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Clin med II exam II Cardio > Infections, HF, shock, vascular dz > Flashcards

Infections, HF, shock, vascular dz Flashcards

1
Q

most common cause of right sided HF

A

left sided HF

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2
Q

si/sx of right sided HF

A

Blood backs up into systemic venous system:

  • Legs
  • Hepatic veins
  • GI tract
  • Elevated JVD and hepatojugular reflex
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3
Q

si/sx of left sided HF

A

Blood backs up into lungs (pulmonary edema) initially

SOB on exertion

orthopena

Paroxysmal nocturnal dyspnea

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4
Q

lab test used as marker for HF

A

•Brain Natriuertic Peptisde (BNP) – measures amount of heart stretch or strain in someone having acute decompensating HF (will be elevated)

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5
Q

patho of right vs left sided HF

A

Right heart is thinner and becomes lax -> starts backing up fluid into right atria and right sided venous system -> lower extremity edema

Acute MI – heart scars and develops regional wall abnormalities -> heart not contracting well -> harder for blood to eject (HFrEF) / (ischemic CM)

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6
Q

Pts w/ known HF – triggers for decompensation:

triggers for new dx HF

A
  • Acute / recent MI
  • Changes in diet – increased salt or fluid
  • Change in medication – reduction in diuretic, missed-dose, non-compliance

new dx

  • Acute MI
  • Recent MI
  • Afib w. RVR or other tachyarrhythmias
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7
Q

in setting of HF when can we order an echo

A

new diagnosis OR decompensating HF that is unexplained

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8
Q

New York Heart Association Functional Classification of HF

I-IV

A
  • Class I – symptoms only with significant activity
  • Class II – symptoms w/ ordinary ADLs
  • Class III – symptoms with minimal exertion
  • Class IV – symptoms at rest
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9
Q

CXR findings in acute decompensated Left sided HF

A
  • Blunting of costophrenic angles
  • Pulmonary valve engorgement (increased interstitial markings)
  • Cephalization – vessels pointing toward head, engorged pulmonary vasculature
  • Kerley B lines – thickened horizontal linear opacities in subpleural region which met at right angles
  • Cardiomegaly
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10
Q

etiology of systolic vs diastolic HF

A

systolic (HFrEF)

  • Dilated CM
  • Ischemic CM
  • Cardiomegaly

•Ischemic heart disease

  • HTN – chronic pressure overload causes remodeling
  • Valvular disease – mitral or aortic valve regurgitation à increased volume in left ventricle (left ventricle is stretched)

diastolic (HFpEF)

  • Restrictive CM
  • HOCM

•Long standing HTN - stiff ventricles

•Valvular disorders – mitral valve stenosis à not able to drive enough blood from atria to ventricle through the tight valve

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11
Q

patho of systolic vs diastolic HF

A

systolic

Impaired ejection of blood from the heart during systole

•Enough volume during diastole, but cannot squeeze well enough get it out during systole

diastolic

Impaired filling of ventricles during diastole

  • Ventricle cannot relax enough to fully fill à so even though EF is preserved the total volume is DEC
  • (DEC stroke volume + CO)
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12
Q

everyone w/ systolic HF should be on what meds

A

ACE - Reduce afterload and improve CO

BB - Improve remodeling (less scar tissue)

Diuretic (loops) - remove excess fluid

  • Furosemide (Lasix) once maxed can add spironolactone
  • Budesonide – stronger then Lasix

AAs - Hydralazine & Isosorbide Dinitrate (Bidil)

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13
Q

meds shown to reduce hospitilizations in HF

A
  • Digoxin
  • Ivabradine – EF <35% on max BB or BBs are CI
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14
Q

Systolic HFrEF Tx

A
  1. Start EVERYONE on ACE at time of diagnosis (or ARB)
  2. Start Furosemide (Lasix) on everyone w/ symptoms
  3. Add Beta-blocker for ALL patients
  4. Add aldosterone antagonist (spironolactone) to Lasix if persistent symptoms
  5. Change from ACE or ARB to ARNI at class II if no CI
  6. Add hydral-nitrates for black patients NYHA class III-IV
  7. Add ICD if EF <35% in class II-III
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15
Q

Tx of Acute Decompensated HF

A

•Hospitalize

•IV Loop Diuretics (furosemide)

  • Strict ins and outs
  • Dailys weights
  • Sodium and fluid restrictions
  • Rate control – BBs or CCB

•Start ACE for systolic dysfunction

  • Monitor electrolytes (k, Mg)
  • Monitor Kidney function
  • Creatinine bumps due to excessive diuresis
  • Acute kidney dysfunction due to INC creatinine – give Lasix
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16
Q

in HF ACE, ARB or ARNI approproate

A

HFrEF

Patients with current symptoms of HFrEF to reduce morbidity and mortality

ARB if intoilerant to ACE

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17
Q

Chronic symptomatic HFrEF NYHA class II or III pts who tolerate an ACE inhibitor or ARB –> replacement of?

A

•replacement by an ARNI is recommended to further reduce morbidity and mortality

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18
Q

meds that make up ARNI

A

Entresto

sacubitril/valsartan.

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19
Q

med for pts w/ HFrEF with an EF <35% who are currently on max dose BB

A

Ivabradine -> reduce hospitalizations

requirements

  • a beta-blocker at max tolerated dose
  • In sinus rhthym
  • and whose HR is >70bpm at rest

EF <35%

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20
Q

most common causes of endocarditis on

native valve

IVDU

A
  • Staph aureus
  • Viridians group Strep
  • Enterococci
  • Coag-negative strep

IDVU

•staph a. MRSA

fungal more common

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21
Q

most common valve affected by endocarditis

most common in IVDU

A

most common aortic

IVDU - tricuspid

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22
Q

3 lesions seen w/ endocarditis

A

Janeway lesions – nontender erythematous macules on palms and soles

Osler nodes – tender SQ violaceus nodules mostly on pads of fingers and toes

Roth spots – exudative, edematous hemorrhagic lesions of retina w/ pale centers seen on fundoscopic examination

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23
Q

what is duke criteria

A
  • Determines who should get an echo
  • Based off of pts w/ left sided native valve endocarditis
  • No tricuspid valve

Only atrial and mitral

Definite IE

Possible IE

Rejected IE

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24
Q

most common pathogrens responsible for endocarditis in prothestic valves

A

staph or strep

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25
Q

Si/Sx of endocarditis

A

nonspecific

usually new or worsening cardiac murmur

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26
Q

complciations of endocarditis

A

cardiac - most common

nuero

septic

metastatic infection - clear infection before surgery

systemic immune reaction

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27
Q

tx for endocarditis

A
  1. Blood cx
  2. Empiric abx therapy – narrow once we have sensitivities (vanco or cefepime)
  • IV 4-6 weeks
  • Can be sent home w/ PICC line
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28
Q

indications for surgery in endocarditis

A
  • Acute HF
  • Unresponsive to therapy after 7-10 days (persistent fevers & positive blood cx)
  • Fungal or gram-neg bacilli endocarditis
  • Recurrent endocarditis
  • Continued embolization despite medical management
  • Prosthetic valve involvement
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29
Q

most common causes of

acute pericarditis

subacute

constrictive (chronic)

A

acute - viral

  • Coxsackievirus
  • Echovirus
  • Influenza

subacute -

M tuberculosis

Dressler’s syndrome

chronic

Radiation

Cardiac surgery

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30
Q

Pleuritic chest pain – alleviated by sitting forwards and worsens by leaning back

dx?

A

pericarditis

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31
Q

on exam on pericarditis you will hear whart sound

acute/subacute

chronic

A

acute/subacute -•Pericardial friction rub

chronic - Pericardial “knock

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32
Q

elevated JVD w/ Kussmal’s sign is assoc w/ what type of pericarditis

A

•Kussmal’s sign – failure of RA pressure to fall w/ inspiration

Constrictive (Chronic) Pericarditis

along w/

Hepatic congestion

Afib – due to enlarged atria

Pericardial “knock”

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33
Q

tx of acute/subacite pericarditis

A

Reduce inflammation

  • Aspirin
  • NSAIDs (indomethican or ibuprofen) for 2 weeks

Resistant cases - Corticosteroids

Dressler’s syndrome – pericarditis after MI

  • Colchicine TID x 3 mo
  • +/- NSAIDs/ aspirin PRN
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34
Q

tx of Constrictive (Chronic) Pericarditis

A

Medication management: diuretics

  • Loops (furosemide, torsemide)
  • Thiazides
  • Aldosterone antag

Surgical interventions: Pericardiectomy

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35
Q

Pt w acute pericarditis should be admitted if:

A
  • Fever >38
  • Subacute course
  • Evidence of cardiac tamponade
  • Large pericardial effusions
  • Immunosuppressed
  • Pts on aticoags
  • Acute trauma
  • Failure to improve outpt
  • Elevated cardiac enzymes
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36
Q

acute, subacute, chronic is described as what length of time

A

acute <2wks

subacute >2wks

chronic >12wks

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37
Q

Inflammation that leads to thickened, fibrotic pericardium

  • Restricts diastolic filling
  • Causes chronically elevated venous pressures -> HF

Dx?

A

Constrictive (Chronic) Pericarditis

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38
Q

define dresslers syndrome and tx

A

Dressler’s syndrome – pericarditis after MI (subacute pericarditis)

  • Colchicine TID x 3 mo
  • +/- NSAIDs/ aspirin
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39
Q

define Pericardial Effusions vs cardiac tamponade

A

p effusions - Accumulation of fluid in pericardium

tamponade - Accumulation of fluids in pericardial space that causes significant hemodynamic changes

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40
Q

EKG findings in pericardial effusions

A
  • Low voltage
  • Electrical alternans pathognomonic à caused by heart swinging in fluid
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41
Q

on exam of pt w/ pericardial effusions you will hear (2)

A
  • Pericardial friction rub
  • Muffles heart sounds
42
Q

gold standard for dx pericardial effusions

A

Echo – gold standard, very sensitive, primary method of dx

43
Q

tx of Pericardial Effusions

A

Small effusions: Observation, Serial echos

Moderate - large: Pericardiocentesis, Pericardial drain placement

R_ecurrent effusions_: Pericardial window

44
Q

define Becks triad

what does it help dx

A

cardiac tamponade

  • Low arterial pressure (hypotension)
  • Dilated neck veins (elevated JVD)
  • Muffled heart sounds
45
Q

si/sx cardiac tamponade

acute vs subacute

A

acute

  • Cool extremities
  • Cyanosis
  • Decreased urine output
  • Decreased end organ perfusion (liver, kidney)

subacute

  • chest fullness
  • Peripheral edema
  • Fatigue

Narrow pulse pressure (80.70) –compressed heart does not contract well

46
Q

what is Pulsus Paradoxus

it is a dx factor of?

A

•Greater then 10mmHg drop in systolic pressure during inspiration due to impaired LV filling

cardiac tamponade

47
Q

dx and tx cardiac tamponade

A

dx - echo gold standard - RV compression and collapse

tx

Emergent pericardiocentesis

  • Needle in apex of heart 5th ICS medial LSB
  • Should get fluid, if red blood you have gone too far and into left ventricle

If s/p cardiac surgery reopen sternotomy

If trauma or surgery relation – pericardial drain is sometimes left in place

48
Q

Types of Aortic Aneurysms

A
  • Fusiform – affects entire circumference of segmented vessel
  • Saccular - involves only a portion of the circumference resulting in outpouching of wall
  • Pseudoaneurysm - intimal and medial layers are disrupted.
  • Dilated segment is lined by adventitia only (occasionally clot)
49
Q

most common ocation of TAA

A

infrarenal -95%

Ascending aortic aneurysm 55%

50
Q

most common etiology of TAA

A

Cystic medial necrosis most common with ascending aortic aneurysms (inherited conditions)

Arteriosclerosis most common with aneurysms of the aortic arch and descending thoracic aorta

51
Q

si/sx TAA

A

Asymptomatic

Tracheal tugging

if rupture:

  • Tachycardia
  • Hypotension
  • Chest pain
  • Left hemothorax
  • Cardiac tamponade
52
Q

gold standard for dx TAA

A

CT angiogram - gold standard

53
Q

tx TAA

A

Control HTN

  • BBs especially in Marfans
  • ACE, ARB

Smoking cessation

Operative repair/ prosthetic graft if symptomatic:

  • >5.5cm diameter asc aorta
  • >6.5 desc aorta
  • Relative aortic size index (aortic diameter /BSA)
54
Q

risk trifecta for AAA

A
  • Age >65
  • PAD – atherosclerosis
  • Smoker
55
Q

why do we screen for AAA and explain screening process

A

they are asymptomatic untul rupture

Screening pts at risk for AAA – abdominal US

•Men 65-74 w/ hx of smoking

•Siblings or offspring w/ AAA
have thoracic or peripheral arterial aneurysms

•Pts w/ hypermobility syndromes (Ehlors-Danlos and Marfans)

56
Q

at what size are we conderned for AAA rupture

A

>5 cm women

>5.5cm males

57
Q

imaging modality of choice in AAA

A

US

58
Q

tx AAA

A

AntiHTN – BBs

Smoking cessation

Surveillance until >5.5cm

  • 3-3.9cm every 3 yrs
  • 4-4.9cm every yr
  • 5-5.4 every 6 mo

Elective repair if >5.5cm if

  • low/acceptable surgical risk
  • Fast growing >1cm in a yr

Open repair - Endovascular repair (EVAR)

REBOA - cross-clamp aorta in field

59
Q

describe process of aortic dissection

A
  1. Tear in the aortic intima
  2. Blood dissects into the media
  3. Intima separates from the surrounding media
  4. False lumen created
  5. Circulation in affected area can be disrupted
60
Q

where do most dissections occur

A
  • 2.2cm above aortic root
  • Distal L subclavian
  • Aortic arch
  • 90% 1st 10cm aorta
61
Q

risk factors for aortic dissection

A

Systemic Hypertension (72%)

• Atherosclerosis(31%)

62
Q

Severe sharp or *”tearing” chest pain in ant/posterior chest or back sudden onset, radiating into anterior chest or neck

A

aortic dissection- classic presentation

63
Q

si/sx of ascending vs descing aorta dissection

A

ascending

  • Aortic valve regurgitation
  • Acute MI
  • Cardiac tamponade
  • Horner syndrome
  • Vocal cord paralysis

descending

  • Chest or backpain
  • Abrupt onset of pain
  • Migrating pain
  • Ischemic peripheral neuropathy
64
Q

gold standard dx aortic dissection

A

CTA gold standard

•MRI if contrast allergy – will prob die

65
Q

tx of aortic dissection

A

Dissection of a_scending aorta_ – surgical emergencies

•Open vs EVAR

Dissection of descending aorta – medical management initially

  • Pain relief (IV morphine)
  • Reduction of SBP (BBs) – drop shearing forces

Surgical candidate if:

  • Progressive dissection w/ end-organ ischemia
  • Continued hemorrhage in pleural or retroperitoneal space
  • Cardiac tamponade – pericardiocentesis
66
Q

2 classification systems for dissections

A

stanford

Type A – arises from ascending aorta

Type B – arises distal to left subclavian

Debakey

Type I - Ascending, descending aorta, Aortic arch

Type II - Only ascending aorta

Type III - Only descending aorta

67
Q

•Mortality untreated type A dissection

A
  • 1% per hour for 72 hours
  • Over 90% at 3 months
68
Q

risk factor for PAD

A

End stage renal disease*

smoking

  • HTN
  • DM
  • Hyperlipidemia
  • Metabolic syndrome
69
Q

si/sx of Peripheral artery disease

A

Asymptomatic

Claudication – get up and walk around legs get sore à improves at rest

  • Buttock and hip
  • Thigh
  • calf
  • Foot

As condition worsens:

Pain at rest

Nonhealing wounds

Gangrene

Erectile dysfunction

70
Q

PE findings in PAD

A
  • Smooth shiny skin – hairless
  • Reduced skin temp
  • Pallor/cyanosis/mottling
  • Ulcers
  • Dependent rubor
71
Q

Ankle-Brachial pulse (ABI) is used in dx of?

A

PAD

compare SBP at ankle w/ systolic brachial pressure

  • 1:1 normal
  • 0.4-0.9 mild PAD
  • 0.0.40 – severe PAD
72
Q

essentials for dx PAD

A
  • Abnormal pulse exam
  • Claudication
  • Ischemic rest pain
  • Tissue loss (ulceration or gangrene)
  • ABI <0.9
73
Q

tx PAD

A

Conservative care

Medical management – ALL Patients on: ASA & Statin

Claudication -Cilostazole or Pentoxifyillne

Angioplasty or stent placement – based on TASC classification

Surgical intervention: Endartectomy (type D, C, B who fail tx)

Aortobifemoral bypass graft (AFBG

amputation - fail all above

74
Q

TASC classification for Angioplasty or stent placement in PAD

A
  • Type A, B, C, D
  • A lesions – short stenosis
  • D lesions – diffuse dz, chronic occlusions
  • Preferred for A or B (possibly C if not surgical candidate
75
Q

6 Ps of limb occlusion

A
  • Pulselessness
  • Pain
  • Poikilothermic – one limb cooler then other
  • Pallor
  • Paresthesia
  • Paralysis
76
Q

tx of arterial occlusion

A
  1. revascularize- IV heparin
  2. Find source of embolus
  • EKG and telemetry
  • US
  • Hypercoagulable evaluation
  • TEE to r/o cardiac source
  • Chest CT
77
Q

Blue toe syndrome

Dx?

A

scattered petechiae or cyanosis on soles of foot or toes

Arterial Occlusion

78
Q

VTE risk factors

A

acquired •Previous VTE*

Inherited Thrombophilia:

79
Q

virchows triad

A

risk fx in venous thromboembolism

  1. Stasis
  2. Endothelial trauma
  3. Hypercoagulable state
80
Q

Superficial Thrombophlebitis most common vein affected

A

GSV

81
Q

superficial vs deep embolism si/sx

A

superficial

  • Pain at site of superficial vein
  • Local erythema and warmth
  • Minimal swelling at site w/ no significant extremity edema

deep

  • Pain
  • Swelling
  • Erythema
  • Warmth

Severity varies – diffuse

82
Q

what is Lemierre syndrome:

A

Superficial Thrombophlebitis

Associated w/ thrombus of internal jugular vein-IVDU

Pharyngitis/tonsilitis infection - significant UR systems

83
Q

Septic thrombophlebitis: Has Trifecta

A
  • Venous thrombosis
  • Inflammation
  • Bacteremia

consult surgery

84
Q

IF in GSV or SSV within ____ near the saphenofemoral junction will need consideration of _______ 45 days and repeat serial imaging -> Hematology consult

A

5cm

anticoagulation

85
Q

define Chronic venous stasis disease

A

patients with chronic venous disease who display more advanced clinical signs, , such as significant edema, skin changes or ulceration

86
Q

si/sx of Chronic venous stasis disease

A

•Leg pain or “aching” and fatigue

  • Leg heaviness
  • Leg swelling

•*Sx worse at end of the day or after prolonged standing

•Edema, skin changes, discoloration

87
Q

etiology of •chronic venous stasis

A
  • Inadequate muscle pump function
  • Incompetent valves (reflux)
  • Venous thrombosis / obstruction
  • Elevated venous pressure
88
Q

dx of Chronic venous stasis disease

A
  • Presence of typical symptoms
  • Possible presence of dilated superficial veins
  • Presence of skin changes, edema or ulcer
  • Confirmation w/ venous duplex study (US)
89
Q

tx of Chronic venous stasis disease

A

Initial – conservative

•Compression therapy *** (no ACE wraps)

  • Multilayer wrap
  • Unna Boot

Stasis dermatitis – topical steroids, wet dressing, compression (unna)

Refer to wound clinic - Abx if infection

Ablation – chemical, mechanical, thermal

90
Q

describe chemical ablation

A

Sclerotherapy (small veins <4mm diameter

•Risks: phlebitis, tissue necrosis, infection

91
Q

describe mechanical ablation

A

tx varicose veins

•Phlebectomy or ligation

92
Q

describe thermal ablation

A
  • Endovenous laser ablation (ELA)
  • Radiofrequency ablation (RFA) saphenous vein ablation – high success & low complications
93
Q

contrast presentation of chronic venous stasis vs lymphadema

A

chronic venous stasis

  • Pitting edema – bilateral
  • Spare dorsal foot

lymphadema

Non-pitting edema – unilateral **

Involves dorsal foot ***

94
Q

describe 3 primary causes of lymphadema and their age of onset

A
  • Congenital lymphedema – birth – 2 yrs
  • Lymphedema pracox – onset during puberty or pregnancy to age 35
  • Lymphedema tarda – onset after age 35
95
Q

most common causes of lymphadema in developed vs developong world

A

developed -•Cancer or cancer tx HUGE risk factor

developing - Filariasis (infection by nematode) Wuchereria bancrofti (elephantiasis)

96
Q

Essentials of Dx of Lymphedema

A
  • Painless persistent edema of one or both lower extremities
  • Pitting or non-pitting edema without ulceration, varicosities, or stasis pigmentation
  • May be episodes of lymphangitis and cellulitis
97
Q

IF patient from an endemic area and presents w/ lymphadema what must you do

A

•blood smears for microfilariae

98
Q

tx Lymphedema

A

No cure but treatment to avoid development interstitial fibrosclerosis

Conservative tx – compression stockings >40mmHg

Pharmacologic treatment

  • Coumarin and flavonoids - Decrease edema, soften limb, decrease # of secondary infections (Hepatotoxic)
  • Diuretics (furosemide, bumex)

physiological vs excisional surgical options

99
Q

physiological vs excisional surgical options in tx lymphadema

A

Physiologic surgical options:

  • Lymphatic-lymphatic bypass
  • Lymphovenous anastomosis
  • Vascularized autologous LN transfer – transfer healthy LN to that area à best if performed early before sclerofibrosis of adipose

Excisional Surgical option:

  • Soft tissue removal of SQ (difficult w/ fibrosis)
  • Stages excision
100
Q

what size should AAA be repaired

A

>5.5cm

101
Q

EKG changes in acute pericarditis

A

diffuse ST elevations

Clin med II exam II Cardio (3 decks)

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