the abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and usually rapid spontaneous recovery is known as what
syncope
which etiology of syncope is neutrally-mediated; this includes vasovagal
reflex (~58%)
which etiology of syncope will cause bradyarrhythmia or tachyarrhythmia, can be due to a structural heart dz leading to abrupt episodic drops in cardiac output by various mechanisms, poorly tolerated supraventricular and ventricular tachycardias and bradycardias
cardiac disease
what is common among the cardiovascular causes of syncope
transient cerebral hypoperfusion
alteration in systemic blood pressure which leads to rapid drop in BP
what are the etiologies of syncope (PASS OUT)
Pressure
Arrhythmias
Seizures
Sugar
Output
Unusual
Transient
what is the most common reflex mediated syncope
vasovagal syncope
this etiology of syncope is when pts usually have no apparent cardiac or neurological dz
vasovagal (neurocardiogenic) syncope
this type of syncope is when there is an episode after eating, coughing, emotional event, hunger, or pain
situational vasovagal syncope
a postural decrease in systolic BP of at least 20mmHg or greater or a postural increase in HR greater than 20bpm with standing is known as what
orthostatic HoTN
what are the causes of pressure caused syncope
decreased intravascular volume
primary autonomic insufficiency or failure (Parkinson Dz)
this test is commonly performed to evaluate syncope, LIMITED specificity/sensitivity and reproducibility, can be used for pts with recurrent episodes of syncope in the absence of heart dz, unexplained single syncopal episode in high risk settings
tilt test
what are the etiologies of arrhythmias
brady-dysrhythmia
tachy-dysrhythmia
SVT
non-sustained Vtach
Afib
pacemaker malfunction
who do you admit with arrhythmias
cardiac sxs
cardiac risk factors
abn ECG
no support network
seizure sxs
injury with syncope
which diagnostic test is recommended for pts at risk or with CAD; abn ECG or those with syncope during or shortly after exertion
exercise test (stress test)
what is the diagnostic test that should be completed prior to a stress test (exercise test)
echo
which diagnostic test is indicated in selected pts with unexplained syncope, especially if they have structural heart dz
EPS (electrophysiology study)
what are some prodromes associated with seizures
auditory or visual phenomena
olfactory phenomena
nausea
what are the gold standards for dx of a seizure
witnessed
sxs (aura)
+ EEG
a partial or complete LOC but without global cerebral hypoperfusion and is usually caused with low glucose is known as what
hypoglycemia
what cardiac sxs are associated with output syncope
CP
tachypnea
dyspnea
what are some cardiac causes of output syncope
valvular (MS, MS, PS)
HoCM
restrictive or dilated cardiomyopathy
atrial myxoma
cardiac tamponade
aortic dissection
MI
CHF
what are the pulmonary causes of output syncope
PE
pulmonary HTN
carbon monoxide
COPD exacerbation
what is the initial testing for the workup of output syncope
SaO2
ABG
CXR
ECG
when would you get an echo with output syncope
structural heart disease
murmurs
exertional syncope
Hx of cardiac output impairment sxs (DOE)
when would you get a lung scan with output syncope
for the evaluation of syncope, when would you order an echo
pre-cardiac stress testing
exertional syncope
r/o cardiac obstruction
for the evaluation of syncope when would you order a stress test
pts at risk for/or hx of CAD
pts with syncope during or shortly after exertion
echo performed PRIOR to testing
which criteria can we use to evaluate high risk syncope pts
ROSE
what is the ROSE criteria used to evaluate a high risk syncopal pt
B-B type natriuretic peptide >300
B- bradycardia of <50bpm
R- rectal exam with positive FOB test
A- anemia (Hb <9g/dL)
C- CP with syncope
E- EKG with Q waves
S- Sat <94% on room air
if the pt is at a high risk for syncope, when should the be admitted
age >65
known structural heart dz or CAD
SOB
syncope in supine position or during exertional without prodrome
palpitations associated with syncope
Fmhx of sudden cardiac death
abn EKG
HCT <30%
the inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure), or the ability to do so only if cardiac filling pressures are abnormally high (backward failure), or both is known as what
heart failure
about half of pts who have HF die within how many years
5 years
this is most commonly due to conditions that lead to impaired left ventricular function, particular CAD and HTN
HF
this is caused when the heart is unable to maintain adequate cardiac output to meet demands and/or able to do so only by elevating filling pressure
forward heart failure
this is caused when the heart is unable to accommodate venous return resulting in vascular congestion (systemic or pulmonary)
backward HF
severe pulmonary congestion secondary to backwards left heart failure is known as what
pulmonary edema
ineffective ventricular filling is known as what
diastolic dysfunction
ineffective ventricular emptying is known as what
systolic dysfunction
poor cardiac output is known as what
low output
increased metabolic demand is known as what
high output
if there is a pressure overload, what is the compensatory response
hypertrophy
if there is a volume overload, what is the compensatory response
cardiac dilatation
this type of HF (systolic/diastolic) is 2/3 of all HF cases, CAD is the underlying etiology, there is impaired myocardial contractile function which leads to decreased EF and SV, and blood backs up into the pulmonary system
systolic dysfunction
this type of HF (systolic/diastolic) is 1/3 of all HF cases, will have a normal EF, decrease compliance (transient by ischemia, permanently by severe hypertrophy, restrictive cardiomyopathy, MI), and has increased LV filling pressures that produce venous congestion upstream
diastolic dysfunction
what are the causes of L HF
CAD
HTN
idiopathic
valvular (AS, AR, MR)
alcohol (toxic cardiomyopathy)
what are the pure forms of right sided HF
RV has increased compliance in order to handle wide differences in volume return to the heart
RV ejects into the low-pressure pulmonary vascular bed and may be susceptible to acute failure with sudden increases in pulmonary pressures
what are the causes of right HF
pulmonary parenchymal dz
COPD
interstitial lung dz
ARDS
chronic pulmonary infx
pulmonary vascular dz
thromboembolic dz
pulmonary HTN
this is associated with conditions that prevent the heart from meeting the body's cardiac output needs
low output failure
this is associated with conditions that initially cause increased cardiac output, is caused by demand for increased cardiac output, often exacerbates existing HF or decompensates a pt with other cardiac pathology
high output failure
what are the neuro-hormonal alterations that are compensatory mechanisms for HF
adrenergic nervous system (baroreceptors, alpha-receptors)
RAAS
antidiuretic hormone (Produced in posterior pituitary gland)
Natriuretic peptides
endothelin
which neuro-hormonal alteration is a positive compensatory effect, and are produced in response to atrial and ventricular stress
natriuretic peptides
which remodeling compensatory mechanism is due to chronic volume overload ⇨ chronic chamber dilation ⇨ synthesis of new sarcomeres in series with old ⇨ myocytes elongate ⇨ proportional increased ventricular chamber radius and wall thickness
eccentric hypertrophy
which remodeling compensatory mechanism is due to chronic pressure overload ⇨ chronic chamber hypertrophy ⇨ synthesis of sarcomeres in parallel with old ⇨ myocytes thicken ⇨ wall thickness increases without proportional chamber dilation ⇨ significant decreased wall stress
concentric hypertrophy
what are the precipitating factors of HF
increased metabolic demands
increased volume
increased afterload
impaired contractility
non-compliance
what are some precipitants of HF (HEARTFAILED)
Hypertension
Endocarditis/environment (heat)
Anemia
Rheumatic heart dz (other valvular dz)
Thyrotoxicosis
Failure to take medications (non-compliance)
Arrhythmias
Infection/ischemia/infarction
Lung problems (PE, pneumonia, COPD)
Endocrine (pheo, hyperaldosteronism)
Dietary indiscretion
what are some s/s of L sided HF
dyspnea
orthopnea
paroxysmal nocturnal dyspnea
nocturnal cough and wheezing
fatigue, exercise intolerance
chest discomfort
what are some s/s of R sided HF
lower extremity edema
RUQ discomfort
abd discomfort, nausea
what are the L sided physical findings
diaphoresis
tachycardia
tachypnea
pulmonary rales
loud P2
S3 gallop
what are the R sided physical findings
JVD
hepatomegaly
peripheral edema
ascites
what are the labs studies ordered during the work up of HF
CBC
metabolic panel
LFT, renal function
TSH
iron studies
cardiac enzymes
BNP
UA
this lab is extremely sensitive for atrial and ventricular stress with great variability in serially measured values even in one pt
BNP
what are the average values for CHF pts by NYHA
Class I: 244 +/- 286 pg/mL
Class II: 389 +/- 374 pg/mL
Class III: 640 +/- 447 pg/mL
Class IV: 817 +/- 435 pg/mL
what is the TOC for diagnosing HF
echo
this diagnostic study may be useful in circumstances requiring precise EF
MUGA
what is the simplest and most widely used method to gauge symptom severity of HF
NYHA
this is a classification system that is a well-established predictor of mortality and can be used at diagnosis and to monitor treatment response of HF
NYHA
this NYHA classification is when ordinary physical activity does not cause symptoms of HF
class I
this NYHA classification is when the pt is comfortable at rest, ordinary physical activity results in symptoms
Class II
this NYHA classification is when there is marked limitation of ordinary activity, less than ordinary physical activity that results in symptoms
class III
this NYHA classification is when the pt has the inability to carry out any physical activity without symptoms, symptoms present at rest
class IV
In systolic HF, what is a powerful predictor of mortality
reduced LVEF
if Framingham criteria are not met or BNP level is normal, _________ is essentially ruled out
systolic HF
if angina is present with HF what is a recommended diagnostic study
coronary angiography
what type of HF is when the EF ≥ 50%, there is elevated LA pressure, decreased LV compliance, and impaired LV relaxation
diastolic HF
what type of HF is when the EF is < 50%
systolic HF
which co-morbidities may be present when there is HF with a preserved EF
HTN
ischemic heart disease
DM
thyroid dysfxn
COPD
obstructive sleep apnea
which class of medications are offered first for pts with HF caused by left ventricular systolic dysfunction
loop diuretics
- furosemide 20-40mg daily
what is the treatment of HF caused by left ventricular systolic dysfunction
loop diuretics
ACE-I (or ARB)
BB
Aldosterone antagonists (if pt is with NYHA class II-IV and LVEF ≤ 35%)
Digoxin
ICD (when appropriate)
what needs to be monitored if you Rx aldosterone antagonists to pts with HF
renal function and plasma potassium concentration
If you have an African American with HF and you have Rx'ed a loop diuretic, ACE-I (or ARB), BB, and an aldosterone antagonist and they still have persistent sxs, what medication is added
hydralazine plus oral nitrate therapy
what are some s/s of pulmonary edema
cough, dyspnea, fatigue which is rapidly worsening
may/may not have chest discomfort
what is the acute treatment of a pulmonary edema
OMI
Lasix (IV 40mg start)
Nitroglycerine (initial dose 5-10 mcg IV)- for pts withouth HTN
positive pressure airway
position- sitting upright with legs hanging down CI in pts that are HoTHN
what vasodilators are used if the pt is not hypotensive, is combined with diuretics, and need close hemodynamic monitoring for HF pts
nitropusside
nitroglycerine
which inotropes are used in hypotensive pts with systolic dysfunction who remain in pulmonary edema despite all previous treatments for HF
dobutamine
phosphodiesterade inhibitors (milrinone)
dopamine (recommended for hypotensive STEMI pts with clinical evidence of shock)
when would you consider pulmonary artery catheterization in HF pts
to monitor PCWP
unstable pt
PCWP >18 indicates cardiac etiology
what are the life saving last resort measures in HF pts
intra aortic balloon pump
ventricular assist device
which co-morbidities are at a high risk for HF but are without structural heart disease or sxs of HF (stage A)
HTN
atherosclerotic disease
DM
obesity
metabolic syndrome
pts using cardiotoxins
Fmhx of co-morbidities
if a pt has had a previous MI, LV remodeling including LVH and low EF, or asymptomatic valvular disease, which stage of at risk heart failure are they
stage B- structural heart disease but without signs or symptoms of HF
if a pt has known structural heart and SOB and fatigue (including exercise intolerance), what stage of HF are they
stage C- structural heart disease with prior or current symptoms of HF
for pts who have marked symptoms at rest despite maximal medical therapy, what stage of HF are they
if the pt has HoTN: when is the systolic pressure to low and what is the recommended solution
asymptomatic pts with dilated cardiomyopathy often tolerate a SBP of 90mHg. if no lightheadedness or undue fatigue, peripheral perfusion is adequate, and BUN and Cr are unchanged, continue the same doses of medications
symptomatic pts, decrease the dose of diuretic. if sxs persist, adjustment of the timing of concomitant medications may be helpful. Decreasing the dose of the ACE-I, BB, ARB or vasodilator is indicated
if the pt is hyperkalemic, what are the recommended solutions
ensure that the pt is taking no exogenous potassium supplement or potassium-containing salt substitute. Avoid hypovolemia. Consider decreasing the dose of a potassium-sparing diuretic. Concomitant use of an ACEI or ARB and spironolactone may increase the risk of hyperkalemia. Avoid high doses of ACEI and ARBS in pts receiving spironolactone. Avoid use of spironolactone in pts with renal failure, and use low doses of ACEI and ARBS
if the pt has increasing azotemia while taking ACE-I, what is the recommended solution
decrease the dose of diuretic. Consider renal-artery stenosis if azotemia persists
if the pt has a cough while taking an ACEI what is the recommended solution
R/O worsening CHF and change to ARB if severe cough persists
should the dose of the ACEI be increased or should the BB therapy be initiated in a symptomatic pt
start BB therapy if there are no CI
should an ARB be added to an ACEI therapy or should a BB be added in a symptomatic pt
start BB therapy if there are no CI
the pt has worsening sxs of CHF after starting BB therapy, what are the recommended solutions
increase the dose of diuretic and slow the titration of the BB
the pt has worsening bronchospasms after starting BB therapy, what are the recommended solutions
decrease the dose of the BB. Consider a beta-selective agent. Discontinue treatment with the drug if the problem persists
if a pt has persistent paroxysmal nocturnal dyspnea or orthopnea or daytime fatigue despite absence or fluid retention on PE, what are the recommended solutions
evaluate the pt for central or obstructive sleep apnea
if the pt requires repeated hospitalization for HF, what are the recommended solutions
a multidisciplinary approach should be initiated, with a visiting nurse in the home. Referral for HF is indicated
what are the conservative measures for symptomatic pts with HF
oxygen if hypoxic
bed rest
elevation of head of bed
what are the lifestyle measures in for HF pts
diet
exercise
DM control
smoking cessation
alcohol control
sodium and fluid restrictions
pneumococcal vaccine and annual influenza vaccine
which medications control systolic and diastolic HTN for pts with HF
individualized to the pt with comorbid dz, DM, or COPD
Diuretic, BB, CCB, ACEI or ARB
what medications control ventricular rate for pts with HF
this diagnostic study determines co-existent CAD, previous MI, elevated left/right diastolic pressures, measures CO, degree of LV dysfunction in pts with dilated cardiomyopathy
cardiac cath
what is obtained when the etiology needs clarification for dilated cardiomyopathy
if after 1 week of no clinical improvement, consider bx
unexplained ventricular hypertrophy (not due to systemic HTN or AS) is known as what
hypertrophic cardiomyopathy
what is the most common pattern of hypertrophy in HCM
septal hypertrophty
this can heart dz can cause sudden death in athletes
HCM
what is the wall thickness measurement is HCM
>15mm (normal is 11mm)
what type of pulse is associated with HCM
bifid carotid pulse
this murmur is a harsh systolic crescendo-decrescendo murmur heard at the LLSB, it is increased with valsalva and squat to stand, decreased with squatting or sitting, handgrip, passive elevation of legs
HCM
why does the valsalva maneuver increase HCM
it increases intrathoracic pressure, decreases venous return, reduces LV size. The septum and MV anterior leaflet are brought closer together, increasing the murmur
why does squatting decrease HCM
it increases preload, increases LV size, decreases LV outflow tract obstruction which decreases the murmur
what is the work-up for HCM
ECG
24 hr or event monitor
CXR
echo (TTE is TOC)
cardiovascular magnetic resonance (CMR)
treadmill exercise testing
cardiac cath
what will an ECG show if a pt has HCM
LVH
high voltage across precordium
prominent q waves in leads looking away from septum (I, aVL, V4-V6)
which diagnostic study should be done if a pt complains of palpitations or lightheadedness, it can identify ventricular arrhythmias, risk for sudden cardiac death or if the pt is a candidate for ICD
24 hr or event monitor
what is the diagnostic test of choice for the workup of hypertrophic cardiomyopathy
TTE
this diagnostic study is used in the assessment of LVOT gradient, determines functional capacity, and determines response to therapy
treadmill exercise testing
if the diagnosis of hypertrophic cardiomyopathy is uncertain or if the pt is being considered for invasive therapy, which diagnostic study is considered
cardiac catheterization
what is the treatment of HCM
avoidance of:
volume depletion
overexertion
vasodilators, diuretics, digoxin
which negative inotropic drugs used in the treatment of HCM slow the heart rate and prolong diastole, allowing increased ventricular filling
Beta blockers and verapamil
which device is usually placed in pts with at least one major risk factor for sudden cardiac death or multiple (3 or more) minor risk factors
ICDs
what are the major risk factors of HCM
cardiac arrest (VFib)
spontaneous sustained Vtach
family history of sudden death
what are the minor risk factors for HCM
unexplained syncope
left ventricular wall thickness >30mm
abnormal BP on exercise
nonsustained vtach
left ventricular outflow obstruction
microvascular obstruction
high-risk genetic defect
this type of cardiomyopathy is when there is restricted ventricular filling in a non-dilated, non-hypertrophied ventricle secondary to myocardial abnormality (stiffening, fibrosis, decreased compliance)
restrictive cardiomyopathy
what are the infiltrative etiologies of restrictive cardiomyopathy
amyloidosis (most common)
sarcoidosis
what are the non-infiltrative etiologies of restrictive cardiomyopathy
scleroderma
idiopathic myocardial fibrosis
what are the storage diseases of restrictive cardiomyopathy
hemochromatosis
fabry's disease
glycogen storage disease
what are the endomyocardial etiologies of restrictive cardiomyopathy
endomycardial fibrosis
loefflers endocarditis
eosinophilic endomyocardial disease
radiation
carcinoid syndrome
what are the helpful historical clues to suggest a diagnosis of constrictive vs restrictive cardiomyopathy
constrictive:
prior history of acute pericarditis
history of active TB
prior cardiac surgery
prior mediastinal radiation therapy
what are the s/s of restrictive cardiomyopathy
CHF usually with preserved LV systolic function
arrhythmias (dilated atria)
elevated JVP with prominent x and y descents
+/- kussmauls sign
S3 is common
S4 early in disease, disappears with Afib or true atrial systolic failure (advanced amyloidosis)
what is the workup of restrictive cardiomyopathy
EKG
CXR
Echo
cardiac cath
endomyocardial biopsy
CT scan
MRI
what will an ECG show on a pt with restrictive cardiomyopathy
low voltage
non-specific, diffuse ST-T wave changes
+/- non-ischemic q waves
heart blocks, A-fib
what will an echo show on a pt with restrictive cardiomyopathy
biatrial enlargement
normal or decreased ventricular volume
normal wall thickness
normal systolic function
impaired ventricle filling
"starry night" or "speckled" pattern seen (due to infiltrative d/o)
what is the essential test in the etiology of restrictive cardiomyopathy (esp with infiltrative disease)
endomyocardial biopsy
what is the test of choice for differentiating restrictive cardiomyopathy from constrictive pericarditis
ct scan
what drugs are used to manage the diastolic dysfunction of restrictive cardiomyopathy
diuretics
what drugs are used to treat the rhythm disturbances of restrictive cardiomyopathy
flecainide
amiodarone
propafenone
digoxin (with great caution)
*also treated with a pacemaker
what is used to treat/prevent thromboembolic events of restrictive cardiomyopathy
anticoagulation therapy
what is the normal measurement of mean pulmonary arterial pressure
8 to 20 mmHg at rest
what measurement of mean pulmonary artery pressure at rest has uncertain clinical implications
21 to 24 mmHg
what is the mean pulmonary arterial pressure at rest for pulmonary HTN
>25 mmHg
what is the mean arterial pulmonary arterial pressure with exercise for pulmonary HTN
> 30 mmHg
what is the systolic pulmonary artery pressure in pulmonary HTN
>40 at rest
what is pulmonary HTN characterized by
elevated pulmonary arterial pressure
secondary right ventricular failure (ie. cor pulmonale)
what is the gold standard for diagnosing sleep breathing disorders like OSA
sleep study
which diagnostic study is used in the predictability of survival in idiopathic PH
exercise testing
this diagnostic study is necessary for a definitive diagnosis and accurately determines the severity and guides treatment
right-heart catheterization
what is the coag of choice in the treatment of PH
warfarin (therapeutic goal INR of 2.0)
which class of the WHO functional classification for PH is when the pts with PH but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue or dyspnea, CP, or heart syncope
class I
which class of the WHO functional classification for PH is when the pts with PH results in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in undue fatigue or dyspnea, CP, or heart syncope
class II
which class of the WHO functional classification for PH is the pts with pulmonary HTN results in marked limitation of physical activity. They are comfortable at rest/ Less than ordinary physical activity causes undue fatigue or dyspnea, CP, or heart syncope
class III
which class of WHO functional classification for PH is when the pts with pulmonary HTN results in inability to carry on any physical activity without sxs. These pts manifest signs of right heart failure. Dyspnea and/or fatigue may be present even at rest. Discomfort is increased by physical activity
class IV
what are the indication for referral to a pulmonary HTN center
unexplained dyspnea or CP on exertion with evidence of PH by transthoracic echo
evidence of moderate to severe pulmonary arterial HTN
clinical or echo evidence of RV dysfunction
parenchymal lung disease
known pulmonary arterial HTN with worsening disease despite therapy
what are the 3 basic mechanisms leading to peripheral vascular disease
what are the common presentation of aortic aneurysms
majority are asymptomatic
pain (chest, abd, flank, back)
syncope
HoTN
palpable mass above umbilicus (in two directions)
airway or esophageal obstruction
what are the clinical findings associated with aortic aneurysms
hoarseness (left recurrent laryngeal nerve)
hemoptysis
hematemesis
distal pulse may be intact
what are the associated diseases with aortic aneurysms
HTN
PVD
CAD
COPD
renal insufficiency
what will a CXR show on a pt with a TAA (thoracic abdominal aneurysm)
widened mediastinum (usually ~8cm at a minimum)
enlargement of the aortic knob
loss of the AP window
if the entire aorta needs to be examined and it is an emergent situation, which diagnostic study should be considered
TEE
what is the procedure of choice for the diagnosis of aortic aneurysms in most centers
CT with contrast/ MRA
what are the clinical findings of an abdominal aneurysm
majority are asymptomatic
pain (atypical abd, back, leg, groin, or flank)
palpable mass above the umbilicus
anorexia, nausea, vomiting
what is the size of most pulsatile abd masses in most adults when it is generally considered aneurysms
>3.0cm
what diagnostic study is up too 100% sensitive for AAA
abd U/S
what is the imaging TOC for non-ruptured AAA
abd U/S
what is the imaging TOC for the diagnosis of ruptured AAA
CT scan
what is the USPSTF screening guidelines for an AAA
recommendation for one-time screening for AAA with US in males aged 65-75 with any smoking hx
no recommendation for or against screening for AAA with US in males who have never smoked
recommendation against screening females of any age for AAA with US
what is the surgical threshold for a TAA (ascending)
5-6cm
what is the surgical threshold for pts with a TAA (descending)
6-7cm
what is the surgical threshold for pts with a AAA
~5.5 cm
what are the CI to surgical repairs
life expectancy <1 year
terminal dz
recent MI
UA
what are the risk factors for aortic dissection
HTN
atherosclerosis
pre-existing aortic aneurysm
inflammatory d/os
bicuspid aortic valve
aortic coarctation
crack cocaine
which Stanford classification type is a proximal aortic dissection, is about 2/3 of pts, and the ascending aorta is involved
type A
which Stanford classification type is a distal aortic dissection, is about 1/3 of pts, and typically is the descending aorta only
type B
what are the clinical findings of an aortic dissection
sudden onset of CP radiating to the back
- tearing or ripping... type A- anterior chest...type B- between the scapula, back and abd
- asymmetric BP or pulse between arms (>20mmHg)
- ischemic sxs (occlusion of coronary arteries, aortic branches, carotids, or splanchnic arteries)
which present sxs if associated with an aortic dissection is associated with a worst outcome
syncope
what will the PE show on a pt with an aortic dissection
HTN
UE BP differential
neurological abnormalities (syncope, AMS)
new diastolic murmur if associated AR present
physical signs of pericardial tamponade in some type A dissections
what is the TOC for an aortic dissection
TEE
what are the 3 sxs that can help you clinically dx an aortic dissection
pain- described as abrupt onset of thoracic/abd pn with sharp, tearing, or ripping sensation
mediastinal widening on CXR
a variation in pulse or BP (>20 mmHg between L and R arm)
what is the acute tx of an aortic dissection
pain control (morphine)
BP control
hemodynamically unstable or airway compromise intubate
obtain a bedside TEE in an unstable pt to comfirm the dx
stable pt CT or MRI/MRA to confirm dx
ADMIT
a type A aortic dissection requires what type of treatment
emergent sx
type B aortic dissection requires what type of tx
can be managed medically
which beta blockers are used in the treatment of an aortic dissection
esmolol IV (fastest onset, short half life, easy to titrate)
propranolol IV or labetalol
IV vasodilators (nitroprusside)
this is a spectrum of disorders typically characterized by abnormal venous dilatation ranging from varicose veins to venous stasis and ulcerations, it is occasionally associated with a discrete etiology, and most cases are related to the progressive degenerative changes in venous structure and function with aging
peripheral venous disease
this is the most important sequelae of DVTs
pulmonary embolism (50%) of untreated cases
chronic venous insufficiency
what is virchows triad
endothelial/vascular damage
venous stasis
hypercoagulability
what are the inherited etiologies of hypercoagulability in a DVT
activated protein C resistance (Factor V leiden)
prothrombin gene mutation
protein C&S deficiency
antithrombin III deficiency
antiphospholipid antibody syndrome
if there is a proximal vein thrombosis, what arteries are/can be involved
popliteal
femoral
iliac
which type of DVT is more commonly associated with the development of a PE
proximal vein thrombosis
if a pt presents with unilateral leg edema, erythema, warmth and tenderness, what is your suspected dx
DVT
what are the most useful test for DVTS
US (Doppler)
D-dimer tests
what score is commonly used for the dx of a DVT
wells score
which diagnostic study provides a definitive diagnosis for a DVT
venography (invasive)
what is the initial therapy for a DVT
LWMH
unfractionated heparin
fondaparinux (arixtra) factor Xa inhibitor
coumadin
when are fibrinolytics used for a pt with a DVT
limb/life threatening thrombosis
very recent sxs
low bleeding risk
what are the different methods for primary prophylaxis for a DVT
intermittent pneumatic compression
graduated compression stockings
unfractionated heparin
LMWH
fondaparinux
warfarin
this is a benign disorder of erythema, induration, and tenderness along a superficial vein, usually is spontaneous, but can follow venous cannulation
superficial thrombophlebitis
what are the risk factors for superficial thrombophlebitis
venous stasis
abnormal coagulation/fibrinolysis
endothelial dysfunction
infection
IV therapy
IV drug use
this is a recurrent migratory superficial thrombophlebitis, associated with adneocarcinomas
trousseau syndrome
which vein is most common for getting superficial thrombophlebitis
greater saphenous
what are some conservative treatments for superficial thrombophlebitis
bed rest and elevation of limb PRN for pain/swelling (otherwise ambulation is encouraged)
moist heat
compression
analgesia
anti-inflammatory
anti-coag
when is a surgical excision indicated in a pt with superficial thrombophlebitis
failure of conservative tx
symptoms > 2 weeks or recurrent sxs
suppurative thrombophlebitis
distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial, or perforator systems is known as what
varicose veins
where is the most common development of varicose veins
greater saphenous vein
what is the most common form of venous disorders of the lower extremity
varicose veins
this is known as a chronic elevation of deep venous pressure and blood pooling in lower extremities
chronic venous insufficiency
what is the most common vascular disorder
chronic lower extremity venous disease
the clinical features of this disorder is when the pt complains of tired or heavy legs, it gets worse with standing or seated with feet dependent for long period of time that IMPROVES with limb elevation and walking
chronic venous insufficiency
what is the test of choice for chronic venous insufficiency
duplex (Doppler and B-mode) US
what are the systemic agents used to treat chronic venous insufficiency
ASA therapy appears to accelerate the healing of chronic venous ulcers
Anbx only when s/s of acute cellulitis or clinically infected ulcer
obstruction of lymphatic drainage resulting in edema with high protein content is known as what
lymphedema
what is the most common cause world wide of lymphedema
filariasis
what is the most common cause of lymphedema within the US
radiation/surgery (axillary or groin lymph node removal)
formation of atherosclerotic plaques in large and medium sized arteries that results in chronic occlusive arterial disease is known as what
peripheral arterial disease
if there is a delay in treatment of acute peripheral arterial disease of greater than 6 hours, what can this result in
ischemia
chronic impairment of under-perfused structures in PAD, can lead to what
muscular atrophy
ischemic non-healing ulcerations
gangrene
what are the traditional risk factors for PAD
smoking (highest risk)
DM (highest risk)
age
hyperlipidemia
HTN
Fmhx
what are the 6 "P"s in acute PAD
Pain
Pallor- within a few hours progresses to mottled cyanosis
Paresthesia
Paralysis/power loss- heralds impending gangrene
Poikilothermia- cool extremity
Pulselessness- least reliable
what are the sxs of chronic PAD
claudication
- pain with exertion (calves most common)
- relieved by rest (2-5 minutes without postural changes)
- reproducible (same distance, same location, same recovery)
