acute coronary syndrome
Card Set Information
acute coronary syndrome
acute coronary syndrome
acute coronary syndrome
what are the stages of atherosclerosis
-Normal Arterial Lumen & normal cell walls
-Lipids in bloodstream
-lipids increase, atheroma occurs accumulates in artery
-Atheroma continues to develop & becomes Lesion (pt will start to have CP, perfusion is decreased)
-Atheroma ruptures, releases lipids in blood stream
-Fresh Clots blocks the vessel (CP not relieved by NTG, No intervention = MI)
True cardiac chest pain left untreated will ...
continue to intensify and escalate!!
Cardiac origin chest pain mat present in various ways
Chest pain (squeezing or crushing)
Radiation (arms, neck, back)
Anxiety (Extreme, impending Doom)
Cardiac symptoms and the Diabetic Patient
because of neuropathy, diabetic patients may not perceive pain so they may not seek treatment.
They may complain or N/V, indigestion.
They usually seek treatment for CHF states and MI is found once EKG is done
What are some NonCardiac Causes of Chest Pain
(inflamm of Intercostal Muscles)
(inflamm pericardial sac)
(Increases risk of dysrhythmias)
(Overstretching muscles of chest wall)
(to chest or organs or chest)
Chest Injuries secondary to Chest Trauma
Tension Pneumothorax (air is trapped in the chest cavity with no possible way to escape, pressure builds)
what is arteriosclerosis?
the hardening of the arteries, Lumens become thick and lose their elasticity
What is Angina?
it is defined as chest pain associated with myocardial ischemia
Symptom of CAD
Most commonly behind the sternum in the chest but can radiate to the arm, neck, back.
Etiology of Angina
Decreased Supply of Oxygen
Increased Demand for Oxygen
What are some things that can cause increased demand for Oxygen?
What are some things that cause decreased supply of Oxygen
Common precipitating factors of Angina include
exercise, Lifting, pushing, Valsalva Maneuver
Emotions, overeating (Oxygen is shunted to the gut)
Extreme Temp Changes (Cold=Vasoconstriction)
Smoking (nicot=↑ HR & BP)
↑ CO2 = ↓ O2
Ischemia leads to _____ metabolism and accumulation of _____
Ischemia leads to
metabolism and accumulation of
Which results in Chest Pain
Angina is associated with 75% occlusion of coronary artery
Subjective Clinical Presentation of Angina
Substernal Chest Pain
Weakness (elderly may have profound weakness as primary symptom)
When people have TRUE Cardaic Chest pain, how long does it last?
No longer than 15 minutes
IS relieved by NTG
Objective Clinical Presentation of Angina
Levine's Sign (grab chest)
S4 (new Onset)
what are diagnostics related to Angina
Isoenzymes (will be negative)
EKG (ST Depression except Prinzmetals elevation)
Graded Stress Test
Myocardial Perfusion scan
Why are isoenzymes negative with Angina patients?
there is no infarction
Angina Patient what will the EKG show
ST Depression unstable angina
ST Elevation with Prinzmetals
ST Depression acute angina episode
**you will see ST DEPRESSION in all angina except prinzmetals angina***
what is the difference in stable and unstable angina?
Stable is predictable, unchanging in freq and duration
Unstable will have more progression of CAD. Pain greater in severity, longer in duration (More difficult to manage and relieve) does not respond to NTG
types of unstable angina
De Novo unstable angina
either New Onset or change in how the angina is occurring
Pain that starts small and increases in frequency, duration, and intensity
Pain that lasts, prolonged duration, and even
occurs during rest
Wellen's Syndrome angina
More specific, it has to do with
highly associated with coronary spasm
Pain can occur at
precipitated by alcohol, cocaine, smoke
longer than 10 mins
ST ELEVATION during the pain
NO BETA BLOCKERS
**GIVE CALCIUM CHANNEL BLOCKERS**
patients that do not report any kind of pain at all, they are put on the monitor and the ST depression or elevation is found
diabetics, elderly, vulnerable populations
Collaborative Pt Management Angina (GOAL)
to relieve chest pain
NTG:Vasodilator (take BP between doses)
Calcium Channel Blockers
: reduce demand of Oxygen by decreasing electrical conduction which decreases work load of heart and increase delivery of Oxygen to the heart because it dilates the arteries
Angina occurs when the heart is not getting enough oxygen, so how can you increase the oxygen supply in the heart?
Oxygen (maintain ↑ 90% sat)
Calcium Channel Blockers or NTG
Possible Blood Transfusion (if caused by Anemia)
Control Dysrhythmias (tachy =↓filling, Brady=↓ Cardiac Output)
IABP (helps heart to beat)
How can the Oxygen Demand be decreased?
Activity Cessation, Bed rest
Beta-Blockers helps decrease HR & contractility (No for Prinzmetals)
Calcium Channel Blockers (help decrease pre-load and after load
Myocardia Infarctions involve ...
death of myocardial tissue in an area deprived of blood flow by a occlusion of a coronary artery
Actual Death of the tissue is the end of a process that begins with ischemia and injury
Pts having an Mi can best be salvaged...
with intervention within 2 to 6 hours, after 6 the tissue is dead
what are the types of MI
Non-Q wave MIs
Transural (entire thickness of the myocardium in one distinct area)
and the usual S/S of MI
***Non Q-Wave MI***
subendocardial (incomplete, not every layer of the myocardium, may only damage inner most layer)
LESS DAMAGE, many go undiagnosed
ST Depression, T-Wave Inversion
The 3 I's of Infarction
3 I's of infarction, what happens in first stage?
Ischemia, T-Wave inverts in the leads overlooking the occluded area. St Depression
Myocardial tissue is starving for blood and oxygen. Tissue becomes pale/whitish in color
3 I's of infarction what happens in stage 2?
once progressed to injury tissue turns bluish in color
Tombstone T's means Injury in progress
3 I's of infarction, what happens in stage 3 ?
after 6 hours with no perfusion the tissue becomes black.
in 6 weeks becomes scar tissue, once necrotic will not rejuvenate.
***ST Segments and T-waves***
ST Depression= Ischemia
ST Elevation & Tombstoone T's= Injury
Non Q MI= ST Depression, T wave inversion
Q wave MI= ST Elevation, T wave inversion, Significant Q waves
ST Depression in Angina except Prinzmetals
Determining Age of MI
Q-Waves always represent Infarction
Walls of LV & Infarct Locations
and front part of the LV
, bottom wall
, left side of LV
RCA & part of CX
, posterior and backside of LV
LAD, CX, Left Main
Etiology of MI (why they occur)
Coronary Artery Thrombosis (Most Common)
Coronary Artery Spasm
Cocaine-Induced (imbalance between supply and demand)
Pathophysiology of MI
Prolonged imbalance between supply and demand
Decreased Contractility and compliance
Ischemia, Injury , and acidosis cause electrical irritability
Healing Process (intervene in 2-6 hours = better prognosis)
How are MI's Classified?
Q-Wave vs Non Q-Wave (more Q-wave)
%'s of occurrence
Degree of muscle dysfunction (depends on size of infarct)
The Bigger the Infarct the more long term complications the patient will have
Subjective clinical presentation of Acute MI
Pain (long duration, not relieved by NTG)
: radiating pain
Atypical Clinical Presentation
: symptoms that you may or may not see but could be caused by something else. N/V, profound weakness
Objective Clinical Presentation of Acute MI
HR, Rhythm (can be tachy or brady) ST elevation, Depression, Q-waves
: may be high, low or normal
Elevated Temp at acute phase
May have JVD (complication of CHF States)
May have Abnormal PMI (inflamm heart can become displaced)
May have Deminished Heart Sounds, Adventitious lung sounds, Murmur, Bruit
*Clinical Indicators of Hypoperfusion
: not enough O2, pallor, cyanosis, decreased renal output, chest pain extremity pain**
Anxiety or impending doom
IABP, what is it?
large bore catheter that is inserted femorally and positioned in the descending aorta below left subclavian artery the treats LV failure that is unresponsive to pharmacological and volume treatment
How does the IABP work?
increases available oxygen supply while decreasing LV work load
which increases Cardiac Output
Balloon works on counter pulsation where helium or Carbon Dioxide moves back and forth to inflate and deflate
When does the IABP inflate
Inflates during Diastole, which increases coronary artery blood flow
When does the IABP deflate
Deflates during ventricular sytole
why would a pt need a IABP?
Recurrent Angina after MI
Ventral Septal Defect
Refractory Ventricular arrhythmias
***Low Cardiac Output Heart needs a break**
When is IABP contraindicated?
Severe Peripheral resistance
Aortafemoral or aortailiac bypass
Diclotic notch triggers inflation, EKG trigger deflation
Weaning pt form IABP
Pt must be hemodynamically stable without vasopressor support
Must have adequate Cardiac Function and Good Arterial Perfusion
Wean Slowly, 1:1, 1:2, 1:3 and so on until off
Complications of IABP include
S/S of poor blood flow
**Limb Ischemia or Neuropathy
Dissection of Aorta = BAD NEWS, worst thing that could happen
Assessment of IABP
Assess MAP, above 60
HR, Wedge pressures
Pulmonary- prob on vent watch infection
**Watch for limb perfusion**