Cardiology Internal Medicine

Congestive Heart Failure

Overview
o Final and most severe manifestation of nearly every form of cardiac disease
o 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 the cardiac filling pressures are abnormally high (backward failure)
o Preventive therapy & patient education is the key to reduction of burden
Pathophysiology of Heart Failure
o Heart failure most commonly results from conditions of impaired left ventricular function (myocardial failure)
= systolic dysfunction
o Summarized as an imbalance in Starlings forces or an imbalance in the degree of end-diastolic fiber stretch
proportional to the systolic mechanical work expended in the ensuing contraction (basically like a rubber band, the
more it is stretched, the greater the releasing velocity)
o Chronic heart failure results from
Impaired ventricular contractility
Systolic dysfunction
Increased afterload
Impaired ventricular filling
Diastolic dysfunction
o Systolic Dysfunction
2/3 of patients
Diminished capacity to eject blood
Impaired contractility
Pressure overload
During diastole, persistently elevated LV pressure transmitted to LA (through the open mitral valve)
pulmonary veins
An elevated pulmonary capillary hydrostatic pressure (> 20 mmHg) results in the transudation of fluid into the
pulmonary interstitium
Symptoms of pulmonary congestion
(Loss of contractility may result from damage to myocytes, abnormal myocyte function, or fibrosis)
o Diastolic Dysfunction
1/3 of patients with clinical heart failure have normal ventricular contractile (systolic) function
Filling of ventricle occurs at higher-than-normal pressures
Display abnormalities of ventricular diastolic function
Impaired early diastolic relaxation
Increased stiffness
Or both
Elevated diastolic pressure transmitted retrograde to pulmonary & systemic veins
Classification
o Heart failure can also be classified as:

Left-sided heart failure

Most common cause is left-sided heart failure
Symptoms
o Dyspnea on exertion
o Orthopnea
o PND (paroxysmal nocturnal dyspnea)
o Nocturnal cough
o Hemoptysis
o Fatigue
o Dulled mental status
o Nocturia
Physical Findings
o Diaphoresis, dusky
o Tachycardia
o Tachypnea
o Pulmonary rales
o Cardiac asthma
o S3 ( S4) (S4 present with diastolic HF)
o Murmur of MR
Right Sided

Susceptible to failure in situations of sudden increase in afterload

RV thin walled, highly compliant accepts blood volume at low pressures and ejects against low
pulmonary vascular resistance
Isolated rt-heart failure is less common, and usually reflects increased RV afterload owing to disease of
the lung itself or pulmonary vasculature
Right-sided heart disease resulting from primary pulmonary process
o Cor pulmonale (isolated RV failure)
When the right ventricle fails, the elevated diastolic pressure is transmitted retrograde to the right
atrium with subsequent congestion of the systemic veins
Indirectly, right-heart failure may also influence left-heart function
o Decreased RV output reduces blood returning to LV (preload)
o Leads to drop in LV stroke volume
Symptoms
o Peripheral edema
o RUQ discomfort
o Anorexia
o Nausea
o Unexpected weight gain
Physical Findings
o JVD
o Hepatomegaly

o Peripheral edema
o Palpable parasternal RV heave
o S3 or S4
o Murmur of TR
o ****pleural effusions may develop with either right sided or left sided failure
Etiology
o Myocardial abnormalities
CAD, MI, ischemia (chronic and silent), cardiomyopathy
o Hemodynamic overload
Pressure AS, HTN, massive PE, COPD
Volume valvular regurgitation, anemia, thyrotoxicosis
o Ventricular filling abnormalities
Mitral stenosis, constrictive pericarditis, LVH
o Cardiomyopathy
Dilated
Hypertrophic
o Arrhythmia
AF, SVT, marked bradyarrhythmias
Causes of HF in Western World
o For a substantial proportion of patients, causes are:
Coronary artery disease
Hypertension
Dilated cardiomyopathy
Aggravating Factors
o Often a lack of response to conventional therapy for heart failure is due to the presence of uncorrected aggravating
or precipitating factors. It is important to always consider the possibility of such factors, particularly in cases of
refractory failure
o Mainly:
Medications
New heart disease
Myocardial ischemia
o Other
Pregnancy
Arrhythmias
Infections
Thromboembolism
Hyper/hypothyroidism
Endocarditis
Obesity
HTN
Noncompliance

Dietary excess
Stages of Heart Failure
o Designed to emphasize preventability of HF
o Designed to recognize the progressive nature of LV dysfunction
o At Risk for Heart Failure:
STAGE A
High risk for developing HF
STAGE B
Asymptomatic LV dysfunction
o Heart Failure:
STAGE C
Past or current symptoms of HF
STAGE D
End-stage HF
o COMPLEMENT, DO NOT REPLACE NYHA CLASSES
NYHA Classes - shift back/forth in individual patient (in response to Rx and/or progression of disease)
Stages - progress in one direction due to cardiac remodeling
Diagnostic Aids
o CXR
Cardiac silhouette
Heart shadow should occupy 50% or less of the maximal width of thorax
Some cases inaccurately reflect heart size
o Elevated diaphragm
o Narrow chest AP diameter
o Pericardial effusion
Therefore chest AP diameter should be assessed on lateral view before frontal view to truly represent an
enlarged heart
Pulmonary Manifestations of Heart disease
Appearance of pulmonary vasculature reflects abnormalities of pulmonary arterial and venous pressures
and pulmonary blood flow.
o Increased vascular markings
o Redistribution of blood flow from bases to apices (cephalization)
o Pulmonary edema (butterfly or bat-wing pattern)
o Abnormal septal lines (Kerley B lines)
o Pleural effusions
o Echocardiography
Safe, noninvasive, relatively inexpensive
High-frequency (ultrasonic) waves
Three types of modalities
M-mode
o First application of ultrasonography
o Provides limited data from one narrow ultrasonic beam
o Valuable for:
Measurement of wall thickness
Chamber diameters

Accurate timing of valve movements

Two-dimensional (2D)
o Multiple ultrasonic beams transmitted through a wide arc
o Returning signals produce 2-D images on screen
o Parasternal and apical views
Some patients with COPD difficult to view subcostal view
Doppler imaging
o Evaluates blood flow direction, velocity, and turbulence
o Permits estimation of pressure gradients
o Colors are superimposed on 2-D images, showing location of stenotic and regurgitant valvular
lesions
o Can also show abnormal communications w/in heart and great vessels

Diagnostic Workup
o In all cases:
History, Physical Exam, EKG
Echo
Etiology
MR?, DD (diastolic dysfunction), RV fxn
Can measure pressures
Chest x-ray
Labs
TSH, Na, K, Cr, BNP
Assessment for CAD
One of few reversible causes
o In selected cases
Labs
Metanephrines
Ferritin
Catheterization
CAD
Hemodynamics
Endomyocardial biopsy
If infiltrative disease considered
o Right-heart catheterization
Right heart
Access from peripheral vein
Measure pressures in RA, RV, & PA
Guided by fluoroscopy
Use specialized balloon-tipped catheter
Recorded pressures identify the catheter tips position

Pulmonary artery wedge pressure

PAWP or PCW
o Closely matches LA pressure in most people
When MV open during diastole
o Pulmonary venous bed, LA, LV normally share same pressure
**Thus, PAWP can be used to estimate LV end-diastolic pressure a measurement of preload**

Treatment
o Overview
Identify and correct underlying conditions
Eliminate acute precipitating factors
Modulation of neurohormonal response
Management of symptoms
Treat congestion
Increase forward cardiac output
Improvement of long-term survival
o Stage A
Treat known risk factors HTN, DM, etc
Lifestyle modifications avoid smoking, excessive use of alcohol, illicit drug use
Periodic eval Echo
Control ventricular rate, restore sinus rhythm
ACE-I, ARBS
o Stage B
Treat known risk factors HTN, DM, etc
Lifestyle modifications avoid smoking, excessive use of alcohol, illicit drug use
Drug therapy for all patients
ACEI or ARBs
Beta-Blockers
ICDs in appropriate patients (implantable cardioverter defibrillator)
Coronary revascularization in appropriate patients
Valve replacement or repair in appropriate patients
Therapies NOT recommended
Digoxin should not be used in patients with low EF, sinus rhythm, and no history of HF symptoms,
because in this population, the risk of harm is not balanced by any known benefit.
Calcium channel blockers with negative inotropic effects may be harmful in asymptomatic patients with
low LVEF and no symptoms of HF after MI
o Stage C
Drug therapy for all patients
Diuretics for fluid retention
ACEI or ARBs
Beta-blockers
Drug therapy for selected patients

Aldosterone Antagonists
Digitalis
Hydralazine/nitrates
ICDs in appropriate patients
Cardiac resynchronization in appropriate patients
Stage D
Recommended Therapies Include:
Control of fluid retention
Referral to a HF program for appropriate patients
Discussion of options for end-of-life care
o Informing re: option to inactivate defibrillator
Device use in appropriate patients
Surgical therapy
o Cardiac transplantation
o Mitral valve repair or replacement
Drug Therapy
o Positive inotrope infusion as palliation in appropriate patients
Several therapies should be avoided when possible, in patients with systolic HF
Thiazoladinediones (glitazones) medication for DM that can worsen HF
Calcium channel blockers
o Except amlodipine and felodipine
NSAIDS and COX 2 inhibitors
o Cause Na and H2O retention
Combination of ACE-inhibitor, ARB and aldosterone blocker
o Increased risk of hyperkalemia
Aggravating factors
Often a lack of response to conventional therapy for heart failure is due to the presence of uncorrected
aggravating or precipitating factors. It is important to always consider the possibility of such factors,
particularly in cases of refractory failure
Other Add-ons if needed
Aldosterone Antagonist Therapy
Chronic excess of aldosterone contributes to cardiac fibrosis and adverse ventricular remodeling
Spironolactone
o substantially reduces mortality rates, reduces hospitalizations, and improves symptoms when
added to ACE inh & diuretics
Chronic therapy using combination of
Venous dilator isosorbide dinitrate plus
Arteriolar dilator hydralazine
Shown to improve therapy of moderate symptoms of HF
Use when intolerance to ACE inh or ARB therapy

 Particular benefit in AA with HF

Inotropic drugs (digitalis)
NOT useful in diastolic dysfunction systolic only
Benefits:
Enhance contractility
Reduces cardiac enlargement
Improves symptoms
Augments cardiac output (with sys. HF)
Added benefit in patients with AFib
Has not been shown to improve long-term survival
o Additional Therapy
Anticoagulation
If AF or LV thrombus
Treatment of atrial or ventricular arrhythmias
Insertion of an implantable cardioverter-defibrillator (ICD)
LVEF 35%
At least 1 month post MI or
3 months post revascularization
NYHA class II or III HF
Above regardless of previous documented ventricular arrhythmia!!
Biventricular pacemaker
Interventricular conduction abnormalities and widened QRS complexes are common in patients with
advanced HF
o Uncoordinated patterns of right and left ventricular contractions
Therapy:
o Augments LV systolic function with an accompanying reduction of LV size
o Improves exercise capacity
o Reduces frequency of HF exacerbations
o Reduces mortality
Indications
o LVEF 35%
o QRS 120 msec, and
o NYHA Class III or IV HF
Diastolic Dysfunction
o Area of ongoing research no clear cut pharmacologic recommendations
o Inotropic drugs or vasodilators usually have no role in the treatment of pure diastolic dysfunction
o Risk of death lower than systolic dysfunction
o Dx: doppler echocardiography
o Treat symptomatically and prevent reversible causes
o Causes:

Pericarditis
Acute
o
o
o

HTN
Hypertrophic cardiomyopathy
Myocardial infarction
Restrictive cardiomyopathy
Aortic stenosis with normal EF
Coronary artery disease

Pericarditis
Most common affliction of pericardium
Inflammation of layers
Etiology
Infectious
Viral / Idiopathic most often
Pneumococcus and staphylococci most frequently responsible; gram-negative infection occurs less often
o Mechanisms of entry for Bacterial Pericarditis
Perforating trauma to chest
Contamination during chest surgery
Extension of intracardiac infection
Extension of pneumonia
Hematogenous spread from remote infection
Tuberculosis
o Low incidence in U.S.
o TB remains problem worldwide
o Important cause in immunosuppressed patients, especially AIDs
Pyogenic bacteria - rare
Noninfectious
Post MI
o Early first few days
Inflammation extending from epicardial surface
Most common with transmural MI
Prognosis following acute MI not affected
< 5% of patients
o Later Dresslers syndrome
2 weeks to several months post MI
? autoimmune
Uremia
Neoplastic disease
Radiation-induced
Connective tissue disorder
Drug-induced

Pathogenesis
Local vasodilation with transudation of protein-poor, cell-free fluid into pericardial space
Increased vascular permeability with leak of protein into pericardial space
Leukocyte exudation
Help contain or eliminate offending agent
Metabolic products released by these cells may
Prolong inflammation
Cause pain and local cellular damage
Mediate somatic symptoms, i.e. fever
The immune response to pericardial injury may significantly contribute to tissue damage and symptomatology
Pathology
The pathologic appearance of the pericardium depends on the underlying cause and severity of inflammation
Serous pericarditis
Characterized by scant polymorphonuclear leukocytes, lymphocytes, and histiocytes
Exudate is thin fluid secreted by mesothelial cells lining the serosal surface of the pericardium
Likely represents early inflammatory response common to all types of acute pericarditis
Serofibrinous pericarditis
Most common
Contains plasma proteins
o Grossly rough and shaggy appearance
Portions of visceral and parietal pericardium may become thickened and fused
o Occasionally this process leads to dense scar
o Restricts movement and diastolic filling
Suppurative (purulent) pericarditis
Intense inflammatory response associated with bacterial infection
Serosal surfaces are erythematous and coated with purulent exudate
Hemorrhagic pericarditis
Grossly bloody form
Most often caused by TB or malignancy
Clinical Features
Most frequent symptoms of acute pericarditis are CP & fever
Chest pain sharp, pleuritic
CP located retrosternal area and left precordium; may also radiate to the back and ridge of the left
trapezius muscle
Aggravated by coughing and inspiration
Fever
Positional sitting / leaning forward eases pain
Dyspnea (nonexertional)
Dyspnea common, but not exertional most likely from a reluctance of pt to breathe deeply b/c of
pleuritic pain

Physical Findings
Tachycardia
Friction rub
Best heard leaning forward while exhaling
Squeaky, high-intensity sound heard best at left lower parasternal edge
Diaphragm
3 components
o Ventricular contraction
o Ventricular relaxation
o Atrial contraction
Diagnostic Studies
EKG abnormal 90% of cases
Diffuse ST segment elevation
PR segment depression
o PR segment depression reflects abnormal atrial repolarization related to atrial epicardial
inflammation

Lab
Elevated WBC count
Elevated ESR
Echocardiography
Assess for pericardial effusion
Treatment
Usually self-limited (1-3 weeks)
Viral/idiopathic usually self-limiting
Rest
Pain relief
Analgesic

Anti-inflammatory
o ASA/NSAIDs
o Corticosteroids severe or recurrent
Corticosteroids should not be given for uncomplicated cases. Potentially severe side
effects and b/c even gradual withdrawal of this form of therapy often leads to recurrent
symptoms of pericarditis
o Purulent pericarditis
More aggressive treatment
Catheter drainage of pericardium
Intensive antibiotic therapy
Mortality rate very high
Constrictive Pericarditis
o As blood passes from the RA into the RV during diastole, the RV size expands and quickly reaches the limit imposed
by the constricting pericardium. At that point, further filling is suddenly arrested, and venous return to the right
heart ceases. Thus systemic venous pressure rises, and signs of right-sided heart failure ensue. In addition, the
impaired filling of the LV causes a reduction in stroke volume and CO, which leads to hypotension
o Results from pericardium becoming fibrosed and thickened
Viral, infectious, post-surgical, autoimmune
o Restricts the normal filling of the heart during diastole
o Restriction results in low-output failure
Initially right-sided
Then left-sided
o Examination
Elevated JVP
Kussmauls sign increase in JVP with inspiration
Kussmauls sign is the opposite of what is found in normal physiology, where inspiration results in a
decline in JVP
Soft heart sounds
Atrial fibrillation common
o Cardiac catheterization is diagnostic
Elevation and equalization of the diastolic pressures in each of the cardiac chambers
Normal left ventricular function on ventriculogram
o Treatment
Pericardectomy
If TB, medical therapy for 1 year
Pericardial Effusion can be a complication of Pericarditis see critical care
Peripheral Vascular Disease
Overview
o Number of diverse pathologic entities affecting arteries, veins, and lymphatics
o PVD results from
Structural changes in vessel wall

 degenerative conditions, infection, or inflammation lead to dilation, aneurysm, disseciton or rupture

Narrowing of vascular lumen
atherosclerosis, thrombosis or inflammation
Spasm
aneurysm
Abnormal localized dilatation of an artery
Diameter has increased by at least 50% compared with normal
Clinical Presentation
Majority asymptomatic
Incidental finding on imaging
Symptoms related to compression of other structures
Thoracic compress mainstem bronchus causing cough, dyspnea, pneumonia
Esophagus compression dysphagia, hoarseness (recurrent laryngeal nerve)
AAA back pain or nonspecific GI symptoms
Physical Exam
Pulsatile mass
Murmur aortic regurgitation
Features of Marfans syndrome
Diagnosis
Ultrasound
Most useful and least expensive mode of diagnosis
Best used to assess progression of AAA size
Average expansion of 0.4 cm/year AAA and 0.1 cm/year thoracic
Contrast-enhanced CT
MRA MRI with contrast
Complication
Rupture in any location produces acute symptoms
Severe pain
LOC
Shock
Death (result of massive internal hemorrhage)
o 15,000 lives per year taken due to rupture
13th leading cause of death
o 40% of 5.5 6 cm AAAs will rupture in 5 years
o Average survival if untreated is 17 months
Natural history Risk of rupture related to size of aneurysm
Treatment
Based on size and patients overall medical conditions
Close monitoring every 6 12 months if asymptomatic
Elective surgical intervention if symptomatic (regardless of size)

Aortic
o
o

Ascending vs Descending vs Abdominal

Etiology
Multifactorial, depends on location
Ascending thoracic aortic aneurysms:
o Aging, HTN, connective tissue disorders (Marfans)
o More common in men
o Fusiform
o Often extend into aortic arch
o Etiology:
Marfans
Inherited disorder, autosomal dominant
Aortic root tends to enlarge in fusiform fashion in association with aortic valvular
regurgitation
Characterized primarily by:
o Dolichostenomelia (long, thin extremities)
o Ligamentous redundancy
o Ectopia lentis
o Ascending aortic dilatation
o Incompetence of aortic &/or mitral valves
Bicuspid aortic valve
Patients born with bicuspid aortic valve have structural abnormalities of the
ascending aorta
o Predisposes to aneurysm and dissection
Aneurysm may develop before clinical symptoms of aortic stenosis
Affects 2% of population (2 in 200)
o Clinical Presentation
Pain anteriorly, under the breast bone
Descending thoracic aneurysms:
o Atherosclerosis & associated risk factors
Majority are atherosclerotic in origin
May develop in patients with aortic coarctation
o Typically fusiform
o May extend to level of abdominal aorta
o Often begin distal to left subclavian artery
o Clinical presentation
Interscapular region / upper back discomfort
abdominal aortic aneurysms
o Atherosclerosis & associated risk factors
o >90% cases distal to renal arteries
Termed infrarenal abdominal aortic aneurysm
o Atherosclerosis

o
o
o
o

Clinical Presentation
Back / left flank pain
Men affected 4x more
2x more common in whites
Average age 69 year for men, 78 years for women
Risks:
Smoking
increases risk 8x in ADAM (Aneurysm Detection and Management)
HTN
present in 40% of patients
Family history and presence of COPD are also cofactors
Cholesterol may play a role

Aortic dissection
o Overview
Life-threatening condition
Blood-filled channel divides medial layers of aorta, splitting intima from adventitia
Any condition that interferes with the normal integrity of the elastic or muscular components of medial layer
can predispose to dissection
Most common in sixth and seventh decades
More frequent in men
> 2/3 have h/o HTN
Cocaine abuse increasingly recognized as a predisposing risk factor
Most common cause for dissection patients <40 yr:
Marfan Syndrome
Pregnancy
Locations
Ascending thoracic aorta 65%
Descending thoracic aorta 20%
Aortic arch 10%
Abdominal aorta 5%
o Type A vs Type B
Type A (proximal)
if ascending aorta involved
2/3 of cases
Type B (distal)
if occurs beyond left subclavian artery
does not involve ascending aorta

o Clinical presentation
Acute vs. Chronic Dissection

Acute dissections
o symptoms of less than 2 weeks duration
Sudden, severe pain
tearing ripping
Anterior, substernal chest pain type A
Scapular/back pain type B
Can radiate anywhere
Consider aortic dissection and ruptured thoracic or abdominal aneurysm in the differential diagnosis of
chest, abdominal or back pain!
Painless occurs in about 15% cases
May present with clinical features of shock if resultant cardiac tamponade or significant blood loss
Imaging
CT angiography
Can effectively exclude the major forms of life-threatening thoracic pathology
D-Dimer
Biomarker indicating activation of the coagulation system
When negative excludes acute aortic dissection
Complications
Pericardial tamponade
Stroke
MI
Renal failure
Limb ischemia
Aortic regurgitation
Treatment
Goal arrest progression of dissection
If suspicion of dissection
Reduce SBP
Decrease force of LV contraction
o IV NTG, sodium nitroprusside, BBs, vasodilators
Type A
Early surgical correction indicated
High risk for death, intrapericardial rupture, aortic reguritation or MI
Type B
Initially aggressive medical therapy alone
o BB + afterload reducer
Early surgical intervention does not improve outcome. Sx indicated if:
o continued propagation
o compromise of major branches of aorta
o impending rupture

o
PAD
o

continued pain

Overview
Formation of atherosclerotic plaques in large and medium-sized arteries
Pathology / pathophysiology is identical to that of CAD
40% w/PAD have clinically significant CAD
2 to 5 fold increase risk of CV death
Problem with oxygen supply / demand
Risk factors
Cigarette smoking
Diabetes mellitus
Dyslipidemia
Hypertension
Clinical Presentation
Buttock, thigh or calf discomfort
Precipitated by walking, relieved by rest
Claudication - Location of claudication corresponds to diseased artery
Severe PAD pain at rest, feet & toes
Prone to ulcerations
Physical Examination
Bruits
Loss of pulses distal to stenotic segment
Muscle atrophy
Pallor
Cyanotic discoloration
Hair loss
Ischemic ulcers toes, lateral malleolus, painful
Arterial
o Trauma heels / toes
o Painful
o Discrete edges - punched out
o Edges covered with crust
o Infected
erythematous
o Rapidly developing
Venous
o Leads to stasis ulceration
o Painless
o Ankle / lower leg above medial malleolus
o Reddened, thickened over medial malleolus
o Cobblestone appearance
o Occurs with slightest trauma

o Slow developing
Diagnostic Studies
ABI
Ankle-brachial index
Measure systolic BP with Doppler in
o each arm and
o dorsalis pedis and posterior tibial pulses
Divide the ankle pressure by the arm pressure bilaterally
1.0 1.3 = Normal which means the ankle pressure is equal to or slightly greater than that in the arms
<0.9
o Diagnostic of PAD
o Usually with symptoms of intermittent claudication
<0.5
o Severe PAD with critical leg ischemia
o Often have pain at rest
Duplex ultrasonography
MRA
CTA
Intra-arterial contrast angiography
Treatment
Antiplatelet therapy**
ASA shown to reduce CV morbidity and mortality
Risk factor modification**
Smoking cessation, lipid management, HTN management, DM management
Supportive care of feet / prevent trauma
Formal exercise program 1st line treatment
Medical therapy
Cilostazol (Pletal)
o Selective phosphodiesterase inhibitor
o Vasodilator and platelet inhibitor properties
o Improves exercise capacity
Pentoxifylline (Trental)
o Improve deformability of RBC & WBC
o May improve claudication symptoms
Area for lot of new and ongoing research
Revascularization
Indicated after failed medical therapy
Or in cases of severe limb ischemia
Goal heal ulcers, prevent limb loss
PTA (percutaneous transluminal angioplasty)

Surgery
** reduce risk of coronary events
Acute Aortic Occlusion
o Caused by embolization or thrombus
Origin of arterial emboli usually cardiac
Mitral stenosis
Atrial fibrillation
Acute AWMI
Infective endocarditis
o Rarely originate from venous circulation
Paradoxical embolism
Arterial embolism from venous circulation
o Clot passes through an abnormal intracardiac communication (ASD, VSD, PFO)
o Symptoms
Abrupt total, or near-total occlusion of terminal aorta or common iliac arteries poses immediate threat to life
and limb
Abrupt onset of severe pain
Lumbar area, buttocks, perineum, abdomen and legs
Diffuse cyanosis
From umbilicus to feet
Lower limbs pale and cold
Numbness, paresthesia, and paralysis
Absent pulses of lower limbs
Muscle necrosis may produce myoglobinuria, renal failure, acidosis, hyperkalemia and death unless circulation
restored promptly
o Treatment
Anticoagulation
Immediate revascularization procedure: limb viability at risk
High mortality rate
Takayasu and Giant Cell arteritis vasculitic syndromes
o Tell difference between two
Takayasu arteritis
Chronic vasculitis, unknown etiology
Targets aorta and major branches
o A.K.A. pulseless disease or aortic arch syndrome
80 90% women, onset age 10 40
o Most cases from Asia and Africa
Clinical presentation
o Pre-pulseless phase
Malaise, fever, nausea, vomiting, weight loss, rash, arthralgia, and Raynaud phenomenon

Once arterial obstruction develops, UE claudication from subclavian artery stenosis

Absent or diminished carotid or limb pulses (85%)
Focal symptoms related to artery affected
Hypertension observed in of the cases
o Sometimes malignant suggesting narrowing of the aorta proximal to renal arteries
Cardiac manifestations result from severe HTN, dilatation of aortic root, or coronary artery stenosis
Diagnosis 6 major criteria
o Onset by age 40
o Upper-extremity claudication
o Diminished brachial pulses
o Greater than 10mmHg difference between SBP in arms
o Subclavian or aortic bruit
o Narrowing of the aorta or a major branch
o Presence of 3 of the 6 carries high diagnostic accuracy
Cell arteritis (temporal)
Chronic vasculitis, medium to large arteries
o Most commonly involve cranial vessels or aortic arch and branches
Uncommon; 24 per 100,000
Onset after age 50, 65% women
May be associated with polymyalgia rheumatica
Clinical Presentation
o Diminished temporal pulses
o Facial pain
o Claudication of jaw while chewing
o Impaired vision (15 20% patients)
Amaurosis fugax
Diagnostic Studies
o ESR and C-reactive protein elevated
o Ultrasound demonstrates hypoechoic halo around involved vessel
o Diagnosis confirmed by biopsy of temporal artery
o

Giant

Treatment
Takayasu Arteritis
Steroid and cytotoxic drugs reduce inflammation
Surgical bypass
Giant Cell arteritis
o Do not wait on result of biopsy to start treatment!!
o High-dose steroids
o 40 60 mg daily
o Self-limited course 1 5 years
Raynaud Phenomenon
o Vasospastic disease of digital arteries
o

Diagnosed by history
Classically defined as episodes of discoloration of white ischemia, then blue stasis, then red hyperemia
(recovery phase)
Extreme vasoconstriction that temporarily obliterates vessel lumen
Cold exposure or emotional stress triggers spasms
Triphasic color response
White finger and/or toes interruption of blood flow
Cyanosis local accumulation of desaturated hemoglobin
Ruddy color blood flow resumes
Raynaud disease
Isolated, primary disorder
Predominantly women
ages 20 40
Most often fingers, 40% toes also
Benign course

o
o

Raynaud syndrome
Secondary Raynaud phenomenon (symptoms caused by another etiology)
Connective tissue disorder
o Scleroderma, SLE
Arterial occlusive disorders
Thoracic outlet syndrome
Blood dyscrasias
Thermal or vibration injuries
Carpal tunnel syndrome
Drugs
Clinical Presentation
Painful, pale, cold extremities
Chronic, recurrent cases
Atrophy of skin, subcutaneous tissues, muscle
Rarely causes ulceration
Ischemic gangrene
General Measures
Avoidance of any environmental triggers, e.g. cold, vibration, etc.
Although emotional stress is a recognized trigger, it tends to be impossible to consciously avoid
Warm clothing for the extremities such as mittens
Smoking cessation
Emergency Measures
If white finger occurs unexpectedly and a source of warm water is available
allow tepid to slightly warm water to run over the affected digits while gently massaging the area.

 Continue this process until the white area turns pink or a normal healthy color.
If triggered by exposure in a cold environment, and no warm water is available
place the affected digits in a warm body cavity - arm pit, crotch, or even in the mouth.
Keep the affected area warm at least until the whiteness returns to pink or a healthy color, avoid
continued exposure to the cold.
o Drug Therapy
Prevent vasospasm
Calcium channel blockers
-adrenergic blockers
Varicose Veins
o Veins: High capacitance vessels
Contain >70% of total blood volume
Deep or superficial
o Overview
Dilated, tortuous superficial vessels
Common in lower extremities, especially saphenous veins
Anorectal area
Lower esophageal veins
Spermatic cord (varicocele)
Women 2 - 3x more than men
patients have family history
Results from
Intrinsic weakness of vessel wall
Increased intraluminal pressure
Congenital defects of valves
o Primary vs Secondary
Primary
Familial
Superficial system
Pregnancy, prolonged standing, obesity
Secondary
Abnormality of deep venous system causes superficial varicosities
o Incompetent perforating veins
o Deep venous insufficiency or occlusion (DVT)
o Arteriovenous fistulas
In such cases, deep venous blood shunted retrograde through perforating channel into superficial veins
o Increases intraluminal pressure and volume
o Symptoms
Many asymptomatic
Burning, bursting, bruised, or aching

Exacerbated by prolonged standing or volume overload states

Elevation relieves symptoms
o Treatment
Sought for cosmetic reasons
Elevate legs while supine
Avoid prolong standing
Wear external compression stockings
Injection of sclerosing agent
Laser small veins
Radiofrequency ablation and surgical vein ligation
Superficial Thrombophlebitis and DVT
o Venous thrombosis
Thrombus formation within superficial or deep vein
Initially thrombus composed of platelets and fibrin
Later RBCs become interspersed within fibrin
Thrombus tends to propagate in direction of blood flow
Two kinds superficial thrombophlebitis and DVT
o Know difference between two
Superficial Thrombophlebitis
Benign disorder
Inflammation and thrombosis of superficial vein
o Tender, erythematos, indurated lesion in the course of a superficial vein
o May occur as a complication of an in-dwelling IV catheter
Clinical Presentation
o Erythema
o Edema
o Tenderness
o Cellulitis is common
Treatment
o Self-limited
o Local heat
o Rest
o ASA or anti-inflammatory
o Abx if cellulitis present
o No need to anticoagulate
Deep Venous Thrombosis
Most commonly veins of calves
May also develop more proximally
o Popliteal, femoral, iliac
Signs and Symptoms
o Nonspecific

o Unreliable
o Objective testing should be obtained whenever the diagnosis is entertained
High index of suspicion
2 major consequences
o Pulmonary embolism
DVT from proximal veins of LE
Pleuritic CP
Tachypnea
Cough, dyspnea
600,000 / year, often fatal
Untreated mortality rate 30 40%
o Postphlebitic syndrome
Chronic deep venous insufficiency
Venous valvular damage and/or persistent occlusion by DVT
Lead to
Chronic leg swelling
Stasis pigmentation
Skin ulcers
Immediate and long-term use of compression stockings to knee or higher drastically
reduces incidence
Triad predisposing to thrombosis Virchows triad
o Stasis
Prolonged inactivity
Immobilized extremity
Heart failure with systemic venous congestion
Hyperviscosity syndromes (polycythemia vera)
o Hypercoagulability
Pregnancy & OCP use
Neoplastic disease
Smoking
Myeloproliferative diseases
Inherited disorders of coagulation
o Vascular damage
Trauma
High risk after fractures of spine, pelvis, and bones of LE
Instrumentation (IV catheters)
Clinical Presentation
o May be asymptomatic
o Calf or thigh discomfort
Standing or walking
o Unilateral leg swelling

Physical Examination
o Edema of involved leg
o Localized warmth and erythema
o Tenderness over course of vein
Palpable deep venous cord
o Homans sign
Calf pain produced by dorsiflexion of foot
Nonspecific and unreliable sign
Diagnosis
o D-Dimer
Byproduct fibrin degradation
Highly sensitive for DVT/PE, but not specific
o Venous compression duplex ultrasonography
95% sensitive in proximal vein
75% sensitive in calf vein
Treatment
o Elevation reduces edema
o Anticoagulation prevents extension of thrombus and PE
LMWH
Warfarin
target INR 2.0 3.0
6 - 12 months
IVC filter
Prophylaxis
o Bedrest following surgery
o Prolonged bedrest
o Give LMWH
Diagnosis and management
o For general surgical patients at low risk (minor operations, less than 40, and no clinical risk
factors), early ambulation after surgery all that is needed
o Higher risk patients or surgeries may require one or a combination of low-dose heparin, lowmolecular-weight (LMW) heparin, elastic stockings, and intermittent pneumatic compression
o Extremely high risk patients or surgeries may require a prophylactic inferior vena cava filter
(umbrella)
o Monitoring of clotting studies may be necessary in higher risk patients