Week 4- Chest Pain Flashcards
1
Q
What is the major cause of mortality and morbidity?
A
- Heart diseases
2
Q
What are the heart diseases?
A
- Congenital heart defects
- Hypertensive heart disease
- Angina
- Heart attacks
- Arrhythmia
3
Q
What is Cardiac Stress?
A
- When the circumstances force the heart to work harder to maintain cardiac output (not necessarily pathological)
- There are fluctuations in cardiac output constantly dependent on metabolic needs of the body
4
Q
What are the 2 categories of cardiac stress?
A
- Direct stress
- Indirect stress
5
Q
What are examples of direct stress?
A
- Structural or functional alterations in the heart that reduce pump effectiveness
- Ischemia
- Infection
- Arrhythmias
- Congenital defects
6
Q
What are examples of indirect stress?
A
- Disorders external to the heart that increase workload
- Anxiety
- Stress from an accident
7
Q
What is ischemia?
A
- Caused by reduction of blood supply to the myocardium caused by degenerative changes to coronary arteries
- Atherosclerosis and Arteriosclerosis
8
Q
What is arteriosclerosis?
A
- Degenerative disorder resulting in vascular obstruction
- Characterized by hardening of the arteries and thickening of the arterial walls
9
Q
What is atherosclerosis?
A
- When arteriosclerosis is accompanied by accumulation of fatty material
- Chronic disease that can remain asymptomatic for decades
10
Q
Atherosclerosis can affect all arteries but predominantly…
A
- coronary, renal, aortic, femoral, carotid and cerebral
- Creates issues as it leads to narrowing of the vessels and reduction of blood flow through them
11
Q
What are the 2 mechanisms?
A
- Chronic gradual narrowing of the arteries can cause ischemia from reduced blood flow
- Acute infarction can be caused by a acute plaque rupture and subsequent thrombus formation and occlusion of coronary arteries (MI)
12
Q
What are the predisposing factors to narrowing of arteries? (factors that CANNOT be changed)
A
- Age: more common after 40, especially in men
- Gender: women are protected by HDL until after menopause
- Genetics: affects fat level, metabolism etc.
13
Q
What are the predisposing factors to narrowing of arteries? (factors that CAN be changed)
A
- Obesity: high levels of LDL
- Cigarette Smoking: decrease HDL, increases LDL, promotes platelet adhesion, increases vasoconstriction
- Sedentary Lifestyle: sluggish blood flow
- Uncontrolled HTN: causes vessel wall damage
14
Q
What are the causes of Ischemia?
A
- Spastic contraction: cold weather, caffeine, nicotine, anxiety, exertion
- Occlusion: degenerative vascular disease, platelets rupture and form clots or thrombosis
15
Q
What are the manifestations of ischemia?
A
- Ischemia= decreased blood supply to the cells= anaerobic metabolism= lactic acid production
- Localized accumulation of lactic acid irritates the nerve endings= cardiac chest pain
16
Q
Angina Pectoris (chest pain)
A
- Occurs when there is a deficiency of O2 for the heart muscle
- Can occur when the heart is working harder than usual and needs more O2 or when blood supply to the myocardium is impaired
- Usually, the heart can adjust its required levels of O2 with vasodilation, however with CAD this function is altered
- “Choking in the chest”
17
Q
Stable Angina
A
- Typically follows the same pattern for the pt. (predictable pain, location, severity, etc.)
- Insufficient O2 supply- anaerobic metabolism and accumulation of lactic acid and CO2
- Typically lasts 1-5 min and is relived by rest
18
Q
How does Angina occur?
A
- At rest, supply is ok in a person with heart disease despite the narrowed arteries, enough to meet the sedentary needs
- As soon as this same person exercises or experiences any type of stress, blood flow is not enough to meet the hearts needs
- Angina results
19
Q
Unstable Angina
A
- Same etiology as stable, however the pain is more severe, different feeling and is not as easily relieved by rest or meds
- Typically lasts >15 mins
- Often indicative of pre-MI angina
- Does not follow the same pattern as their usual angina
20
Q
What are the symptoms of Angina?
A
- Recurrent, intermittent episodes of substernal chest pain, usually triggered by physical or emotional stress
- Tightness or pressure in the chest that often radiates into the neck or left arm
- Pallor, diaphoresis, and nausea
- Can last a few seconds to much longer
21
Q
What is the treatment for Angina?
A
- Full assessment, detailed questioning (try to rule in/out differential diagnosis)
- Assess for need for O2
- ASA
- 12 lead
- Nitro
- IV therapy
- Vital every 5 mins- mininmum
22
Q
What is Acute Coronary Syndrome?
A
- Results from prolonged cardiac disorder myocardial ischemia or infarction (STEMI, Non-STEMI and unstable angina)
- Typically caused by a rupture of the plaque in the arteries and subsequent thrombosis of the coronary artery
23
Q
What is Acute Myocardial Infarction?
A
- Parts of the coronary muscle is deprived of blood flow until that part subsequently dies (infarcts)
- Most common cause is plaque rupture and thrombus formation
- Can also occur from spasm of a coronary artery with angina-arteries and already narrowed
- 3rd cause is the thrombus size blocks the artery
24
Q
What is a AMI classified as?
A
- STEMI or Non-STEMI
- Clinical presentation is the same, only an ECG differentiates them
- Blood work- troponin is typically the distinguishing factor
25
Q
Location and size of the MI depends on what?
A
- It depends on which coronary artery is blocked
- Infarcted tissue area is inevitably surrounded by a ring is ischemic tissue. This is relatively deprived of O2 but is still viable
- Ischemic tissue often is electrically unstable, this causes cardiac arrhythmias
- Of all deaths from MI’s- 90% are due to arrhythmias (usually v-fib)
26
Q
What are the signs of a heart attack?
A
- Pain- sudden, sub sternal chest pain that can radiate into the jaw, neck and left arm. Usually described as severe, steady and crushing- no relief with vasodilators
- Non pain- (Silent MI) Gastric discomfort, described as indigestion. Often in women
- Pallor
- Diaphoresis
- Dizziness, weakness
- Anxiety and fear
- Hypotension (especially if RV MI)
- Rapid and weak pulse
- Dyspena
27
Q
What is the prehospital management for ACS upon arrival?
A
- Assessment and management for possible ACS should occur simultaneously
- Be calming and place the patient at rest
- Determine the presence of possible ACS
- OPQRST
- Care must begin immediately
- Limit the size of the infarct
28
Q
Confirm possible ACS
A
- Preform a 12-lead ECG, and assess for ASA and oxygen administration
- Rapid acquisition of the 12-lead ECG before the secondary assessment and before anti-ischemic therapy (nitro) is preferred
- Consider rapid transport now if your patient has evidence of a STEMI
- Early ECG prior to treatment can document ischemic ECG changes that may normalize after treatment is started
- If aspirin has not been taken before your arrival, give the patient aspirin to chew and swallow
- Oxygen should be administered only if needed
29
Q
Preform cardiac monitoring (ACS)
A
- Document initial rhythm
- Record vital signs
30
Q
Secondary Assessment (ACS)
A
- Detailed history: find out of the patient has a history of cardiac disease, heart medications, or heart attack or heart surgery
- Obtain a more complete description of the present symptoms (especially onset)
- Do not delay transport to hospital; do this en route to the hospital
- If a serious arrhythmia or cardiac arrest occurs during transport, pull over and start treatment immediately
- Look for other potential causes of the patient’s symptoms and for complications of ACS
- While you are assessing the patient for further therapies, start an IV line
31
Q
What is the prehospital treatment for MI?
A
- Full assessment (vitals, detailed questioning OPQRST, Chest assessment- palpation)
- Assess for ASA- chest pain medical directive
- Assess for O2- BLS standard
- 12 Lead- needs to be done prior to nitro
- Assess for nitro- chest pain medical directive
- Transport to PCI if possible, otherwise closest ER
32
Q
What is ASA?
A
- Platelet aggregation inhibitor (anticlotting)
- Interferes with the production of clotting factor
- Has been shown to significantly decrease mortality with MI
- Orally administered
33
Q
What is nitro?
A
- Vasodilator that dilates the coronary vasculature
- Can relive vasospasm and improve blood flow
- Relaxes peripheral vasculature and may reduce afterload to reduce the cardiac workload
- Typically won’t relive the pain in an MI as it has little to no effect on the blockage
- Does not reduce mortality- not life saving
- Side effects: hypotension, headache
- Should never be used in patients with RVI
- Sublingually administered (under tongue)
34
Q
What is Dissecting Aortic Aneurysm?
A
- Aorta is subjected to massive hemodynamic forces, leads to degenerative changes in the middle layer of the aorta
- These are more dominant in older people with HTN and patient with connective tissue disorders
- Over time, these changes in the middle layer lead to an “ungluing” of the inner layer of the aorta, tears (once this is torn, dissection often begins)
- Blood gets pumped int the unnatural layer between the inner and middle layer, this then chronically stretches and weakens the vessel
35
Q
What happens if the dissecting aortic aneurysm, dissects?
A
- If it dissects into the valves, may prevent the valve from closing and results in blood entering back into the left ventricle during systole
36
Q
What are the s/s of dissecting aortic aneurysm?
A
- Middle aged or older- chronic hypertension
- Main complaint is chest pain- often described as “the worst pain I have ever felt”, “ripping or tearing”, “like a knife”
- Pain usually comes on suddenly
- Located in the anterior chest or the back, between the shoulder blades- can radiate into the back or abdomen
- Difference in BP between the 2 arms- disruption of blood flow through the innominate artery
37
Q
What is the management for aortic dissection?
A
- Main objective is pain relief- Morphine if possible
- Calm and reassure the pt
- O2
- IV
- Cardiac monitor
- Transport without delay: nothing can be done prehospital to stabilize the condition
