Infections, HF, shock, vascular dz Flashcards
1
Q
most common cause of right sided HF
A
left sided HF
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
3
Q
si/sx of left sided HF
A
Blood backs up into lungs (pulmonary edema) initially
SOB on exertion
orthopena
Paroxysmal nocturnal dyspnea
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)
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)
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
7
Q
in setting of HF when can we order an echo
A
new diagnosis OR decompensating HF that is unexplained
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
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
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
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)
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)
13
Q
meds shown to reduce hospitilizations in HF
A
- Digoxin
- Ivabradine – EF <35% on max BB or BBs are CI
14
Q
Systolic HFrEF Tx
A
- Start EVERYONE on ACE at time of diagnosis (or ARB)
- Start Furosemide (Lasix) on everyone w/ symptoms
- Add Beta-blocker for ALL patients
- Add aldosterone antagonist (spironolactone) to Lasix if persistent symptoms
- Change from ACE or ARB to ARNI at class II if no CI
- Add hydral-nitrates for black patients NYHA class III-IV
- Add ICD if EF <35% in class II-III
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
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
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
18
Q
meds that make up ARNI
A
Entresto
sacubitril/valsartan.
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%
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
21
Q
most common valve affected by endocarditis
most common in IVDU
A
most common aortic
IVDU - tricuspid
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
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
24
Q
most common pathogrens responsible for endocarditis in prothestic valves
A
staph or strep
25
Si/Sx of endocarditis
nonspecific
usually new or worsening cardiac murmur
26
complciations of endocarditis
cardiac - most common
nuero
septic
metastatic infection - clear infection before surgery
systemic immune reaction
27
tx for endocarditis
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
28
indications for surgery in endocarditis
* 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
29
most common causes of
acute pericarditis
subacute
constrictive (chronic)
acute - viral
* Coxsackievirus
* Echovirus
* Influenza
subacute -
M tuberculosis
Dressler’s syndrome
chronic
**Radiation**
Cardiac surgery
30
Pleuritic chest pain – alleviated by sitting forwards and worsens by leaning back
dx?
pericarditis
31
on exam on pericarditis you will hear whart sound
acute/subacute
chronic
acute/subacute -•Pericardial friction rub
chronic - Pericardial “knock
32
elevated JVD w/ Kussmal’s sign is assoc w/ what type of pericarditis
•Kussmal’s sign – failure of RA pressure to fall w/ inspiration
## Footnote
Constrictive (Chronic) Pericarditis
along w/
Hepatic congestion
Afib – due to enlarged atria
Pericardial “knock”
33
tx of acute/subacite pericarditis
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
34
tx of Constrictive (Chronic) Pericarditis
Medication management: diuretics
* Loops (furosemide, torsemide)
* Thiazides
* Aldosterone antag
Surgical interventions: Pericardiectomy
35
Pt w acute pericarditis should be admitted if:
* Fever \>38
* Subacute course
* Evidence of cardiac tamponade
* Large pericardial effusions
* Immunosuppressed
* Pts on aticoags
* Acute trauma
* Failure to improve outpt
* Elevated cardiac enzymes
36
acute, subacute, chronic is described as what length of time
acute \<2wks
subacute \>2wks
chronic \>12wks
37
Inflammation that leads to thickened, fibrotic pericardium
* Restricts diastolic filling
* Causes chronically elevated venous pressures -\> HF
Dx?
Constrictive (Chronic) Pericarditis
38
define dresslers syndrome and tx
Dressler’s syndrome – pericarditis after MI (subacute pericarditis)
* Colchicine TID x 3 mo
* +/- NSAIDs/ aspirin
39
define Pericardial Effusions vs cardiac tamponade
p effusions - Accumulation of fluid in pericardium
tamponade - Accumulation of fluids in pericardial space that causes _significant hemodynamic changes_
40
EKG findings in pericardial effusions
* Low voltage
* Electrical alternans pathognomonic à caused by heart swinging in fluid
41
on exam of pt w/ pericardial effusions you will hear (2)
* Pericardial friction rub
* Muffles heart sounds
42
gold standard for dx pericardial effusions
Echo – gold standard, very sensitive, primary method of dx
43
tx of Pericardial Effusions
_Small effusions:_ Observation, Serial echos
_Moderate - large_: Pericardiocentesis, Pericardial drain placement
R_ecurrent effusions_: Pericardial window
44
# define Becks triad
what does it help dx
cardiac tamponade
## Footnote
* Low arterial pressure (hypotension)
* Dilated neck veins (elevated JVD)
* Muffled heart sounds
45
si/sx cardiac tamponade
acute vs subacute
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
what is Pulsus Paradoxus
it is a dx factor of?
•Greater then 10mmHg drop in systolic pressure during inspiration due to impaired LV filling
cardiac tamponade
47
dx and tx cardiac tamponade
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
Types of Aortic Aneurysms
* 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
most common ocation of TAA
infrarenal -95%
Ascending aortic aneurysm 55%
50
most common etiology of TAA
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
si/sx TAA
Asymptomatic
Tracheal tugging
if rupture:
* Tachycardia
* Hypotension
* Chest pain
* Left hemothorax
* Cardiac tamponade
52
gold standard for dx TAA
CT angiogram - gold standard
53
tx TAA
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
risk trifecta for AAA
* Age \>65
* PAD – atherosclerosis
* Smoker
55
why do we screen for AAA and explain screening process
they are asymptomatic untul rupture
## Footnote
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
at what size are we conderned for AAA rupture
\>5 cm women
\>5.5cm males
57
imaging modality of choice in AAA
US
58
tx AAA
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
describe process of aortic dissection
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
where do most dissections occur
* 2**.2cm above aortic root**
* Distal L subclavian
* Aortic arch
* 90% 1st 10cm aorta
61
risk factors for aortic dissection
Systemic Hypertension (72%)
• Atherosclerosis(31%)
62
Severe sharp or \*”tearing” chest pain in ant/posterior chest or back sudden onset, radiating into anterior chest or neck
aortic dissection- classic presentation
63
si/sx of ascending vs descing aorta dissection
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
gold standard dx aortic dissection
CTA gold standard
•MRI if contrast allergy – will prob die
65
tx of aortic dissection
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
2 classification systems for dissections
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
•Mortality untreated type A dissection
* 1% per hour for 72 hours
* Over 90% at 3 months
68
risk factor for PAD
End stage renal disease\*
smoking
* HTN
* DM
* Hyperlipidemia
* Metabolic syndrome
69
si/sx of Peripheral artery disease
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
PE findings in PAD
* **Smooth shiny skin – hairless**
* Reduced skin temp
* Pallor/cyanosis/mottling
* Ulcers
* Dependent rubor
71
Ankle-Brachial pulse (ABI) is used in dx of?
PAD
## Footnote
compare SBP at ankle w/ systolic brachial pressure
* 1:1 normal
* 0.4-0.9 mild PAD
* 0.0.40 – severe PAD
72
essentials for dx PAD
* Abnormal pulse exam
* Claudication
* Ischemic rest pain
* Tissue loss (ulceration or gangrene)
* ABI \<0.9
73
tx PAD
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
TASC classification for Angioplasty or stent placement in PAD
* 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
6 Ps of limb occlusion
* Pulselessness
* Pain
* Poikilothermic – one limb cooler then other
* Pallor
* Paresthesia
* Paralysis
76
tx of arterial occlusion
1. revascularize- IV heparin
2. Find source of embolus
* EKG and telemetry
* US
* Hypercoagulable evaluation
* TEE to r/o cardiac source
* Chest CT
77
Blue toe syndrome
Dx?
scattered petechiae or cyanosis on soles of foot or toes
## Footnote
Arterial Occlusion
78
VTE risk factors
acquired •Previous VTE\*
Inherited Thrombophilia:
79
virchows triad
risk fx in venous thromboembolism
1. Stasis
2. Endothelial trauma
3. Hypercoagulable state
80
Superficial Thrombophlebitis most common vein affected
GSV
81
superficial vs deep embolism si/sx
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
what is Lemierre syndrome:
Superficial Thrombophlebitis
Associated w/ thrombus of internal jugular vein-IVDU
Pharyngitis/tonsilitis infection - significant UR systems
83
Septic thrombophlebitis: Has Trifecta
* Venous thrombosis
* Inflammation
* Bacteremia
consult surgery
84
IF in GSV or SSV within ____ near the saphenofemoral junction will need consideration of _______ 45 days and repeat serial imaging -\> Hematology consult
5cm
anticoagulation
85
define Chronic venous stasis disease
patients with chronic venous disease who display more advanced clinical signs, , such as significant edema, skin changes or ulceration
86
si/sx of Chronic venous stasis disease
**•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
etiology of •chronic venous stasis
* Inadequate muscle pump function
* Incompetent valves (reflux)
* Venous thrombosis / obstruction
* Elevated venous pressure
88
dx of Chronic venous stasis disease
* Presence of typical symptoms
* Possible presence of dilated superficial veins
* Presence of skin changes, edema or ulcer
* Confirmation w/ venous duplex study (US)
89
tx of Chronic venous stasis disease
_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
describe chemical ablation
Sclerotherapy (small veins \<4mm diameter
•Risks: phlebitis, tissue necrosis, infection
91
describe mechanical ablation
tx varicose veins
## Footnote
•Phlebectomy or ligation
92
describe thermal ablation
* Endovenous laser ablation (ELA)
* Radiofrequency ablation (RFA) saphenous vein ablation – high success & low complications
93
contrast presentation of chronic venous stasis vs lymphadema
chronic venous stasis
* Pitting edema – bilateral
* Spare dorsal foot
lymphadema
Non-pitting edema – unilateral \*\*
Involves dorsal foot \*\*\*
94
describe 3 primary causes of lymphadema and their age of onset
* Congenital lymphedema – birth – 2 yrs
* Lymphedema pracox – onset during puberty or pregnancy to age 35
* Lymphedema tarda – onset after age 35
95
most common causes of lymphadema in developed vs developong world
developed -•Cancer or cancer tx HUGE risk factor
developing - Filariasis (infection by nematode) *Wuchereria bancrofti (elephantiasis)*
96
Essentials of Dx of Lymphedema
* 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
IF patient from an endemic area and presents w/ lymphadema what must you do
•blood smears for microfilariae
98
tx Lymphedema
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
physiological vs excisional surgical options in tx lymphadema
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
what size should AAA be repaired
\>5.5cm
101
EKG changes in acute pericarditis
diffuse ST elevations
