aortic stenosis as

8/9/2019 Aortic Stenosis as...

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- Anamnesis - The symptoms- The physical examination

- The cardiovascular disorders:

Angina pectoris

Myocardial infarction

Valvular disorders:1-aortic valvular stenosis2-aortic regurgitation 3-mitral stenosis4-

mitral regurgitation 5-mitral valve prolapse

Congestive heart failure

CV examination

1.general observation:

-Breathlessness

-body habitus (characteristics developing into a disease)

-body mass(obese/weight loss)

-Cyanosis

-Distress, demeanour (=the way person behaves towards others)

-sweating

-syndroms - Marfan's

*Hyperlipidemia- (3 signs)

CORNEAL ARCUS (white (creamy-yellow( rim around middle part of

eye,=precipitated ch crystals

XANTHELASMA - yellowish ch plaques around eyes, on skin in periorbital area

XANTHOMATA=yellow nodules w/ lipid deposits ex. in achilles tendon/patella - over

the knee!!(sign in skin&tendon)

*Infective endocarditis- look for:

SPLINTER HEMORHAHES= multiple, linear, redis-brown, along axis of finger&toe

nails!!

ROTH SPOTS- flame-shaped retinal hemorhhages(also in anemia&leukemia) - seen

on ophtalmoscopy

Multiple Capillary hemorrhages = PETECHIAE- FOUND ON SKIN(LEGS) &

CONJUNCTIVA(white part) - caused by vasculitis


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Other signs: finger clubbing - very rare in endocarditis!!

microscopic hematuria

2.Hands-clubbing

-tremor*

-skin temp*

-splinter hemorhages (on nail - in endocarditis, 1/6 patients; clots migrate from

affected valve!!)

-peripheral cyanosis on hands (normal, if exposed to cold, abn if assoc. w/ clubbing-

> HF or congenital R to L shunting )

3.Pulse and pressure: characteristics: (rate, rhytm, volume, character); check in

order:

-Radial- use 3 middle fingers-press on same side w/ patients thumb-on wrist, count

over 15 s and multiply by 4; on both hands simultaneously--> to see volume

differences + feel "collapsing radial pulse"-when hand raised up!!!

-Brachial-use thumb (cuz is deeper) - press elbow level on ant side -ANTECUBITAL

FOSSA (medial to biceps tendon)

-Carotid- tell p' what u doing& never press both simultaneously! + listen for bruits

w/stetoscope (its diaphragm) - in semirecumbent position (=half seat1ed-half layed

down)

-Femoral- midway betw pubic symphysis & ASIS - (=mid-inguinal point)

& listen for bruits w/stethoscope

-->*check for radiofemoral delay-(palpate both - radial and femoral pulses on one side ofthe body at the same time. The pulsation should occur at the same time, any delay may suggest

coarctation of the aorta!!!!!!!!!

-popliteal -post to knee joint (flexed1 knee to~45 degrees, foot on the bed, place bothhands on the front of the knee and place your fingers in the popliteal space.

-Post tibial-2cm post & below to medial maleolus!!

-dorsalis pedisdorsum ant of the foot, lateral to the extensor tendon of the great toe

4.Neck :

JVP


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Carotid bruits

5. Face

6.Eyes

- hypertensive retinopathy* -"etinal hemorrhages

Diabetic retinopathy*- #$ percent of all patients %ho ha&e had diabetes for 1$ years

7.Precordium -inspect/ palpate/asc

8.Lung bases - crackles& pleural effusion

9.abd - hepatomegaly, ascites

-aortic aneurysm*/bruits

-sacral edema

10.Legs-femoral pulses & bruits* radio-femoral dealy** ('ruits are (s%ishing( sounds heard

o&er ma)or arteries during systole or, less commonly, systole and diastole.*or bruits + check o&er the aorta, both renal arteries. and the iliac arteries

ankle edema

leg ulcers* -a yello%, bro%n, grey or black color and usually does not bleed.

n the feet - often on the heels, tips of toes, bet% toes %here rub against one another + if rub against bed

sheets, socks or shoes common the nail bed

ULC1ERS ON LEGS 3 TYPES

Venous statis ulcers

Neurotrophic (ia!etic"

#rterial (ische$ic ulcers"

%T C#USES L1E1G ULCERS

Poor circulation' oten cause !) arteriosclerosis

Venous insu*cienc) (a ailure o the +al+es in the +eins o the le, that causes con,estion an

slo-in, o !loo circulation in the +eins"

Other isorers o clottin, an circulation that $a) or $a) not !e relate to atherosclerosis

.ia!etes

Renal (/ine)" ailure

&)pertension (treate or untreate"

L)$phee$a (a !uilup o 0ui that causes s-ellin, in the le,s or eet"

n0a$$ator) iseases incluin, +asculitis' lupus' scleroer$a or other rheu$atolo,ical conitions

Other $eical conitions such as hi,h cholesterol' heart isease' hi,h !loo pressure' sic/le cell

ane$ia' !o-el isorers

&istor) o s$o/in, (either current or past"

Pressure cause !) l)in, in one position or too lon,

Genetics (ulcers $a) !e hereitar)"

# $ali,nanc) (tu$or or cancerous $ass"

nections


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SYMPTOMS

-most CV diseases - asymptomatic initially (silent - many yrs)

-severity of discomfort - doesnt correlate w/


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AORTIC DISSEECTION

2.PALPITATION TACHYARRYTHMIAS -anxiety/drugs

ECTOPIC BEATS -hyperthyroidism

3.SYNCOPE ARRHYTMIAS/ AORTIC STENOSIS - anxiety/simple

faints/epilepsy

/DIZZINESS POSTURAL HYPOTENSION

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY!!

ATRIAL MYXOMA

4.DYSPNEA CHF, Angina -anxiety, resp dis,

obesity&ANEMIA!!

Pulmonary embolism& hypertension

5.EDEMA venous stastis (=slow flow in veins) -immobility

constrictive pericarditis -liver disease

CHF -nephrotic syndrome

CHEST PAIN - CV CAUSES------------------TYPE - CAUSE - CHARACTERISTICS

ANGINA - CAD

AS

Hypertrophic cardiomyopathy

MI - CA Occlusion only!! - similar sites to angina, but more severe& persists at rest

+RESTLESSNESS, BREATHLESSNESS,

+feeling of impending death

+ANS stimul: sweating, pallor, nausea, vomit, diarrhoea!! pain can be absent 30% p, esp. DM & elderly!!!

PERICARDITIC PAIN- pericarditis - sharp, raw/STUBBING ANT CENTRAL chest

pain; varies w/ respiration& movement

+worst on: inspiration/swallowing

+relieved by: sitting up& lean forward

+can be secondary to ;2MI (can coexist),

2viral infection,

-after surgery


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2catheter ablation (re$o+in, electrical path-a) in arrh)th$ias4atrial5!rillation etc"

2angioplasty/radiotherapy

AORTIC PAIN- dissection of aorta!! - SUDDEN ONSET, severe, tearing, radiates toback (typical intrascapular!)

+profound autonomic stimulation!

+*if tear involves coronary a's-->may cause MI/syncope/focal neurological signs!

STABLE ANGINA -CLASSIFICATION ACC. TO SEVERITY (GRADE 1-4)

1.walking& climbing ok, angina w/STRENOUS / PROlonged excersise

2.physical activity SLIGHTLY LIMITED -1= after rapid walking/climbing

AFTER MEALS, in COLD/WIND/EMOTIONS/ AFTER AWAKING*

3.physical activity MARKELY LIMITED - walking only 1-2 blocks, climbing 1 level

4. AT REST (no physical activity possible)!!!!!!!!

DYSPNEA- awareness of increase drive to breath, abn if at rest (normal at

excersise)

-path. if occurs at lower threshold than expected,

-non-specif symptom (may b also by resp/metabolic/neuroM conditions

+toxins+anxienty)

-w/ ANGINA - relieved by nitroglycerine

-w/ CHF - assoc. w/ FATIGUE!

-w/ L increased atrial end diastolic presure!! --> fluid stucked in alveoli-

pulmonary edema-w/elevated pressure in pulmonary v's/capillaries

ORTHOPNEA- sign of advanced increased venous return to pulmonary congestion & pulmonary edema

PAROXYSMAL NOCTURNAL DYSPNEA- mech sim to orthopnea-gradual accumul.

of fluid in alveoli

+frothy blood-stained sputum present (differentiate it form asthma awaking fromsleep)


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PALPITATION

-ASK ABOUT - onset - gradual/sudden,

-precipitating factors-coffe, excersise, alcohol/drugs

-due to sustained arrhytmia:

PALPITATION IN TACHYARRHYTMIA - sudden, lasts for minutes/hours

-NOT trigerred by stress/anxiety!

-ASK ABOUT: fam history- CAD, RF, previous problms/smoking/caffeine/alc/drugs

-if recent ill health - suggests infective endocarditis

*CAD & cardiomyopathic . - risk for V arrhtymia**

(=&entricular tachycardia /T-15$-05$ bpm - one electrical short circuit that races in

a circle&entricular fibrillation /* + o&er 2$$ bpm + origin many different locations in the&entricles, each one trying to signal the heart to beat 32 doesnt contract but ui&ersshi&ers

SYNCOPE&DIZZINESS(=vertigo=light-headness, rarely cause by MALIGNANT VASO-VAGAL SYNDROME (+a,usner+e runs o-n throu,h the centre o the chest an a!o$en controllin,

!reathin,' the re6uenc) o the heart!eat an the circulation"

227 &CSS 2 &)persensiti+e Caroti Sinus S)nro$e

-arrhytmias: -supraventricular (ex. atrial fibrilation) - rarely cause syncope

- bradyarrythmias - most common - due to Sick Sinus Syndrom/ AV bloks

--> Stokes Adams attack (sudden faint)

-mech obstr to CO!:- esp. after excersise when CO cant meet demands:

severe aortic stenosis


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hypertrophic cardiomyopathy obstructing flow

& others: pulmonary embolism (w/freq fainting)

atrial myxoma & other tumors

precipitationg factors: getting up/sitting quickly,starting/increasing ant-hypertensive drugs

EDEMA

-usually dependent, seen in ankles, legs, sacrum (if lying in bed)

-causes: CHF & vasodilator meds!

*if JVP NOT elevated - edema NOT carcinogenic!!!!!********************************!

*in CHF -


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-myxedema (severe hypothyroidism)

CARDIAC EDEMA is pitting & dependent

Order of occurrence: LEGSFACEASCITIS

If due to R 1side


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--> pericarditis

CV diseases also present NON cardiac symptoms:

Endocardits& Hypertension--> CNS-->Stroke***

Liver congestion (due to HF-->jaundice!!!

HF-->oliguria-->renal fail

GENITICAL CV DISORDERS

single-gene defect

1.Hypertrophic cardiomyopathy!

2.Marfans syndrom

3.Familial hyperh--> premature cardiac & peripheral a disease

4.M dystrophies

5. Long Q-T syndrom = delayed repolarization (following HR speeds up; on exp HR

falls

tachycardia-causes: excers, pain, excitement, FEVER, hyperthr, meds:

sympatomimetics& vasDILATORS


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BRADYCARDIA-during sleep,athletic person, hypothyr, meds: B-BLOCKERS,

DIGOXIN, VERAPAMIL, DITIAZEM

&BRADYARRHYTMIA: carotid sinus hypersensitivity,

SSS-sick sinus syndrom,

2nd degree block*complete


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HEART FAILURE; mech- cause

systolic dysfunction - ischemia, MI,

=reduced contractility -cardiomyopathy. myocarditis

-inotropic effect indced by drugs; b-blockers

diastolic dysf.

impaired v filling -LVhypertrophy & constrictive pericarditis!

increased demand -thyrotoxicosis, (pregnacny, anemia, fever-all 3 aggrev. factors

rarely cause CHF alone)

metabolic&cardiac -Arteriovenous fistulas** (how is the process??)

-Paget's disease (bone re-modeling-->embolism)

ARRHYTMIAS -tachy/brady

vulvular& -all

structural lesions -Hypertrophic Obstructive Cardiomyopathy-ventricular septal defect

fluid overload -excessive IV infusions, drugs NSAIDS, steroids


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MS-Mitral Stenosis

narrowing of the valve passage by thickening of valve (=INCOMPLETE

OPENING) obstr flow from LA LV

Normal cross-section of mitral valve 4-5 cm2

Severe MS >less than 1cm !!

Moderate 1,5 2 cm

Mild 2 cm

*Symptoms start if valve less than 2,5 cm-surgery indicated if symptoms occur or PA

SYSTOLIC PRESSURE>50 mmHg at rest

>60 in excersise

Pressure increased in:

LA (in diastole)

Pulmonary vasculature (fluid goes back there)

R tage "enal


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-Chest pain

-Infective endocarditis (in Mild MS)

-R


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Physical Exam: Neck eins!"echni#ue for Examining$epato%ugular &eflux '$(&)

;epato)ugular reflux distension of the neck &eins- precipitated by the maneu&er of firm pressure o&er theli&er. !!-seen in tricuspid regurgitation, heart failure due to other non-&al&ular causes

constricti&e pericarditis, cardia tamponade, and inferior &ena ca&a obstruction.

The ;@" maneu&er may be performed as follo%s

1. The patient is positioned supine %ith ele&ation of the head at 45 degrees.

2. Aook at )ugular pulsations during uiet respirations

3. 9pply gentle pressure 2$-4$ mm ;g o&er the right upper uadrant or middle abdomen for at least 1$

seconds some suggest to 1 minute.

9n increase in @/ of B2 cm is a positi&e ;@" test.

alsalva manoeuvre forceful attemptedexhalationagainst a closedair%ay,

blo%ing up a balloon, %ith blocked nose and mouth

- test of cardiac function andautonomic ner&ouscontrol of theheart'

or to (clear( theearsandsinusesthat is, to euali6e pressure bet%een them %henambient pressure changes, as indi&ing' hyperbaric oxygen therapy, orair tra&el!!

-%orks by decreasing preload to the heart.

Effect of alsalva ardiac +inding

ostly -ecreases

urmur...

9ortic stenosis

ulmonic stenosis

Tricuspid regurgitation

/ncreases urmur ;ypertrophic cardiomyopathy' mitral &al&e

prolapse

complementary maneu&er for differentiating disorders is thehandgrip maneu&er, %hich

increases afterload-clenching one7s fist forcefully for a sustained time until fatigued
http://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Airwayhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Earhttp://en.wikipedia.org/wiki/Aerosinusitishttp://en.wikipedia.org/wiki/Scuba_divinghttp://en.wikipedia.org/wiki/Hyperbaric_oxygen_therapyhttp://en.wikipedia.org/wiki/Air_travelhttp://en.wikipedia.org/wiki/Aortic_Stenosishttp://en.wikipedia.org/wiki/Pulmonic_Stenosishttp://en.wikipedia.org/wiki/Tricuspid_insufficiencyhttp://en.wikipedia.org/wiki/Hypertrophic_cardiomyopathyhttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Handgrip_maneuverhttp://en.wikipedia.org/wiki/Exhalationhttp://en.wikipedia.org/wiki/Airwayhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Earhttp://en.wikipedia.org/wiki/Aerosinusitishttp://en.wikipedia.org/wiki/Scuba_divinghttp://en.wikipedia.org/wiki/Hyperbaric_oxygen_therapyhttp://en.wikipedia.org/wiki/Air_travelhttp://en.wikipedia.org/wiki/Aortic_Stenosishttp://en.wikipedia.org/wiki/Pulmonic_Stenosishttp://en.wikipedia.org/wiki/Tricuspid_insufficiencyhttp://en.wikipedia.org/wiki/Hypertrophic_cardiomyopathyhttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Handgrip_maneuver


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$andgripping maneuver ardiac +inding

/ncreased murmur intensity

9ortic regurgitation

?itral regurgitation

/entricular septal defect

?itral &al&e prolapse8

>T=C>D>

-ecreased murmur

intensity

9ortic stenosis

;ypertrophic cardiomyopathy

>ince increasing afterload %ill pre&ent blood from flo%ing in a normal for%ard path, it %ill

increase any murmurs that are due to back%ards flo%ing blood. E0FThis includes aortic

regurgitation 9", mitral regurgitation ?", and a &entricular septal defect />


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?"-/al&e doesnLt close completely during systoleA/ contracts, but blood goes back to A9 8

makes it congested, cu6 at same time recei&es from pulmonary circulatio

?itral prolapse leaflets protrude into A9

9> + &al&ular tisse thickens, opening narro%s flo% pre&ented from A/ to aorta

-----------------------------------------

/"&01 01E P&210P3 4 50&laws syndrome 4 +loppy itral valve 6 occurs when 1

contracts 4 /"&01 01E 50122N3 /N"2 10

/"&01 01E 0PP0&0"73 '8 components) 6 any disf to those can cause prolapse

9yo!cardium 6 to which papillary attaches

;Papillary 6 in dysfunction

yndrom:";eptal


18/24

Aortic Stenosis

usually- pathol simmil. to Atherosclerosis!!

1. Calcific vulvular disease - common in elderly, esp. western word

-valve inflamm--> many MACROpahues&LYPPHocytes-->valve thickening,

fibrosis&lipoprotein deposits

2. Congenital bicuspid valve (Normally should be tri!)

=fused aortic valve

3.RHD = Reumatic

-produces stenosis & fusion

-esp. in Mitral but also Aortic

Aortic Stenosis-->obstr to outflow-->pressure overload-->LV hypertrophy

-->low pressure in Aorta, systolic pressure fillin v.flow-> SLOW RISING PULSE OF

AORTIC STENOSIS

*ECHOcardiography - useful, cuz measures pressure

AS can caue excersise-induced death (hypertrophy-->high 02 demands & also

squeezes its own supply

->ischemiaexcersise-->bv dilatation-->flow to M--> not to


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apex beat: heaving (on palpation) - LV pumps against obstruction in slow, sustained

mannes

sounds:

Loop - sssssss-Doop

ssss=murmur in ventricular systole

'

'

'

'

'

'S4- as always found in pressure overload (s3 in volume overl)

-caused by strong A contraction to push blood into V

AS is treated w/ valve replacement or baloon valvuloplasty

88888888888888888888888888888888888888888888888888888888888888888888888888888888

2222222222222222222222222222222222222222222222222222222222222222222222222222222222222222222222

R less 02 to tissues--> BP i --> LV hypertrophy & stretching --> LVHypertrophy--> LHF


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NV: max 140/90 - risk to develop hypertension

- 160/95

hypertension-->stroke/MI

-contributes to artherosclersis! (circulatiom"bombards the wall harder, so causes

erosions & thrombus sticks better"

-Smoking accelarates atherosclerosis!! And kils the action of ANTI hypertensive

meds**

-adrenalin release-->vasoconstriction-->BPi

NO - Nitric Oxide is a molecule protecting from atherosclerosis- works like TEFLON

ATHEROSCLEROSIS: (4 RISK FACTORS)

1.smoking

2.hyperch

3.hyperT

4.DM

hypertension is a SLENT KILLER - has no symptms till organs& vessels involved

(20% PPL HAS IT)

95% is primary hypertension (pathology of regulatory mechanism -

hormonal/nervous/electrical)

factors: noise (ppl close to airports)/stress (drivers/boss)/anger/salt in diet (japanese

ppl)

5%secondary hypertension - due to diseases: -kidney dis./tubular dysf -adrenal glands tumors

-COARCTATION of aorta

(=narrowing--> CO i ; usually congenital)

-hormonal pills oral

MARFAN SYNDROME = abn CT due to def of FIBRILIN (protein that together

w/elastin form elastic tissue)

1.Skin

2.Skeletal changes - (long fingers, extra fingers - congenital Aracnodactyli*3.


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Aortic--II--

- best diagnosed w/ echocardiography

-treat w/ B-blockers--> less powerful blood ejection--> less risk for aorta dissection

AORTA DISSECTION=DISSECTING HEMATOMA

within wall of aorta!! = SEPARATION OF LAYERS IN AORTA

most risk: M> 50 w/ hypertension!

pregnancy!**

young person w/ marfan syndrome or other abn CT

coarctation of aorta=narrowing-->abn. flow dynamics

tear in media--> new-formed false blood channel within aortic wall = Pseudochannel

-poosible evolutions: - rupture back ;)

- rupture out--> hemorrhage-->emergncy!

AORTIC DISSECTION ACC. TO REGION:

1.In Asc. aorta - Type A - w/ high mortality! - ust distal to AORTIC ROOT (where

aorta meets rapid damage to may cause PERICARDIAL TAMPONADE

-->compressed ventricles&L venous return cant go back to JVP i

COMPLICATIONS OF DISSECTION1.Cardiac tamponade

2.MI - inf wall (suppl. by R Coronary a.)

3. Acute Aortic valve regurgitation (insuff. due to loosenesness around it)

4.Transverse Myelitis (if inv. aortic branch going to spine)

AORTIC DISSECTION - assoc. CHEST PAIN-sudden


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-excrutiationg (=cutting)

-radiates to back

-upward and downward (to abd - if abd aorta involved)

-->renal failure (if renal a. involved)

-HEMIplegia!!**-->check BP ON BOTH ARMS - if unequal BP&Pulse-->diasnosis - dissection

AORTIC DISSECTION - WAYS FOR BLOOD - PERICARDIUM-->CARDIAC

TAMPONADE--> VENTRICLES SQUEEZED-->their collapse-->CO cant be

maintained by L BP I -->SHOCK

- PERITONEUM/PLEURA

-compressing R coronary a.--> MI!!

LV HYPERTROPHY - any disease w/ i afterload* that LVH (as compensatory mech!)

ATHEROSCLEROSIS -frequency

1/abd aorta

2.Coronary a's -->IHD--> MI/CHF

popliteal a--> embolism to legs-->ischemia

carotid a & circle of Willis->CNS thrombi


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not

sufficient),

pregnancy, Paget's disease (bone metabolism very fast!-->req lots of blood flow),

beri-beri (thiamine def.; arterio-venous shunting, very low peripheral resistance,

blood passes very fast from artery to veins-->not enough dilution!!)

arterio-venous fistulas (microcirculation doesnt get enough nutrients, cuz doesnthave time; passess to fast from a-->v)

2. low CO

-myo


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>less efficient pump

aortic regurgitation

-rate and rhytm problems - both brady and tachy - nvole R and LV simultaneously!!

-------------

3.LVF4.RVF

5.Biventriclar VF

---------------

systolic failure

diastolic

---------------

aortic stenosis as

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