue is already O2 deprived. This can cause ventricular dysrhythmias
When is tx of MI needed
within 4-6 hours, physical changes to the heart occur after 6 hours
ventricular remodeling
when scar tissue permanently changes the heart, can cause dysrhythmias
CK-MB lab
most specific test for MI but doesn’t peak until 24 hours after
Priority problems for Pts with CAD
Acute pain (r/t < myocardial O2), inadequate tissue perfusion, activity intolerance, ineffective coping
Additional potential problems for a Pt having an MI
Potential for dysrhythmias
Potential for HF
Potential for recurrent symptoms and extension of injury
New onset a-fib
May signal MI in patients with DM and CAD, they may not experience chest pain or pressure because of neuropathy.
Drugs given in acute MI
ASA, Nitro, morphine, O2
Reperfusion therapy
uses thrombolytics to restore blood flow, best used within 6 hours of onset
percutaneous transluminal coronary angioplasty (PTCA)
Stent placement to re-open the clotted artery, should be done within 2-3 hours
Signs the clot was lysed and the artery reperfused
Abrupt cessation of pain, Sudden onset of ventricular dysrhythmias, Resolution of ST-segment depression/elevation or T-wave inversion, A peak at 12 hours of markers of myocardial damage
Complication after clot lysis
vessel reocclusion due to high thrombin release into the blood
S/Sx of left ventricular failure and pulmonary edema
crackles, wheezing, tachypnea, and frothy sputum
Listen for S3 sound
S/Sx of inadequate organ perfusion
change in mental status, Urine output less than 30mL/hr, Cool clammy extremities with decreased or absent pulses, Unusual fatigue or recurrent chest pain
Medications to reduce preload
diuretics and nitroglycerin
S/Sx of Rt ventricular failure
Decreased cardiac output with a paradoxical pulse, clear lungs, and JVD
ST segment elevation indicates what?
Infarction
ST segment depression indicates what?
Ischemia
When does the S3 heart sound occur?
during the rapid ventricular filling of diastole; low pitched; use bell
When does the S4 heart sound occur?
linked to resistance in ventricular filling or a vibration caused by atrial contraction; low- pitched; use bell
Contraindications of reperfusion therapy
any hx of bleeding disorders, anticoagulation therapy or HTN > 180/110
How to calculate CO and average CO
SV X HR
averages 4-8 L
Preload
amount of stretch on myocardial muscle fibers at end diastole determined by amount of blood in the ventricles
Afterload
Sum of all forces against which the ventricle muscle must contract to eject blood into the pulmonary and systemic circulation
SVR`
measures afterload
Factors that affect afterload
heart size, qty of resistance overcome by heart muscle to eject blood, qty of disease
When is preload increased?
hypervolemia, valvular regurgitation
When is afterload increased?
HTN, vasoconstriction
HR at which CO declines
160 BPM
Normal ejection fraction
55-70%
Acute coronary syndrome
refers to unstable angina, Non STEMI or STEMI MI
CO changes in sepsis
in earlier stages your CO will rise because of vasodilation and more fluids moving in, in the later stages, your CO drops
Do beta blockers reduce preload or afterload?
Afterload because they dilate the arterial beds
Are ACE and ARB preload or afterload reducers
Afterload
Does aldoactone reduce preload or afterload
proload because it will help move fluid out of the body
Ways to measure SVR (systemic vascular resistance)
Crudest is BP
Pulmonary artery catheter
How does the size of the heart affect afterload
The larger your heart gets, the more it increases the arterial resistance
What happens to myocardial O2 demand with increased afterload?
O2 demand goes up
What drugs depress cardiac contractility?
Beta Blockers (mild negative inotrope)
Test to measure ejection fraction
Echo
Cardiac cath
S/Sx seen in low EF %
Dyspnea, cool skin, edema, JVD, low BP, crackles
What reading can be obtained from the cardiac cath?
pulmonary artery pressure, Rt atrial pressure, central venous pressure, HR, BP
Wedge pressure only when balloon is inflated
Average arterial BP
Systolic 90-140
Diastolic 60-90
Mean arterial BP range
70-11 mmHg
Rt arterial pressure range
2-6 mmHg
Measures preload
Pulmonary artery pressure range
25/10
a quarter over a dime
Systolic range 15-25
Diastolic range 8-15
Neurohormonal factors for preload
1st- SNS
2nd- RAAS
Factors effecting preload levels
blood volume, decreased fluid excretion by kidneys, SV, contractility, HR
Steps of management in HF
1st- Preload
2nd- Afterload
3rd- Contractility
Correlation to high BP to afterload
afterload will be high
very high BP = increased SVR
Interventions in the home to decrease proload
lower legs, restrict fluid, give diuretic
Interventions to reduce afterload
vasodilator/antihypertensive (ACE, Nitro, etc.)
Interventions in acidosis and decreased CO
must fix acidosis 1st or drugs won’t work
Acidosis is detrimental to contractility
Can give insulin
Functions of echocardiogram
gives EF
Diagnose valve disorders
Diagnose cardiac tamponade
Normal pulmonary capillary wedge pressure
4-12 mmHg
What is the significance of PCWP (pulmonary artery wedge pressure)
shows L side heart function
If pressure is up, then pressure is up in the L side of the heart
First intervention when high PA pressure is seen
put them on O2
then look at pre-load and address that
SVR
represents arterial bed constriction
What 3 symptoms seen together should be reported together for ACS?
Increased HR
No HTN
Pulmonary congestion
Heart sound heard with exces fluid
S3
Common w/ previous MI or HTN
What condition is indicated with S3 and S4 heart sounds
severe HF
Priority interventions with suspected cardiac issues
1. VS and cardiac monitoring/12 lead 2 Labs 3 IV (saline lock) 4 Physical exam and chest x-ray Give MONA when 12 lead is positive
What is the biggest risk for CV issues
DM (type I or II)
Classic clinical manifestations of cardiac disease
Chest, jaw, left arm pain (esp. men), N/V, diaphoretic, cool, clammy, temp (mild)
Common sx of MI in women
SOB (biggie for women), extreme fatigue, pain/discomfort centered low in chest or upper abdomen, shoulder blade/back pain, pain/discomfort in left arm, shoulder, jaw (like men), weakness, nausea, hot, flushed, dizziness, syncope
3 inflammatory markers to test for
Homocystiene, lipoprotein and C-reactive protein (#1, high is 3)
Causes of increased imflammation (which increases CV risk)
poor nutrition, sugar, sedentary lifestyle, psoriasis, migraines, sleep apnea, gum disease
Labs to get when MI is possible
cardiac markers, comprehensive metabolic panel, CBC, coags, C-RP, Mg+, cholesterol
When to give morphine for an MI
after 3 doses of nitro have not relieved pain
What does ST depression indicate?
Ischemia, possibly some myocardial death but ischemia may be reversed
What does ST elevation indicate
Infarction (MI)
must be significant in 2 leads
What does an inverted/flattened T wave indicate?
ischemia
When to gove TpA
within 12 hours of onset
if not going to cath lab/delayed
if no bleeding risk (injury/trauma, CPR, recent surgery or stroke)
Time frame and what is needed in the H&P for cardiac injury
10 minutes
onset?, syncope?, CV Hx? DM? renal disease? smoking and diet?
Where is the PMI and how do you palpate?
Left MCL 5th intercostal
palpate with palm
S1 sound
Tricuspid and mitral valve close
heard best at 5th intercostal MCL
S2 sound
aortic and pulmonic closure
heard best at 2nd ICS rt of sternum
S3
Occurs during rapid ventricular filling, use bell
= fluid overload/ HF
S4
resistance to ventricular filling or vibration from atrial contraction, use bell
= HF and aortic stenosis
Where to best hear murmurs
3rd ICS on L side (erbs point)
Best Pt position to hear heart sounds
Pt sit up and lean forward (to the left a little too maybe)
If have to lie down, lay on left side (left lying probably best, but often having trouble breathing, etc so sit up)
