acute coronary syndrome
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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
- Pleurisy (inflammation)
- Costochondritis (inflamm of Intercostal Muscles)
- Pericarditis (inflamm pericardial sac)
- Myocardial Contusion (Increases risk of dysrhythmias)
- Muscle Strain (Overstretching muscles of chest wall)
- Trauma (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?
- Hypertensive States
- Valve disease
- CHF States
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 anaerobic metabolism and accumulation of lactic acid.
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?
- 1-4 minutes
- No longer than 15 minutes
- IS relieved by NTG
Objective Clinical Presentation of Angina
- Hypertensive, Hypotension
- 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
- Wellen's Syndrome
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 LAD stenosis
- Variant, spasmodic, highly associated with coronary spasm
- Pain can occur at rest
- precipitated by alcohol, cocaine, smoke
- Lasts 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
- Decrease Stimuli
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
- Transural (entire thickness of the myocardium in one distinct area)
- Results in ST Elevation, T-Wave Inversion, Significant Q-Waves 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
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
- ST Elevation
- 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.
- Significant Q-Waves
- 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
- Anterior: LAD and front part of the LV
- Inferior: RCA, bottom wall
- Lateral: CX, left side of LV
- Posterior: RCA & part of CX, posterior and backside of LV
- Anterior-Lateral: LAD, CX, Left MainAnteroseptal: LAD
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
- Anaerobic metabolism
- Prolonged Ischemia
- 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)
- Associated Symptoms: 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
- BP: 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?
- LV Failure
- Unstable Angina
- Recurrent Angina after MI
- Cardiogenic Shock
- Ventral Septal Defect
- Refractory Ventricular arrhythmias
- ***Low Cardiac Output Heart needs a break**
When is IABP contraindicated?
- Aortic insufficiency
- 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
- Manage Arrhythmias
- Dissection of Aorta = BAD NEWS, worst thing that could happen
Assessment of IABP
- Assess MAP, above 60
- HR, Wedge pressures
- renal output
- Pulmonary- prob on vent watch infection
- **Watch for limb perfusion**
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