aortic stenosis as
TRANSCRIPT
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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
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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
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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
---------------