firecracker 11/28 Flashcards
RHF
right ventricle cannot pump blood into lungs
blood accumulates in systemic venous system
most common cause of RHF
left heart failure
also:
pulmonary HTN, L2R shunt, Tricuspid valve regurg
most common cause of RHF if no LSHF
COPD
cor pulmonale
rhf due to chornically elevated pulmonary artery pressures
RSHF symptoms
HSM
peripheral edema
jugular venous distension
hepatomegaly in RSHF
venous congestion of hepatic veins of liver
can cause portal htn
hepato-jugular reflux
pressing on RUQ elcitis distension of right jugular vein
peripheral edema cause
increase in venous hydrostatic pressure
jugular venous distension
increased venous pressure in superior venous cava
>4cm abnormal
severe pulmonary hypertension ECG
P pulmonale
peaked P waves >2.5 in inferior leads II, III, avf
right axis deviation
right ventricular hypertrophy
treatment for cor pulmonale
adequate oxygenation
correct respiratory acidosis
treat underlying infections
decrease work of breathing using positive pressure or bronchodilators
HIT
immune mediated reaction after exposure to heparin products
paradoxically pro-thrombotic state
pathophysiology of HIT
auto-antibodies to platelet factor 4:heparin complex Ab cross react with platelets peripheral activation (thrombosis) and destruction (thrombocytopenia)
HIT risk factors
unfractionated (vs LMWH)
higher doses
female
recent surgery
timing of hit
5-10 days after exposure
early onset within 24 hrs if exposed to heparin in past 3 months
thrombocytopenia in HIT
drop in platelet count >50%
thrombosis in HIT
venous>arterial
skin necrosis at injection sites
limb gangrene
organ ischemia or infarction
4 T score of HIT
thrombocytopenia
timing
thrombosis
oTher causes not present
HIT diagnosis
immunoassay test anti-PF4 antibodies
serotonin release assay
management of HIT
stop heparin
start direct thrombin inhibitor (argatroban or bivalirudin)
fondaparinux
HIT - pts with renal dysfunction
argratroban
HIT - pts with hepatic dysfunction
fondaparinux
gout
deposition of monosodium urate crystals in joints
primary gout
hyperuricemia due to nucleic acid metabolism disorders or underexcretion of uric acid
secoundary gout
diseases with high metabolic turnover (leukemia, psorasis)
gout age groupd
men, 40-60
overproduction of uric acid
obesity, cancer, hemoglobinopathies
underexcretion of uric acid
renal disease
diuretic use
podagra
first metatarsophalangeal joint
gout diagnosis
needle shaped negatively birefringent crystals
not uric acid
tophi
x ray imaging that shows bony erosions and soft tissue crystal deposition
gout treatment
nsaids, colchicine, corticosteroids
chronic gout treatment
allopurinol (decrease UA production)
probenecid (inhibit renal UA reabsorption)
pleural effusion
collection of fluid between parietal and visceral pleura
causes of exudative pleural effusions
lung infections, tb
cancer
pulmonary embolism
impaired pleural lymphatic drainage
transudative
increased hydrosatatic pressure or decreased serum oncotic pressure
exudate
increased vessel permeability
causes of transudative pleural effusion
CHF
nephrosis, cirrhosis
injuries to pleural lining
injuries to pleural lining
central venous catheter misplacement
pulmonary emobolism - type of pleural effusion
trans or exud
chylous effusions
iatrogenic (surgery)
traumatic
malignant
pleural effusion symptoms
dyspnea
pleuritic chest pain
worsens with time
associated symptoms (night sweats, wt loss, swelling)
pleural effusion physical exam
decreased breath sounds
dullness to percrussion
decreased fremitus
pleural effusion cxr
blunting of costophrenic angle
transudative - bilateral, exudative - unilateral
lateral decubitus cxr
most sensitive
light’s criteria
pleural prot/serum >.5
pleural ldh/serum ldh >.6
pleural ldh greater than 2/3 of normal serum ldh
treatment of parapneumonic effusions (around a pneumonia)
antibiotics if uncomplicated
chest tube drainage if complicated
ischemic atn most common cause
pre renal failure
- decreased effective circulating load/preload
- decreased cardiac output
- nsaids
DKA potassium levels
low total body levels
normal/high on labs
common cause of nephrotoxic ATN
aminoglycosides, amph b, cisplatinum
heavy metals, contrast, gram negative sepsis, myoglobinuria
meds for pts with coronary interventions
clopidogrel
gb11a/111b inhibitor
decreased effective circulating blood volume
hypovolemia
systemic vasodilation/septic shock
cirrhosis
chylous pleural effusion
iatrogenic (surgery)
traumatic
malignant
CXR RSHF
right ventricular enelargement
pulmonary artery dilatation
delta gap
AG - 12
/
24 - HCO3
ATN - ischemic and nephrotoxic have in common…
disturbances in renal blood flow
tubular injury
RSHF echo
tricuspid regurg
paradoxical displacement of IV septum into LV during systole
agents that cause CAP
streptococcus pnemoniae haemophilus influenzae klebsiella pneumonia pseudomonas aeruginosa staphylococcus aureus
most common cause of pneumonia
streptococcus pneumoniae
risk factors for streptococcus pneumoniae
smoking
copd
immunocompromised
H influenzae risk factors
sickle cell dz
copd, smoking
immunocomprimised
alcoholism, diabetes
klebsiella risk factors
alcoholics, strokes, elderly, decreased LOC
pseudomonas risk factors
structural lung dz: bronchiectasis, cystic fibrosis, copd
hosp or nursing home residents
pts who have received broad spectrum antibiotics or high dose steroid therapy
s. aureus risk factors
recent flu or viral illness
skin colonization or staph infection
laryngeal cancer
immunosuppressoin
pseudomonas treatment
piperacillin/tazobactam
cefepime
imipenem
meropenem + fluroquinolone
symptoms for pneumonia
increased tactile fremtius
dullness to percussion
pleural friction rub
atelectasis is
decrease in lung volume secondary to partial collapse of lung tissue
atelectasis caused by
operations, impaired inspiratory ability, lack of cough reflex, obstructions/tumors, foreign body in children
resorption atelectasis
airway obstructed by foreign object, tumor or thick mucus plug
devoid of lung sounds
compression atelectasis
space occupying lesion in pleural caivty (air or fluid) increases pressure
atelectasis symptoms
dyspnea, fever
pleuritic chest pain
tachycardia, hypoxia
atelectasis physical exam
dullness to percuss
decreased breath sounds
crackles on ausuclation
atelectasis CXR
raised diaphram in lower lobe atelectasis
tracheal deviation towards atelectasis in upper lobes
fluffly infiltrates
atelectasis treatment
incentive spirometry
deep breathing
ambulation
(bronchoscopy)
atelectasis complications
damange to lung parenchyma
pneumonia
resp failure
maintaining body ph
bicarbonate buffer in ECF
proteins and phosphates in ICF
phosphate regulation
PTH decreases
insulin lowers
vit D increases
signs of pulmonary emoblism - later
resp alkalosis with hypoxia, hypocarbia
loud p2
right heart failure
unstable angina
1) chest pain at rest >10 min
2) severe and new onset
3) cresendo pattern
most common cause of UA/NSTEMI
rupture of coronary artery plaque –> down stream occlusion
unstable angina cause
incomplete stenosis or presence of well-perfused collaterals
st depression
subendocardial ischemia
NSTEMI vs UA
elevations in cardiac enzymes in NSTEMI
pts w/ UA/NSTEMI admit
- telemetry
- serial cardiac enzymes
- possible coronary angiography if indicated
Thrombolysis Infarction Risk score
> /= 3 consider LMWH, angiography
Severe angina, coronary artery stensosi >50%, age >65, aspirin use within past 7 days, three or more Risk factors for cad, enzymes elevated, ST segment changes
cardiac stress test
- diagnose ischemic heart disease
cardiac stress test, how test is performed
exercise –> increase cardiac oxygen demand
dobutamine – cardiac INOTROPE
stress test with adenosine or dipyridamole
coronary vasodilators
stenotic vessels will dilate less
blood flow through stenotic vessels will be decreased and those tissues will get less oxygen –> “cardiac steal”
pre test probability of coronary artery disease
age
sex
typical/definitive AP vs atypical probably AP
nonagnial chest pain
high probability patients
more likely to have false negative
diagnostic testing for CAD warranted in
pts with symptoms of CAD
asymptomatic pts with high pre test CAD probability
pts with newly diagnosed heart failure
asymptomatic pts who should undergo stress testing
> 20% 10-year CAD risk
exercise ECG
symptomatic pts with low or intermediate pre-test probability
if able to exercise and have interpretable ECG –> undergo stress exercise testing
test of choice for symptomatic pts unable to exericse or uninterpretable ECG
stress radionuclide imaging or echo
stress cardiac mri
symptomatic high pre test
symptomatic pt with high pre test probability should receive
stress radionucleide imaging, stress echo, stress MRI, or coronary angiography
not exercise ecg
newly diagnosed CHF pts
evaluated similarity to symptomatic with high pre test probability
exercise stress test that diagnose coronary artery stenosis show
greater than 2mm ST segment depression
greather than 10mmhg drop in systolic blood pressure
drugs that should be held before exercise stress test
beta blockers, non-dihydropyridine calicum channel blockers
certain antiarrhthm - amiodaraone, sotalol
digoxin, nitrates
exercise stress testing contraindicated in
unstable patients
patients who cannot exercise
patients with uninterpreable EKGs
nuclear stress testing
thallium
accumulates in well-perfused heart tissue
approriate in pts with baseline EKG abnormalities
coronary angiography
most sensitive and specific for CAD
allows immediate intervention (stent placement)
A fib
signal from SA node is overwhelmed by disorganized signals from other areas
myocytes contracting at different times
most important risk factor for A fibrillation
mitral valve stenosis
A fib incidence increases with
age
atrial rate vs ventricular rate
500bpm vs 120-180
A fib symptoms
palpitations
exercise intolerance
venous statsis –> SOB, edema
A fib EKG/PE
> 100 bmp
irregularly regular rhythm with ventricular rate >100 bmp
absence of p waves
narrow QRS complexes
lab tests for A fib
renal function
electrolytes
TSH
CBC
complications of a fib arise from
reduced CO
increased cardiac oxygen demand
thromboembolism
A fib - blood remains
in atrium, may lead to clot –> emoblic event –> stroke
increased cardiac oxygen demand
can lead to MI
reduced cardiac output can lead to
CHF symptoms like pulmonary or lower leg edema
treatment of a fib - ventricular rate
beta blocker, calcium channel blocker
chemical cardioversion of a fib
class IC (propafenone, flecainide) class III (ibutilide, dofetilide > amiodarone, sotalol)
electric cardioversion in afib
delivery of DC synchronized with QRS complex
CHADS
CHF, HTN, Age > 75 (2 pts)
DM
Previous stroke or TIA (2)
VASC
vascular dz
age >65 but less than 75
sex cateogry - female
anticoagulation with a fib
warfarin
dabigatran
warfarin causes prolongation of
PT/INR, aPTT
a fib rate control
class II (BB) class IV (CCBs)
ventricular rate ontrol
slows conduction from fibrilating atria to ventricles
pts >65
rhythm control
propafenone, dofetilide, amiodarone
alter cardiac potential
CHADSVASC of 1
aspirin
CHADSVASC of 2
anticoagulation
TTP and HUS characterized by
microangiopathic hemolytic anemia
+
thrombocytopenia
TTP vs HUS
neuro symptoms - TTP
renal symptoms - HUS
TTP/HUS pentad
F - fever A - micoangiopathic anemia T - thrombocytopenia R - acute kidney injury N - neuro abnormalities (AMS)
MAHA
non-immune hemolysis
RBC fragmentation = schitocytes
TTP/HUS associated symptoms
bloody diarrhea ( e coli 0157h7)
pregnancy
meds - mitomycin C, cyclosporine, gemcitabine
lab studies for TTP/HUS
schistocytes
elevated LDH
decreased haptoglobin
<10% ADAMTS13
TTP/HUS treatment
plasma exchange
normalize platelet count, LDH level
