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perfusion Flashcards

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1
Q

What is CSA

A

Episodes or paroxysms of pain or pressure in the anterior chest, not enough O2 to heart when active or stress

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2
Q

What caused CSA

A

Atherosclerotic, CAD, physical exercise extreme temps/ emotion, heavy meals

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3
Q

What are the signs of symptom CSA

A

Ischemia (pain (deep in chest) (neck, jaw, shoulders, usually upper left arm), mild indigestion, choking, heavy sensation in the upper chest, severe apprehension, impending death)

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4
Q

What are the risk factors for CSA

A

Age, gender, ethnic, menopause, hyperlipidemia, HTN, Obesity, Tobacco use, diabetic, metabolic disorder, cocaine use

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5
Q

How is CSA diagnosised

A

clinical manifestations of ischemia, 12-lead ECG (T-wave inversion, ST-segment elevation, abnormal Q wave) (exercise or pharmacologic stress), cardiac catheterization, coronary angiography, cardiac biomarker (rule out ACS), Xray

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6
Q

Treatment for CSA

A

Nitro, Beta blockers, Calcium channel blockers, Antiplatelet/ anticoagulant, stent, CABG.

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7
Q

What do you see in NSTEMI

A

S/S, no definite ECG (ST depression/T wave inversion), lab are bad troponin (necrosis), Antiplatelet, anticoagulants, beta blockers, PCI

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7
Q

What is ACS

A

is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death, unstable angina, NSTEMI, and ST-segment elevation myocardial infarction (STEMI)

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8
Q

What do you see in unstable angina

A

S/S, but ECG (slight ST depression) and labs are good (plaque has ruptured), Antiplatelet and anticoagulated, beta blockers

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9
Q

What causes ACS

A

unstable a reduced blood flow in a coronary artery, due to rupture of an atherosclerotic plaque. A clot begins to form on top of the coronary lesion, but the artery is not completely occluded, MI, plaque rupture and subsequent thrombus formation result in complete occlusion of the artery

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10
Q

What do you see in a STEMI

A

S/S, ECG, (ST elevation) and labs are bad (clot has developed, severe damage), emergency PCI, thrombolytic therapy, CABG

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11
Q

What are the S/S ACS

A

Chest pain (PQRST) that occurs suddenly and continues despite rest and medication, S3&S4, shortness of breath, crackles, indigestion, vomiting, nausea, and anxiety. cool, pale, and moist, anxiety, skin (diaphoresis), increase HR, RR, feeling of impending doom, or denial that anything is wrong

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12
Q

Risk Factors ACS

A

patient history (cardiac illness and family), Age, gender, ethnic, menopause, hyperlipidemia, HTN, Obesity, Tobacco use, diabetic, metabolic disorder

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13
Q

Diagnosis ACS

A

S/S 12 lead ECG (T-wave inversion, ST-segment elevation, abnormal Q wave, ST depression), and

serial cardiac biomarkers

Troponin 1&2, onset 4-6, peak 10-24, duration 10-14 days (about 2 weeks) best for MI

three CK isoenzymes: CK-MM (skeletal muscle), CK-MB ), onset 6, peak 18, duration 24–36 hours

myoglobin onset 2, peak 2-15H, duration 24 H

Coronary angiography, chest X-ray

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14
Q

Nursing management for ACS

A

Avoids stress, heavy meal, educate on S/S of MI and lifestyle management, bed for 12–24-hour gradual increase it

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14
Q

Treatment options ACS

A

Oxygen, aspirin, nitroglycerin, and morphine. (MONA)

STEMI- s taken directly to the cardiac catheterization laboratory for an immediate Percutaneous Coronary Intervention  

Thrombolytics 

aspirin, a beta-blocker, and an angiotensin-converting enzyme (ACE), or ARB, antidysrhythmic, lipid lowering agents, stool softeners  

Blood pressure, urine output, serum sodium, potassium, and creatinine levels need to be monitored closely.
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15
Q

Complication ACS

A

Dysrhythmia (most common)
Heart failure
Cardiogenic shock
Papillary muscle dysfunction (sudden and severe mitral valve regurgitation)

LV auteurism (infarcted heart wall thin and bulges out)
LV and septal wall rupture (loud systolic murmur) Emergent; can lead to rapid death
Pericarditis
Dressler syndrome (Pericarditis and fever. Can have pericardial effusion)
Death

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16
Q

What is CAD

A

is a narrowing or blockage of your coronary arteries, which supply oxygen-rich blood to your heart.

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17
Q

S/S CAD

A

schemia, Angina pectoris, epigastric distress and pain that radiates to the jaw or left arm dyspnea/ women indigestion, nausea, palpitations, and numbness

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18
Q

Preventing CAD

A

our modifiable risk factors—cholesterol abnormalities, tobacco use (increase HR, BP, oxidation of LDL, decrease O2), hypertension, and diabetes (Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function)

Mediterranean diet/ plant food/minimal process food/Fish or vegy diet/ low red meat and sugar// low fat// high fiber (dietician) 

Physical activity- Regular, moderate physical activity increases HDL levels and reduces triglyceride levels, moderate 150 minutes or vigorous 75 minute per week, be able to talk/ right cloth  

Medication
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18
Q

Risk Factors CAD

A

Family history, increase age, men, race, history of premature menopause, high LDL, Hyperlipidemia, Tobacco use, Hypertension, Diabetes, Metabolic syndrome, Obesity, Physical inactivity, Chronic inflammatory conditions (e.g., rheumatoid arthritis, lupus, HIV/AIDS), chronic kidney disease

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18
Q

Causes CAD

A

Smoking or tobacco use, hypertension, and hyperlipidemia can trigger an inflammatory response, damaging the endothelium, which normally produces antithrombotic and vasodilating agents. Macrophages ingest lipids move into the arterial wall, causing further damage by oxidizing LDL (moves into the arteries) (100mg/dL) HDL (male greater 40mg/dL females 50mg/dL) moves then out with exercise. Total cholesterol < 200 mg/dL, triglycerides < 150mg/dL

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19
Q

CAD Diagnosised

A

Blood test (blood sugar, cholesterol, C-reactive protein) lipid panel, stress test

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20
Q

Treatment for CAD

A

Statins, Fibrates, Bile Acid Sequestrate

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21
What is CHF
a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of a ventricle to fill (diastolic dysfunction) or eject blood (systolic)
22
Causes CHF
Impairment of ventricular filling or ejection of blood [1], which results in the inability of the heart to provide adequate perfusion to the tissues while maintaining normal cardiac filling pressures. In pediatric most causes by congenital defects (pulse rate higher, sound higher in ptch and intensity)
23
S/S of left/right CHF
(left) Dyspnea, orthopnea, Paroxysmal, nocturnal dyspnea, cough, crackle, lightheadedness/dizziness, confusion, resting tachycardiac. Cold extremities, air hunger, fatigue rapids weight gain, peripheral venous pressure (right)edema, ascites, hepatomegaly and spleen, JVD Low Cardiac Output- decrease exercise, muscle wasting, anorexia/nausea, unplan weight loss,
24
Risk factors for CHF
- African Americans and Hispanics, adults over 60 years of age, men, cigarette smoking, obesity, poorly managed diabetes, and metabolic syndrome, morbid consequence of another disease or disorder, including coronary artery disease (CAD), hypertension, cardiomyopathy, valvular disorders, and renal dysfunction, Myocardial infarction (MI)
25
Diagnosed in CHF
look at S/S, hypertension, Comorbid conditions such as obesity, CAD, diabetes, atrial fibrillation, and hyperlipidemia/ echocardiogram, a chest x-ray and 12-lead electrocardiogram (ECG)/ serum electrolytes, stress test, blood urea nitrogen (BUN), creatinine, liver function tests, thyroid-stimulating hormone, complete blood count (CBC), (b-type natriuretic peptide) BNP, and routine urinalysis. BNP being key
26
Treatment CHF
Low salt/fluid diet, high omega 3, Diuretics (loop diuretic, thiazide, aldosterone), an angiotensin system blocker (ACE, ARB, ARNI), and a beta-blocker, Ivabradine, Hydralazine-isosorbide dinitrate, Digitalis underlying CAD, coronary artery revascularization with PCI or coronary artery bypass surgery cardiac resynchronization therapy (CRT) Transplantation Nursing intervention- (education, weight daily, fluid restriction, rest periods)
27
Preventing CHF
Lifestyle recommendations include restriction of dietary sodium; avoidance of smoking, including secondhand smoke; avoidance of excessive fluid and alcohol intake; weight reduction when indicated; and regular exercise, vaccines
28
Complication of CHF
Pulmonary edema is an acute event, reflecting a breakdown of physiologic compensatory mechanisms; hence, it is sometimes referred to as acute decompensated heart failure Pleural effusion: fluid in the pleural cavity Dysrhythmias: atrial fibrillation, ventricular tachycardia/fibrillation Left ventricular thrombus: blood clot in left ventricle Hepatomegaly: enlargement of liver Renal failure
29
What is PAD
egs or lower extremities (most common in femoral popliteal area) is the narrowing or blockage of the vessels that carry blood from the heart to the legs
30
Causes PAD
Atherosclerosis is an important cause of peripheral artery disease (PAD) and is common in the lower extremities
31
S/S of PAD
aching, cramping, or inducing fatigue or weakness that occurs with some degree of activity or exercise (caudation)(10 minutes of rest to stop), which is relieved with rest. Pain is distal to area of stenosis or occlusion, may affect walking cause pain, ischemia (worst at night), dependent position reduces pain , paresthesia
32
Risk factors for PAD
Cigarette smoking contributes to the progress of atherosclerosis of the lower extremities and development of symptoms of ischemia. People with diabetes mellitus develop more extensive and rapidly progressive vascular disease, HTN, obesity, hyperlipidemia, family history, age stress, CKD, sedentary
33
Diagnosis for PAD
Test CW /duplex Doppler and ABIs (ankle -branchial index), treadmill testing for claudication, duplex ultrasonography, angiography/ MRI or other imaging studies, lipid panel, CRP, blood glucose
34
Treatment for PAD
Pharmacological - Cilostazol, Antiplatelet agents, such as aspirin or clopidogrel, and statins  Endovascular management- balloon angioplasty, stent, stent graft, or an atherectomy  Surgery is reserved for the treatment of rest pain, severe and disabling claudication, or when the limb is at risk for amputation because of tissue necrosis.  Percutaneous Transluminal Angioplasty, Femoral popliteal graft, atherectomy
35
Complication of PAD
Chronic rest pain, Ulceration () usual of bony prominence, gangrene infection, amputation, 6-7 times higher risk of heart, stoke
36
What is CVI
is a condition in which veins have problems moving blood back to the heart
37
cause of CVI
increased venous hydrostatic pressure (as with prolonged standing), incompetent valves in the veins, deep vein obstructions (as with DVT), decreased skeletal muscle pump function, inflammatory processes, and endothelial dysfunction.
37
S/S CVI
chronic venous stasis, resulting in edema, altered pigmentation (Leathery looking skin), pain (aching/tenderness), and stasis dermatitis (ulcers), new varicose veins, eczema/itching, ulcers with irregular shape
38
Risk factors for CVI
history of DVT, Age, Obesity, pregnancy, Sitt/stand for too long
39
Diagnosis CVI
Duplex ultrasound with doppler, CT venogram
40
Complication for CVO
venous ulceration (drainage of ulcer yellow/irregular wound edges), osteomyelitis, amputation
40
Treatment for CVI
The three EEE Elevating, Encourage walking, Elastic stockings
41
the cause of DVT
is associated with stasis of blood, increased blood coagulability, and vessel wall injury. Bed rest/immobilization, hip fracture, joint replacement, or spinal cord injury, impaired cardiac function, older adults, long airplane, Oral contraceptives and hormone replacement therapy 
41
What is DVT
is the presence of thrombus and the accompanying inflammatory response in the vein wall, Virchow triad- endothelial damage, venous stasis, and altered coagulation 
42
Diagnosis DVT
CBC (platelet, WBC, prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR), D-Dimer hypercoagulation-CRP, factor V Leiden, prothrombin G20210A mutation, antithrombin III, protein C, and protein S venography, ultrasonography (larger than normal/noncompressible), and plasma d-dimer assessment
42
S/S of DVT
Swollen, tense, painful, and cool to the touch), deep vein - edema, swelling, warmer, superficial vein appear more prominent, tenderness
42
Risk Factors for DVT
venous stasis- Age > 65, Bed rest/immobilization, HF, obesity, spinal injury, Endothelial damage- Central venous catheters, Dialysis catheter, local vein damage, trauma, Altered Coagulation- cancer, polytheremia, pregnancy
43
Treatment for DVT
Warfarin/heparin mechanical thrombectomy and ultrasound-guided thrombolytic therapy Nursing intervention- elevate above heart, gradual compression and analgesic pain relief////// DEEP (don’t massage, elevate, ensure bedrest, pharmacologic intervention)
44
Preventing DVT
early ambulation and leg exercises, the application of graduated compression stockings, and the use of intermittent pneumatic compression devices subcutaneous unfractionated heparin or low-molecular-weight heparin (LMWH). weight loss, smoking cessation, and regular exercise
45
Complication of DVT
bleeding, thrombocytopenia, and drug–drug interactions.
45
What causes a PE
dislodged or fragmented DVT, air, fat, amniotic fluid, and septic (from bacterial invasion of the thrombus
46
What is a pulmonary embolism
Refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originate(s) somewhere in the venous system or in the right side of the heart.
46
Risk factors for PE
venous stasis Endothelial damage Altered Coagulation
47
diagnosis PE
chest x-ray (usually normal but infiltrates, atelectasis, elevation of the diaphragm on the affected side, or a pleural effusion), ECG (sinus tachy, nonspecific ST-T waves), pulse oximetry, arterial blood gas analysis (hypoxemia, hypercapnia), D-dimer assay and MDCTA or pulmonary arteriogram or V./Q. scan.
48
treatment option
Unstable PE - Emergency measures - Thrombolytic therapy (Unfractionated Heparin, Low-Molecular-Weight Heparin (LMWH), Oral Anticoagulant, Factor Xa Inhibitor, Oral Direct Factor Xa Inhibitor, Direct Thrombin Inhibitor, Oral Direct Thrombin Inhibitor, Thrombolytic) Stable PE- LMWH (e.g., enoxaparin), unfractionated heparin, or a direct oral anticoagulant (DOAC), such as a direct thrombin inhibitor (e.g., dabigatran), or a factor Xa inhibitor (e.g., fondaparinux, rivaroxaban, apixaban, edoxaban)
49
nursing intervention for PE
thrombolytic therapy- bed rest, vitals, INR/aPTT 3-4/ manage pain-chest pain- semi-fowler, and opioid agents/ Oxygen therapy- Deep breathing and incentive spirometry-Nebulizer therapy or percussion and postural drainage/ relieving anxiety /
50
Complication of PE
cardiogenic shock or right ventricular failure subsequent to the effect of PE on the cardiovascular system.

Exam 2 (4 decks)

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