Cardiology FM

8/17/2019 Cardiology FM

1/25

Cardiology – Internal MedicineCongestive 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 sucient rate to meet the metabolic demands of the body (forward

failure) or the ability to do so only if the cardiac lling pressures are abnormally high (bacward failure)o !reventive therapy " patient education is the ey to reduction of burden

•

!athophysiology of Heart Failureo Heart failure most commonly results from conditions of impaired left ventricular function (myocardial failure)

# systolic dysfunction

o $ummari%ed as an imbalance in $tarlings forces or an imbalance in the degree of end&diastolic ber stretch

proportional to the systolic mechanical wor e'pended in the ensuing contraction (basically lie a rubber band themore it is stretched the greater the releasing velocity)

o Chronic heart failure results from

Impaired ventricular contractility

• $ystolic dysfunction

Increased afterload

Impaired ventricular lling

• iastolic dysfunctiono $ystolic ysfunction

*+, of patients

iminished capacity to e-ect blood

• Impaired contractility

• !ressure overload

uring diastole persistently elevated ./ pressure transmitted to .0 (through the open mitral valve)

pulmonary veins 0n elevated pulmonary capillary hydrostatic pressure (1 *2 mmHg) results in the transudation of 3uid into the

pulmonary interstitium $ymptoms of pulmonary congestion (.oss of contractility may result from damage to myocytes abnormal myocyte function or brosis)

o iastolic ysfunction

4+, of patients with clinical heart failure have normal ventricular contractile (systolic) function

Filling of ventricle occurs at higher&than&normal pressures

isplay abnormalities of ventricular diastolic function

• Impaired early diastolic rela'ation

• Increased sti5ness

• Or both

6levated diastolic pressure transmitted retrograde to pulmonary " systemic veins

• Classication

o Heart failure can also be classied as7


2/25

.eft&sided heart failure

• 8ost common cause is left&sided heart failure

• $ymptoms

o yspnea on e'ertion

o Orthopnea

o !9 (paro'ysmal nocturnal dyspnea)

o 9octurnal cough

o Hemoptysis

o Fatigueo ulled mental status

o 9octuria

• !hysical Findings

o iaphoresis dusy

o :achycardia

o :achypnea

o !ulmonary rales

o Cardiac asthma

o $, (; $ accepts blood volume at low pressures and e-ects against low

pulmonary vascular resistance

• Isolated rt&heart failure is less common and usually re3ects increased =/ afterload owing to disease ofthe lung itself or pulmonary vasculature

• =ight&sided heart disease resulting from primary pulmonary process

o Cor pulmonale (isolated =/ failure)

• ?hen the right ventricle fails the elevated diastolic pressure is transmitted retrograde to the right

atrium with subse@uent congestion of the systemic veins• Indirectly right&heart failure may also in3uence left&heart function

o ecreased =/ output reduces blood returning to ./ (preload)

o .eads to drop in ./ stroe volume

• $ymptomso !eripheral edema

o =AB discomfort

o 0nore'ia

o 9ausea

o Ane'pected weight gain

•

!hysical Findingso /

o Hepatomegaly


3/25

o !eripheral edema

o !alpable parasternal =/ heave

o $, or $<

o 8urmur of :=

o DDDDpleural e5usions may develop with either right sided or left sided failure

• 6tiology

o 8yocardial abnormalities

C0 8I ischemia (chronic and silent) cardiomyopathy

o Hemodynamic overload !ressure > 0$ H:9 massive !6 CO!

/olume > valvular regurgitation anemia thyroto'icosis

o /entricular lling abnormalities

8itral stenosis constrictive pericarditis ./H

o Cardiomyopathy

ilated

Hypertrophic

o 0rrhythmia

0F $/: mared bradyarrhythmias

• Causes of HF in ?estern ?orldo For a substantial proportion of patients causes are7

Coronary artery disease

Hypertension

ilated cardiomyopathy

• 0ggravating Factorso Often a lac of response to conventional therapy for heart failure is due to the presence of uncorrected aggravating

or precipitating factorsE It is important to always consider the possibility of such factors particularly in cases ofrefractory failure

o 8ainly7

8edications 9ew heart disease

8yocardial ischemia

o Other

!regnancy

0rrhythmias

Infections

:hromboembolism

Hyper+hypothyroidism

6ndocarditis

Obesity

H:9

9oncompliance


4/25

ietary e'cess

• $tages of Heart Failureo esigned to emphasi%e preventability of HF

o esigned to recogni%e the progressive nature of ./ dysfunction

o 0t =is for Heart Failure7

$:06 0 High ris for developing HF

$:06 G 0symptomatic ./ dysfunction

o Heart Failure7

$:06 C !ast or current symptoms of HF $:06 6nd&stage HF

o CO8!.6869: O 9O: =6!.0C6 9H0 C.0$$6$

9H0 Classes & shift bac+forth in individual patient (in response to =' and+or progression of disease)

$tages & progress in one direction due to cardiac remodeling

• iagnostic 0ids

o C=

Cardiac silhouette

• Heart shadow should occupy J2K or less of the ma'imal width of thora'

• $ome cases inaccurately re3ect heart si%e

o 6levated diaphragmo 9arrow chest 0! diameter

o !ericardial e5usion

• :herefore chest 0! diameter should be assessed on lateral view before frontal view to truly represent an

enlarged heart !ulmonary 8anifestations of Heart disease

• 0ppearance of pulmonary vasculature re3ects abnormalities of pulmonary arterial and venous pressures

and pulmonary blood 3owEo Increased vascular marings

o =edistribution of blood 3ow from bases to apices (cephali%ation)

o

!ulmonary edema (butter3y or bat&wing pattern)o 0bnormal septal lines (Lerley G lines)

o !leural e5usions

o 6chocardiography

$afe noninvasive relatively ine'pensive

High&fre@uency (ultrasonic) waves

:hree types of modalities

• 8&mode

o First application of ultrasonography

o !rovides limited data from one narrow ultrasonic beam

o /aluable for7

8easurement of wall thicness

Chamber diameters


5/25

0ccurate timing of valve movements

• :wo&dimensional (*)o 8ultiple ultrasonic beams transmitted through a wide arc

o =eturning signals produce *& images on screen

o !arasternal and apical views

$ome patients with CO! dicult to view > subcostal view

• oppler imagingo 6valuates blood 3ow direction velocity and turbulence

o !ermits estimation of pressure gradientso Colors are superimposed on *& images showing location of stenotic and regurgitant valvular

lesionso Can also show abnormal communications w+in heart and great vessels

• iagnostic ?orup

o In all cases7

History !hysical 6'am 6L

6cho

• 6tiology

• 8=M (diastolic dysfunction) =/ f'n

• Can measure pressures Chest '&ray

.abs

• :$H 9a L Cr G9!

0ssessment for C0

• One of few reversible causes

o In selected cases

.abs

• 8etanephrines

• Ferritin

Catheteri%ation

• C0

• Hemodynamics

6ndomyocardial biopsy

• If inltrative disease considered

o =ight&heart catheteri%ation

=ight heart

• 0ccess from peripheral vein

• 8easure pressures in =0 =/ " !0

• uided by 3uoroscopy

• Ase speciali%ed balloon&tipped catheter• =ecorded pressures identify the catheter tipNs position


6/25

!ulmonary artery wedge pressure

• !0?! or !C?o Closely matches .0 pressure in most people

• ?hen 8/ open during diastole

o !ulmonary venous bed .0 ./ normally share same pressure

• DD:hus !0?! can be used to estimate ./ end&diastolic pressure > a measurement of preloadDD

• :reatment

o Overview

Identify and correct underlying conditions 6liminate acute precipitating factors

8odulation of neurohormonal response

8anagement of symptoms

:reat congestion

Increase forward cardiac output

Improvement of long&term survival

o $tage 0

:reat nown ris factors > H:9 8 etc

.ifestyle modications > avoid smoing e'cessive use of alcohol illicit drug use

!eriodic eval > 6cho

Control ventricular rate restore sinus rhythm

0C6&I 0=G$

o $tage G

:reat nown ris factors > H:9 8 etc

.ifestyle modications > avoid smoing e'cessive use of alcohol illicit drug use

rug therapy for all patients

• 0C6I or 0=Gs

• Geta&Glocers

ICs in appropriate patients (implantable cardioverter debrillator)

Coronary revasculari%ation in appropriate patients /alve replacement or repair in appropriate patients

:herapies 9O: recommended

• igo'in should not be used in patients with low 6F sinus rhythm and no history of HF symptoms

because in this population the ris of harm is not balanced by any nown benetE

• Calcium channel blocers with negative inotropic e5ects may be harmful in asymptomatic patients withlow ./6F and no symptoms of HF after 8I

o $tage C

rug therapy for all patients

• iuretics for 3uid retention

•

0C6I or 0=Gs• Geta&blocers

rug therapy for selected patients


7/25

• 0ldosterone 0ntagonists

• igitalis

• Hydrala%ine+nitrates

ICs in appropriate patients

Cardiac resynchroni%ation in appropriate patients

o $tage

=ecommended :herapies Include7

• Control of 3uid retention

• =eferral to a HF program for appropriate patients• iscussion of options for end&of&life care

o Informing re7 option to inactivate debrillator

• evice use in appropriate patients

• $urgical therapy >

o Cardiac transplantation

o 8itral valve repair or replacement

• rug :herapy >o !ositive inotrope infusion as palliation in appropriate patients

$everal therapies should be avoided when possible in patients with systolic HF

• :hia%oladinediones (glita%ones) > medication for 8 that can worsen HF• Calcium channel blocers

o 6'cept amlodipine and felodipine

• 9$0I$ and CO * inhibitors

o Cause 9a and H*O retention

• Combination of 0C6&inhibitor 0=G and aldosterone blocer

o Increased ris of hyperalemia

0ggravating factors

• Often a lac of response to conventional therapy for heart failure is due to the presence of uncorrected

aggravating or precipitating factorsE It is important to always consider the possibility of such factors

particularly in cases of refractory failureo Other 0dd&ons if needed

0ldosterone 0ntagonist :herapy

• Chronic e'cess of aldosterone contributes to cardiac brosis and adverse ventricular remodeling

• $pironolactoneo substantially reduces mortality rates reduces hospitali%ations and improves symptoms when

added to 0C6 inh " diuretics Chronic therapy using combination of

• /enous dilator > isosorbide dinitrate plus

• 0rteriolar dilator > hydrala%ine

• $hown to improve therapy of moderate symptoms of HF• Ase when intolerance to 0C6 inh or 0=G therapy


8/25

• !articular benet in 00 with HF

Inotropic drugs (digitalis)

9O: useful in diastolic dysfunction systolic only

Genets7

• 6nhance contractility

• =educes cardiac enlargement

• Improves symptoms

• 0ugments cardiac output (with sysE HF)

• 0dded benet in patients with 0Fib• Has not been shown to improve long-term survival

o 0dditional :herapy

0nticoagulation

• If 0F or ./ thrombus

:reatment of atrial or ventricular arrhythmias

Insertion of an implantable cardioverter&debrillator (IC)

• ./6F ,JK

• 0t least 4 month post 8I or

• , months post revasculari%ation

• 9H0 class II or III HF

• 0bove regardless of previous documented ventricular arrhythmiaPP

Giventricular pacemaer

• Interventricular conduction abnormalities and widened B=$ comple'es are common in patients with

advanced HFo Ancoordinated patterns of right and left ventricular contractions

• :herapy7o 0ugments ./ systolic function with an accompanying reduction of ./ si%e

o Improves e'ercise capacity

o =educes fre@uency of HF e'acerbations

o =educes mortality• Indications

o ./6F ,JK

o B=$ Q 4*2 msec and

o 9H0 Class III or I/ HF

• iastolic ysfunction

o 0rea 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 =is of death lower than systolic dysfunction

o '7 doppler echocardiography

o :reat symptomatically and prevent reversible causeso Causes7


9/25

H:9

Hypertrophic cardiomyopathy

8yocardial infarction

=estrictive cardiomyopathy

0ortic stenosis with normal 6F

Coronary artery disease

!ericarditis

• 0cute !ericarditis

o 8ost common aRiction of pericardiumo In3ammation of layers

o 6tiology

Infectious

• /iral + Idiopathic > most often

• !neumococcus and staphylococci most fre@uently responsibleS gram&negative infection occurs less ofteno 8echanisms of entry for Gacterial !ericarditis

!erforating trauma to chest

Contamination during chest surgery

6'tension of intracardiac infection

6'tension of pneumonia Hematogenous spread from remote infection

• :uberculosiso .ow incidence in AE$E

o :G remains problem worldwide

o Important cause in immunosuppressed patients especially 0Is

• !yogenic bacteria & rare

9oninfectious

• !ost 8I

o 6arly > rst few days

In3ammation e'tending from epicardial surface

8ost common with transmural 8I

!rognosis following acute 8I not a5ected

T JK of patients

o .ater > resslerNs syndrome

* wees to several months post 8I

M autoimmune

• Aremia

• 9eoplastic disease

• =adiation&induced

• Connective tissue disorder• rug&induced


10/25

o !athogenesis

.ocal vasodilation with transudation of protein&poor cell&free 3uid into pericardial space

Increased vascular permeability with lea of protein into pericardial space

.euocyte e'udation

• Help contain or eliminate o5ending agent

8etabolic products released by these cells may

• !rolong in3ammation

• Cause pain and local cellular damage

• 8ediate somatic symptoms iEeE fever :he immune response to pericardial in-ury may signicantly contribute to tissue damage and symptomatology

o !athology

:he pathologic appearance of the pericardium depends on the underlying cause and severity of in3ammation

$erous pericarditis

• Characteri%ed by scant polymorphonuclear leuocytes lymphocytes and histiocytes

• 6'udate is thin 3uid secreted by mesothelial cells lining the serosal surface of the pericardium

• .iely represents early in3ammatory response common to all types of acute pericarditis

$erobrinous pericarditis

• 8ost common

• Contains plasma proteinso rossly rough and shaggy appearance

• !ortions of visceral and parietal pericardium may become thicened and fusedo Occasionally this process leads to dense scar

o =estricts movement and diastolic lling

$uppurative (purulent) pericarditis

• Intense in3ammatory response associated with bacterial infection

• $erosal surfaces are erythematous and coated with purulent e'udate

Hemorrhagic pericarditis

• rossly bloody form

• 8ost often caused by :G or malignancyo Clinical Features

8ost fre@uent symptoms of acute pericarditis are C! " fever

Chest pain > sharp pleuritic

• C! located retrosternal area and left precordiumS may also radiate to the bac and ridge of the left

trape%ius muscle

• 0ggravated by coughing and inspiration

Fever

!ositional > sitting + leaning forward eases pain

yspnea (none'ertional)

• yspnea common but not e'ertional > most liely from a reluctance of pt to breathe deeply b+c ofpleuritic pain


11/25

o !hysical Findings

:achycardia

Friction rub

• Gest heard leaning forward while e'haling

• $@ueay high&intensity sound heard best at left lower parasternal edge

• iaphragm

• , componentso /entricular contraction

o /entricular rela'ationo 0trial contraction

o iagnostic $tudies

6L > abnormal U2K of cases

• i5use $: segment elevation

• != segment depression

o != segment depression re3ects abnormal atrial repolari%ation related to atrial epicardial

in3ammation

•

.ab

• 6levated ?GC count

• 6levated 6$=

6chocardiography

• 0ssess for pericardial e5usion

o :reatment

Asually self&limited (4&, wees)

• /iral+idiopathic usually self&limiting

=est !ain relief

• 0nalgesic


12/25

• 0nti&in3ammatory

o 0$0+9$0Is

o Corticosteroids > severe or recurrent

Corticosteroids should not be given for uncomplicated casesE !otentially severe side

e5ects and b+c even gradual withdrawal of this form of therapy often leads to recurrentsymptoms of pericarditis

o !urulent pericarditis

8ore aggressive treatment

Catheter drainage of pericardium Intensive antibiotic therapy

8ortality rate very high

• Constrictive !ericarditis

o 0s blood passes from the =0 into the =/ during diastole the =/ si%e e'pands and @uicly reaches the limit imposed

by the constricting pericardiumE 0t that point further lling is suddenly arrested and venous return to the rightheart ceasesE :hus systemic venous pressure rises and signs of right&sided heart failure ensueE In addition theimpaired lling of the ./ causes a reduction in stroe volume and CO which leads to hypotension

o =esults from pericardium becoming brosed and thicened

/iral infectious post&surgical autoimmune

o =estricts the normal lling of the heart during diastole

o =estriction results in low&output failure

Initially right&sided

:hen left&sided

o 6'amination

6levated /!

LussmaulNs sign > increase in /! with inspiration

• LussmaulNs sign is the opposite of what is found in normal physiology where inspiration results in a

decline in /! $oft heart sounds

0trial brillation common

o Cardiac catheteri%ation is diagnostic 6levation and e@uali%ation of the diastolic pressures in each of the cardiac chambers

9ormal left ventricular function on ventriculogram

o :reatment

!ericardectomy

If :G medical therapy for 4 year

• !ericardial 65usion > can be a complication of !ericarditis see critical care

!eripheral /ascular isease

• Overview

o 9umber of diverse pathologic entities a5ecting arteries veins and lymphatics

o !/ results from $tructural changes in vessel wall


13/25

• degenerative conditions infection or in3ammation > lead to dilation aneurysm disseciton or rupture

9arrowing of vascular lumen

• atherosclerosis thrombosis or in3ammation

$pasm

• 0ortic aneurysm

o 0bnormal locali%ed dilatation of an artery

iameter has increased by at least J2K compared with normal

o Clinical !resentation

8a-ority asymptomatic• Incidental nding on imaging

$ymptoms related to compression of other structures

• :horacic > compress mainstem bronchus causing cough dyspnea pneumonia

• 6sophagus compression > dysphagia hoarseness (recurrent laryngeal nerve)

• 000 > bac pain or nonspecic I symptomso !hysical 6'am

!ulsatile mass

8urmur aortic regurgitation

Features of 8arfanNs syndrome

o iagnosis Altrasound

• 8ost useful and least e'pensive mode of diagnosis

• Gest used to assess progression of 000 si%e

• 0verage e'pansion of 2E< cm+year 000 and 2E4 cm+year thoracic

Contrast&enhanced C:

8=0 > 8=I with contrast

o Complication

=upture in any location produces acute symptoms

• $evere pain

• .OC• $hoc

• eath (result of massive internal hemorrhage)o 4J222 lives per year taen due to rupture

4,th leading cause of death

o V cm 000s will rupture in J years

o 0verage survival if untreated is 4W months

9atural history > =is of rupture related to si%e of aneurysm

o :reatment

Gased on si%e and patientNs overall medical conditions

Close monitoring every V > 4* months if asymptomatic

6lective surgical intervention if symptomatic (regardless of si%e)


14/25

o 0scending vs escending vs 0bdominal

6tiology

8ultifactorial depends on location

• 0scending thoracic aortic aneurysms7

o 0ging H:9 connective tissue disorders (8arfanNs)

o 8ore common in men

o Fusiform

o Often e'tend into aortic arch

o 6tiology7 8arfanNs

• Inherited disorder autosomal dominant

• 0ortic root tends to enlarge in fusiform fashion in association with aortic valvular

regurgitation

• Characteri%ed primarily by7

o olichostenomelia (long thin e'tremities)

o .igamentous redundancy

o 6ctopia lentis

o 0scending aortic dilatation

o Incompetence of aortic "+or mitral valves Gicuspid aortic valve

• !atients born with bicuspid aortic valve have structural abnormalities of the

ascending aortao !redisposes to aneurysm and dissection

• 0neurysm may develop before clinical symptoms of aortic stenosis

• 05ects *K of population (* in *22)

o Clinical !resentation

!ain anteriorly under the breast bone

• escending thoracic aneurysms7

o 0therosclerosis " associated ris factors 8a-ority are atherosclerotic in origin

• 8ay develop in patients with aortic coarctation

o :ypically fusiform

o 8ay e'tend to level of abdominal aorta

o Often begin distal to left subclavian artery

o Clinical presentation

Interscapular region + upper bac discomfort

• abdominal aortic aneurysms

o 0therosclerosis " associated ris factors

o

1U2K cases distal to renal arteries :ermed > infrarenal abdominal aortic aneurysm

o 0therosclerosis


15/25


16/25

• 0cute dissections

o symptoms of less than * wees duration

$udden severe pain

YtearingZ YrippingZ

• 0nterior substernal chest pain > type 0

• $capular+bac pain > type G

Can radiate anywhere

• Consider aortic dissection and ruptured thoracic or abdominal aneurysm in the di5erential diagnosis of

chest abdominal or bac painP !ainless occurs in about 4JK cases

8ay present with clinical features of shoc if resultant cardiac tamponade or signicant blood loss

o Imaging

C: angiography

• Can e5ectively e'clude the ma-or forms of life&threatening thoracic pathology

&imer

• Giomarer indicating activation of the coagulation system

• ?hen negative e'cludes acute aortic dissectiono Complications

!ericardial tamponade $troe

8I

=enal failure

.imb ischemia

0ortic regurgitation

o :reatment

oal > arrest progression of dissection

If suspicion of dissection

• =educe $G!

• ecrease force of ./ contractiono I/ 9: sodium nitroprusside GGs vasodilators

:ype 0

• 6arly surgical correction indicated

• High ris for death intrapericardial rupture aortic reguritation or 8I

:ype G

• Initially aggressive medical therapy alone

o GG [ afterload reducer

• 6arly surgical intervention does not improve outcomeE $' indicated if7

o continued propagation

o compromise of ma-or branches of aortao impending rupture


17/25

o continued pain

• !0

o Overview

Formation of atherosclerotic pla@ues in large and medium&si%ed arteries

!athology + pathophysiology is identical to that of C0

• toes lateral malleolus painful

• 0rterial

o

:rauma heels + toeso !ainful

o iscrete edges & Ypunched outZ

o 6dges covered with crust

o Infected erythematous

o =apidly developing

• /enous

o .eads to stasis ulceration

o !ainless

o 0nle + lower leg above medial malleolus

o =eddened thicened over medial malleolus

o Cobblestone appearance

o Occurs with slightest trauma


18/25

o $low developing

o iagnostic $tudies

0GI

• 0nle&brachial inde'

• 8easure systolic G! with oppler in

o each arm and

o dorsalis pedis and posterior tibial pulses

• ivide the anle pressure by the arm pressure bilaterally

• 4E2 > 4E, # 9ormal which means the anle pressure is e@ual to or slightly greater than that in the arms• T2EU

o iagnostic of !0

o Asually with symptoms of intermittent claudication

• T2EJ

o $evere !0 with critical leg ischemia

o Often have pain at rest

uple' ultrasonography

8=0

C:0

Intra&arterial contrast angiographyo :reatment

0ntiplatelet therapyDD

• 0$0 > shown to reduce C/ morbidity and mortality

=is factor modicationDD

• $moing cessation lipid management H:9 management 8 management

$upportive care of feet + prevent trauma

Formal e'ercise program > 4st line treatment

8edical therapy

• Cilosta%ol (!letal)

o $elective phosphodiesterase inhibitoro /asodilator and platelet inhibitor properties

o Improves e'ercise capacity

• !ento'ifylline (:rental)

o Improve deformability of =GC " ?GC

o 8ay improve claudication symptoms

• 0rea for lot of new and ongoing research

=evasculari%ation

• Indicated after failed medical therapy

• Or in cases of severe limb ischemia

•

oal > heal ulcers prevent limb loss• !:0 (percutaneous transluminal angioplasty)


19/25

• $urgery

DD reduce ris of coronary events

• 0cute 0ortic Occlusion

o Caused by emboli%ation or thrombus

Origin of arterial emboli usually cardiac

8itral stenosis

0trial brillation

0cute 0?8I

Infective endocarditis

o =arely originate from venous circulation

!arado'ical embolism

• 0rterial embolism from venous circulation

o Clot passes through an abnormal intracardiac communication (0$ /$ !FO)

o $ymptoms

0brupt total or near&total occlusion of terminal aorta or common iliac arteries poses immediate threat to life

and limb 0brupt onset of severe pain

• .umbar area buttocs perineum abdomen and legs

i5use cyanosis• From umbilicus to feet

• .ower limbs pale and cold

9umbness paresthesia and paralysis

0bsent pulses of lower limbs

8uscle necrosis may produce myoglobinuria renal failure acidosis hyperalemia and death unless circulation

restored promptlyo :reatment

0nticoagulation

Immediate revasculari%ation procedure7 limb viability at ris

High mortality rate• :aayasu and iant Cell arteritis > vasculitic syndromes

o :ell di5erence between two

:aayasu arteritis

• Chronic vasculitis unnown etiology

• :argets aorta and ma-or brancheso 0ELE0E Ypulseless diseaseZ or Yaortic arch syndromeZ

• X2 > U2K women onset age 42 >


20/25

o Once arterial obstruction develops A6 claudication from subclavian artery stenosis

0bsent or diminished carotid or limb pulses (XJK)

• Focal symptoms related to artery a5ected

• Hypertension observed in \ of the cases

o $ometimes malignant > suggesting narrowing of the aorta pro'imal to renal arteries

• Cardiac manifestations result from severe H:9 dilatation of aortic root or coronary artery stenosis

• iagnosis > V ma-or criteria

o Onset by age demonstrates hypoechoic halo around involved vesselo iagnosis conrmed by biopsy of temporal artery

o :reatment

:aayasu 0rteritis

• $teroid and cytoto'ic drugs reduce in3ammation

• $urgical bypass

iant Cell arteritis

o o not wait on result of biopsy to start treatmentPP

o High&dose steroids

o V2 mg daily

o $elf&limited course 4 > J years

• =aynaud !henomenono /asospastic disease of digital arteries


21/25

iagnosed by history

Classically dened as episodes of discoloration of white ischemia then blue stasis then red hyperemia

(recovery phase)o 6'treme vasoconstriction that temporarily obliterates vessel lumen

Cold e'posure or emotional stress triggers spasms

o :riphasic color response

?hite > nger and+or toes interruption of blood 3ow

Cyanosis > local accumulation of desaturated hemoglobin

=uddy color > blood 3ow resumeso =aynaud disease

Isolated primary disorder

!redominantly women

• ages *2 >


22/25

• Continue this process until the white area turns pin or a normal healthy colorE

If triggered by e'posure in a cold environment and no warm water is available

• place the a5ected digits in a warm body cavity & arm pit crotch or even in the mouthE

• Leep the a5ected area warm at least until the whiteness returns to pin or a healthy color avoid

continued e'posure to the coldEo rug :herapy

!revent vasospasm

• Calcium channel blocers

• ]&adrenergic blocers• /aricose /eins

o /eins7 High capacitance vessels

Contain 1W2K of total blood volume

eep or supercial

o Overview

ilated tortuous supercial vessels

Common in lower e'tremities especially saphenous veins

• 0norectal area

• .ower esophageal veins

• $permatic cord (varicocele) ?omen * & ,' more than men

\ patients have family history

=esults from

• Intrinsic weaness of vessel wall

• Increased intraluminal pressure

• Congenital defects of valves

o !rimary vs $econdary

!rimary

• Familial

• $upercial system• !regnancy prolonged standing obesity

$econdary

• 0bnormality of deep venous system causes supercial varicosities

o Incompetent perforating veins

o eep venous insuciency or occlusion (/:)

o 0rteriovenous stulas

• In such cases deep venous blood shunted retrograde through perforating channel into supercial veins

o Increases intraluminal pressure and volume

o $ymptoms

8any asymptomatic Gurning bursting bruised or aching


23/25

6'acerbated by prolonged standing or volume overload states

6levation relieves symptoms

o :reatment

$ought for cosmetic reasons

6levate legs while supine

0void prolong standing

?ear e'ternal compression stocings

In-ection of sclerosing agent

.aser > small veins =adiofre@uency ablation and surgical vein ligation

• $upercial :hrombophlebitis and /:o /enous thrombosis

:hrombus formation within supercial or deep vein

Initially thrombus composed of platelets and brin

.ater =GCs become interspersed within brin

:hrombus tends to propagate in direction of blood 3ow

:wo inds > supercial thrombophlebitis and /:

o Lnow di5erence between two

$upercial :hrombophlebitis

• Genign disorder

• In3ammation and thrombosis of supercial vein

o :ender erythematos indurated lesion in the course of a supercial vein

o 8ay occur as a complication of an in&dwelling I/ catheter

• Clinical !resentation

o 6rythema

o 6dema

o :enderness

o Cellulitis is common

• :reatmento $elf&limited

o .ocal heat

o =est

o 0$0 or anti&in3ammatory

o 0b' if cellulitis present

o 9o need to anticoagulate

eep /enous :hrombosis

• 8ost commonly veins of calves

• 8ay also develop more pro'imally

o !opliteal femoral iliac

• $igns and $ymptomso 9onspecic


24/25

o Anreliable

o Ob-ective testing should be obtained whenever the diagnosis is entertained

• High inde' of suspicion

• * ma-or conse@uenceso !ulmonary embolism

/: from pro'imal veins of .6

!leuritic C!

:achypnea

Cough dyspnea V22222 + year often fatal

Antreated mortality rate ,2 >


25/25

• !hysical 6'amination

o 6dema of involved leg

o .ocali%ed warmth and erythema

o :enderness over course of vein

!alpable deep venous cord

o Homans sign

Calf pain produced by dorsi3e'ion of foot

9onspecic and unreliable sign

•

iagnosiso &imer

Gyproduct brin degradation

Highly sensitive for /:+!6 but not specic

o /enous compression duple' ultrasonography

UJK sensitive in pro'imal vein

WJK sensitive in calf vein

• :reatmento 6levation reduces edema

o 0nticoagulation > prevents e'tension of thrombus and !6

.8?H

?arfarin

• target I9= *E2 > ,E2

• V & 4* months

I/C lter

• !rophyla'iso Gedrest following surgery

o !rolonged bedrest

o ive .8?H

• iagnosis and management

o For general surgical patients at low ris (minor operations less than

Date post:	06-Jul-2018
Category:	Documents
Upload:	trusha
View:	217 times
Download:	0 times

Cardiology FM

Documents