Flashcards in cards test 1 Deck (191):
major risk factors for HTN
chronic kidney disease
is the majority of HTN essential or secondary?
essential (90% of cases)
common causes of secondary HTN
chronic kidney disease, renovascular disease, Rx drugs, street drugs
is the sphygmomanometry a direct or indirect BP measurement?
formula for BP
BP= CO x TPR (total peripheral resistance)
peripheral resistance is dependent on what factors?
cardiac output is dependent on what?
stroke volume and heart rate
what does Angiotension II do?
acts directly on the kidneys to retain salt and water
increases aldosterone release from the adrenals to further increase salt and water reabsorption
SBP > 140 mmHg and/or
DBP >90 mmHg
based on the average of two or more properly measured, seated BP readings on each of two or more office visits
JNC 8 recommendations
60 or older 18 with CKD or diabetes
equipment regularly inspected and validated
operator should be trained and regularly retrained
patient must be properly prepared and seated quietly for at least 5 minutes in a chair
auscultatory method should be used
caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP measurement
appropriately sized cuff should be used
how to measure BP cuff
inflatable bladder = 80% around circumference of the arm
width = should cover roughly 40%
which drugs should you treat stage 1 hypertension without compelling indication?
thiazide-type diuretics. may consider ACEI, ARB, BB (usually more for compelling), CCB, or combination
t or f: prehypertension is not a disease category, rather a designation for individuals at high risk of developing HTN
not candidates for drug therapy but should be advised to practice lifestyle modification
those with pre-htn, who also have diabetes or kidney disease, drug therapy is indicated if a trial of lifestyle modification fails to reduce their BP to 130/80 mmHg or less
when is systolic BP a more important cardiovascular risk factor?
after age 50
when is diastolic BP an important cardiovascular risk factor?
before age 50
target organs affected by prolonged uncontrolled HTN
CVS (heart and blood vessels)
effects of prolonged HTN on CVS
ventricular hypertrophy, dysfunction and failure
CAD, Acute MI
arterial aneurysm, dissection, and rupture
effects of prolonged HTN on kidneys
glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease
ischemic kidney disease especially when renal artery stenosis is the cause of HTN
effects of prolonged HTN on nervous system
stroke, intracerebral, and subarachnoid hemorrhage
cerebral atrophy and dementia
effects of prolonged HTN on the eyes
retinopathy, retinal hemorrhages and impaired vision
vitreous hemorrhage, retinal detachment
neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction
*if dx with HTN, should always have eye exam right away
stages of HTN eye manifestations
I - arteriolar narrowing
II - AV nicking
III - hemorrhages, cotton wool spots and exudates
IV - papilledema - HTN emergency, usually associated with headach
cardiovascular risk factors
obesity (BMI > or equal to 30)
microalbuminuria or estimated GFR
identifiable causes of HTN
drug-induced or related causes
chronic steroid therapy and cushings syndrome
coarcation of the aorta
thyroid of parathyroid disease
T or F : beta blockers aggravate claudication and PVD
what does the JNC-8 recommend for patients over the age of 18 with CKD for medications?
ACEI or ARB to improve kidney outcomes. this applies to all CKD patients with hypertension regardless of race of diabetes status
if goal BP is not reached within a month of treatment, what does the JNC-8 recommend doing?
increase the dose of the initial drug or add a second drug from one of the classes in recommendation 6 (thiazine-type diuretic, CCB, ACEI, or ARB) if goal BP cannot be reached within 2 drugs, add and titrate a 3rd drug from the list
should you use ACEI and ARBs together in same patient?
follow up recommendations for different BP stages
normal - recheck in 2 years
pre-HTN- recheck in 1 year
HTN stage 1- comfirm within 2 months
stage 2 HTN- evaluate or refer to source of care within 1 month.
recommended salt intake/day
dietary approach to stop hypertension clinical trial
diet rich in fruits, vegetables, and low fat diary foods
clues that HTN is secondary
resistant to treatment or severe
young non obese patient
onset before puberty
acute rise when previously stable with or without treatment
common causes of secondary HTN
intrinsic renal disease
sleep breathing disorder
uncommon causes of secondary HTN
co-arcation of aorta
features indicative of secondary HTN
variable pressure with tachycardia, sweating, tremor
family history of renal disease
most common cause of secondary HTN?
chronic renal disease - activation of RAAS and SNS
unexplained hypokalemia is indicative of what?
what is pheochromocytoma?
A pheochromocytomais a rare, usually noncancerous (benign) tumor that develops in cells in the center of an adrenal gland. You have two adrenal glands, one above each kidney. Your adrenal glands produce hormones that give instructions to virtually every organ and tissue in your body.
If you have a pheochromocytoma, an adrenal gland releases hormones that cause persistent or episodic high blood pressure
if epinephrine: systolic HTN, tachycardia, sweating, flushing, apprehension
if norepinephrine: systolic and diastolic HTN from peripheral vasoconstriction. less tachycardia, palpitations, anxiety
who should pheochromocytoma be suspected in?
patients with labile HTN and/or paroxysms of HTN or orthostatic hypotension
headache, palpitations, pallor and perspiration
how do you diagnose pheochromocytoma?
laboratory confirmation done by plasma free metanephrine essay. tumor localized by CT or MRI
weak femoral pulses and inconsistant BPS in upper and lower BP in a child is indicative of what?
coarctation of the aorta- dx by echo, surgical repair
difference between hypertensive urgencies and emergencies
urgencies - no progressive target-organ dysfunction...no longer considered a term according to JNC-8- can be managed outpatient with oral meds
emergencies - progressive end-organ dysfunction (malignant HTN)
hypertensive emergencies require what?
hospitalization and parenteral medication
hypertensive emergencies present like what?
CNS- encephalopathy, intracranial hemorrhage, AMS
Kidneys - acute kidney injury, microscopic hematuria, rise in serum creatinine
vasculature - dissection or clot
heart - CHF, angina, MI
**pulmonary edema, hypertensive encephalopathy, CHF**
who is more likely to have a HTN emergency?
elderly, African Americans, men (2 x more than women)
BP for hypertensive emergencies
>180/120 with progressive target organ dysfunction
examples of HTN emergences
severely elevated BP with:
hypertensive encephalopathy (confused and combative)
acute left ventricular failure with pulmonary edema
acute MI or unstable angina pectoris
dissecting aortic aneurysm
what is the hallmark pathology of malignant hypertension?
fibrinoid necrosis of the arterioles occurring mostly in the kidneys
may include hemolytic anemia from the destruction of RBCs as they travel through small vessels occluded with fibrin
what is hypertensive encephalopathy
initially constricted vessels become stretched and dilated when mean arterial pressures reach 180 mm Hg
hyperperfusion of brain with high pressure
cerebral edema: encephalopathy
may occur at lower BPs with eclampsia and acute glomerulonephritis
what is unique about malignant HTN?
always accompanied by ocular changes - papilledema, flame hemorrhages. other presentations include encephalopathy and impaired renal function
other causes may be secondary HTN, acute thyroid disease, cocaine or amphetamine abuse, head injury
malignant HTN treatment?
admit (usually ICU)
reduce mean arterial BP by no more than 25% within minutes to 1 hour
if pt is stable, reduce the BP to 160/100-110 within the next 2-6 hours
avoid using short-acting nifedipine in initial treatment bc risk of rapid, unpredictable hypotension
once stabilized, the pt's BP may be gradually reduced over the next 24-48 hours
treatment for HTN with associated CVA
avoid abrupt falls in pressure
ischemic stroke - 10-15% decrease if systolic levels are above 220 mm Hg
hemorrhagic stroke - no lower than 180 mm Hg stystolic
drug treatment for HTN urgency
can use oral agents in most cases
drug of choice for HTN emergency
sodium nitroprusside (duration is 1-2 min, immediate onset)
hydralazine : onset 10-20 min, duration 60-240 min - be careful if pt is on beta blockers though bc can make heart block worse
drug of choice for stage 1 hypertension with no compelling indications
ACE inhibitor, ARB, CCB, or combination
drug of choice for stage 2 hypertension with no compelling indications
two drug combination for most. usually thiazide-type diuretic with an ACE inhibitor, or ARB, or CCB
what is preeclampsia and what is the treatment?
BP >140/90 after 20 weeks gestation with proteinuria
treatment: restricted activity, bed rest, close monitoring beneficical
methyldopa is drug of choice
***cannot be on ACE inhibitors or ARBs if pregnant - fetal toxicity, death
how do diuretics work?
exact hypotensive mechanism unknown
initial BP drop caused by diuresis - reduced plasma and stroke volume decreases CO and BP. causes compensatory increase in peripheral vascular resistance
extracellular and plasma volume return to near pretreatment levels with chronic use ->peripheral vascular resistance becomes lower than pretreatment values, which results in chronic antihypertensive effects
where do thiazide diuretics work?
on distal convulated tubule and inhibit Na+ - Cl- symport
particularly useful for elderly patients but not effective when kidney function is inadequate
what is the renin-angiotensin system (RAAS) important for?
regulating blood volume, arterial pressure, and cardiac and vascular function
most important site for renin release?
where is angiotensinogen released from?
mainly the liver
where is ACE released from?
vascular endothelium, particularly in the lungs - this enzyme helps forms angiotensin II
what does angiotensin II do?
constricts vessels thereby increasing vascular resistance and arterial pressure
stimulates the adrenal cortex to release aldosterone, which acts upon the kidneys to increase sodium and fluid retention
stimulates the release of vasopressin (ADH) from pituitary
stimulates cardiac and vascular hypertrophy
ARBs block angiotensin II receptors**
what do ACE inhibitors do?
block angiotensin I to angiotensin II conversion
2nd line to diuretics
can give patients cough
block bradykinin degradation; stimulate vasodilating substances such as protaglandin E and prostacyclin
what do you do after you prescribe ACE inhibitor to pt?
monitor serum K and SCr within 4 weeks of initiation or dose increase
side effects; hyperkalemia, acute renal failure
what are ARBs?
Angiotensin II Receptor Blockers
inhibit angiotensin II from all pathways - directly block angiotensin II type 1 receptor (ACE inhibitors partially block effects of angiotensin II)
do ARBs block bradykinin breakdown?
no - so less cough than ACE inhibitors
side effects of ARBs
who should not take ACE inhibitors and ARBs?
people with severe bilateral renal artery stenosis - can cause acute kidney failure
what do renin inhibitors do?
inhibits angiotensinogen to angiotensin I conversion
does not block bradykinin breakdown
adverse effects: orthostatic hypotension
what do B-blockers do?
inhibit renin release - weak association with antihypertensive effect
negative chronotropic and inotropic cardiac effects reduce CO
B-blockers with intrinsic sympathomimetic activity (ISA) do not reduce CO, lower BP, decrease peripheral resistance
adverse effects of B-blockers
atrioventricular conduction abnormalities
abrupt discontinuation may cause rebound hypertension or unstable angina
bronchospastic pulmonary disease exacerbation - COPD contraindicator
may aggravate intermittent claudication, Raynaud's phenomenon
cardioselective B-blockers have a greater affinity for what receptors?
Beta- 1 - so safer in patients with bronchospastic disease, peripheral arterial disease, diabetes
cardioselective beta blockers
what do nonselective beta-blockers do and who should they not be used for?
inhibit B1 and B2 receptors at all doses, but can exacerbate bronchospastic disease
additional benefits: essential tremor, migraine headache, thyrotoxicosis
what do CCBs do?
inhibit influx of Ca across cardiac and smooth muscles cell membranes. - muscle contraction requires increased free intrcellular Ca concentration and CCBs block high-voltage Ca channels resulting in coronary and peripheral vasodilation
dihydropyridines (almodipine) and non-dihydropyridines are different pharmacologically but similar antihypertensive efficacy
what should alpha-blockers be used for?
not appropriate monotherapy for HTN
used with diuretics to minimize edema - use caution with elderly patients
inhibit smooth muscle catecholamine uptake in peripheral vasculature: vasodilation and BP lowering
what do central alpha2 agonists do?
stimulate a2-adrenergic receptors in the brain
reduce sympathetic outflow from the brains vasomotor center - increases vagal tone
decrease HR, CO, TPR, plasma renin activity, baroreceptor activity
adverse effects of central a2-agonists
abrupt discontinuation may cause rebound HTN
clonodine: anticholinergic side effects - cheap and potent and can get in a patch but if you stop will go into HTN emergency
when are central alpha2-agonists most effective?
if used with a diuretic - minimizes fluid retention
what do direct arterial vasodilators do?
direct arterial smooth muscle relaxation causes antihypertensive effect (little or no venous vasodilation)
use with diuretic (preferable thiazide) and beta blocker to reduce fluid retention and reflex tachycardia
in which patients is orthostatic hypotension more prevalent?
adverse effects of direct arterial vasodilators
hydralazine can cause lupus-like syndrome
minoxidil can cause hypertrichosis
failure to achieve BP goal on full doses of 3 drug regimen including diuretic is what?
to control BP, what should almost every patient be on?
a thiazide diuretic unless contraindicated
most patients require 2 or more agents to control BP
where is the most common aneurysm location?
infrarenal abdominal aorta
who is more likely to have a TAA?
men, and those with lung disease
where is the most common location for a TAA?
pathophysiology of TAA
degeneration of elastic layers within the media (collagen and elastin)
cystic medial degradation and smooth muscle cell necrosis
which ultimately leads to weakening
signs and symptoms of TAA
most are asymptomatic - many diagnosed incidentally after routine chest film
common signs and symptoms:
-substernal chest pain (most common)
-upper back, jaw, or neck pain
-local mass effect (ie cmpression of adjacent mediastinal structures) - coughing, wheezing, dyspnea, hoarseness
-superior vena cava (SVC) syndrom
-aortic regurgitation or insufficiency
imaging if you suspect a TAA
CT of chest with or without contrast (depending on kidney function) is standard- repeat every 6-12 months to monitor aneurysm expansion
chest x-ray - will see **** silhouettte enlargement of the aortic knob, or displacement of the trachea from midline
Transthoracic echocardiogram - good for patients with marfan's who are at risk for TAA
treatment for TAA
depends on location, size and symptoms
Ascending TAA >5.5 cm should be surgically repaired
Descending TAA>6.5 should be surgically repaired
Asymptomatic patients less than 5.5 cm - serial CT imaging, control HTN and other conditions, STOP SMOKING
other considerations for TAAs
rapid expansion (growth >1 cm/yr)
aneurysm size in relation to body surface area (women more at risk for rupture if they are smaller)
patients with other risk factors (Marfan's, mycotic, etc)
what is used to surgically repair TAA?
endoluminal stent (endo stent)
focal dilation in an artery with at least 50% increase over its normal diameter
normal abdominal aorta size
difference between fusiform and saccular aneurysm
fusiform - there is symmetrical dilation of the aorta
saccular - when the dilation involves mainly one wall
when the aorta is enlarged as a consequence of dilation of only the outer layers of the vessel wall, such as occurs with an contained rupture of the aortic wall
false aneurysm or pseudoaneurysm
who is most likely to get a AAA?
elderly, white males
90% of AAA's are where?
infrarenal (below renal arteries)
do genetics play a role in AAA?
yes, 15-25% of first degree relatives of patients with AAA's affected - relatives need to get ultrasound
signs and symptoms of AAA
most are asymptomatic
"pulatile mass" in abdomen
classic triad for diagnosis of AAA rupture
acute onset abdominal, flank, or back pain
"pulsatile abdominal mass"
who should be screened for AAA?
all males over age 65 with hx of smoking should be screened with ultrasound. begin screening at age 50 with other risk factors
what is the workup for AAA?
CT scan***: almost 100% sensitivity
- defines aortic size, length, involvement of other arteries, visualization of retroperitoneum
-use only if pt is considered relatively stable
disadvantages: cost, longer study time, radiation and contrast exposure
ultrasound :sensitive and specific
what is the treatment for AAA?
depends on size, symptoms and location
AAA> 5.5 cm should be surgically repaired
AAAs 4.5-5.4 should be monitored every 6 months - should be referred to a vascular surgeon at this time
AAAs 3.0-4.4 should be monitored yearly (ultrasound)
separation of the layers within the aortic wall is what?
which type of dissection require emergent or urgent surgery?
Standford type A (2/3)
standford type B can be medically managed
classic presentation of aortic dissection
sudden onset, severe chest pain
described as "tearing" or "ripping" quality
pt presents with "tearing" or "ripping" in anterior chest area, where is the aortic dissection likely?
aortic arch or aortic root dissection
pt presents with neck or jaw pain, where is the aortic dissection likely?
aortic arch and extension into the great vessels
pt presents with tearing/ripping intrascapular pain. where is the aortic dissection likely?
physical exam findings in aortic dissection
hypertension (70%), interarm blood pressure differential
imaging to diagnose aortic dissection
chest x-ray - abnormal aortic contour/knob or widened mediastinum
TEE: most useful in ascending aortic dissections. high sensitivity and specificity
CT chest with contrast: most definitive test for suspicion of aortic dissection - use in a hemodynamically stable pt
MRI- most sensitive
what labs should you order for an aortic dissection?
WBC : to determine infectious process
Hgb/Hct: in case of leak or rupture
BUN/Creat: renal involvement
CK-MB/troponins: myocardial ischemia, coronary artery involvement
LDH : hemolysis in the false lumen
chronic inflammatory disease of unknown cause, which involves the aorta and its branches, and causes areas of arterial stenosis and aneurysms. more common in women, mean onset is 29 years old
signs and symptoms of takayasu arteritis
symptoms of inflammatory process - fever, night sweats, arthalgias, weight loss
loss of upper extremities pulses - "pulseless" disease
pain in upper extremities
what is the diagnostic evaluation for tikayasu arteritis?
Elevated ESR, elevated C-reactive protein, mild leukocytosis, mild anemia
chest x-ray - rim of calcification around involved vessels
what is the treatment of takayasu arteritis?
high dose corticosteroids
balloon angioplasty of stenotic lesions
very good prognosis
this disease typically affects medium-sized arteries, and the temporal artery is commonly involved. mean age of 67 years old. diagnosis is usually done by temporal artery biopsy
giant cell arteritis
treatment for giant cell arteritis
high-dose corticosteroid therapy
what is PVD?
arterial narrowing or occlusion caused by the accumulation of atherosclerotic plaque elements in the vessel wall. result of atherosclerosis.
PVD is commonly associated with what?
3-10 fold increase risk of MI or death. often co0exists with CAD, afib, TIA, stroke, and renal disease
what are the clinical presentations of PVD?
claudication of the thigh, hip or buttock occurs with disease where?
aorta or illiac arteries
calf claudication comes from stenosis of what arteries?
popliteal and femoral
pedal claudication comes from stenosis of what arteries?
tibial and peroneal artery
what is intermittent claudication?
- used to be able to walk 2 blocks to store and now has to stop after one block until pain goes away
blood supply does not meet demand of muscle
discomfort, pain, fatigue, or heaviness that is felt in an extremity during walking and resolves within a few minutes of resting
this occurs when the blood supply does not adequately meet the basic nutritional requirements of the tissues of the affected extremity, typically occurs i ntoes or foot, initially pain is WORSE AT NIGHT, with legs in neutral position and sitting up and dangling the leg alleviates the discomfort
what are physical exam findings of rest pain?
skin breakdown, ulceration, necrosis and gangrene
what will a venous ulcer look like?
painless or painful
what will an arterial ulcer look like?
what is a normal peripheral pulse exam?
2+ easily palpabler
non-invasive diagnosis of PAD
ABI (ankle/brachial index) - should be 1:1
carotid doppler identifies patients who are at risk for stroke
what are the invasive ways to diagnose PAD?
CT angiogram - send to vascular so not getting double bolus
what is ABI?
simple, reliable means for diagnosis PVD. blood pressure measurements are taken at the arms and ankles using a doppler.
gold standard for evaluation of PVD
what are the risks of getting an angiogram?
renal failure, bleeding, limb loss, arterial embolism or thrombosis, false aneurysms, stroke
what is the preferred treatment in amenable vascular lesions?
percutaneous transluminal angioplasty (PTCA)
- lower peri-procedural mortality and morbidity.
-more cost effective than surgery
PTCAs have best outcomes with what vascular lesions?
pharmacological uses in PVD
cilostazol (pletal) - phosophodiesterase inhibitor and vasodilator increases distance to claudication - has vasodilatory and platelet inhibitory properties
antiplately therapy - aspirin or plavix (used only after intervention)
where do the majority of arterial embolisms come from?
heart (90%) - atrial fibrillation, valvular heart disease, etc
where do most arterial emboli end up?
what is arterial thrombosis
occurs in atherosclerotic vessels. propagates up or down the artery. occasionally rupture of arteriosclerotic plaque. inflammation of the arterial wall may lead to thrombosis. secondary to hypotension or cardiac failure
how would you determine if a pt had a thrombosis or an embolus?
thrombosis - evidence of occlusive arterial disease in other areas. contralateral pulses absent. evidence of bilateral disease, history of intermittent claudication and or PVD. history of cancer/hypercoaguable disorder
embolus - history of afib, valvular disorder, IV drug use, rheumatic fever, endocarditis. sudden onset, normal contralateral pulses
how do you treat arterial embolism if neurological or motor involvement is present?
emergent surgery - immediate embolectomy
how do you treat arterial embolism if no neurological or motor involvement is present?
consider tPA or IV anticoagulation (heparin drip)
what should you be concerned about when treating a patient who has arterial embolism?
them developing compartment syndrome (reperfusion injury) post-op - pressure too high so muscles die off. may lead to gangrene and ultimately amputation, so continue to monitor closely
most common type of syncope?
vasovagal- sympathetic inhibition and parasympathetic activation
carotid sinus syndrome- at bifurcation, external pressure on the external body can make you pass out
second most common type of syncope?
what is cardiac syncope?
often with palpitations preceding, abrupt, often exertional
hypertrophic cardiomyopathy - left ventricle becomes hypertrophic. in younger people. wall abnormally thick, doesn’t contract well. low cardiac output, so pass out when working out
fluttering, pounding, rapid heartbeat in neck or chest. can also have breathlessness
when are palpitations more serious?
if accompanied by pre-syncope or syncope, or dizziness - this suggests a tachyarrhythmia
sudden breathlessness or single "pounding"sensation may indicate what?
what should you do for a palpitation workup?
stress test if associated with exercise
holter or event monitor
what can cause sinus bradycardia?
excessive vagal stimulation (valsalva, vomiting, cold water)
hypoxia, MI, meds (beta blockers), athletic heart, OSA
treatment for sinus bradycardia
none unless symptomatic, treat the cause. if acutely symptomatic (MI, ischemia) consider atropine acutely and a pacer long-term
two drugs for bradycardia
atropine- inhibits action of Ach on autonomics - antimuscarinic
epinephrine - positive inotropic effect on heart, increases HR and contractility, CO. acts below AV node
what will show up on an EKG with a bundle branch block?
wide QRS, because conduction is slow
which leads do you assess for bundle branch block?
precordial - v1-v6
what usually causes RBBB?
CAD, conduction system lesion, R ventricle disease
usually no symptoms - treat the cause
what is worse, LBBB or RBBB?
LBBB - should be treated as an MI, as they may mask EKG findings of MI
what shows up on the EKG for an AV block?
prolonged PR interval - due to ischemic or supressed AV node (most common site of block)
treatment for first degree AV block?
EKG findings of second degree type I AV block/wenckebach
Normal P waves, PR interval progressively elongates until a QRS is dropped
treatment of wenckebach
rate usually slow, if symptoms of decreased CO are present emergently atropine and pacer long term. no treatment if asymptomatic
where do tachyarrhythmias arise from?
atria, AV node, or from ventricle
causes of sinus tachycardia
stress, meds, fever, hypoxia, hyperthyroidism, etc
what do B-blockers do?
Reduce heart rate and contractility, reduce cardiac output, reduce renin release, depress SA and AV node function
uncommon, most associated with underlying heart disease (CAD, PE, valvular disease)
EKG atrial flutter
atrial rate 250-350
no P waves present, saw tooth flutter wave present and narrow QRS
how do you treat atrial flutter?
rate control - Ca channel blocker, b-blocker
rhythm control - radiofrequency ablation
clot prevention - those with sustained a flutter should be treated like those with pure a fib and anticoagulated with warfarin
what is the most common arrhythmia generating from the atria?
pathophys of afib
Multiple reentrant circuits prevent synchronous atrial contraction
chaotic rhythm in the atria not controlled by the SA node, atria cannot contract to fully empty due to the high rate of impulse
causes of afib
HTN, CHD, MI, valvular disease
*not associated with caffeine intake
*not common in children
different classes of afib
paroxysmal - recurrent, >2 episodes, self terminates in less than 7 days
persistent - fails to self terminate in 7 days
long standing persistent > than 1 year
permanent -- persistent a fib in which a rhythm control strategy is no longer being pursued
what is "lone" afib?
in those less than 60 w/out structural heart disease
male predominance, associated with "triggers"
least risk for complications
important questions for afib
Duration and frequency of symptoms
Precipitating factors: exertion, sleep, caffeine
Termination of symptoms: vagal maneuvers, rest
Antiarrhythmics and rate-controlling meds?
Underlying heart disease?
atrial rate usually between 400-650
p wave not present, wavy baseline is seen instead
normal or narrow QRS
Further workup for Afib
TTE - evaluate atrial volume, function and presence of thrombi
stress test - eval for CAD
labs - TSH, BUN, CRT, glucose
what is usually first choice, rate or rhythm control?
rate - antiarrythmics have many side effects and rhythm control does not reduce embolic risk
When to (carefully) choose rhythm control
Younger patients who are active to increase exercise tolerance
Failure of rate control
Continued symptoms despite rate control
Patients early in their history of a fib
what is DC cardioversion?
direct current discharged in synch with the R wave, depolarizes most cardiac cells and allows SA node to resume pacing
what are indications for urgen cardioversion?
pre excitation syndroms
what should you do for non urgent cardioversion?
antigoagulate prior to procedure- one month pre and post
control rate prior to procedure
antiarrhythmic prior to procedure
what are rhythm control drugs?
amiodarone - appears to be most effective but does have side effects (thyroid disease, arrythmias, cataracts, pulmonary disease)
-lower rates due to beta and calcium and channel blocking properties of the drug
Score of 0- no anticoagulation (no proven benefit from ASA)
Score of 1- anticoagulant or ASA (anticoagulation more effective)
Score of 2 or more- oral anticoagulation
most effective oral anticoagulation
warfarin (pradxa and xarelto not usually covered under insurance)