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Cardiology,HTN, HF, and Pharm > HTN, HF, Carditis, hypotension, syncope > Flashcards

HTN, HF, Carditis, hypotension, syncope Flashcards

1
Q

Difference between essential (primary) and secondary HTN

A

Essential-Onset between 25-50
95% of HTN
Exacerbating factors (obesity, NSAIDS, sleep apnea, Increased Na+, Excessive ETOH, Smoking, Polycythemia)

Secondary causes think someone, not between 20-50, had well controlled and now has an increase, refractory HTN on multiple meds
Causes(OCPs, NSAIDs, decongestants, SSRIs and tricyclic, glucocorticoids, weight loss meds, erythropoietin, illicit drugs, Primary renal disease(most comon cause) renal artery stenosis, hyper/hypothyroid, pregnancy, coarctation of aorta(children))

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2
Q

Metabolic Syndrome

A 
Abdominal Obesity
Triglycerides >150mg/dL
HDL <40mg/dL in Men
HDL <50mg/dL in women
Systolic BP >130 or diastolic BP >85
Fasting BGL >100mg/dL
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3
Q

Hypertensive urgency

A

Severe HTN in asymptomatic Pt no evidence of EOD
SBP>180
DBP>120

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4
Q

Hypertensive Emergency

A

Severe HTN with evidence of acute EOD
Life threatening needs immediate treatment
SBP>180
DBP>120

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5
Q

Lab tests for R/O secondary HTN

A 
TSH-thyroid issues
UA-checking for protein
Renal artery bruits-stenosis
Polysomnography-sleep apnea
Excessive cortisol, moon face, obesity-bushings
UA- illicit drugs
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6
Q

120-129/80

A

JNC 7-preHTN

2017 elevated

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7
Q

130-139/80-89

A

JNC 7-preHTN

2017 Stage 1 HTN

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8
Q

140-159/90-99

A

JNC-7-Stage 1 HTN

2017-Stage 2 HTN

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9
Q

> 160/>100

A

JNC7-STage 2 HTN

2017-Stage 2 HTN

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10
Q

HTN screening

A

Over 40 or with risk factors yearly

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11
Q

Ambulatory BP monitoring

A

24 hr BP monitoring, expensive

Preferred method for confirming the diagnosis oHTN/white coat HTN

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12
Q

How to diagnose HTN

A

Pt presents with HTN urgency or emergency

initial screening of >160/100 with target EOD

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13
Q

2ndary HTN causes

A 
Sleep apnea
Drug induced/related
CKD
Primary aldosteronism
renovascular disease
longterm corticosteroid use/ bushings syndrome
pheochromocytoma
coarctation of aorta
thyroid/parathyroid
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14
Q

Think 2ndary HTN in Pt

A

Less than 20 older than 50
well controlled HTN with spike
HTN refractory to multiple treatments

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15
Q

Meds that causes 2ndary HTN

A

OCP, NSAIDs, Decongestants, Antidepressants, Glucocorticoids, Weight loss meds, EPO, Cyclosporine, stimulants

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16
Q

Most common cause of 2ndary HTN

A

Primary Renal disease

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17
Q

Complications of Untreated HTN

A

ESKD,
Strokes,
dementia/alzheimers
CVD-LVH, HF, arrhythmias, MI, sudden death

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18
Q

End Organ Damage(EOD)

A 
LVH(early finding)
CHF-
AMI/CAD
Demand ischemia
Stroke
Aortic dissection
retinal hemorrhage
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19
Q

EOD on fundoscopy

A

optic disc swelling, cotton wool patches, hard exudates

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20
Q

HTN Pt clinical presentation

A

Asymptomatic for years-nonspecific headaches

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21
Q

Hypertensive Encephalopathy

A

HTN with somnolence, confusion, visual disturbances, N/V

EMERGENCY

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22
Q

Goal of initial assessment

A

Determine extent of EOD
Determine overall CVD risk
RO identifiable 2nd causes/often curable causes of 2nd HTN

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23
Q

Nonpharm approach

A 
Weight reduction
DASH diet
Na reduction
physical activity
decrease alcohol/smoking
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24
Q

JNC 8 HTN goals >60 no DM or CKD

A

<150/90
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB

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25
Q

JNC 8 HTN goals<60 no DM/CKD

A

<140/90
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB

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26
Q

JNC 8 HTN goals DM or CKD

A

<140/90
DM no CKD
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB

CKD- ACE or ARB along with another class

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27
Q

Hypotension-BP criteria

A

BP<90/60 MAP <65

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28
Q

Shock-definition

A

state of cell and tissue hypoxia due to a decrease in O2 delivery

Hypoperfusion state

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29
Q

Features of Hypotension

A 
Tachycardia
oliguria
hyperlactatemia
AMS
Tachypnea
Cool/clammy
Cyanosis-Perioral cyanosis
metabolic acidosis
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30
Q

Orthostatic/postural hypotension

A

After 5 min of lying down, delay of the normal compensatory mechanism of ANS

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31
Q

Clinical presentation of orthostatic hypotension

A

SBP drops >20mmHg

DBP drops>10mmHg

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32
Q

Orthostatic Hypotension-etiology

A 
Drop in blood volume
Drop in cardiac output
Arrhythmia
Medications
endocrine, neurological or metabolic disorders
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33
Q

Orthostatic Hypo initial work up

A

CBC, BMP, ECG,

Consider- tilt test, echo, neuro and cardiology consults

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34
Q

Management of orthostatic hypotension

A 
treat underlying cause
asymptomatic pt may not need treatment
D/C causative med
IV or PO fluid
treat infection, arrhythmia, anemia
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35
Q

Orthostatic hypotension Pt ed

A

Stand up slowly, maintain hydration, increase Na+ intake, raising head of bed, compression socks, reduce alcohol, increase caffine

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36
Q

Vasovagal hypotension

A

Stimulation of vagus nerve causes drop in BP and HR(stimulation of parasympathetic nervous system)

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37
Q

DVT etiology

A

prolonged immobilization, thrombophilia, neoplasm, Fhx, increases with age

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38
Q

DVT clinical finding

A

swelling of leg or calf, warmth and erythema

pain increasing with standing or walking

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39
Q

DVT diagnosis

A

H&P Hollman’s test, ultrasound, can do d Dimer

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40
Q

DVT treatment

A

Depends on location
Fem-pop or more distal- determine if provoked or unprovoked- Anticoag with warfarin or DOAC/NOAC-
Ileofemoral- refer for mechanical thrombectomy vs thrombolysis

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41
Q

chronic Arterial occlusive disease etiology/pathology

A

chronic and progressive- atherosclerotic plaques, stenosis, ruptured plaques(emboli)

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42
Q

chronic arterial occlusive disease- clinical findings

A

typically chronic and progressive-claudication, collateral circulation
PAD is normally asymptomatic-can progress to become life-threatening if risk factors are not treated

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43
Q

chronic Arterial occlusive disease- Dx

A

H&P, specific pattern Pt has with Sx development,
Ankle-brachial index
imaging if indicated

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44
Q

Chronic arterial occlusive disease treatment

A

Tx risk factors- Especially statins and controlling DM. Walking program can help to create collateral circulation and train muscles to depend on less O2.

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45
Q

acute arterial occlusive disease treatment

A

emergency(NPO) discuss anticoag with surgeon(heparin) Angiogram, open embolectomy vs endovascular

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46
Q

Acute arterial occlusive disease -Dx

A

Cardiac exam, abdominal exam, pulse exam, imaging -CT

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47
Q

acute arterial occlusive disease clinical findings

A

cold leg, painful, no collateral flow

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48
Q

acute arterial occlusive disease etiology

A

result of clot

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49
Q

phlebitis/thrombophlebitis-eti

A

a clot formed in superficial venous return-no risk of DVT

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50
Q

phlebitis/thrombophlebitis clinical findings

A

pain, redness, and inflammation (locally not to entire lower limb as with DVT)

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51
Q

phlebitis/thrombophlebitis Dx

A

Clinical, use duplex ultrasound if suspicious for DVT

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52
Q

phlebitis/thrombophlebitis treatment

A

NSAIDs and localized heat

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53
Q

Chronic venous insufficiency etiology/pathology

A

MC FMHx, then DVT and trauma, occurs in men and women equally-rarely congenital
Venous insufficiency, reflux of blood flow through valves

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54
Q

Chronic venous insufficiency clinical findings

A

spider or reticular telangiectasia, varicose veins, edema, skin changes, ulceration, thrombophlebitis
-pain edema, aching, throbbing fatigue-consider venous stasis ulcer

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55
Q

chronic venous insufficiency Dx

A

Ultrasound can measure size and flow (antegrade/retrograde)-reflux is retrograde flow for more than 500ms

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56
Q

chronic venous insufficiency Tx

A

lifestyle modifications- elevation and compression socks
minimally invasive techniques- ablation
invasive- vein stripping

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57
Q

varicose veins pathology

A

venous insufficiency- causing dilation of veins and blood pooling

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58
Q

Varicose veins clinical findings

A

squishy +/-painful veins

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59
Q

Varicose veins Dx and Tx

A

Ultrasound- minimally invasive (ablation) to invasive(vein stripping)

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60
Q

Venous ulceration EPI/Patho

A

the result of venous insufficiency

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61
Q

Venous ulceration clinical /Dx

A

typically on medial malleolus, will have swelling, will have a palpable pulse

62
Q

Reynaud’s disease Epi/

A

F>M, FMHx, smoking, autoimmune disease, some meds

63
Q

Reynaud’s pathology

A

vasospastic disorder

64
Q

Reynaud’s clinical and Dx

A

pallor, cyanosis, hyperemia

H&P Sx

65
Q

Reynaud’s treatment

A

Lifestyle changes-gloves and socks-smoking cessation, D/C BB if HTN and give CCB

66
Q

Temporal arteritis EPI/ETI

A

Autoimmune vasculitisF>M 4:1

caucasions

67
Q

temporal arteritis clinical findings

A

HA, malaise/fatigue, some fever and neck/jaw claudication

68
Q

Temporal arteritis Dx

A

ESR/CRP- Rheumatology referral

69
Q

Temporal arteritis Tx

A

temporal artery biopsy, Oral corticosteroids (PO Prednisone)

70
Q

Aortic Aneurysm Epi/Eti

A

M>F >60yo, Caucasians, Hx of smoking, FMHx

71
Q

Aortic Aneurysm Clinical findings

A

Usually none - can cause back and abd pain
can embolize to legs
RUPTURE- very rapidly becomes hemodynamically unstable
Pulsatile mass in abd

72
Q

Aortic Aneurysm Dx

A

Imaging or ultrasound

73
Q

Aortic Aneurysm Tx

A 
Treat HTN (BB) antiplatlets and statins(prevent emboli and further stenosis)
Endovascular repair:  stent graft EVAR
or open repair
74
Q

Aortic Dissection Epi/Eti

A

Trauma, penetrating atherosclerotic plaque, HTN

75
Q

Aortic Dissection Patho

A

Fenestrated intima allows blood into other layers of the blood vessel creating a false lumen

76
Q

Aortic Dissection Clinical findings

A

Ripping, tearing pain in back, depending on location can have unequal BP(check bilateral BP)

77
Q

Aortic Dissection Dx

A

Imaging

78
Q

Aortic Dissection Tx

A

BP management, may need endovascular or open repair if causing end organ damage

79
Q

HF NYHA Class I

A

Pt with heart disease w/o limitation of physical activity-no signs of HF

80
Q

HF NYHA Class II

A

Pt with heart Disease resulting in slight limitation of physical activity-Symptoms of HF develop with activity but go away with rest

81
Q

HF NYHA class III

A

Pt with heart disease resulting in marked limitation of physical activity, Symptoms develop w/ less than ordinary physical activity- no symptoms at rest

82
Q

HF NYHA Class IV

A

Symptoms of HF at rest

83
Q

HF AHA Stage A

A

At high risk for HF no structural damage and no Sx of HF

84
Q

HF AHA Stage B

A

Structural HD w/o signs or symptoms of HF,

85
Q

HF AHA Stage C

A

Structural HD w/ prior or current signs and symptoms of HF

86
Q

HF AHA Stage D

A

Refractory HF requiring specialized intervention

87
Q

HFpEF

A

Diastolic HF-enlarged muscle doesn’t allow enough blood into the ventricle, Ejection fraction is normal but Cardiac output is decreased-dizziness, orthostatic hypotension

88
Q

HFrEF

A

Systolic HF- weak ventricular muscle is not able to push out causing a decrease in CO and EF

89
Q

Left-sided HF

A

SOB, pulmonary edema

Can have right sided failure symptoms as well due to the severity of HF

90
Q

Right Sided HF

A

Systemic edema-JVD-

Can have Left sided symptoms as well depending on the severity

91
Q

HF ECHO

A

Can monitor proper contraction and movement of heart and valves- can give an EF and determine which part of the heart is damaged

92
Q

HF Brain Natriuretic peptide(BNP)

A

Is released from the ventricle in response to increases in ventricular stretch

93
Q

Acute HF

A

Decompensated HF

94
Q

Chronic HF

A

Stable- treat underlying causes

95
Q

Treatment approach to Chronic HF

A

1-ACE, ARB or ARNI
2-BB-carvedilol or metoporlol ER
3-Aldosterone Antagonist-Spironolactone

96
Q

ACE/ARB-MOA

A

afterload reducers

97
Q

ARNI-moa

A

potentiate ARB effects

98
Q

Aldosterone antagonist MOA

A

Diuretic

99
Q

BB moa

A

decrease afterload and myocardial O2 demand

100
Q

Loop diuretics

A

Symptom relief

101
Q

Digoxin moa

A

positive inotrope and negative chronotrope

102
Q

Non pharm treatments of HF

A 
ICD-
BiVentricular pacing
Case management- daily weigh-ins
Coronary revascularization
LVAD
Transplants
103
Q

Treatment of acute HF

A

O2, BiPAP-CPAP
Vascular support- MSO4-venodilation, Nitrates-venodilation, Diuretics-excrete fluid, Dobutamine-increase inotropy, Slowly reintroduce ACE, BB and other meds once stablized

104
Q

S1

A

Closure of the AV valves-beginning of systole

105
Q

S2

A

Closure of the Semilunar valves- the beginning of diastole

106
Q

S3

A

Extra sound- HF or dilated cardiomyopathy-blood rushing into the ventricle “Ken Tuck Y”
Gallop

107
Q

S4

A

Extra heart sound- immediately precedes S1- stiff ventricle, infiltrate-HFpRF
“Ten es see”
Gallop

108
Q

Systolic murmurs

A

Aortic stenosis
Pulmonic Stenosis
Mitral/tricuspid insufficiency/regurge
Mitral valve prolapse

109
Q

Diastolic murmurs

A

Always pathologic
Aortic/pulmonic insufficiency/regurge
mitral/tricuspid stenosis

110
Q

Aortic Stenosis murmur

A

Harsh crescendo/decrescendo over aortic region

111
Q

Aortic Stenosis eti/

A

MC valve disease, degeneration due to calcification

RHD, congenital bicuspid aortic valve, atherosclerosis, elderly-radiation/collagen diseases(rare)

112
Q

Aortic stenosis signs

A

rales- cool extremities, angina, syncope-Life expectancy decreases rapidly when symptoms arise

113
Q

Aortic stenosis Dx

A

Murmur heard best with Pt leaning forward, decreased w/volume reduction(standing) and increased with volume increase(squating)

114
Q

Aortic stenosis grading

A

Normal-3-4cm^2
Mod 1.15cm^2
Severe<1cm^2

115
Q

Aortic stenosis Tx

A

Valve replacement or repair

116
Q

Aortic stenosis management

A

Avoid Negative inotropes
Observe yearly w/echo-asymptomatic every 2-5 years
Replacement for severe(10-30y expectancy)

117
Q

Aortic stenosis Pt ed

A

Pt needs to tolerate elevated BP to maintain CO

118
Q

Pulmonic stenosis murmur

A

crescendo/decrescendo over pulmonic area

with Pt leaning forward and with the release of Valsalva

119
Q

Pulmonic stenosis ETI

A

heart surgery or congenital MC

Tetralogy of Fallot

120
Q

Mitral insufficiency/ regurge murmur

A

Best heard at apex-radiates to axilla
systolic murmur-opening snap blowing holosystolic murmur
increases with increased peripheral resistance

121
Q

Mitral regurge insufficiency ETI

A

leaflet, annulus chordae tendonae/papillary muscle abnormalities

122
Q

Mitral regurge Sx

A

Asymptomatic —exercise intolerance, IHD(angina), severe dyspnea(L HFrEF) afib

123
Q

Mitral regurge management

A

yearly echo, avoid atrial remodeling

124
Q

Mitral valve prolapse murmur

A

late systolic click with a crescendo murmur

click will occur sooner when standing, later with squatting

125
Q

Tricuspid regurge murmur

A

difficult to hear-use bell when standing

126
Q

tricuspid regurge eti

A

pulmonary HTN leading to HF

infective endocarditis, Epstein barr, pacemaker leads, Rheumatic fever

127
Q

Aortic insufficiency/regurge

A

Quiet blowing decrescendo heard on left sternal border, increases with peripheral resistance

128
Q

Aortic insufficiency ETI

A

congenital leaflet-bicuspid aortic valve

endocarditis, marfans, Rheumatic HD, dilation of aortic root, rarely syphilis

129
Q

Aortic insufficiency sings/sx

A

exercise intolerance, dyspnea, orthopnea, CHF, angina, bounding peripheral pulses

130
Q

Aortic stenosis tx/management

A

yearly echos

replacement

131
Q

Mitral valve stenosis murmur

A

Opening snap, diastolic murmur, rumbling decrescendo low pitch heard best at apex with bell in left recumbent

132
Q

Mitral valve stenosis ETI

A

second most common murmur-
Rheumatic fever, 4x more males-females have more symptoms
endocarditis

133
Q

Mitral valve stenosis sx/signs

A

rales, cool extremities, subtle exercise intolerance, palpitations, chf, hoarsness, a fib

134
Q

Mitral valve stenosis Dx

A

EKG, Echo, CBC, BMP, Mg++, TSH, CXR, BNP

135
Q

Mitral valve stenosis grading

A

Normal 4-5 cm^2
mild <2.5cm^2
Critical<1 cm^2

136
Q

Mitral valve stenosis Tx and Management

A

Replacement
prevent clots, control HR(BB, CCB), prophylaxis against endocarditis(dental procedures)
Yearly echo

137
Q

Pulmonic regurge murmur

A

caused by pulmonary HTN MC

quiet murmur low flow- Descrescendo best heard in pulmonic area increases with release of valsalva

138
Q

Tricuspid stenosis murmur

A

Pan diastolic at L sternal border

increases with exercise(increased venous return to heart

139
Q

Dilated cardiomyopathy

A

MC type- ischemia, HTN, thick ventricular walls with dialation inside then becomes thin and weak

140
Q

Hypertrophic cardiomyopathy HOCM

A

think sudden cardiac death by athlete, inborn deffect of left ventricle hypertrophy near the outflow track into the aorta
need exercise restriction(can have surgery to remove portion(Septal myomectomy)
ICD and BB

141
Q

Restrictive cardiomyopathy-

A

rare -deposits of things in the heart muscle, amylooidosis-plaques heart muscle causing issues with conduction and contraction

142
Q

tako tsubo cardiomyopathy

A

broken heart-after catecholamine discharge dilation and ballooning of LV-mainly postmenopausal women

143
Q

EKG findings in cardiomyopathy

A

50% sensitive 90% specific
Criteria for LVH
V1 S+V5/6 R >35mm(7big boxes)

144
Q

Radiology findings in cardiomyopathy

A

CXR- gives an indication of an enlarged heart but no cause
Echo can calculate EF and specify which part of Heart is affected
Cardiac MRI-expensive and slow-more detailed than echo

145
Q

Lab studies in cardiomyopathy

A

BNP/Nt-ProBNP-higher the BNP the more stretch of the ventricles- causes vasodilation-drop in BP
Causes decrease in renin causing more diuresis decreasing blood volume

146
Q

Endocarditis

A

Patho-Infection/inflammation of valve or prosthetic valve
ETI-TB, mycobacteria, HACEK, Staph and Strep
Risks-indwelling catheters, central lines, iv drug users, prolonged infections
S/S- fever, malaise, splinter hemorrhages, Osler nodes(painful) Janeway lesions(not painful), new murmur, sepsis
Dx-blood culture(3 separate locations), echo
Tx-based on blood culture results, replace valve if damaged

147
Q

Myocarditis

A

Patho-inflammation/infection of muscle
ETI- HX recent uri, febrile illness, drugs, vaccination
Dx- Echo, MRI, myocardial biopsy
Tx- typically self limiting, if not treat as HF and treat cause

148
Q

Pericarditis

A

Patho- inflammation/ infection of pericardial sac
ETI- viral infection, systemic disease, infrections, autoimmune, drugs, uremia
Clinical pres- pericardial friction rub, fever, tamponade, tachypnea, tachycardia, narrow pulse pressure, pulsus pardoxus, diffuse ST elevation, pleuritic chest pt increases in supine position decreases when leaning forward
Dx- elevated erythrocyte sediment rate(ESR) and c reactive protein(CRP)
Tx NSAIDs, ASA, colchicine(post MI), ABX for infective, dialysis for uremic
Consideration- Colchicine can cause severe ADE, effusion vs tamponade

149
Q

Rheumatic heart disease tx

A

PCN, Tx chorea, CHF management, surgery to replace valves

150
Q

Endocarditis prophlylaxis

A

Dental procedures, respiratory tract procedures, procedures on infected skin/tissue -prosthetic cardiac valve, previous infective endocarditis, Congenital heart disease, cardiac transplants

Cardiology,HTN, HF, and Pharm (3 decks)

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