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Myocardial Infaract
Pn 141 Test 1 book med surg pg 618
Question | Answer |
---|---|
Def of coronary occlusion | Closing off of blood vessels on the heart, results in MI |
Def of MI | Death of muscle tissue (Cells in area of cardiac muscle necrose due to lack of oxygen and blood), secondary to coronary occlusion |
Why is an MI life threatening | B/c is circulation to cardiac muscle is not restored, functioning muscle is lost and heart rate maybe unable to maintain effective cardiac output |
What can an MI lead to (2 serious consequences) | cardiogenic shock, death |
what percent of Mi are fatal | 50% |
Risk factors for MIs | age, gender, smoking, heredity, obesity, hyperlipidemia, HTN, DM, Stress, sedentary lifestyle |
What happens to the injured ischemic tissues if the blood flow is restored | it can recover and heal |
What happens to the infarcted tissues if the blood flow is restored | it no longer conducts electrical energy and ceases to contract |
when a larger coronary artery is occluded what is done in the collateral blood vessels in order to conpensate | the collateral blood vessels connect to smaller arteries in coronary system, the collateral dilate to maintain blood flow to cardiac muscle (then the larger coronary arteries will progressively narrow) |
What ventricle is normal affected with an mi, why | the left ventricle, b/c it is the work horse of the heart, here the muscle mass is greater & so is oxygen demand |
Def of infarcts | death of tissure/ |
In an MI why do cells in areas of cardiac muscle die | due to lack of blood and oxygen |
is it a life threatening event | yes |
what happens if circulation to affected cardiac muscle is not rapidly restored | functional muscle is lost and the heart may be unable to maintain and effective cardiac output |
Most deaths from a mi occur with in the ______ hour/s of onset | first |
risk factors for MI are the same ones for what disease | CAD/CHD |
occlution of a coronary artery is caused by the development of what | a clot (thrombus) in area of athersclerosis narrowing |
there is irreversable damage to the cells when they are deprived from oxygen and nutrients for how long? | 20-45 min |
The necrotic tissue is surrounded by an area of what kind of tissue | injured and ischemic tissue |
what tissue is stunned/ hybernating | the injured tissue |
what tissue contracts ineffectively | the injured tissue |
what causes the cardiac output to fall | the stunned/ hybernating tissue that is contracting ineffectively |
what tissue (injured, ischemic, infarcted) tissue recovers and heals if blood flow is restored | the injured an ischemic |
What tissue no longer conducts electrical energy and ceases to contract | the infarcted |
_______ vessels connect to the smaller arteries to maintain blood flow ot cardiac muscle when an MI occurs | collateral |
What ventricle is usually affected and why? | Left, because it is the workhorse of the heart (muscle mass is greater and so is it's oxygen demand |
Def of transmural infarction | an MI that effects all layers of the heart (endocardium, myocardium, and epicardium) |
Def of subendocardial infarction | MI that only involes the inner layer of the heart |
What is the #1 s/s of an MI | Chest pain |
How would a person describe the pain of an MI | tight, crushing, severe, heavy, sqeezing, burning |
Where does the s/s of pain normally begin in the body, where does the pain radiate to | in the center of the chest, pain radiates to the shoulders jaw, neck or arms |
You know it is a MI when it lasts > ______ minutes | 15-20 |
Is the pain of an MI relieved by NTG or rest | no |
S/s of am mi | tachycardia, SOB, cool, clammy skin, diaphoresis, anxiety, N/V, dysrhythmias |
Who may have the atypical S/S of an mi (upper abdominal pain) | Wm and older adults |
Complications of an MI depend on what? | The size and location of the mi |
The most frequent complication of an MI is | Dysrhythmias |
Def of Dyrsrhythmias | DISRUPTION OF of the electrical conduction system of the heart and or its rhythm |
S/s of a very slow HR | SOB, dizziness, altered mental state |
The risk for v-fib is greatest during what time after an MI | the first hour |
Heart failuer can develop, particularily wen there are larger portions of what chamber of the heart affected | the left ventricle |
S/s of left sided ht failure | dyspnea, fatigue, weakness, respiratory crackles |
Cardiogenic shock occurs when more than ______ % of the left ventricle is infarcted | 40% |
Def of cardiogenic shock | impaired tissue perfusion due to pump failure |
s/s of impaired tissue perfusion | hypotensive, decrease urinary output, decreased LOC, cool clammy skin |
Def of pericarditis | inflammation of the pericardium |
What day/s does pericarditis usually develop after an MI | 2-3 days |
s/s of pericarditis | chest pain (stabbing, sharp, agrevating by deep breathing and movement) |
Why does a ventricular aneurysm occur | b/c the scar tissue that replaces necrotic muscle is thinner than the ventricular muscle mass |
Def of a vetricular aneurysm | an outpouching of the ventricular wall |
when does a myocardial rupture normally occur after an MI | day 4-7 |
Why is it important to reopen the occluded artery ASAP | time is muscle: the quicker it is reopened and blood flow is restored, the more myocardium can be saved and fewer complications |
What is the major issue in the delay of medical care given for an MI | delay of pt to seek medical care |
LAbs: Serum Cardiac markers: how long are the ordered for | adminssion- 3 days |
LAbs: Serum Cardiac markers: why is it done | to establish Dx and eval the extent of myocardial damage |
LAbs: Serum Cardiac markers: What two markers are specific for the Diagnosis of an MI | Creatine kinase and cardiac- specific troponin |
LAbs: Serum Cardiac markers: to creatine kinase levels rise or fall faollowing an mi | rise |
LAbs: Serum Cardiac markers: what marker remains in the blood for several days and is useful for diagnosis an MI where Treatment was delayed | the cardiac specifc troponins |
_______ vessels connect to the smaller arteries to maintain blood flow ot cardiac muscle when an MI occurs | collateral |
What ventricle is usually affected and why? | Left, because it is the workhorse of the heart (muscle mass is greater and so is it's oxygen demand |
Def of transmural infarction | an MI that effects all layers of the heart (endocardium, myocardium, and epicardium) |
Def of subendocardial infarction | MI that only involes the inner layer of the heart |
What is the #1 s/s of an MI | Chest pain |
How would a person describe the pain of an MI | tight, crushing, severe, heavy, sqeezing, burning |
Where does the s/s of pain normally begin in the body, where does the pain radiate to | in the center of the chest, pain radiates to the shoulders jaw, neck or arms |
You know it is a MI when it lasts > ______ minutes | 15-20 |
Is the pain of an MI relieved by NTG or rest | no |
S/s of am mi | tachycardia, SOB, cool, clammy skin, diaphoresis, anxiety, N/V, dysrhythmias |
Who may have the atypical S/S of an mi (upper abdominal pain) | Wm and older adults |
Complications of an MI depend on what? | The size and location of the mi |
The most frequent complication of an MI is | Dysrhythmias |
Def of Dyrsrhythmias | DISRUPTION OF of the electrical conduction system of the heart and or its rhythm |
S/s of a very slow HR | SOB, dizziness, altered mental state |
The risk for v-fib is greatest during what time after an MI | the first hour |
Heart failuer can develop, particularily wen there are larger portions of what chamber of the heart affected | the left ventricle |
S/s of left sided ht failure | dyspnea, fatigue, weakness, respiratory crackles |
Cardiogenic shock occurs when more than ______ % of the left ventricle is infarcted | 40% |
Def of cardiogenic shock | impaired tissue perfusion due to pump failure |
s/s of impaired tissue perfusion | hypotensive, decrease urinary output, decreased LOC, cool clammy skin |
Def of pericarditis | inflammation of the pericardium |
What day/s does pericarditis usually develop after an MI | 2-3 days |
s/s of pericarditis | chest pain (stabbing, sharp, agrevating by deep breathing and movement) |
Why does a ventricular aneurysm occur | b/c the scar tissue that replaces necrotic muscle is thinner than the ventricular muscle mass |
Def of a vetricular aneurysm | an outpouching of the ventricular wall |
when does a myocardial rupture normally occur after an MI | day 4-7 |
Why is it important to reopen the occluded artery ASAP | time is muscle: the quicker it is reopened and blood flow is restored, the more myocardium can be saved and fewer complications |
What is the major issue in the delay of medical care given for an MI | delay of pt to seek medical care |
LAbs: Serum Cardiac markers: how long are the ordered for | adminssion- 3 days |
LAbs: Serum Cardiac markers: why is it done | to establish Dx and eval the extent of myocardial damage |
LAbs: Serum Cardiac markers: What two markers are specific for the Diagnosis of an MI | Creatine kinase and cardiac- specific troponin |
LAbs: Serum Cardiac markers: to creatine kinase levels rise or fall faollowing an mi | rise |
LAbs: Serum Cardiac markers: what marker remains in the blood for several days and is useful for diagnosis an MI where Treatment was delayed | the cardiac specifc troponins |
ECG: what are some common changes in the wave with an MI | inversion of the t wave, depression of the st segment, formation of a q wave |
Medical care: why is the pt on bedrest for 12 -24 hrs? | to reduce cardiac workload |
Meds" why is pain relief vital in the Tx of a pt with an MI | b/c pain stimulates the SNS, increasing the heart rate and BP (yhus in the hearts workload) |
Meds: What is the drug of choice for pain relief | Morphine sulfate |
Meds: Why is valium given | to promoate rest |
Meds: def of fibrolytic agents | drugs that dissolve or break up blood clots to restaore blood flow to the obstructed artery |
MEds: Fibrolytics: complications of them | serious bleeding |
Meds: what is given to a pt with a suspected mi in emergency | chewable aspirin |
Meds: why are beta blockers given | to decrease the HR and reduce cardiac work and myocardial oxygen demand |
cardiac rehab: Whst is it | A planned program of activities and exercise, and education for pt who have had an MI |
cardiac rehab: goal of it | to improve quality of life by reducing risk factors for heart disease |
What are the highest priorities of a PT who had an MI | maintaining cardiac output, and tissue perfusion, and eliminateing pain |
Why use morphine for the pain | along with pain relief it decreases to workload of the heart |
s/s of decreased tissue perfusion | changes in LOC, decreased uirinary output, moist, cool, pale skin and MM, diminished or absent peripheral pulses, delayed cap refill |
with out oxygen what happens to the cells and tissue of theheart | they die |
what does MONA stand for | 1st four steps of ER visit: morphine, oxygen, nitrate, asprin |
after ER visit, when MI happens, how long is it before you are discharged | 24 hours |
what labs are drawn | troponin, cpk, bnp |
pain from pericarditis is different from an MI how | the chest pain will occur when pt takes a deep breath |
how is a ventricular rupture similar to a hole in a water balloon | it leaks and gets larger and it spills into the chest cavity, with force |
meds: when do you only give thrombolytics? | in the first 6 hours of mi, *** only if known emboli origin (cath lab should Dx) |