Cardiovascular Disease Flashcards
What is the #1 cause of death in men and women in the US?
cardiovascular disorders
What are the top 3 cardiovascular disorders?
HTN, hypercholesterolemia, atherosclerosis
HTN stats
affects 1 in 3 adults and 50% are adequately controlled
What is the most common primary diagnosis in the US?
primary/essential HTN– aka silent killer
What is primary HTN?
the most common 95%; idiopathic, potential genetic or racial predilection; diet and lifestyle play an impact
What is secondary HTN?
increased bp secondary to another cause like medication, kidney, endocrine disorders, drug use
What is malignant hypertension?
call 911, end organ damage to cardiovascular system, CNS, or kidney
What is labile HTN?
BP that fluctuates repeatedly in response to emotional stress; HTN medications are normally not effective, instead Rx stress-relieving meds and monitor for 24 hrs
What is white coat syndrome?
can increase bp 20/10 mmHg; acute spike in bp due to the fact they know their bp is being taken
When does gestational HTN return to normal?
within 12 weeks of delivery (begins 1st trimester)
What are symptoms of acute HTN?
HA, nausea, vomiting, dizziness, sweating, loss of consciousness
What are some causes of acute hypertension?
exogenous etiologies: caffeine, nicotine, sodium intake, pregnancy, alcohol, medications; endogenous: tumor like adrenal gland tumor
Normal BP
<120 over <80
Elevated BP
120-129 and <80
Stage 1 BP
130-139 or 80-89
Stage 2 BP
> 140 or >90
Hypertensive crisis BP
> 180 and/or >120
T/F pt must be seated for 5 minutes before bp measurement
true
Every 20/10 mmHg increase in BP over 115/75, increases the risk for cardiovascular disease ___ fold
2 fold
HTN urgency
180/100 or greater, organ damage may occur; check for HA, SOB, nosebleeds or severe anxiety
HTN crisis
> 180/>120, organ damage WILL occur
What can a HTN crisis do to the body?
CVA, loss of consciousness, memory loss, MI, ESRD, aortic dissection, angina, pulmonary edema, eclampsia, blindness
What organs are primarily effected by HTN?
those with the most microvascular beds; brain, retina, heart, kidneys
What percent of HTN morbidity is from coronary artery disease?
50%
What percent of HTN morbidity is from cerebral vascular accident?
33%
What percent of HTN morbidity is from renal failure and end stage renal disease?
10%
What are HTN risk factors?
male, increased age, african american, family hx, sympathetic over-activity, sleep apnea, concomitant disease, lifestyle
Why is sympathetic over-activity an issue?
vasoconstriction, increased heart rate; from stress of pheochromocytoma which has the hallmark impending sense of doom
What diseases are concomitant to HTN?
dyslipidemia, diabetes
What lifestyle factors increase risk of HTN?
alcohol, obesity, sedentary lifestyle, smoking, salt intake
How do you calculate BMI?
weight (lbs)/height (in^2) x 703 OR kg/m^2
What is the BP equation?
BP = CO x VR
CO=cardiac output
VR= peripheral resistance
How do you calculate cardiac output?
CO = SV x HR which describes the amount of blood pumped by the ventricle per minute
What affects peripheral resistance?
blood volume and blood vessel size
What are some functions of angiotensin II?
up-regulates sympathetic tone, increases absorption of Na and Cl, excretion of Ca to increase volume of blood, stimulates aldosterone release from adrenal gland, arteriolar constriction, increase ADH from anterior pituitary
Increased BP creates a negative feedback loop to the kidney causing
reduced renin release
What does renin do?
transforms angiotensinogen to angiotensin I
What does ACE do?
converts angiotensin I to II
Where is ACE from?
surface of renal and pulmonary endothelium
What are manifestations of secondary HTN?
pitting edema, truncal obesity, foot ulcers, numbness of extremities, muscle weakness, tachycardia
What are lifestyle modifications of HTN?
weight reduction, mediterranean diet, sodium decrease, physical activity, moderation of alcohol
What is a normal BMI?
18.5-24.9
What are first line agents?
diuretics, ACE inhibitors, Angiotensin receptor blockers, Ca channel blockers
What are diuretics?
furosemide, hydrochlorothiazide
What are ACE inhibitors?
captopril
What are ARBs?
valsartan
What are Ca channel blockers?
diltiazem, nifedipine, verapamil
What are second line agents?
beta blockers, alpha agonist/antagonist, methyldopa, vasodilators
What is a beta blocker?
metoprolol
What are alpha agonist/antagonist?
clonidine/terazonsin
What is a vasodilator?
hydralazine
What is first line in African americans?
Ca channel blockers
What is first line in whites?
beta blocker
What is the effect of HTN on heart muscle?
increased work load and stronger stroke which can lead to left ventricular hypertrophy and congestive heart failure
What is bad news on an EKG?
inverted T wave means current or past MI
What are you looking for in an urinalysis?
RBCs, WBCs, protein or glucose in urine
On the bp cuff, if the white line on the cuff doesn’t overlap with the other white line, you need…
a larger cuff
What is the desirable total cholesterol level?
<200
What is the desirable LDL level?
<100
What is the desirable HDL level?
> 45
What is the desirable triglyceride level?
<150
What is homocysteine level measuring?
amino acid in blood that converts cholesterol to LDL… causes damage to arterial walls and blood clots
What is a normal homocysteine level vs increase risk for CVD?
normal <12 micro mol/L; risk 12 to 15
What is the treatment for elevated homocysteine?
B vitamins like folic acid/b9, cobalamin/b12 and pyridoxine/b6
What does C reactive protein measure?
inflammation, promoting globulin in blood that is produced when blood vessel walls become damaged
What is normal C reactive protein?
<0.11 mg/dL
What is high C reactive protein?
0.20 to 1.50 mg/dL
What factors increase CRP?
HTN, BMI, smoking, metabolic syndrome, hyperglycemia, low HDL, high triglycerides, estrogen use, chronic infection, RA, genetic mutation
What is the progression toward MI?
HTN –> CAD –> MI
What is coronary artery disease?
atherosclerosis, coronary revascularization, heart failure, angina, MI
What is the most fatal MI?
left ventricular ischemia aka widow-makers heart attack
Define arteriosclerosis
the thickening and hardening of the walls of the arteries, occurring typically in old age; will happen to everyone but HTN increases the rate
Define atherosclerosis
preventable; a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls, produce emboli
When does arteriosclerosis start
shortly after birth, intervene as young as possible
What is a fibro-atheroma?
larger atheroma with calcification
What is peripheral vascular disease?
arteriosclerotic type disease of the femoral/popliteal artery of the distal portion of superficial femor
What are symptoms of peripheral vascular disease?
intermittent claudication limited to the calf/foot
What are signs of peripheral vascular disease?
affected area has hair loss, thinning of skin, decreased muscle mass, coolness to touch, good to fair femoral pulses, no popliteal or pedal pulse
What are renal effects of HTN?
renal artery stenosis, renal insufficiency, decreased GFR
What is the result of decreased glomerular filtration rate and tubular dysfunction?
hematuria and proteinuria
What occurs when a renal artery has stenosis
focal restriction results in decrease blood supply to kidneys and renal necrosis… may develop neo
What is the increased risk of stroke CVA from HTN?
4x increased risk
Which CVA is more common, hemorrhagic or ischemic?
ischemic 87%
What is HTN encephalopathy?
swelling of the brain with HA, nausea, vomiting, HTN retinopathy, CN palsy, altered mental status
How many people with TIA will stroke?
1/3
How long does a TIA last?
< 24 hours but usually 15 mintues
What are symptoms of a TIA?
vertigo, dizziness, light headedness, focal deficit, weakness contralateral, speech disturbance, visual disturbance
What are the 3 types of ischemic CVA?
thrombotic 35% embolic 30% And lacunar/hypoxic 20%
What is a thrombotic CVA?
plaque decreases the lumen aka stenosis
What is an embolic CVA?
plaque/ fibrous cap is liberated and lodged in the artery
What is lacunar and hypoxic CVA?
secondary to hypoxic events (fine vessels in the brain), difficult to dx
What are signs of lacunar and hypoxic CVA?
INO and weird saccadic dysfunction
What is the cause of a hemorrhagic CVA?
rupture of an intracranial artery
How does damage occur in a hemorrhagic CVA?
hypoxia, hydraulic pressure, toxicity of blood to brain tissue
What may hydraulic pressure cause?
herniation of the brain through the foramen magnum
What are risk factors for hemorrhagic CVA?
HTN, vessel damage, aneurysm, trauma, vasculature malformation
What is the strongest portion of the cranium?
the petrous portion of the temporal bone
What is epidural?
between cranium and dura mater; trauma is the most common cause; 80% involve the middle meningeal artery
Where is the most common location of damage for the middle meningeal artery?
the most temporal area of the skull (thinnest area) results in epidural hemorrhagic CVA
What is subdural?
the most common type of hemorrhagic stroke, caused by acceleration injuries
What is the highest risk factor group for subdural stroke?
alcoholics, blood thins and brain shrinks in alcoholics
What is subarachnoid?
commonly caused by congenital malformations and berry aneurysms that lead to leaks in CSF and increased ICP= worse headache ever
What age group is subarachnoid stroke more common in?
young patients
What is the FAST acronym for stroke?
face asymmetry, arm hangs, speech slurred, time call 911
How to differentiate bell’s palsy and stroke
bell’s palsy cannot raise their eyebrows
Is bell’s palsy a lower or higher brainstem problem?
lower, idiopathic– leads to paralysis of half of the face
What fibers does a stoke affect?
with brain lesion, retain ipsilateral fibers to upper portion of the face aka the patient can raise their eyebrows
General stroke treatment
anti-platelet medication, cholesterol lowering statins and anti HTN meds
Ischemic stroke treatment if within first 4 hours
clot-dissolving medicine tissue plasminogen activator (gold standard), ASA, endovascular device to remove clot
Hemorrhage stroke treatment
endovascular procedure, surgery to secure aneurysm
If a patient presents with a homonymous visual field defect respecting the vertical midline…
think CVA or cerebral lesion and perform a cranial nerve screening
What is treatment of homonymous VF defect?
yoked prism base towards field defect
Ocular effects of HTN
second only to diabetic retinopathy in prevalence
What does the clinical presentation of ocular HTN depend on?
severity, duration and degree of control
What are retinal vascular changes?
constriction, crossing changes, micro-aneurysms, and sclerosis
What is HTN retinopathy?
hemorrhages, exudates, CWS, papilledema
What is grade 1 HTN?
minimal vessel change, arterial narrowing
What is grade 2 HTN?
sclerosis, thickened arterial wall, attenuated arteries, widened ALR, ciking/banking at AV crossings
What is grade 3 HTN?
exudates, hemes, CWS, occlusions, micro-aneurysms and macro-aneurysms
What is grade 4 HTN?
optic nerve head edema, macular edema
T/F malignant hypertensive retinopathy correlates with severe systemic disease
true, 3 year survival of grade 4 ret is approximately 6% (worse than choroidal melanoma)
T/F chronic hypertension w/ a significant elevation in diastolic pressure has been directly related to the narrowing of the caliber of the vessel
true
What causes arterial attenuation?
arteries have a large tunica media and the more stressed they are the more muscular they become, this leads to rigidity and straightness
What causes venous tortuosity?
venules have thin walls and are flimsy, increased pressure causes the venule to twist and turn
What is vasoconstriction controlled by?
autoregulation
What is the appearance of arterial attenuation?
reduced caliber of retinal arterioles, nicking/banking possible
T/F focal constrictions are most commonly seen in patients with a diastolic BP greater than 100mmHg
true, secondary to acute rise in bp
Will focal constrictions disappear with reduction in bp?
possibly, they’re due to hypertonus not atherosclerosis
What causes sclerosis?
prolonged HTN, this is irreversible damage and thickening of the arterial wall, best observed 1DD out
What is the appearance of sclerosis?
attenuation of arterioles, thickening of ALR, nicking and banking at AV crossings
What is the normal arterial to vein ratio?
2/3
What is the normal ALR?
1/3
What does compression of the retinal vein at their common sheath with arteries lead to?
BRVO
What is a micro-aneurysm?
small out-pouch of a venule wall, may be the direct result of an increase in pressure from a sclerosed arteriole
Where are micro-aneurysms located?
usually near AV crossings and often associated with CWS, best seen with IVFA
Appearance of micro-aneurysm and dot-blot hemes on IVFA?
micro-A light up while dot-blot hemes show up as darkened areas
What is exudation from?
prolonged HTN or abrupt acute episode; tight junctions are damaged and blood + hard exudates leak into retina
What is a CWS?
sign of ischemia of the NFL
What is the most common etiology of BRVO?
vascular occlusion from complication of sclerosis in HTN
What is a fusiform retinal macro-aneurysm?
spindle shaped, typically associated with exudation
What is a saccular retinal macro-aneurysm?
shaped like a small sac, more likely to result in hemorrhage
What is HTN encephalopathy?
optic nerve swelling + hemes secondary to acute spikes in bp; bilateral disc edema and venous engorgement
What is acute HTN?
rapid rise in BP leading to arteriolar constriction and damage to small vessel endothelium causing leakage of plasma protein into the posterior retina and a breakdown fo the BRB resulting in hard exudate formation
What is a macular star?
leakage of plasma into macular area in a radiating pattern, lipid exudates in the OPL
What grade is macular star?
technically grade 3
What is HTN choroidopathy?
grade 3/4; necrosis of choroidal capillaries and arterioles, elschnig spots
What are elschnig spots?
round, deep, grayish-yellow spots that become hyper-pigmented over time; RPE infarction
What are vascular sources of emboli?
cholesterol plaque at bifurcation of ECA and ICA
What are cardiac sources of emboli?
calcification of cardiac valves; chalk white, non-refractile, permanent, central artery
What are fibrin and endogenous sources of emboli?
atrial fibrillation, infectious endocarditis, acute MI
What is a hollenhorst plaque?
cholesterol, yellow-golden color, refractile, small, multiple, near arterial branches, transient
How to evaluate for Hollenhorst plaque?
bruit eval, carotid doppler and bifurcation of ICA/ECA
What is a calcific plaque?
chalky while, large, non-refractile, near ONH
How to evaluate for calcific plaque?
cardiology consult for echocardiogram to r/o valvular stenosis
What is a fibrinoplatelet?
capsule shaped, fuzzy, plug-like
What is fibrinoplatelet associated with?
auto-immune, hyper coagulable, vegetative
What is a talc emboli?
multiple tiny, glittering, grouped around macula from IV drug abuse
What is a fat emboli?
purtscher’s retinopathy, from long bone fracture, acute pancreatitis, or post-liposuction
What is a tumor emboli?
metastatic neoplasm
How to diagnose a retinal emboli?
ophthalmoscopy, carotid auscultation
How to treat a retinal emboli?
ocular digital massage, aspirin therapy, breathe into paper bag, paracentesis
Why do you breathe into a paper bag with a retinal emboli?
increased CO2 dilates retinal vasculature
How to perform a carotid auscultation?
palpate carotid pulse at carotid triangle and listen with bell at carotid triangle
Bruit sounds at <50, 50-90 and >90?
<50% stenosis = no sound; 50-90% swishing sound; >90% no heart beat sound
When do you perform a carotid endarterectomy?
if >70% stenosed and symptomatic
