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1

major risk factors for HTN

stroke
MI
vascular disease
chronic kidney disease

2

is the majority of HTN essential or secondary?

essential (90% of cases)

3

common causes of secondary HTN

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

4

is the sphygmomanometry a direct or indirect BP measurement?

indirect

5

formula for BP

BP= CO x TPR (total peripheral resistance)

6

peripheral resistance is dependent on what factors?

vascular structure
vascular function

7

cardiac output is dependent on what?

stroke volume and heart rate

8

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

9

HTN definition

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

10

JNC 8 recommendations

60 or older 18 with CKD or diabetes

11

accurate BP

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

12

how to measure BP cuff

inflatable bladder = 80% around circumference of the arm
width = should cover roughly 40%

13

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

14

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

true

15

pre-htn treatment

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

16

when is systolic BP a more important cardiovascular risk factor?

after age 50

17

when is diastolic BP an important cardiovascular risk factor?

before age 50

18

target organs affected by prolonged uncontrolled HTN

CVS (heart and blood vessels)
kidneys
nervous system
eyes

19

effects of prolonged HTN on CVS

ventricular hypertrophy, dysfunction and failure

arrhythmias

CAD, Acute MI

arterial aneurysm, dissection, and rupture

20

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

21

effects of prolonged HTN on nervous system

stroke, intracerebral, and subarachnoid hemorrhage

cerebral atrophy and dementia

22

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

23

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

24

cardiovascular risk factors

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

25

identifiable causes of HTN

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

26

T or F : beta blockers aggravate claudication and PVD

true

27

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

28

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

29

should you use ACEI and ARBs together in same patient?

no

30

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.

31

recommended salt intake/day

2400 mg/day

32

DASH diet

dietary approach to stop hypertension clinical trial

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

33

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

34

common causes of secondary HTN

intrinsic renal disease
renovascular disease
mineralocorticoid excess
sleep breathing disorder

35

uncommon causes of secondary HTN

pheochromocytoma
glucocorticoid excess
co-arcation of aorta
hyper/hypothyroidism

36

features indicative of secondary HTN

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

37

most common cause of secondary HTN?

chronic renal disease - activation of RAAS and SNS

38

unexplained hypokalemia is indicative of what?

hyperaldosteronism

39

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

40

who should pheochromocytoma be suspected in?

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

headache, palpitations, pallor and perspiration

41

how do you diagnose pheochromocytoma?

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

42

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

43

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)

44

hypertensive emergencies require what?

hospitalization and parenteral medication

45

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**

46

who is more likely to have a HTN emergency?

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

47

BP for hypertensive emergencies

>180/120 with progressive target organ dysfunction

48

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

49

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

50

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

51

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

52

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

53

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

54

drug treatment for HTN urgency

captopril
clonidine
furosemide
labetalol
nifedipine
propranolol/metoprolol

can use oral agents in most cases

55

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

56

drug of choice for stage 1 hypertension with no compelling indications

thiazide-type diuretics

ACE inhibitor, ARB, CCB, or combination

57

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

58

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

59

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

60

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

61

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

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

62

most important site for renin release?

kidney

63

where is angiotensinogen released from?

mainly the liver

64

where is ACE released from?

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

65

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**

66

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

67

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

68

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)

69

do ARBs block bradykinin breakdown?

no - so less cough than ACE inhibitors

70

side effects of ARBs

orthostatic hypotension
renal insufficiency
hyperkalemia

71

who should not take ACE inhibitors and ARBs?

pregnant women

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

72

what do renin inhibitors do?

inhibits angiotensinogen to angiotensin I conversion

does not block bradykinin breakdown

adverse effects: orthostatic hypotension

73

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

74

adverse effects of B-blockers

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

75

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

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

76

cardioselective beta blockers

atenolol
betaxolol
bisoprolol
metroprolol
nebivolol

77

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

78

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

79

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

80

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

81

adverse effects of central a2-agonists

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

when are central alpha2-agonists most effective?

if used with a diuretic - minimizes fluid retention

83

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

hydralazine andminoxidil

84

in which patients is orthostatic hypotension more prevalent?

diuretics
ACE inhibitors
ARBs

85

adverse effects of direct arterial vasodilators

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

86

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

resistant hypertension

87

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

88

where is the most common aneurysm location?

infrarenal abdominal aorta

89

who is more likely to have a TAA?

men, and those with lung disease

90

where is the most common location for a TAA?

ascending aorta

91

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

92

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

93

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

94

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

95

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)

96

what is used to surgically repair TAA?

endoluminal stent (endo stent)

97

AAA definition

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

98

normal abdominal aorta size

2-3 cm

99

difference between fusiform and saccular aneurysm

fusiform - there is symmetrical dilation of the aorta
saccular - when the dilation involves mainly one wall

100

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

101

who is most likely to get a AAA?

elderly, white males

102

90% of AAA's are where?

infrarenal (below renal arteries)

103

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

104

signs and symptoms of AAA

most are asymptomatic

"pulatile mass" in abdomen

back/abdominal/flank pain

nausea/vomiting

urinary symptoms

venous thrombosis

105

classic triad for diagnosis of AAA rupture

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

106

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

107

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

108

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)

109

separation of the layers within the aortic wall is what?

aortic dissection

110

which type of dissection require emergent or urgent surgery?

Standford type A (2/3)

standford type B can be medically managed

111

classic presentation of aortic dissection

sudden onset, severe chest pain

described as "tearing" or "ripping" quality

112

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

aortic arch or aortic root dissection

113

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

aortic arch and extension into the great vessels

114

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

descending aorta

115

physical exam findings in aortic dissection

hypertension (70%), interarm blood pressure differential

116

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

117

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

118

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

takayasu arteritis

119

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

hypertension

HF

120

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

narrow-wide-narrow

121

what is the treatment of takayasu arteritis?

high dose corticosteroids

balloon angioplasty of stenotic lesions

very good prognosis

122

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

123

treatment for giant cell arteritis

high-dose corticosteroid therapy

124

what is PVD?

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

125

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

126

what are the clinical presentations of PVD?

intermittent claudication
rest pain

127

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

aorta or illiac arteries

128

calf claudication comes from stenosis of what arteries?

popliteal and femoral

129

pedal claudication comes from stenosis of what arteries?

tibial and peroneal artery

130

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

131

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

rest pain

132

what are physical exam findings of rest pain?

skin breakdown, ulceration, necrosis and gangrene

133

what will a venous ulcer look like?

normal pulses
woody leg
hemosiderin deposition
painless or painful
fibrinous exudate

134

what will an arterial ulcer look like?

decerases pulses
hairless leg
pale color
painful
necrotic base

135

what is a normal peripheral pulse exam?

2+ easily palpabler

136

non-invasive diagnosis of PAD

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

137

what are the invasive ways to diagnose PAD?

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

138

what is ABI?

ankle-brachial index

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

139

gold standard for evaluation of PVD

angiogram

140

what are the risks of getting an angiogram?

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

141

what is the preferred treatment in amenable vascular lesions?

percutaneous transluminal angioplasty (PTCA)
- lower peri-procedural mortality and morbidity.
-more cost effective than surgery

142

PTCAs have best outcomes with what vascular lesions?

femoral

143

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)

statin therpy

144

where do the majority of arterial embolisms come from?

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

145

where do most arterial emboli end up?

femoral

146

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

147

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

148

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

emergent surgery - immediate embolectomy

149

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

consider tPA or IV anticoagulation (heparin drip)

150

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

151

most common type of syncope?

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

second most common type of syncope?

cardiac

153

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

154

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

palpitations

155

when are palpitations more serious?

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

156

sudden breathlessness or single "pounding"sensation may indicate what?

PVC

157

what should you do for a palpitation workup?

EKG
stress test if associated with exercise
holter or event monitor

158

what can cause sinus bradycardia?

excessive vagal stimulation (valsalva, vomiting, cold water)

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

159

treatment for sinus bradycardia

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

160

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

161

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

wide QRS, because conduction is slow

162

which leads do you assess for bundle branch block?

precordial - v1-v6

163

what usually causes RBBB?

CAD, conduction system lesion, R ventricle disease

usually no symptoms - treat the cause

164

what is worse, LBBB or RBBB?

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

165

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)

166

treatment for first degree AV block?

none

167

EKG findings of second degree type I AV block/wenckebach

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

168

treatment of wenckebach

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

169

where do tachyarrhythmias arise from?

atria, AV node, or from ventricle

170

causes of sinus tachycardia

stress, meds, fever, hypoxia, hyperthyroidism, etc

171

what do B-blockers do?

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

172

atrial flutter

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

173

EKG atrial flutter

atrial rate 250-350

usually REGULAR

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

174

how do you treat atrial flutter?

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

what is the most common arrhythmia generating from the atria?

atrial fibrillation

176

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

177

causes of afib

HTN, CHD, MI, valvular disease

*not associated with caffeine intake
*not common in children

178

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

179

what is "lone" afib?

in those less than 60 w/out structural heart disease

male predominance, associated with "triggers"

least risk for complications

"holiday heart"

180

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?

181

afib EKG

atrial rate usually between 400-650

p wave not present, wavy baseline is seen instead

normal or narrow QRS

IRREGULARLY IRREGULAR

182

Further workup for Afib

TTE - evaluate atrial volume, function and presence of thrombi

stress test - eval for CAD

labs - TSH, BUN, CRT, glucose

holter

183

what is usually first choice, rate or rhythm control?

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

184

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

Patient preference

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what is DC cardioversion?

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

186

what are indications for urgen cardioversion?

active ischemia
hypoperfusion
heart failure
pre excitation syndroms

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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

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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

dofetilide

flecainide

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chads2 score

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

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most effective oral anticoagulation

warfarin (pradxa and xarelto not usually covered under insurance)

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contraindications for anticoags

alcoholics, noncompliant, pregnancy