- Anamnesis - The symptoms- The physical examination

- The cardiovascular disorders:

Angina pectoris
Myocardial infarction
Valvular disorders:1-aortic valvular stenosis2-aortic regurgitation 3-mitral stenosis4mitral 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

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 of
the 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 both
hands on the front of the knee and place your fingers in the popliteal space. )

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

-dorsalis pedis dorsum (ant) of the foot, lateral to the extensor tendon of the great toe
4.Neck :
JVP

Carotid bruits
5. Face
6.Eyes
- hypertensive retinopathy* - Retinal hemorrhages
Diabetic retinopathy* - 80 percent of all patients who have had diabetes for 10 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** ( Bruits are "swishing" sounds heard
over major arteries during systole or, less commonly, systole and diastole.
For bruits check: over the aorta, both renal arteries. and the iliac arteries

ankle edema
leg ulcers* - a yellow, brown, grey or black color and usually does not bleed.
On the feet - often on the heels, tips of toes, betw toes where 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 (diabetic)
Arterial (ischemic ulcers)
WHAT CAUSES L1E1G ULCERS

Poor circulation, often caused by arteriosclerosis

Other disorders of clotting and circulation that may or may not be related to atherosclerosis

History of smoking (either current or past)

Venous insufficiency (a failure of the valves in the veins of the leg that causes congestion and
slowing of blood circulation in the veins)
Diabetes
Renal (kidney) failure
Hypertension (treated or untreated)
Lymphedema (a buildup of fluid that causes swelling in the legs or feet)
Inflammatory diseases including vasculitis, lupus, scleroderma or other rheumatological conditions
Other medical conditions such as high cholesterol, heart disease, high blood pressure, sickle cell
anemia, bowel disorders
Pressure caused by lying in one position for too long
Genetics (ulcers may be hereditary)
A malignancy (tumor or cancerous mass)
Infections

SYMPTOMS
-most CV diseases - asymptomatic initially (silent - many yrs)
-severity of discomfort - doesnt correlate w/<3 problem severity
ANGINA PERCTORIS - most common cardiac pain, caused by Myo<3 ischemia:
-obstr. flow in Epi-cardial* coronary vessel
-aortic stenosis ( how about others ??)
-hypertrophic cardiomyopathy (w/ i 02 demand)
characteristics;
=ache in ant chest (center of it)
=diffused dull discomfort
-lasting less than 10 min!
-described by patient as 'heavy weight", tight, pressing-band like sensation'
-confused w/ indigestion
-radiation: down ONE or BOTH arms,
up: throat, jaw, teeth
-unaffected by; inspiration, twisting/turning
-aggravating factors: all that raises 02 demands/ <3 contraction/ HR, BP
=exercise (likely early after starting)
=cold weather (peripheral vasoconstriction!!)
=heavy food (redistributed blood to digestive s.)
-relieving: rest &nitroglycerin
UNSTABLE ANGINA - recent onset w/ increasing: severity/duration/freq!
may trigger MI
NOCTURNAL/DECUBITUS ANGINA - when lie flat->increased !! venous return!!
or reduced efficacy of anti-anginal drugs - often taken in morning

5 SYMPTOMS CV DISESES
symptom - cv cause - other possible cause
1.Chest discomfort - ANGINA
MI
PERICARDitits

-esophageal spasm
-pneumothorax
-M-skeletal pain

AORTIC DISSEECTION
2.PALPITATION

TACHYARRYTHMIAS
ECTOPIC BEATS

-anxiety/drugs
-hyperthyroidism

3.SYNCOPE
faints/epilepsy
/DIZZINESS

ARRHYTMIAS/ AORTIC STENOSIS - anxiety/simple

4.DYSPNEA
obesity&ANEMIA!!

CHF, Angina

POSTURAL HYPOTENSION
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY!!
ATRIAL MYXOMA
-anxiety, resp dis,

Pulmonary embolism& hypertension

5.EDEMA

venous stastis (=slow flow in veins)

constrictive pericarditis
CHF

-immobility
-liver disease
-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 ;-MI (can coexist),
-viral infection,
-after surgery <3

-catheter ablation (=removing electrical pathway in arrhythmias/atrial

fibrillation etc)
- angioplasty/radiotherapy
AORTIC PAIN - dissection of aorta!! - SUDDEN ONSET, severe, tearing, radiates to
back (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<3 failure--> increased atrial end diastolic presure!! --> fluid stucked in alveolipulmonary edema-w/elevated pressure in pulmonary v's/capillaries
ORTHOPNEA - sign of advanced <3 failure!
-despnea when lye flat-->increased venous return to <3
-if LV failure --> 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 from
sleep)

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**
(= ventricular tachycardia (VT)-150-250 bpm - one electrical short circuit that races in
a circle
=ventricular fibrillation (VF) over 300 bpm origin: many different locations in the
ventricles, each one trying to signal the heart to beat <3 doesnt contract but quivers
(=shivers)
SYNCOPE&DIZZINESS(=vertigo=light-headness, rarely cause by <3 disease!! but
may be CV origin:
-postural hypotension - fall of 20 mmHg in systolic BP ON STANDING - caused by:
hypovolemia,
antihypertensive drugs (esp diuretcs&vasodilators);
also symptom of autonomic neuropathy
-neurocardiogenic syncope - faint results from sudden bradycardia & vasodilation
(in normal ppl on emotions) / freq fainting by trivial stimuli:
-->MALIGNANT VASO-VAGAL SYNDROME (vagus
nerve runs down through the centre of the chest and abdomen controlling
breathing, the frequency of the heartbeat and the circulation)
--> HCSS - Hypersensitive Carotid Sinus Syndrome
-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

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 - <3 slows downfluid build up in legs (if occurs fast may also cause
pulmonary edema!!!!!!!!!!!!!!!)
unilateral - causes
DVT
Soft tissue infection
trauma
immobility e.g-hemiplegia (porazanie polowiecze=paralysis 1 side of body)
lymphatic obstruction
BILATERAL EDEMA - causes:
CHF
Chronic venous insuff./immobility
Hypoproteinemia - eg. nephrotic syndrom, cirrhosis
lymphatic obstr eg. pelvic tumor, filariasis (asia/africa parasite)
drug-INDUCED EDEMA:
NSAIDS (ibuprofen)
nifedipine*= calcium channel blocker -antianginal(esp. in Prinzmetal's angina) &
antihypertensive,

amlodipine= calcium channel blocker; to lower blood pressure and to treat anginal chest pain
FLUDROCORTISONE-corticosteroid; to replace the missing hormone aldosterone in
various forms of adrenal insufficiency such as Addison's disease

GENERALISED EDEMA = ANASARCA in CHF, constrictive pericarditis

Or other conditions: diseases: renal/liver/hypoproteinemia

-myxedema (severe hypothyroidism)

CARDIAC EDEMA is pitting & dependent
Order of occurrence: LEGSFACEASCITIS
If due to R 1side <3 failure systemic congestion and generalized edema
L sided <3 failure1 initially pulmonary congestion, later generalized
*Other signs to estimate if edema due to cardiac failure:
-EDEMA ASSOCIATED CONDITIONS IN CARDIAC FAILURE
-exertional dyspnea
-jugulars are engorge=congested w/ blood
-tender hepatomegaly
-----------------------------------------------------------------------------------------------------------*Prinzmetal angina (/sounds like "prints metal")
(also known as variant angina, angina inversa, or coronary vessel spasm)
=syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles
caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the
smooth muscle tissue in the vessel walls rather than directly by atherosclerosis (buildup
of fatty plaque and hardening of the arteries)
more in older women

------------------------------------------------ANAMNESIS: ask about RF, childhood murmurs, smoking, hyperT, DM, kidney d.,
drugs
thyrotoxicosis (atrial fibrilation)
alcohol (arrhytmias and cardiomyopathy)
Marfans (aortic dissection & regurgitation)
*suspected endocarditiss--> ask about previous dental other bacteremias sorcesskin infections, drug used by IV, penetrating trauma
*p w/ chronic resp disease - can develop R<3 failure (=cor pulmonale) or atrial
fibrilation!!! why??
*Reumatoid arthritis (autoimmune, inflamm) -->Raynaud phenomenon* (=reduced
blood flow to extremities - fingers/toes-->discoloration& numbness)

--> 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 <3 beat) & risk for
ventricular <3 beats!--> ventricular fibrilation, sudden death
polygenic inheritance
-ischemic <3
-Hypertenion!! & Hyperlipidemia
-type 2 DM
-Abd Aortic Aneurysm!
--------------------------------------------------------PULSE- normal findings
40 bpm - can be normal in FIT, YOUNG!!
65 bpm - abn in Acute HF!!

PULSE ACC TO RATE

NV resting HR 60-100 bpm 9BELOW 60 - BRADYCARDIA, OVER 100 TACHY..)
*during inspiration-->parasympathetic tone falls******-->HR speeds up; on exp HR
falls
tachycardia-causes: excers, pain, excitement, FEVER, hyperthr, meds:
sympatomimetics& vasDILATORS

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

DIGOXIN, VERAPAMIL, DITIAZEM
&BRADYARRHYTMIA: carotid sinus hypersensitivity,
SSS-sick sinus syndrom,
2nd degree block*
complete <3 block
irreg pukse causes: sinus arrhytmias,
extrasysystoles*(from A & V)
atrial flutter & fibrilation
2nd degree heart block w/ variable response
PULSE ACC. TO RATE - brady/tachycardia
RHYTM - regular/ irreg
VOLUME - changes in atrial fibrilation (ex not enough time to fill in)
-large pulse volume - reflexion of large pulse pressure-very
common due to atherosclerosis! (vascular diseases/ old age/hypertension)
-low pulse volume - due to low stroke volume - in L<3 failure /
hypovolemia / peripheral vascular disease*
*COARCTATION OF AORTA-congenital
narrowing of aorta, usually distal to L subclavian
*PULSUS ALTERANS= beat to beat variation in pulse volume w/ normal rhyth - in
ADVANCED HF
*PULSUS PARADOXUS - respiratory cycle exagerates normal pulse volume;
normally - increases in expiration,
-decreases in inspiration (itrathorasic pressure-->venous return)
-in cardiac tamponade, acute severe asthma (things that restrict venous return even
more????
COLLAPSING PULSE - risines - early reaches peak & drops sudden!--in severe
aortic regurgitation!!!***
SLOW-RISING PULSE - gradual unstroke+reduced peak (occurs late in systole**)-in
severe aortic stenosis!!**
BISFERIENS PULSE - 2 systolic peaks separated by distinct mid-systolic dip -in
mixed aorit steosis & regurgitation**!!

HEART FAILURE; mech- cause

systolic dysfunction
=reduced contractility

diastolic dysf.
impaired v filling

- ischemia, MI,
-cardiomyopathy. myocarditis
-inotropic effect indced by drugs; b-blockers

-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&
structural lesions

-all
-Hypertrophic Obstructive Cardiomyopathy
-ventricular septal defect

fluid overload

-excessive IV infusions, drugs NSAIDS, steroids

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 <3
Causes:
-almost always w/ RHD! typically 20 yrs after = p~30 yrs old
-antibodies attack the valve except of bacteria
Other possible causes:
-Mitral Annular calcification (chronic degenerative process, assoc. w/ complete <3
block/ RHD)
-ESRD - End Stage Renal Disease mostly due to DM or high blood pressure
Symptoms: dyspnea(all3: ortopnea & PND)
*hemoptysis so much pressure going back to lungscapillary rupture in lungsPINK
FROTHY SPUTUM
-LA enlargement AF (atrial fibrillation) (HOW??)
thrombus formation
enlargement in upper part obstr to bronchial tree PNEUMONIA
-if MS severe LV enlargement also
Complications:
-AF-Atrial FibrilationPalpitation 30% cases
-Thromboembolism

-Chest pain
-Infective endocarditis (in Mild MS)
-R<3 failurehepatomegaly
increased JVP
BILATERAL LEG EDEMA
-hoarsness&dysphagia if laryngeal n. compressed by LA
Management
1.Diuretic therapy to decrease preload
2.Beta blockers to decrease CO/HR<100 bpm
3. Anticoagulants if p has AF** or embolic event
Physical diagnose-signs:
Apex NORMAL POSITION, BUT CAN BE TAPPING=CAN BE FELT
DUE TO LOUD S1
MALAR FLUSH
RAISED JVPHEPATOMEGALY
PEDAL EDEMA
*HEPATOJUGULAR REFLUX
Physical diagnose MS-ascultation:
S1 I louder (cuz valve has long way to go as pressure rises in LV**)
(normally S1=simultaneous closure of mitral & Tricuspid valves)
Opening snap (the ealier the worst) barely audible
Diastolic murmur low-pitched, rumbling (as blood passess to LV)
esp heart at L Lateral decubitus (why?)
(same as in AR aortic regurgitation but there called Austin Flint)
P2 I due to pulmonary hypertension
Exhalation sound even louder! (cuz septum pressured to L side***)
After valsalva manoeuvre-s1 lowered (makes <3 smaller on both sides**)

Physical Exam: Neck Veins-Technique for Examining

Hepatojugular Reflux (HJR)
Hepatojugular reflux = distension of the neck veins- precipitated by the maneuver of firm pressure over the
liver. !!-seen in: tricuspid regurgitation, heart failure due to other non-valvular causes:
constrictive pericarditis, cardia tamponade, and inferior vena cava obstruction.
The HJR maneuver may be performed as follows:

1.

The patient is positioned supine with elevation of the head at 45 degrees.

2.

Look at jugular pulsations during quiet respirations

3.

Apply gentle pressure (30-40 mm Hg) over the right upper quadrant or middle abdomen for at least 10
seconds (some suggest to 1 minute).
An increase in JVP of >3 cm is a positive HJR test.

Valsalva manoeuvre = forceful attempted exhalation against a closed airway,

blowing up a balloon, with blocked nose and mouth
- test of cardiac function and autonomic nervous control of the heart,
or to "clear" the ears and sinuses (that is, to equalize pressure between them) when
ambient pressure changes, as in diving, hyperbaric oxygen therapy, or air travel!!
-works by decreasing preload to the heart.
Effect of Valsalva

Cardiac Finding

Aortic stenosis
Mostly Decreases
Murmur!!!

Pulmonic stenosis

Tricuspid regurgitation

Increases Murmur

Hypertrophic cardiomyopathy, mitral valve

prolapse

complementary maneuver for differentiating disorders is the handgrip maneuver, which

increases afterload-clenching one's fist forcefully for a sustained time until fatigued

Handgripping maneuver

Cardiac Finding

Aortic regurgitation

Mitral regurgitation
Increased murmur intensity
Ventricular septal defect

Mitral valve prolapse&

STENOSIS

Decreased murmur

Aortic stenosis

intensity
Hypertrophic cardiomyopathy

Since increasing afterload will prevent blood from flowing in a normal forward path, it will
increase any murmurs that are due to backwards flowing blood. [2] This includes aortic
regurgitation (AR), mitral regurgitation (MR), and a ventricular septal defect (VSD).
Mitral valve prolapse: The click and the murmur of mitral valve prolapse are delayed because of
the increased left ventricular volume
Murmurs that are due to forward flowing of blood such as aortic stenosis, and hypertrophic
cardiomyopathy decrease in intensity.
Mitral stenosis: The diastolic murmur of mitral stenosis increases because of an increased heart
rate, blood pressure and cardiac output
-------------------------------------------------------------------------------------------------------------------

MR most common valvulopathy

*REGURGITATION=INSUFFICIENCY = INCOMPETENCE = not complete closure
MS thickened valve; flow prevented from LA to LV

MR-Valve doesnt close completely during systoleLV contracts, but blood goes back to LA &
makes it congested, cuz at same time receives from pulmonary circulatio
Mitral prolapse= leaflets protrude into LA
AS valvular tisse thickens, opening narrows flow prevented from LV to aorta
----------------------------------------MITRAL VALVE PROLAPS = BARlaws syndrome = Floppy Mitral valve occurs when LV
contracts = MITRAL VALVE BALOONS INTO LA
MITRAL VALVE APPARATUS (5 components) any disf to those can cause prolapse
1.Myo-cardium to which papillary M attaches
2.Papillary M in M dysfunction
3.Corda tendinae (<3 strings)
4.Leaflets
5.ANNULLUS (FIBROUS) if too loose in hypertrophy
*M prolapsed more in female, Marfan Syndrom/RHD/IHD. HOCM*, ASD (Atrial Septal Defect)
-in hyperthyroidism I T3&T4- WHY?

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
->ischemia
excersise-->bv dilatation-->flow to M--> not to <3
excersise induced:
1.Angina
2.Syncope(low suppl to brain=transient loss of consciousness due to global cerebral
hypoxia
3.Dyspnea - blood from lungs CANT ENTER EASILY to <3 by PV- due to high
pressure
AS S&S: pulse: slow volume & slow rising

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
8888888888888888888888888888888888888888888888888888888888888888
8888888888888888

---------------------------------------------------------------------------------------------R <3 - recives - from systemic v'v & pulmonary a's (trunk) - low pressure
myocardium=<3 M - thicker in ventricles - generates higher pressures
& thicker in L <3
AV valves - tRicuspid - R side /
-attach. to papillary M's in V myo<3 via chordae tendinae (f; prevent from prolapse
into A)
Pulmonary valve (R <3) & Aortic (L<3) - separate from arterial circulation
-each 3 cusps!-half-moon shaped = semilunar valves
----------------------------------------------------------------------------------------------<3 contraction-->arteries - away from <3--> to body-->by veins back to <3
Pressure in arteries depends on how far they r from LV
Aorta
120/80
Arteries 120/40!
Arterioles 40/25
Narrowed vessel's lumen-->less 02 to tissues--> <3 tries to make up and works
harderCO i--> BP i --> LV hypertrophy & stretching --> LVHypertrophy--> LHF

NV: max 140/90 - risk to develop hypertension

- 160/95

hypertension-->stroke/<3 ischemia--->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.<3 - Mitral valve regurgitation=( prolapse due to stretching)

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 <3) -->rapid damage to <3
type B - distal to L subclavian
PROGRESSION OF DISSECTION
some part of aortic root - covered w/ percardium - if hemorrhage thereHEMOPERICARDIUM--> may cause PERICARDIAL TAMPONADE
-->compressed ventricles&<3
-->L<3 cant maintain its output
--> venous return cant go back to <3
->JVP i
COMPLICATIONS OF DISSECTION
1.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

-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 <3-->BP I -->SHOCK
- PERITONEUM/PLEURA
-compressing R coronary a.--> MI!!

LV HYPERTROPHY - any disease w/ i afterload* that <3 has to contract against

3 causes: aortic-stenosis/insufficiency
hypertension
*long-standing mitral insuff-->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

<3 failure
fail to generate enough CO to meet min metabolic demand of body
CO=HRxStroke volume
SV det by:
1. Intrinsic health of myocardium
2.preload (=amount of blood in ventricles at the end of diastol=EDV;
=blood accumulated in V, just before their contraction - systole)
*ejection friction
2.afterload = peripheral resistance against which blood had to be pumped out to
circulation **

<3 failure causes:

1.increased preload-EDV (p=T/R-->pressure goes down if Radius increases-in LV
hypertrophy)
2.increased afterload-ex. aortic stenosis/hypertension
3.Increased metabolic needs- hyperthyroidism
4.unhealthy myocardium
types of chf 0 classif accto diff criteria
NV CO=5L/
1. high CO -thyrotoxicosis, severe anemia (low oxygen carring capacity-->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 doesnt
have time; passess to fast from a-->v)
2. low CO
-myo<3 contractilit loss, due to intrinsic (ischemic <3,infiltrative problem-ex
amyloidosis)
extrinsic factors ex. severe acidosis/
cardiotoxic drugs/ / toxicity of negatively inotropic
agents (B-blockers,all for arrhytmias)
alcohol-induced cardiotoxicity!!
-increased preload-volume overload - in mitral regurgitation-->dilatation of chaber--

>less efficient pump

aortic regurgitation
-rate and rhytm problems - both brady and tachy - nvole R and LV simultaneously!!
------------3.LVF
4.RVF
5.Biventriclar VF
--------------systolic failure
diastolic
---------------