Class 20: Intro to CAD Flashcards
what should be asked during the health interview for CVS assessment
- Hx of heart problems, surgeries, meds, etc.
- family Hx
- personal habits
- comorbid disease?
what is another word for chest pain
- angina
what is angina a sign of
- cardiac tissue ischemia –> decreased blood flow
what can angina be described as
- tightness
- squeezing
- pressure
- clenched fist
- crushing
- elephant on chest
- sense of impending doom
how can we distinguish from pleuritic pain, muscular chest wall pain, gastric upset, and angin?
- pleuritic pain: follows breathing pattern
- gastric upset/gallbladder: go away with antacid
- angina: does not change w breathing, can be brought on by exertion and relieved w rest
what are some questions to ask regarding angina?
- OPQRSTU
- brought on by activity? relieved w rest?
- associated symptoms?
- referred or radiating pain?
what are some associated symptoms w angina?
- sweating/diaphoresis
- pale/ashen grey
- heart skipping a beat
- heart fast or slow
- SOB
- N&V
how come SOB is associated w angina
- compensation for decreased blood flow & O2 to tissues
what causes the associated symptoms of angina
- visceral pain in ischemic heart
- SNS/PSNS stimulation
where might you feel radiated pain w angina?
- lower jaw (NOT upper)
- midsternal
- left should
- down both arma
- neck
- epigastric
- intrascapular
how come radiated pain occurs with angina?
- nerve impulses from the heart and other places get mixed up in the spine
- this causes the pain to misinterpret where the pain is
how is angina graded
4 classes
describe class 1 of angina
- angina not caused by ordinary physical activity
ex. walking, climbing stairs - angina occurs with strenuous, rapid, and prolonged exertion
describe class 2 of angina
- slight limitation of normal activity
- occurs when walking or climbing stairs rapidly
- walking uphill
- walking or climbing stairs after meals
- in cold, wind, or under emotional stress
- during few hours after awakening
- walking 2 blocks on level
- climbing more than 1 flight of ordinary stairs at normal pace
describe class 3 of angina
- marked limitations of physical activity
- walking 1 or 2 blocks on level
- climbing 1 flight of stairs under normal conditions & at normal pace
describe class 4 of angina
- inability to carry on any physical activity without discomfort
- may be present at rest
describe dyspnea r/t CVS assessment
- SOB
- SOBOE or at rest
- what type of activity brings it on
- how does it affect ADLs
- paroxysmal nocturnal dyspnea = awaken at night, occurs w heart failure
what is orthopnea? what are indicators of it
- SOB when lying down
- causes inability to sleep flat
- ask if the number of pillows they sleep w at night has changed
describe cough r/t CVS assessment
- productive?
- dry?
- hacking?
- hemopytsis? (pulmonary disorder)
- what meds? ACE inhibitor can have side effect of cough
describe fatigue r/t CVS assessment
- recent change?
- affect ADLs?
- walk stairs?
- 6 min walk test
what causes cyanosis or pallor?
- cyanosis = lack of oxygenation
- pallor = anemia or vasoconstriction of blood vessles
- both occur with MI & low CO
describe edema r/t CVS assessment
- dependent when caused by heart failure
- bilaterial if cardiac
- gets better w elevation
- can be peripheral, pulmonary, or abdominal
describe nocturia r/t CVS assessment
- if have to awaken at night with urgency to void
- occurs w HF
describe auscultation of the carotid arteries
- assess for bruit (swooshing sound)
- press lightly
describe palpation of the carotid artery
- avoid carotid sinus –> can cause vagul stimulation = slowed down HR
- do not do simultaneousloy
why is the carotid artery important
- yields important info about cardiac function
what does jugular venous pressure tell us
- fluid gage
- can tell us about central venous pressure
what should the jugular vein look like normally
- should be flat
- distended = build up of fluid
what is hepatojugularr eflux test
- do if venous pressure is elevated or suspect HF
- push in the right upper quadrant on abdomen
- if heart functioning normal, will pump out this additional volume = jugular vein rises for few seconds then recedes
- if HF is present, jugular vein will stay elevated entire time
what is a heave or lift
- sustained forceful thrusting of ventricle during systole
= visible at the sternal border or apex
what is the PMI
- point of maximal impulse
- AKA the apical impulse (if normal)
what is a thrill
- palpable vibration
- feels like purring cat
- signifies turbulent flow & often accompanies murmurs
what are the S1 and S2 heart sounds
- S1 = mitral & tricupsid valve closing = beginning of systole = beginning of systole
- S2 = aortic & pulmonic valve closing = beginning of diastole
what is the splitting of S2
- normal
- occurs toward end of inspiration
- occurs when aortic & pulmonic valve do not close together
= T-DUB sound
what is a murmur
- blowing, swishing sound
- occurs with turbulent blood flow
what is the S3 heart sound
- ventricular gallop
- heard after S2
- LUB DUB-T
- sound of blood hitting the ventricles
- can be due to volume overload or HF
what is the S4 heart sound
- atrial gallop
- before S1
- T-LUB DUB
- due to atria trying to push blood into resistant ventricles
what is hyperlididemia
- condition of having too many lipids in the blood
why is hyperlipidemia problematic
- high amounts of specific lipids can cause atherosclerosis
what is astherosclerosis
- hardening, occlusion, or damage to the arteries
what can atherosclerosis lead to
- CAD
what are the 3 types of serum lipids
- cholestrol
- triglycerides
- phospholipids
what is cholestrol
- steroid used in plasma membranes to build vit D, bile acids, cortisol, estrogen, and testosterone
what are lipoproteins? why are they important?
- lipid carrying proteins
- imp bc water insoluble fats (such as cholestrol) must be bound to apolipoproteins
what are the different types of lipoproteins? which are good vs bad>
- high density lipoproteins = good
- very low density lipoproteins = bad
- low density lipoproteins = bad
what do LDLs do`
- carry cholestrol from liver to other tissues
- major carrier of cholestrol
what do HDLs do
- returns excess cholestrol to the liver
what do high levels of LDL cause
- associated w cholestrol plaque build up & cardio diseases
what are triglycerides
- lipid stored in the body as a source of energy
how do triglycerides contribute to the development of CAD
- when body is in fasting state, they are bound to VLDL
- inceased triglyceride level = increased risk of CAD
- increased levels cause LDL particles to become more atherogenic
how do HDL contribute to CAD
- low levels = increased risk
what can cause increased triglyceride & LDL levels
- obesity
- inactivity
- diabetes
- increased alcohol intake
what are phospholipids
- lipids used for plasma membranes
- not used as a clinical indicator for hyperlipidemia in the context of atherscleritis disease
what is the primary risk factor for atherosclerotic disease
- elevated LDL
why are LDLs the primary risk factor for atherosclerotic disease
- deposit cholestrol in vessel walls for storage
- strongly associated w plague formation & PAD/heart disease
what do low HDL levels cause
- less removal of cholestrol from the vessels
what is the goal for lipid levels
- maximize HDL
- minimize LDL <2.5 mmol/L
what is total cholestrol? what is the target range
- ratio of total cholestrol in blood
- want to be less than 4.0
what are optimal triglyceride levels
- 1.7 mmol/L
describe the transpot of lipids
- lipids are hydrophobic = problem because they need to get into the blood
- to be transported, they are put into lipoproteins
describe the structure of lipoproteins
- fat surrounded by proteins
what do VLDLs do?
- transport lipids from liver to body cells
- contain high levels of triglycerides
what do high VLDLs indicate
- high levels of TG = increased risk of CAD
what is ischemic pain in the heart called
- angina
how do supply & demand affect angina
- narrowing of blood vessels = decreased supply of O2 and blood
- activity = increased demand for O2 and blood
how does rest affect demand
- rest reduces demand = pain goes away
what is a primary mechanism for narrowing of arteries
- development of atherosclerosis in the arteries
what is atherosclerosis
- changes in the vessel wall that lead to thickening & plague formation in the vessel wall
what can narrowing of the vessel wall lead to
- can trap small arterial emboli, that cause further/fast blocking of blood flow & greater ischemia to distal (down stream) tissue
how does hypertension r/t atherogenesis
- causes increased pressure = injure vessel wall & start inflammatory process
how does high cholestrol r/t atherogenosis
- provides material needed to develop the plagues
what are the developmental stages of atherosclerosis
- fatty streak
- fibrous plague
- complicated lesion
describe the stage of fatty streak
- damaged endothelium = increased permeability of wall = lipids accumulate and migrate into sm. m cells
- yellow tinge
what may cause endothelial damage
- hypertension
- high cholestrol
- hyperlipidemia
- smoking
- obesity
- diabetes
- infections
- toxins
what forms a fibrous plague
- collagen covers the fatty streak
= vessel lumen narrowed = blood flow reduced - may form a fissure
- fibrous plague = grey or white
describe a complicated lesion
- plague ruptures = thrombus formation = further narrowing or total occlusion of vessel
what is collateral circulation
- when the body creates new circulation in the heart around a blockage
what can cause collateral circulation
- atherosclerosis
what 2 factors contribute to the growth & extent of collateral circulation
- inherited predisposition to develop new blood vessels (angiogenesis)
- presence of chronic ischemia
how does chronic ischemia lead to collateral circulation
- when an occlusion of a coronary artery occurs slowly over time, there is greater chance of developing collateral circulation = allows myocardium to recieve an adequate intake of O2
what causes where atherosclerotic plaques form
- forms wherever they are the most stressed
- typically bending & branching points
what is the current theory for the development of atherosclerosis
- plaque formation involves an inflammatory event stimulated by vessel wall injury
what are 2 ways the intima of an artery can become injured
- mechanical stress
2. oxidative stress
what is mechanical stress
- high bp
- high viscosity
what is oxidative stress
- high levels of reactive oxygen species which damage cell structures
what are ROS
- reactive chemicals containing O2
what is associated with increased production of ROS
- hyperlipidemia
- hyperglycemia
how do ROS damage the artery wall
- oxidize LDL
what is superoxide
- type of ROS
- O2-
what does superoxide do
- destroys nitric oxide which has protective mechanisms on arteries bc it causes vasodilation
how do phagocytes affect the artery wall
- produce superoxide during inflammation
- when the vessel wall is damaged the inflammatory response brings WBCs to the area
describe macrophages r/t to oxidized LDL
what happens when they die?
- consume the oxidized LDL
- macrophages die & become lipid filled foam cells that form a bulge in the side of the artery wall = plaque
describe how inflammation forms plaque r/t oxidative stress
- vessel wall damaged = inflammation
- inflammation brings WBCs to the area
- phagocytes produce superoxide when oxidize LDL
- oxidized LDLs are consumed by macrophages
- macrophages die & become lipid filled foam cells & form a bulge = plaque
what is coronary artery disease
- condition where blood vessels that supply the heart muscle w blood (coronary arteries) become narrowed due to plaque in the artery wall
= prevent blood flow
what is a myocardial infarction
- heart attack
what causes a myocardial infarction
- when the blood supply to an area of the heart is interrupted due to blocked coronary arteries
- causes myocardial tissue to die or become necrosis
- caused by CAD
describe the damage to heart muscle: is it temp? permanent? what does this mean
- will be permanently damaged
- heart muscle does not have the ability to regenerate
= heart will not able to function properly
what is cardiac arresr
- when the heart stops pumping completely
- medical emergency
- after recovery may develop heart failure
what is heart failure
- heart cannot pump blood properly
symptoms of heart failure
- sob
- edema
- fatigue
what is the end result of CAD
- myocardial infarction
- cardiac arrest
define atherosclerosis
- formation of plaque that causes narrowing or blockage of the blood vessels
what is the difference between CAD and atherosclerosis
- CAD = specifically refers to athero in the coronary arteries
- atherosclerosis = general term that describes a condition that can affect anywhere in the body
how can atherosclerosis cause an MI
- plaque that forms can rupture forming a blood clot
- this can get lodged in the coronary arteries
what does a blood clot in the brain cause
- stroke
is CAD progressive or sudden
- progressive
what are the 2 types of risk factors for CAD
- nonmodifiable
2. modifiable
what are nonmoodifiable risk factors for CAD
- increasing age
- sex (men > women until 65 y.o)
- ethnicity (white> black)
- genetic predisposition
- family history of heart disease
what are the major modifiable risk factors of CAd
- serum lipid alteration: high LDL, triglyc & low HDL
- high bp: >140/90
- DM
- tobacco use
- physical inactivitiy
- obesity
what is defined as obesity
- waist circumference >102 in men
- >88cm women
what are contributing modifiable risk factors for CAD
- fasting blood glucose >10 mmol/L
- psychosocial factors
- elevated homocysteine levels
what psychosocial factors contribute to CAD
- depression
- hostility
- anger
- stress
compare risk factors for atherosclerosis in the heart & PVS
- the same
what is the Framingham Risk tool
- tool that provides an estimation of 10 year risk of CAD
describe supply & demand of the heart in normal conditions
- normally, the amount of blood delivered to the heart via coronary artiers matches the myocardial o2 demand
what determines the heart’s demand
- heart rate
- contractility
- preload
- afterload
what does it mean if the lumen size is reduced to 75%
- ischemia can occur during times of elevated myocardial o2 demand
ex. physical activity, emotional stress, hot or cold exposure, large meal
what occurs if the lumen size is reduced to 90%
- ischemia can occur at rest
describe supply & demands role in ischemia
- ischemia can be caused by icnreased demand or decreased supply or both
how long does it take for the myocardium to become hypoxic on a cellular level?
- within the first 10 sec
contractility stop after ____ min with total occlusion
several
what occurs when the myocardium becomes hypoxic? what does this cause?
- anerobic metabolism
= lactic acid accumulates
= pain fibers stimulated
= cross over = referred pain, specifically to left shoulder & arm
how long does it take for cardiac cells to die
- 20 min
what happens to cardiac cells if blood flow returns in time
- process reverses & contracility is restored
- repair begins
what might cardiac ischmemia result in (5 things)
- diastolic dysfunction
- systolic dysfunction
- electrical disturbance in heart rhythmn
- angina pectoris
- cardiac muscle death = MI
what is diastolic dysfunction
- muscle becomes stiff = reduced muscle relaxation & filling
= reduced preload = reduced SV, CO, and BP
what is systolic dysfunction
- failure of heart to properly contract = decreased contracility
= reduced SV, CO, BP
how do electrical disturbances occur as a result of cardiac ischemia
- conduction moves around ischemic tissue
- or heart muscle is irritable
= ECG changes, irregular pumping, ineffective pumpin - brady and tachy = altered CO
what causes angina pectoris
- visceral pain from cardiac muscle ischemia
what can cause high blood viscosity
- polycythemia
- hyperglycemia
how does tobacco use cause endothelial injury
- effect platelet agg
what is hyperhomocysyteinemia? what can it cause?
- high homocysyteine
- linked to inflammation
= endothelial injury
how does diabetes cause endothelial injury
- creates thicke blood = mechanical stress
how do infections & toxins cause endothelial injury
- trigger inflammation
when will we open a blockage
- only if 75% or greater
what do free radicals of o2 cause
- steal protons or electrons from healthy cells = destabilize the cells = cell death
ex. superoxide can do this - also elicit the inflammatory resposne
what can cause increased ROS
- hyperlipidemia
- hyperglycermia
what does increased triglyceride cause
- causes LDLs to become more atherogenic
why do low HDL cause risk of athersclerosis
- provides less removal of cholestrol from the vessels
what is the total cholestrol ratio
total cholestrol: HDL cholestrol
- want to be <4.0
what age groups should be screened for CAD
- men > 40
- women > 50 or postmenopausal
people with which conditions should be screened for CAd
- smoking
- diabetes
- HTN
- family history of hyperlipid or premature CVD
- erectile dysfunction
- chronic kidney disease
- inflammatory disease
- HIV infection
- obesity (BMI > 27)
- manifestations of hyperlipid
- clinical evidence of atherosclerosis
what does a framingham risk score of <5% mean? > 5%
- <5 = repeat every 3-5 years
- >5% = repeat every year
what tests should be run for screening for CAD
- history
- examination
- LDL, HDL, TG levels
- glucose
- GFR
what does an increased in BUN or Cr mean
- decreased kidney function
what are antilipemic drugs? what are they used as an adjunct with?
- drugs used to lower lipid levels
- used as an adjunct to diet therapy
what influences drug choice for antilipemic
- based on the specific lipid profile of the pt
what are the classes of antilipemic
- HMG-CoA reductase inhibitors (HMGs or statins)
- bile acid resins
- nicotinic acid
- fibric acid derivatives (fibrates)
- misc.
what drugs are the most potent LDL reducers
- statins (HMG-CoA Reductase inhibitors)
what is the MOA of statins
- inhibit HMG-CoA reductase (enzyme)
- this enzyme is used by the liver to produce cholestrol = reduced cholestrol production
- causes liver to produce more LDL receptors on surface of liver = collect more LDL = less circulating in blood
what do statins result in
- decreased LDL and TG
- increased HDL
what are statins the first line drug therapy for
- hypercholesterolemia
what are 2 types of statins
- atorvastatin (lipitor)
- simvastatin (zocor)
what types of hyperlipidemias do statins work on
- type 2a
- type 2b
= familial or genetic
how do statins effect LDL
- decreases by 30-40%
how statins effect HDL
- increased by 2-15%
how statins effect TG
- reduced by 10-30%
how long must statins be taken for
- take for lifetime
- or until diet/lifestyle changes permanently lower cholestrol levels
when is most cholestrol produced? how does this effect med administration?
- most produced at night
= short acting lovastatin must be taken hs
what is a drug interaction w statins
- grapefruit
what are adverse effects of statins
- myopathy (muscle pain) & muscle breakdown lead to
- rhabdomyolysis
- rash
- mild GI symptoms
- elevated liver enzymes or liver disease= avoid with liver dysfunction
- insomnia
- lens opacities
what is rhabdomyolysis? what can it lead to?
- breakdown of skeletal muscle
- may lead to renal failure due to blockage of kidneys by myoglobin
why should serum CK levels by monitored when taking statins?
- monitor for rhabdomyolysis
- product of muscle damage
what liver enzymes are increased with statins
- LDH
- lactate dehydrogenase
describe nursing considerations with statins
- monitor w eye exams
- monitor liver function tests
- monitor serum CK levels
what is the MOA of bile acid resins
- in small bowel, binds to bile acids containing dietary cholestrol to form insoluble complex
- prevent absorption
= increased bowel excretion of cholesterol
what is a type of bile acid resins
- cholestyramine (questran)
why are bile acid resins not first line
- adverse effects
what are bile acid resins used for
- relief of pruritus associated w partial biliary obstruction
- may be used along w statins
what are side effects of bile acid resins
- unpleasant gritty taste
- GI disturbances (nausea, dyspepsia, constipation, belching)
- may cause increase in TG levels
what are nursing considerations regarding bile acid resins
- avoid other meds/vit 1h before and 4 hr after (bc will bind & excrete them)
- adverse effects diminish with time
- take with lots of water to help w GI upset
what meds do bile acid resins interact w
- digoxin
- thiazides
- B blockers
- fat soluble vitamins
- folic acid
- vanocmyosin
what is a type of nicotinic acid
- nicotinic acid = niacin, vit B3
what is the MOA of nicotinic acid
- inhibit synthess & secretion of VLDL and LDL
- enhances HDL
how does nicotinic acid effect lipid level
- reduced VLDL = reduced LDL
- reduced TG levels
- increases HDL
describe the dose required for niacin
- lipid-lowering properties require much higher doses than when used as a vitamin
describe the use of niacin
- effective
- inexpensive
- often used in combo w other lipid-lowering drugs
what are the adverse effects of niacin
- histamine release = hot flashes, flushing, pruritis in upper torso & face
- GI upset
- hepatotoxicity
- gout
- hyperglycemia in diabetes
what are nursing considerations regarding niacin
- most adverse effects subside w time
- decreased liver function & arrthymias may occur w high doses
- aspirin 30 min to 1 hr before niacin may reduce flushing
- taken w food
what is a type of fibric acid derivitative (fibrate)
- gemofibrozil (lopid)
- fenofibrate (lipidil)
what is the MOA of fibrates
- decrease TG by decreasing VLDL
- suppress release of free FA from adipose tissue
- may elevate HDL levels
what are adverse effects of fibrates
- GI upset & cramping
- increased risk of gallstones
- increase effect of warfarin & anticoagulants & hypoglycemics
- liver studies may show increased function
what are nursing considerations for fibrates
- monitor PT/INR (bc of effect on warfarin & anticoagulants)
what are misc agents from antilipemics
- cholestrol absorption inhibitor
- omega-3 FA
- orlistat
what are cholestrol absorption inhibitors
- inhibit abs of cholesterol & related sterols from the SI
= reduced total cholesterol, LDL, and TG - increased HDL
- often combined w statins
what is a type of cholesterol absorption nhibitors
- ezetimibe (Zetia)
what do omega-3 FA do
- decrease CAD
what are types of omega-3 FA
- tuna
- salmon
- halibut
- flaxseed
- soybeans
- walnuts
- pumpkin seeds
what is the MOA of orlistat
- prevents ab of TG
- may promote weight loss & lower LDL
what are side effects of orlistat
- oily fecal spotting
- oily stools
- flatulence
- urgency
- pain
describe the decision tree used to determine how to manage cholestrol
- assess LDL-C and total CV risk
- indication for drug treatment?
- if yes = define LDL-C target & give statin - LDL-C target reached?
- yes = stay
- no = consider adding ezetimibe - LDL-C target reached?
- no = consider PCSK9 inhibitor
- or consider bile acid sequestrant
what are 3 basic cardiac diagnostic studies
- 6 min walk test
- stress-exercise test
- angiogram
describe a 6 minute walk test
- sees how far the pt can walk in 6 min
- also see if they have any chest pain, SOB
describe the stress-exercise test
- pt on treadmill or bike
- put ECG leads, gradually increase resistance & look at ECG for signs of ischemia
- if cant get on treadmill or bike = stress heart with drugs that increase HR
what is an angiogram
- use catheter to put dyes in arteries of heart to see heart in xray
- aka cardiac cathetrization
- uses fluroscopy
what is the myocardium
- muscular tissue of the heart
how does the myocardium receive blood
- from the 2 coronary arteries coming from base of aorta
- left & right coronary arteries
what does the left main (coronary artery) split into
- circumflex
2. left anterior descending
what does the left anterior descending (LAD) supply?
- the anterior left ventricle & septum
what does the circumflex supply
- the lateral & posterior LV
which coronary artery is more dangerous to obstruct
- left
what does blockage of the right coronary artery cause
- can affect SA node if up high
= arrythmia
what does the right coronary artery & branches supply
- the anterior & posterior right ventricle
- SA/AV nodes
what is the posterior descending artery? what does supply
- branch of the right coronary artery
- supplied the inferior & apex of the myocardium
describe the progression of CAD
- unpredictable
- manifests as a broad range of unpredictable clinical symptoms
how might CAD manifest
- chronic stable angine
- acute coronary syndrome
- MI
- cardiac arrythmias
- HF
- sudden cardiac death
what can acute coronary syndrome be split into
- unstable angina/nonSTEMI
- STEMI
what is the difference between a STEMI and non-STEMI
- stemi = full thickness effected = more dangerous
- nonstemi = partial thickeness
