Perfusion Flashcards
What causes Angina?
Reduced coronary blood flow. Identified by a identifiable event. Relieved by rest
Types of Angina (3)
Stable: caused by physical exertion, stress, or exposure to cold. most common.
prinzmetal (variant): caused by coronary vasospasm
Unstable: Caused by transient formation and dissolution of a blood clot.
What does decreased coronary blood flow cause?
Vasospasm, fixed stenosis (althersclerosis), thrombosis (blood clot)
What does increase need for O2 cause?
Increased heart rate, increased contractility, increased preload/afterload
What are the clinical manifestations of myocardial infarction?
sudden, continuous chest pain that lasts 15-20 mins.
pain that radiates to shoulder, neck, arms, jaw
chest pain that gets worse
What is the pathopysiology of myocardial infarction?
plaque formation –> plaque rupture –> endothelial cell injury and inflammation –> decreased blood supply and increased O2 demand –> myocardial ischemia –> myocardial cell necrosis
Ischemia Definition
Blood flow is restricted or reduced
Myocardial Ischemia Signs & Symptoms
BF to portion of cardiac muscle is completely blocked.
angina, hypoxia, tachycardia, extra heart sound (S3)
Acute Coronary Syndrome
Unstable angina, NSTEMI, STEMI
Difference between CAD, angina, and heart attack
CAD: plaque builds up in an artery
Angina: plaque makes it harder for blood to get through an artery
Heart Attack: plaque cracks and a blood clot blocks the artery
CAD Risk Factors
Age, gender, race, ethnicity, family history, DM, hyperlipidemia, HTN, smoking, inactivity, obesity, unmanaged stress
Electrocardiogram
Performed and interpreted within 10 min. Most common. Repeat ECG every 10-15 minutes if first time with angina
Tropinin
Protein found in muscles of heart.
hs-cTn should be <14 if >14 ICU
Check troponin at 0-2-6 hours
Echocardiogram - Normal EF
Checks how heart chambers and valves are pumping blood
Normal EF is 50-70%
Stress Echocardiogram
Treadmill test and echocardiogram. Dobutamine test for pt. who cannot excercise
Nuclear scan-myocardium perfusion imaging
shows how well blood flows to the heart.
3-part test
lexiscan dilates BV
CAD Treatment Goals
Relieve chest pain, reduce extent of myocardial damage, maintain cardiovascular stability, manage risk factors
Statins
Lower cholesterol by increasing LDL excretion from circulation
Nitrates
Treat angina. Produce coronary artery and peripheral vasodilation. Take 3.
Beta Blockers
Manage stable angina. “lol” suffix. Blocks the effect of epinephrine.
Non-Pharmocological Therapy (2)
- Percutaneous Coronary Intervention prev. known as angioplasty w/ stent
- Coronary Artery Bypass Grafting - use veins or artery to create connection to construct a detour around blocked portion of artery
What is a good diet for somebody with CAD?
Low-fat diet rich in antioxidants. Foods containing bioflavinoids. Supplement C, E, B6, B12, Folic Acid
What is HTN a risk factor for?
CHD, heart failure, stroke, renal failure
Elevated BP category
120-129, <80
Stage 1 HTN
130-139 or 80-89
Stage 2 HTN
> 140 or >90
hypertensive crisis
BP > 180/120
HTN risk factors
age, ethnicity, smoking, high salt intake, health problems, inactive lifestyle, alcohol, high stress, obesity
HTN complications
Stroke, heart failure, sexual dysfunction, vision loss, heart attack, kidney disease
Primary HTN symptoms
Usually asymptomatic
headache, confusion, nausea/vomiting, visual distrubances (most common), nocturia
Treating HTN - Diuretics
First drug of choice. Thiazide. Watch K+ levels
Treating HTN: Beta Blockers
metoprolol, atenolol. For newly diagnosed pt.
Treating HTN: ACE inhibitors
lisinopril, benazepril, Block angiotensin, which causes BV to open
Treating HTN: Angiotensin 2 receptor blockers
losartan, valsartan
Treating HTN; Calcium Channel Blockers
diltiazem, amlodipine. block CA from entering smooth muscle cells of heart.
Treating HTN: Alpha Blockers
not common. doxazosin, prazosin. reudce the arteries resistance
Treating HTN: alpha 2 receptor agents
clonidine, methyldopa.
Treating HTN: combined alpha and beta blockers
carvedilol, labetalol
vasodilators
last effort. hydralazine. for HTN emergency
Drug regime for HTN
1 antihypertensive medication given at low dose and slowly increased until optimal BP reached.
What is a good diet for somebody with HTN?
Low calorie, low fat, low sodium
What is preload?
Stretch of vesicle. Amount of blood in vesicles at end of distole
What is afterload?
Relaxation. The resistance left ventricle must overcome to circulate blood.
Left Sided Heart Failure
Prevents delivery of oxygenated blood. Main cause of right sided heart failure. There are 2 types: systolic heart failure, diastolic heart failure
Left sided heart failure symptoms
- paroxysmal nocturnal dyspnea (most common)
- cough,
- pulmonary congestion: cough, crackles, wheezes, blood tinged sputum, tachapnea
- restlessness
- confusion
- tachycardia
- exertional dyspnea
- fatigue
- cyanosis
Systolic Heart Failure
- pumping problem
- reduced ejection fraction
- inability of heart to contract enough to push blood foward
- stretch and thin chambers 0 heart gets bigger
- increased afterload
- impaired contrile ability
- incompetent valves
- cardiomyopathy
Diastolic Heart Failure
- filling problem
- preserved ejection fraction - it could remain normal
- inability of left ventricle to relax, resulting in fluid backing up into lungs
- increased preload
- left ventriclular hypertrophy
Right Sided Heart Failure
- Oxygen depleted blood
- heart loses ability to move o2 depleted blood into lungs
- Caused by left sided heart failure
Right sided heart failure symptoms
- edema
- ascites
- fatigue
- enlarged liver and spleen
- distended jugular vein
- anorexia and GI distress
- weight gain
heart failure risk factors
atherosclerosis, HTN, DM, fautly heart valves/muscles, smoking, alcohol, obesity
HF Compensatory Mechanism: Nervous System
- Catecholamines released (help body respond to stress)
- alpha and beta effects activated - lead to increased HR, increased BP, increased cardiac output
- baroreceptors stimulated: sense pressure change by response to changes in tension in arterial wall
HF Compensatory mechanism: hormones
Renin - decreases fluid eliminated as urine
Angiotensin: narrows BV to increase BP
Aldosterone: sends signals to organs to regulate sodium they send to the blood stream
HF Compensatory mechanisms: Cardiovascular System
- Ventricular Dilation: initial cardiact response to pump more blood
- myocardial hypertorphy: stronger, thicker muscles
- Frank Starling Mechanism: hypertrophy of L ventricle
PRO BNP normal value
<100. Detects hormone released from the ventricles in response to increased wall tension
Ejection Fraction Values
Normal: 55-70%
Less blood is ejected: 40-54%
Mild heart failure: 35-39%
Severe Heart Failure: <35%
Managing HF: ACE Inhibitors
Lisonopril, benzepril
Managing HF: beta Blockers
Metoprolol, atenolol
Managing HF: diuretics
Furosemide, HCTZ
Managing HF: Vasodilators
hydralazine
Managing HF: Cardiac Glycoside
Digoxin (monitor for toxicity. Arrythmia, visual disturbances, tiredness, loss of appetite, confusion)
Lanoxin
Goals of HF Therapy
improve cardiac output, reduce pulmonary and systemic congestion, prevent complications, improve quality of life, educate pt. and family
Abdominal Aortic Aneurism
arterial walls weak, enlarged
Types of aneurisms
- Fusiform: bulge on all sides
- Saccular: 1 side has bulge
- pseudo: BV injured and leak
AAA Etiology
altherosclerosis, hypertension, BV disease (CVD, MI, ANGINA), Trauma, Genetic diseases
AAA risk factors
High BP, High Cholesterol, Smoking, sedentary, family history
AAA clinical manifestations
Back, leg, abdominal pain
pulsing sensation in abdomen
IF RUPTURED: clammy, sweaty skin. dizziness. fainting, tachycardia, dyspnea, nausea/vomiting
When is surgical management recommened for AAA?
when it’s 4-5 cm
6 P’s of peripheral vascular disease
Pain Paresthesia poikilothermia paralysis pallor pulselessness
Peripheral Artery Disease
Narrow, weak, blocked arteries
Result of build up of fat and cholesterol
Arterioslerosis
Atheroslecrosis
PAD Patho
athermatous plaque formation in intima of vessel –> calcification of medial layer and loss of elasticity –> inadequate blood supply to tissues leads to tissue hypoxia
PAD manifestations
Claudation
rest pain
ulceration
gangrene
PAD Risk Factors
CAD/PAD Diabetes HTN obesity smoking > 50
PAD Risk Factor Modifaction
Antiplatelet Therapy Lipid lowering agents glycemic control BP control smoking cessation lifestyle modication heart healthy diet Excercise
CVI (DVT)
vein blockage or valve leakage in leg veins, blood flows back and pools in legs
DVT most common
DVT patho
hemdynamic changes/veno status –> endothelial injury/dysfunction –> hypercoagulability
CVI/DVT manifestions
edema, vericous veins, skin changes/discoloration, skin ulceration
DVT Risk Factors
> 50 obesity smoking family history hormonal fluctuation poor lyfestyle choices
DVT nursing management
avoid long periods of sitting or standing elevate legs exercise regularly lose weight hygiene
Vessel Differation DVT
Ateriole: dangle legs, pain sharp and worse at night, intesne pain, intermittent claudation, skin cool to touch, skin thin/dry/scaly/hairless, rubor, poor or absent pulse, edema not common, located toes/feet/shin
Venous: elevation of legs, aching, throbbing, pain worse when sitting/standing/dangling/walking, skin warm to touch, skin thick/tough/leathery, pulse present, edema present, located over ankle
Diabetes Patho
Food is broken down into glucose, the pancrease produces insulin. Type 1 no insulin is produced due to damage of B cells. Type 2, over production of insulin so body becomes desnsitized.
Diabetes Type I etiology
Autoimmune Juvenile DM Insuin Dependent Exposure to virus Climate (oceanic)
Type I Diabetes Manifestations
3 P’s : polyuria, polydipsia, polyphagia
Diabetes Type II Clinical Manifestations
Increased urination, increased thirst, increased hunger, fatigue, blurred vision, frequent infections, erectile dysfunction, pain/tingling in hands and feet
Increased BP Risk for Diabetes
130/85 or higher
High Triglycerides for Diabetes
150 mg/Dl or above
Large Waistline Risk for Diabetes
Men: 40” or more
Women: 35” or more
LOW HDL risk for diabetes
Men: <40
Women: <50
Elevated Fasting BS Risk for Diabetes
100 or more
C-Peptide Test
0.5-2.7 NG/mL. Increased in Type 2 DM, insulinoma, cushings, kidney disese
decreased in Type 1 DM, Addisons disease, liver disease
Hemoglobin A1C
<5.7 normal
>6.5 diabetes
Fasting Blood Sugars
70-100 normal
100-125 risk of diabetes
126 or higher diabetes
Glucose Tolerance Test
200 or above
Hypoglycemia Symptoms
45-60 mg/DL
sweating, pallor, irritability, hunger, lack of coordination, sleepiness
Hypoglycemia Management
15 g fast acting carb. Avoid protein it slows absorption of sugar
Wait 15 min. If Blood glucose <70 repeat
Hyperglycemia Symptoms
180-200
Dry mouth, increased thirst, weakness, headache, blurred vision, frequent urination
HHS
Common in Type II Dm BS >600 Osmality >340 Shallow breaths ALOC Dehydration Develops slowly
DKA
Type I Diabetes Common BS >300 Osmality >340 Kassumauls respiration Abdominal pain Nausea/vomiting Develops quickly
Hyperglycemia Etiology (8 I’s)
Infection Infarction Infraction (non-compliant) Ischemic Illegal Iatrogenic Idiopathic
DKA/HHS management
- maintain airway
- decrease blood glucose
- Blood glucose monitor every 1-2 hours
- improve dehydration
Acute Diabetes Complications
DKA, HHS
Microvascular Diabetes Complications
Retinopathy
Nephropathy
Neuropathy
Macrovascular (Chronic) Diabetes Complications
Atherosclerosis
Cardiovascular/Peripheral Vascular
Cerebrovascular
Retinopathy
Microvascular damage and occulsion of retinal capillaries due to changes in retina. Have eyes dilated every year
Nephropathy
Albumin in urine
Detioration of kidney function to overfiltering of glucose
Peripheral Neuropathy
numbness/tinling in lower extremities.
Managing Diabetes: Biguanides
Control hepatic glucose production
Metformin. Do not use in pt. with kidney, liver, or heart failure. Cautious with contrast medium
Sulfonylureas
stimulate pancreas to make more insulin. Glyburide, glizipizide, glimepiride, take with meals, watch for hypoglycemia
Glucose Inhibitors
Slows the absorption of starches/CHO. Best used for those with normal FBS, but elevated post prandial blood sugars. Arcabose, miglitol
Incretin Mimetics
Insulin pen. Do not use with insulin. May combine with oral agents
Rapid Acting Insulin
Bolus. Lispro (humalog)
Short-Acting Insulin
Bolus/Prandial. Regular Insulin (humulin R)
Intermediate acting insulin
NPH (humulin N)
Long-Acting Insuin
Basal. Lantus
Diabetes Dietary Recommendation
Non Starchy Veggies, grains and starchy foods, protein, high fiber, non fat dairy
