Week 4- Chest Pain Flashcards
(37 cards)
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
Location and size of the MI depends on what?
- 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
What are the signs of a heart attack?
1. 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
2. Non pain- (Silent MI) Gastric discomfort, described as indigestion. Often in women
3. Pallor
4. Diaphoresis
5. Dizziness, weakness
6. Anxiety and fear
7. Hypotension (especially if RV MI)
8. Rapid and weak pulse
9. Dyspena
27
What is the prehospital management for ACS upon arrival?
- 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
Confirm possible ACS
- 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
Preform cardiac monitoring (ACS)
- Document initial rhythm
- Record vital signs
30
Secondary Assessment (ACS)
- 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
What is the prehospital treatment for MI?
- 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
What is ASA?
- Platelet aggregation inhibitor (anticlotting)
- Interferes with the production of clotting factor
- Has been shown to significantly decrease mortality with MI
- Orally administered
33
What is nitro?
- 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
What is Dissecting Aortic Aneurysm?
- 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
What happens if the dissecting aortic aneurysm, dissects?
- 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
What are the s/s of dissecting aortic aneurysm?
- 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
What is the management for aortic dissection?
- 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
