Cardiology Terms Mi

Front 1

Dressler syndrome

Back 1

Post MI syndrome
characterized by pericarditis with effusion and fever that develops one to four weeks after MI

Front 2

Myocardial infarction

Back 2

Myocardial tissue destroyed due to diminished blood supply. Caused by sustained ischemia causing your reversible cellular death.

Front 3

Area of bull's-eye

Back 3

Area of damage works out like a bull's-eye -- area away from the injury is less irritated

Front 4

Necrosis to heart

Back 4

Cells can withstand ischemic conditions for up to 20 minutes before cell death begins

Front 5

Transmural MI

Back 5

Full thickness of myocardium in the region is involved

Front 6

Subendocardial MI

Back 6

Damage has not penetrated through the entire thickness of the myocardial wall

Front 7

Inferior wall infarctions

Back 7

Result from right coronary artery lesions

Front 8

Anterior wall infarctions

Back 8

Result from lesions in the left anterior descending artery

Front 9

Lateral/posterior/inferior wall infarctions

Back 9

Result from lesions in the left circumflex artery

Front 10

Healing process after MI

Back 10

-- inflammatory process
-- 24 hours leukocytes infiltrate the area
-- enzymes are released by the dead cardiac sails
-- enzymes of neutrophils and macrophages remove all necrotic tissue by the second or third day

Front 11

Healing Process of MI

Back 11

-Lipolysis & Glycogenolysis
-Collagn Matrix forms scar tissue after necrotic tisue is cleared
-By 6 weeks area is usually healed

Front 12

Lipolysis

Back 12

release of glucose
(will see rise in serum glucose levels)

Front 13

Glycogenolysis

Back 13

release of fatty acids

Front 14

Clinical Manifistations of MI

Back 14

-Pain, Severe, immobilizing not relieved by repositioning, rest, nitrates
-Anxious, restless
-^ HR & RR
-N/V
-Fever may ^ 1st 24hr & last for 1 week

Front 15

Site of MI pain

Back 15

Substernal
Epigastric
Retrosternal

Front 16

MI presentation in Women

Back 16

-c/o discomfort
-SOB
-Fatigue
**MI in women is usually mis-diagnosed

Front 17

MI presentation in Elderly

Back 17

-SOB
-Edema
-AMS
-Dysrrhythmias

Front 18

MI presentation in Diabetic

Back 18

May not experience pain
**Silent MI**

Front 19

Cardiovascular manifistations of MI

Back 19

-^BP initially -- then drop due to decreased CO
-HR may ^ initially
-Urine output may decrease (r/t decrease perfusion of kidneys
-Crackles to lungs may last hours - days
-hepatic enlargement, peripheral edema (may indiciate cardiac failure)
-Jugular vein distention (early ventricular dysfunction & pulmonary congestion)

Front 20

Assessment & Diagnostics of MI

Back 20

-HX:
Details of current episode of pain: where, intesity/description, duration, percipitating factors
Risk Factors: (family, stress, activity)
Previous Illness (similar symptoms)

Front 21

Diagnostics of MI

Back 21

-ECG
*ST segment ^
*Q wave or Non-Q wave (1-3 days)
*Serial measurement of cardiac markers

Front 22

Diagnostic examination to establish or r/o MI

Back 22

-Cardiac Markers
*CK (creatine kinase)
*CK-MB
*LDH (lactic dehydrogenase)
*Myoglobin
*Troponin

Front 23

Cardiac Markers

Back 23

Proteins released into the blood as a result of the necrotic hear muscle after an MI

Front 24

Main enzyme released after MI

Back 24

CK
Begin to rise in 3-12 hrs
Peak in 24hrs
Return to normal 2-3 days

Front 25

Myocardial Specific Enzyme

Back 25

CK-MB
>3% ^ indicative of MI

Front 26

Troponin

Back 26

Myocardial muscle protein released into the blood stream after MI tissue injury

Front 27

Troponin

Back 27

Troponin T
Troponin I
-rises as quickly as CK
-remains ^ for 2 weeks
-^ 3-12 hrs
-Peak 24-48 hrs
-Returns to baseline 5-14 days

Front 28

Myoglobin

Back 28

-Released within few hrs of MI
-Lacks cardia specificity
-Rapidly excreted in urine resulting in blood levels returning to normal within 24hrs

Front 29

Management of patient with MI

Back 29

-minimize myocardial damage
-preserve myocardial function
-prevent complications

Front 30

Medication tx for MI

Back 30

-Nitroglycerine IV
-Morphine
-ASA

Front 31

Nitroglycerine IV

Back 31

-promotes peripheral vasodilation, decreasing preload and afterload
-Coronary artery vasodilation

Front 32

Morphine

Back 32

-Acts as an analgesic and sedative
-Reduces preload and myocardial O2 consumption

Front 33

Aspirin

Back 33

Inhibits platelet aggregation

Front 34

Angiotensin-converting enzyme
(ACE) inhibitors

Back 34

-Decreases mortality and prevents onset of CHF
-MOnitor B/P, urine output, serum sodium and potassium

Front 35

Thrombolytics TNKase

Back 35

-Dissolve & lyse thrombus in coronary artery
*must be given within very short period of time of onset of MI

Front 36

Other collaborative Care/Tx of patient with MI

Back 36

-O2
-IV therapy
-Continuous monitoring
-Hemodynamic monitoring
*EKG, labs, v/s, Swans (pressures)

Front 37

Complications of MI

Back 37

-Dysrrhythmias
*#1 complication of MI - most common cause of death
-Cardiogenic Shock
-CHF
-Papillary muscle dysfunction
-Ventricle aneurysm
-Pericarditis
-Dressler Syndrome
-PE

Front 38

Pericarditis

Back 38

-inflammation of visceral and/or parietal pericardium.
-may occur 2-3 days after acute MI
-Chest pain is aggravated by inspiration, coughing and movement of upper body
*Pain may be relieved by sitting in forward position
-Friction rub over pericardium

Front 39

Nitropusside

Back 39

-Glass bottle
-Very sesnitive to light
*bottle and tubing must be covered and protected from light

Front 40

Papillary muscle dysfunction

Back 40

-Systolic murmur over apex of heart
-causes mitral valve regirgitation (^ volume of blood in left atrium)

Front 41

Nursing Process for patient with MI

Back 41

-Cardiac & Resp. Asessment
-Nursing Dx

Front 42

Nursing Dx in patient with MI

Back 42

-decrease myocardial perfusion r/t reduced coronary blood flow
-Potential impaired gas exchange r/t fluid overload from left ventricular dysfunction
-Potential altered peripheral tissue perfusion r/t decreased cardiac output
-Anxiety r/t fear of death
-Knowledge deficit about post MI self care

Front 43

CABG

Back 43

Myocardial Revascularization:
*primary surgical tx for CAD
--usually patient had failed medical management

Front 44

Reasons for Cardiac Surgery

Back 44

-Improve blood flow to the heart
-Repair/replace cardiac valves
-Congenital Anatomic Heart defects
-Cardiac Transplant

Front 45

MIDCABG

Back 45

-minimally invasice direct coronary artery bypass grafting
-used for patients with LAD or single vessel dz (medical management not effective)
-several small incisions between ribs
-heart slowed with IV Beta adrenergic or calcium channel blockers
-Lt internal mammary artery is used for anasomosis to LAD

Front 46

Care of patient with MIDCABG

Back 46

-postop - like other cardiac surgery's
-IV nitro to minimize ischemia/coronary spasm
-Recovery time shorter
-Performed without cardiopulmonary bypass

Front 47

Transmyocardial Laser

Back 47

-indirect revascularization procedure using laser to make channels between lt ventricular activity & the cornary microcirculation
*channels allow blood to flow into ischemic areas
-may be performed during cath/surgery using lt anterior thoscotomy incision
_current tx for patients with CAD who are not candidates for bypass/failed medical therapy

Front 48

Risk of "on pump" vs "off pump"

Back 48

has been found that "on pump" can result in deminished memory, decreased mental function in later years

Front 49

Graft sites for bypass

Back 49

-Saphenous vein
-Internal Mammary Artery
(Internal Thoracic Artery)
-Radial Artery
-Gastroepiploic Artery
-Inferior Epigastric Artery

Front 50

Most common artery for used for bypass

Back 50

Internal Mammary Artery
-patency rate is ^

Front 51

Cardiac Surgery Complications

Back 51

-Infection
-Collapse of graft
*patient will c/o heart pain
-Dysrrhytmias