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cards test 1 Flashcards

1
Q

major risk factors for HTN

A

stroke
MI
vascular disease
chronic kidney disease

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2
Q

is the majority of HTN essential or secondary?

A

essential (90% of cases)

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3
Q

common causes of secondary HTN

A

chronic kidney disease, renovascular disease, Rx drugs, street drugs

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4
Q

is the sphygmomanometry a direct or indirect BP measurement?

A

indirect

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5
Q

formula for BP

A

BP= CO x TPR (total peripheral resistance)

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6
Q

peripheral resistance is dependent on what factors?

A

vascular structure

vascular function

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7
Q

cardiac output is dependent on what?

A

stroke volume and heart rate

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8
Q

what does Angiotension II do?

A

acts directly on the kidneys to retain salt and water

increases aldosterone release from the adrenals to further increase salt and water reabsorption

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9
Q

HTN definition

A

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

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10
Q

JNC 8 recommendations

A

60 or older 18 with CKD or diabetes

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11
Q

accurate BP

A

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

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12
Q

how to measure BP cuff

A

inflatable bladder = 80% around circumference of the arm

width = should cover roughly 40%

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13
Q

which drugs should you treat stage 1 hypertension without compelling indication?

A

thiazide-type diuretics. may consider ACEI, ARB, BB (usually more for compelling), CCB, or combination

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14
Q

t or f: prehypertension is not a disease category, rather a designation for individuals at high risk of developing HTN

A

true

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15
Q

pre-htn treatment

A

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

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16
Q

when is systolic BP a more important cardiovascular risk factor?

A

after age 50

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17
Q

when is diastolic BP an important cardiovascular risk factor?

A

before age 50

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18
Q

target organs affected by prolonged uncontrolled HTN

A

CVS (heart and blood vessels)
kidneys
nervous system
eyes

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19
Q

effects of prolonged HTN on CVS

A

ventricular hypertrophy, dysfunction and failure

arrhythmias

CAD, Acute MI

arterial aneurysm, dissection, and rupture

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20
Q

effects of prolonged HTN on kidneys

A

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

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21
Q

effects of prolonged HTN on nervous system

A

stroke, intracerebral, and subarachnoid hemorrhage

cerebral atrophy and dementia

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22
Q

effects of prolonged HTN on the eyes

A

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

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23
Q

stages of HTN eye manifestations

A

I - arteriolar narrowing
II - AV nicking
III - hemorrhages, cotton wool spots and exudates
IV - papilledema - HTN emergency, usually associated with headach

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24
Q

cardiovascular risk factors

A 
hypertension
cigarette smoking
obesity (BMI > or equal to 30)
physical inactivity
dyslipidemia
DM
microalbuminuria or estimated GFR
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25
Q

identifiable causes of HTN

A 
sleep apnea
drug-induced or related causes
CKD
primary aldosteronism
renovascular disease
chronic steroid therapy and cushings syndrome
pheochromocytoma
coarcation of the aorta
thyroid of parathyroid disease
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26
Q

T or F : beta blockers aggravate claudication and PVD

A

true

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27
Q

what does the JNC-8 recommend for patients over the age of 18 with CKD for medications?

A

ACEI or ARB to improve kidney outcomes. this applies to all CKD patients with hypertension regardless of race of diabetes status

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28
Q

if goal BP is not reached within a month of treatment, what does the JNC-8 recommend doing?

A

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

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29
Q

should you use ACEI and ARBs together in same patient?

A

no

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30
Q

follow up recommendations for different BP stages

A

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.

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31
Q

recommended salt intake/day

A

2400 mg/day

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32
Q

DASH diet

A

dietary approach to stop hypertension clinical trial

diet rich in fruits, vegetables, and low fat diary foods

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33
Q

clues that HTN is secondary

A

resistant to treatment or severe
young non obese patient
onset before puberty
acute rise when previously stable with or without treatment

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34
Q

common causes of secondary HTN

A

intrinsic renal disease
renovascular disease
mineralocorticoid excess
sleep breathing disorder

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35
Q

uncommon causes of secondary HTN

A

pheochromocytoma
glucocorticoid excess
co-arcation of aorta
hyper/hypothyroidism

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36
Q

features indicative of secondary HTN

A

unprovoked hypokalemia
abdominal bruit
variable pressure with tachycardia, sweating, tremor
family history of renal disease

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37
Q

most common cause of secondary HTN?

A

chronic renal disease - activation of RAAS and SNS

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38
Q

unexplained hypokalemia is indicative of what?

A

hyperaldosteronism

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39
Q

what is pheochromocytoma?

A

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

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40
Q

who should pheochromocytoma be suspected in?

A

patients with labile HTN and/or paroxysms of HTN or orthostatic hypotension

headache, palpitations, pallor and perspiration

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41
Q

how do you diagnose pheochromocytoma?

A

laboratory confirmation done by plasma free metanephrine essay. tumor localized by CT or MRI

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42
Q

weak femoral pulses and inconsistant BPS in upper and lower BP in a child is indicative of what?

A

coarctation of the aorta- dx by echo, surgical repair

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43
Q

difference between hypertensive urgencies and emergencies

A

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)

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44
Q

hypertensive emergencies require what?

A

hospitalization and parenteral medication

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45
Q

hypertensive emergencies present like what?

A

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

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46
Q

who is more likely to have a HTN emergency?

A

elderly, African Americans, men (2 x more than women)

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47
Q

BP for hypertensive emergencies

A

> 180/120 with progressive target organ dysfunction

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48
Q

examples of HTN emergences

A

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

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49
Q

what is the hallmark pathology of malignant hypertension?

A

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

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50
Q

what is hypertensive encephalopathy

A

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

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51
Q

what is unique about malignant HTN?

A

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

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52
Q

malignant HTN treatment?

A

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

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53
Q

treatment for HTN with associated CVA

A

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

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54
Q

drug treatment for HTN urgency

A 
captopril
clonidine
furosemide
labetalol
nifedipine
propranolol/metoprolol

can use oral agents in most cases

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55
Q

drug of choice for HTN emergency

A

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

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56
Q

drug of choice for stage 1 hypertension with no compelling indications

A

thiazide-type diuretics

ACE inhibitor, ARB, CCB, or combination

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57
Q

drug of choice for stage 2 hypertension with no compelling indications

A

two drug combination for most. usually thiazide-type diuretic with an ACE inhibitor, or ARB, or CCB

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58
Q

what is preeclampsia and what is the treatment?

A

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

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59
Q

how do diuretics work?

A

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

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60
Q

where do thiazide diuretics work?

A

on distal convulated tubule and inhibit Na+ - Cl- symport

particularly useful for elderly patients but not effective when kidney function is inadequate

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61
Q

what is the renin-angiotensin system (RAAS) important for?

A

regulating blood volume, arterial pressure, and cardiac and vascular function

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62
Q

most important site for renin release?

A

kidney

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63
Q

where is angiotensinogen released from?

A

mainly the liver

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64
Q

where is ACE released from?

A

vascular endothelium, particularly in the lungs - this enzyme helps forms angiotensin II

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65
Q

what does angiotensin II do?

A

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**

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66
Q

what do ACE inhibitors do?

A

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

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67
Q

what do you do after you prescribe ACE inhibitor to pt?

A

monitor serum K and SCr within 4 weeks of initiation or dose increase

side effects; hyperkalemia, acute renal failure

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68
Q

what are ARBs?

A

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)

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69
Q

do ARBs block bradykinin breakdown?

A

no - so less cough than ACE inhibitors

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70
Q

side effects of ARBs

A

orthostatic hypotension
renal insufficiency
hyperkalemia

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71
Q

who should not take ACE inhibitors and ARBs?

A

pregnant women

people with severe bilateral renal artery stenosis - can cause acute kidney failure

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72
Q

what do renin inhibitors do?

A

inhibits angiotensinogen to angiotensin I conversion

does not block bradykinin breakdown

adverse effects: orthostatic hypotension

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73
Q

what do B-blockers do?

A

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

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74
Q

adverse effects of B-blockers

A

bradycardia

atrioventricular conduction abnormalities
acute HF

abrupt discontinuation may cause rebound hypertension or unstable angina

bronchospastic pulmonary disease exacerbation - COPD contraindicator

may aggravate intermittent claudication, Raynaud’s phenomenon

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75
Q

cardioselective B-blockers have a greater affinity for what receptors?

A

Beta- 1 - so safer in patients with bronchospastic disease, peripheral arterial disease, diabetes

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76
Q

cardioselective beta blockers

A 
atenolol
betaxolol
bisoprolol
metroprolol
nebivolol
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77
Q

what do nonselective beta-blockers do and who should they not be used for?

A

inhibit B1 and B2 receptors at all doses, but can exacerbate bronchospastic disease

additional benefits: essential tremor, migraine headache, thyrotoxicosis

78
Q

what do CCBs do?

A

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

79
Q

what should alpha-blockers be used for?

A

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

80
Q

what do central alpha2 agonists do?

A

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

81
Q

adverse effects of central a2-agonists

A

sodium/water retention

abrupt discontinuation may cause rebound HTN

depression

orthostatic hypotension

dizziness

clonodine: anticholinergic side effects - cheap and potent and can get in a patch but if you stop will go into HTN emergency

82
Q

when are central alpha2-agonists most effective?

A

if used with a diuretic - minimizes fluid retention

83
Q

what do direct arterial vasodilators do?

A

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

hydralazine andminoxidil

84
Q

in which patients is orthostatic hypotension more prevalent?

A

diuretics
ACE inhibitors
ARBs

85
Q

adverse effects of direct arterial vasodilators

A

sodium/water retention
angina
hydralazine can cause lupus-like syndrome
minoxidil can cause hypertrichosis

86
Q

failure to achieve BP goal on full doses of 3 drug regimen including diuretic is what?

A

resistant hypertension

87
Q

to control BP, what should almost every patient be on?

A

a thiazide diuretic unless contraindicated

most patients require 2 or more agents to control BP

88
Q

where is the most common aneurysm location?

A

infrarenal abdominal aorta

89
Q

who is more likely to have a TAA?

A

men, and those with lung disease

90
Q

where is the most common location for a TAA?

A

ascending aorta

91
Q

pathophysiology of TAA

A

degeneration of elastic layers within the media (collagen and elastin)

cystic medial degradation and smooth muscle cell necrosis

which ultimately leads to weakening

92
Q

signs and symptoms of TAA

A

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
93
Q

imaging if you suspect a TAA

A

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

94
Q

treatment for TAA

A

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

95
Q

other considerations for TAAs

A

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)

96
Q

what is used to surgically repair TAA?

A

endoluminal stent (endo stent)

97
Q

AAA definition

A

focal dilation in an artery with at least 50% increase over its normal diameter

98
Q

normal abdominal aorta size

A

2-3 cm

99
Q

difference between fusiform and saccular aneurysm

A

fusiform - there is symmetrical dilation of the aorta

saccular - when the dilation involves mainly one wall

100
Q

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

A

false aneurysm or pseudoaneurysm

101
Q

who is most likely to get a AAA?

A

elderly, white males

102
Q

90% of AAA’s are where?

A

infrarenal (below renal arteries)

103
Q

do genetics play a role in AAA?

A

yes, 15-25% of first degree relatives of patients with AAA’s affected - relatives need to get ultrasound

104
Q

signs and symptoms of AAA

A

most are asymptomatic

“pulatile mass” in abdomen

back/abdominal/flank pain

nausea/vomiting

urinary symptoms

venous thrombosis

105
Q

classic triad for diagnosis of AAA rupture

A

acute onset abdominal, flank, or back pain
“pulsatile abdominal mass”
hypotension/tachycardia/shock

106
Q

who should be screened for AAA?

A

all males over age 65 with hx of smoking should be screened with ultrasound. begin screening at age 50 with other risk factors

107
Q

what is the workup for AAA?

A

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

108
Q

what is the treatment for AAA?

A

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)

109
Q

separation of the layers within the aortic wall is what?

A

aortic dissection

110
Q

which type of dissection require emergent or urgent surgery?

A

Standford type A (2/3)

standford type B can be medically managed

111
Q

classic presentation of aortic dissection

A

sudden onset, severe chest pain

described as “tearing” or “ripping” quality

112
Q

pt presents with “tearing” or “ripping” in anterior chest area, where is the aortic dissection likely?

A

aortic arch or aortic root dissection

113
Q

pt presents with neck or jaw pain, where is the aortic dissection likely?

A

aortic arch and extension into the great vessels

114
Q

pt presents with tearing/ripping intrascapular pain. where is the aortic dissection likely?

A

descending aorta

115
Q

physical exam findings in aortic dissection

A

hypertension (70%), interarm blood pressure differential

116
Q

imaging to diagnose aortic dissection

A

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

117
Q

what labs should you order for an aortic dissection?

A 
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
118
Q

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

A

takayasu arteritis

119
Q

signs and symptoms of takayasu arteritis

A

symptoms of inflammatory process - fever, night sweats, arthalgias, weight loss

loss of upper extremities pulses - “pulseless” disease

pain in upper extremities

hypertension

HF

120
Q

what is the diagnostic evaluation for tikayasu arteritis?

A

Elevated ESR, elevated C-reactive protein, mild leukocytosis, mild anemia

chest x-ray - rim of calcification around involved vessels

narrow-wide-narrow

121
Q

what is the treatment of takayasu arteritis?

A

high dose corticosteroids

balloon angioplasty of stenotic lesions

very good prognosis

122
Q

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

A

giant cell arteritis

123
Q

treatment for giant cell arteritis

A

high-dose corticosteroid therapy

124
Q

what is PVD?

A

arterial narrowing or occlusion caused by the accumulation of atherosclerotic plaque elements in the vessel wall. result of atherosclerosis.

125
Q

PVD is commonly associated with what?

A

3-10 fold increase risk of MI or death. often co0exists with CAD, afib, TIA, stroke, and renal disease

126
Q

what are the clinical presentations of PVD?

A

intermittent claudication

rest pain

127
Q

claudication of the thigh, hip or buttock occurs with disease where?

A

aorta or illiac arteries

128
Q

calf claudication comes from stenosis of what arteries?

A

popliteal and femoral

129
Q

pedal claudication comes from stenosis of what arteries?

A

tibial and peroneal artery

130
Q

what is intermittent claudication?

A
  • 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

131
Q

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

A

rest pain

132
Q

what are physical exam findings of rest pain?

A

skin breakdown, ulceration, necrosis and gangrene

133
Q

what will a venous ulcer look like?

A 
normal pulses
woody leg
hemosiderin deposition
painless or painful
fibrinous exudate
134
Q

what will an arterial ulcer look like?

A 
decerases pulses
hairless leg
pale color
painful
necrotic base
135
Q

what is a normal peripheral pulse exam?

A

2+ easily palpabler

136
Q

non-invasive diagnosis of PAD

A

ABI (ankle/brachial index) - should be 1:1
carotid doppler identifies patients who are at risk for stroke
vascular ultrasound

137
Q

what are the invasive ways to diagnose PAD?

A

CT angiogram - send to vascular so not getting double bolus
MRA
peripheral angiograms

138
Q

what is ABI?

A

ankle-brachial index

simple, reliable means for diagnosis PVD. blood pressure measurements are taken at the arms and ankles using a doppler.

139
Q

gold standard for evaluation of PVD

A

angiogram

140
Q

what are the risks of getting an angiogram?

A

renal failure, bleeding, limb loss, arterial embolism or thrombosis, false aneurysms, stroke

141
Q

what is the preferred treatment in amenable vascular lesions?

A

percutaneous transluminal angioplasty (PTCA)

  • lower peri-procedural mortality and morbidity.
  • more cost effective than surgery
142
Q

PTCAs have best outcomes with what vascular lesions?

A

femoral

143
Q

pharmacological uses in PVD

A

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)

statin therpy

144
Q

where do the majority of arterial embolisms come from?

A

heart (90%) - atrial fibrillation, valvular heart disease, etc

145
Q

where do most arterial emboli end up?

A

femoral

146
Q

what is arterial thrombosis

A

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

147
Q

how would you determine if a pt had a thrombosis or an embolus?

A

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

148
Q

how do you treat arterial embolism if neurological or motor involvement is present?

A

emergent surgery - immediate embolectomy

149
Q

how do you treat arterial embolism if no neurological or motor involvement is present?

A

consider tPA or IV anticoagulation (heparin drip)

150
Q

what should you be concerned about when treating a patient who has arterial embolism?

A

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

151
Q

most common type of syncope?

A

neurally mediated

vasovagal- sympathetic inhibition and parasympathetic activation

postural

situational

carotid sinus syndrome- at bifurcation, external pressure on the external body can make you pass out

152
Q

second most common type of syncope?

A

cardiac

153
Q

what is cardiac syncope?

A

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

154
Q

fluttering, pounding, rapid heartbeat in neck or chest. can also have breathlessness

A

palpitations

155
Q

when are palpitations more serious?

A

if accompanied by pre-syncope or syncope, or dizziness - this suggests a tachyarrhythmia

156
Q

sudden breathlessness or single “pounding”sensation may indicate what?

A

PVC

157
Q

what should you do for a palpitation workup?

A

EKG
stress test if associated with exercise
holter or event monitor

158
Q

what can cause sinus bradycardia?

A

excessive vagal stimulation (valsalva, vomiting, cold water)

hypoxia, MI, meds (beta blockers), athletic heart, OSA

159
Q

treatment for sinus bradycardia

A

none unless symptomatic, treat the cause. if acutely symptomatic (MI, ischemia) consider atropine acutely and a pacer long-term

160
Q

two drugs for bradycardia

A

atropine- inhibits action of Ach on autonomics - antimuscarinic

epinephrine - positive inotropic effect on heart, increases HR and contractility, CO. acts below AV node

161
Q

what will show up on an EKG with a bundle branch block?

A

wide QRS, because conduction is slow

162
Q

which leads do you assess for bundle branch block?

A

precordial - v1-v6

163
Q

what usually causes RBBB?

A

CAD, conduction system lesion, R ventricle disease

usually no symptoms - treat the cause

164
Q

what is worse, LBBB or RBBB?

A

LBBB - should be treated as an MI, as they may mask EKG findings of MI

165
Q

what shows up on the EKG for an AV block?

A

prolonged PR interval - due to ischemic or supressed AV node (most common site of block)

166
Q

treatment for first degree AV block?

A

none

167
Q

EKG findings of second degree type I AV block/wenckebach

A

Normal P waves, PR interval progressively elongates until a QRS is dropped

168
Q

treatment of wenckebach

A

rate usually slow, if symptoms of decreased CO are present emergently atropine and pacer long term. no treatment if asymptomatic

169
Q

where do tachyarrhythmias arise from?

A

atria, AV node, or from ventricle

170
Q

causes of sinus tachycardia

A

stress, meds, fever, hypoxia, hyperthyroidism, etc

171
Q

what do B-blockers do?

A

Reduce heart rate and contractility, reduce cardiac output, reduce renin release, depress SA and AV node function

172
Q

atrial flutter

A

uncommon, most associated with underlying heart disease (CAD, PE, valvular disease)

173
Q

EKG atrial flutter

A

atrial rate 250-350

usually REGULAR

no P waves present, saw tooth flutter wave present and narrow QRS

174
Q

how do you treat atrial flutter?

A

rate control - Ca channel blocker, b-blocker
rhythm control - radiofrequency ablation
maintaining NSR
clot prevention - those with sustained a flutter should be treated like those with pure a fib and anticoagulated with warfarin

175
Q

what is the most common arrhythmia generating from the atria?

A

atrial fibrillation

176
Q

pathophys of afib

A

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

177
Q

causes of afib

A

HTN, CHD, MI, valvular disease

  • not associated with caffeine intake
  • not common in children
178
Q

different classes of afib

A

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

179
Q

what is “lone” afib?

A

in those less than 60 w/out structural heart disease

male predominance, associated with “triggers”

least risk for complications

“holiday heart”

180
Q

important questions for afib

A

Duration and frequency of symptoms

Precipitating factors: exertion, sleep, caffeine

Termination of symptoms: vagal maneuvers, rest

Antiarrhythmics and rate-controlling meds?

Underlying heart disease?

181
Q

afib EKG

A

atrial rate usually between 400-650

p wave not present, wavy baseline is seen instead

normal or narrow QRS

IRREGULARLY IRREGULAR

182
Q

Further workup for Afib

A

TTE - evaluate atrial volume, function and presence of thrombi

stress test - eval for CAD

labs - TSH, BUN, CRT, glucose

holter

183
Q

what is usually first choice, rate or rhythm control?

A

rate - antiarrythmics have many side effects and rhythm control does not reduce embolic risk

184
Q

When to (carefully) choose rhythm control

A

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

Patient preference

185
Q

what is DC cardioversion?

A

direct current discharged in synch with the R wave, depolarizes most cardiac cells and allows SA node to resume pacing

186
Q

what are indications for urgen cardioversion?

A

active ischemia
hypoperfusion
heart failure
pre excitation syndroms

187
Q

what should you do for non urgent cardioversion?

A

antigoagulate prior to procedure- one month pre and post

control rate prior to procedure

antiarrhythmic prior to procedure

188
Q

what are rhythm control drugs?

A

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

dofetilide

flecainide

189
Q

chads2 score

A

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

190
Q

most effective oral anticoagulation

A

warfarin (pradxa and xarelto not usually covered under insurance)

191
Q

contraindications for anticoags

A

alcoholics, noncompliant, pregnancy

clin med (12 decks)

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