Left Atrial

C/P
Young female Recurrent syncope Embolism Intermittent M.S

12 8

CARDIOLOGY

Myxoma

Benign tumor from the interatrial septum encroaches to left atrium.

Investigations Echo - ESR Treatment Resection. N.B. Primary cardiac tumors are rare but the heart and mediastinum
may be the site of metastases. Most tumors are benign e.g. fibsomas, lipomas and haemangioma.

Mitral Valve Prolapsed

C/P
Degenerative disease of mitral valve (myxomatous) . prolapsed of mitral valve cusps into left atrium (mostly post leaflet). Young female Atypical chest pain Recurrent arryhmia Palpitation

Diagnosis

Mid systolic click. Late systolic murmur. Echo. Treatment Inderal (prophylaxis against arrythmia). Valve replacement (if severe). Prophylaxis against endocarditis with significant M.I. N.B. Mild mitral valve prolapse is so common that it should be regarded as a normal variant.

MVP sometimes thyrotoxicosis.

12 9

CARDIOLOGY

associated

with

marfans

and

A.S

A) Org Causes
1. Valvular *Rh. child *Cong. Child *Calcific old age, isolated history isolated young (calcific M.V.D. other cong. Bicuspid valve) (Usually associated) anomalies 2. Subvalvular A.S e., HocM. 3. Supravalvular A.S Elfin facies, Mental R usually associated (williams syndrome).

B) Functional causes In severe AI hperdynamic ciculation Haemodynamics

A.S. Pr.L. on left V left V. + + ischaemia heart failure

C/P
Triad cop Chest pain Due to Lt. V. F. * COP (syncope) exertional occur in any A.S At rest in calcific type calcification in conductive system (AVB) heart. block * Chest pain A.S Itself COP associated coronary atherosclerosis esp with calcific type (old age) Lf. V hypertrophy cop Lt. V. + +

 O/E

Pulse platuae (small volume and is slow-rising) * Insp. & palp: Lt. V. + + , apex sustained and localized Due Concentric hypertrophy i.e. Lt. V. + + , apex at 5th space (diagnosed by ECG and echo) late, dilatation apex shifted

13 0

CARDIOLOGY

* Thrill (base murmur

neck) = Org. A.S A1 A2 neck apex Allover loud harsh

S1 (Lt. V. + +) muscle. Component of S1 S2 Aortic Pr. S2 S3 Lt. V. failure (late) (S3 Apex) S4 A.S. Lt. V. pr. Vigorous atcial contraction (S4 apex)

Investigation
1- E.C.G., X-ray Lt. V. + + with strain in severe cases 2- Catheter: to measure pr. Gradient across Aortic valve. Pr. Gradient > 50 mm. Hg = severe A.S. 3- Echo * valve area < 0.7 cm2 * Normally 2.5 cm2 * Also it can measure pressure gradient across Aortic valve

Treatment
(No role for medical ttt, digit & diuretics may sympt) Surgery V.R. Indications (sympt + pr. Gr > 50). Valvotomy (sympt + pr. Gr > 50). Aortic balloon valvoplasty transient improvement. Mild A-S follow up with echo to detect the progression of stenosis. Angina best treated with BB, vasodilators or nitrates are better avoided as they aggravate exertional syncope

A.I
Causes

13 1

CARDIOLOGY

1. Rh. fever 2. $ aneurysm in ascending Aorta A.I. 3. valvotomy (post valvotomy) 4. collagen D (Aorta is rich in collagen fibers) ankylosis spondylitis. marfan $ weak wall of the Aorta rheumatoid D. 5. Endocarditis dilatation 6. Dissection of the aorta A.I

Heamodynamics
Regurged blood to Lt. V. Lt. V. dilatation Forceful contraction systolic pressure reflex periph. V.D. diastolic wide pulse pr.

C/P
Chest pain + palpitation due to diastolic pressure v. load coronary filling Late sympt of heart failure. Mild case may be a sympt except for palpitation.

 Peripheral

13 2

CARDIOLOGY

signs of A.I

3 H & neck 3 U.L. 3 L.L. 1- Corrigans sign: Marked carotid pulsation.

2- De-Musset sign: Nodding of the head 3- Systolic thrill over the carotid: Artery may be present due to rapid
flow of blood (carotid shuddering).

4- Water hammer pulse: This may be absent in the following

conditions: COP. d.t. A.S. or Lt. V.F. diastolic bl pr due to systemic hypertension. Mild A.I. 5- B.P.: Systolic Wide pulse pressure Diastolic

6- capillary pulsation: (Quinckes) may be detected in nails, lips, the

lobule of the ear and uvula (Mullers) 7- Pistol shot femoralis: Femoral is a loud sound heard with each pulse beat over the femoral artery (traubes sign).

8- Duroziezs sign: Systolic & diastolic murmurs are heard over the
femoral artery if a slight pr. is applied to it.

9- Hills sign: normally bl. Pr. In L.L. is higher than in U.L. by 20 mm.

Local exam

Hg in A.I the difference is > 40 mm. Hg.

Lt. V. ++ (dilatation). Hyperdynamic apex. Murmur - A2 - A1 soft, high pitched decrecent character - Apex.

Murmur over the apex

A. I. Functional M.I due to Lt. V. dilatation. Austin flint murmur (M.S)

N.B.

Causes

of

13 3

CARDIOLOGY

absence of periph Signs

M.S. A.S. why ? Lt. V.F. COP. Mild A.I. syst. Bl. Pr narrow pulse pr. P. signs if present = Lt. V is compensated.

Investigation E.C.G., echo, x-ray Lt. V.++ with

dilatational the ascending aorta. Mild symptoms ttt Mild Severe P. signs not evident + ve sympt Lt v is not enlarged th enlarged Lt.v (apex at 5 space) Medical ttt Surgery (valve R) Prophylaxis for Rh. F. Digit & diuretics!?

Infective endocarditis

Tricuspid Stenosis
Etiolo
gy

C/P

O/E Echo ttt

Rheumatic usually associated with mitral or aortic valve disease Carcinoid $ COP. S.V.C. If associated with M.S. it will decrease P.V.C, and P++ mid diastolic rumbling murmure on tricuspid area-signs of S.V.C. Rt. Atrium is enlarged Valvotomy (occasionally possible) V.R. (often necessary)

Tricuspid
Cause

13 4

CARDIOLOGY

Regurge

s
General exam O/E Tretm ent

Rt. V. ++ (functional) Rheumatic. Endocarditis esp in I.V. drug abusers (staph) Ebsteins anomally Neck veins congested cyanoicterus Ascites precox - +ve hepatojugular reflux Pansystolic murmur left to the xiphisternum. It increase in intensity with inspiration

ttt of the underlying cause reduce the severity to T.R. tricuspid valve annuloplasty if sever functional T.R., it can be done for example during mitral V.R. V.R. for organic T.R. Irrythemia Rh, activity Pulm embolism

Complication of Rh. H. disease

Infective endocarditis Heart failure DVT Systemic embolisation

Heart Transplantation
Indication
End stage heart disease for which all medical & surgical trials had been exhausted with no response (pump failure)

Patient
* age < 60 yrs. Heart disease grade 3,4 (symp. at mild exertion or at rest) * Medications after transplantation: Cyclosporine Cortisone

Pulmonary Hypertension
The pulmonary vascular bed is normally of low pressure the systolic pressure is about 25mm. Hg and the diastolic about 10.

Azathioprine.

13 5

CARDIOLOGY

Causes of P++
123Hyperkinetic P++ ASD, VSD, PDA. Post capillary Lf VF or MVD Obstructive Embolic Vasculitis. 1ry reactive GOAD- High altitude sleep apnea.

4-

C/P
Cause Rt V++. Rt sided failure.

Investigations cause echo P++, Rt V+, ECG Rt

V++

Treatment

cause

1ry Pulmonary Hypertension

This is a rare condition (female >male) esp children and young adult

Aet
unknown embolic or thrombotic events in pulm arterioles!?

C/P

* dyspnea * Rt V failure

 ttt

* Vasodilators have little efficacy. * Heart lung transplantation should be considered early.

13 6

CARDIOLOGY

Hyperlipidaemia
Serum lipoprotein by electrophoresis
1Chylomicrons: Which transport dietary (exogenous) triglycerides from intestine to blood. 2VLDL: Transports endogenous triglycerides from the liver to blood. It also contains cholesterol. 3IDL: Transports 60% of plasma cholesterol from liver to tissue. 4HDL: Trasports 40% of plasma cholesterol from tissue to liver.

13 7

CARDIOLOGY

I. Classification of 1ry Hyperlipidaemia

Type 1 ( Chylomicrons) Creamy plasma. Due to lipoprotein lipase. Triglycerides pancreatitis. ttt by fat in diet. 2Type II ( LDL) It is a familial hypercholesterolemia. Due to LDL receptors. Liable to I.H.D. ttt by educing cholesterol rich diet & by drugs e.g. cholestyramine & HMG COA reductase inhibitors (stations) HMG COA i.e. (hydroxymethyl Glutaryl coenzyme A). 3Type III ( LDL, VLDL) Familial hypercholesterolemia & triglyceridemia. Liable to I.H.D. TTT by cholesterol in diet & by bezafibrate. Type IV (endogenous Hyperlipemia) VLDL, triglycerides. I.H.D & pancreatitis. TTT fat, CHO in diet & nicotonic. A. 5- Type V ( Chylomicrons & VLDL) 4-

1-

 Plasma triglycerides

13 8

CARDIOLOGY

pancreatitis.

Associated with obesity. Liable to pancreatitis. TTT by fat, CHO, Wt reduction & nicotinic acid (triglycerides lowering agent).

II. Causes of 2ry Hyperlipidaemia

1- D.M. VLDL, IDL, triglycerides. 2- Alcohol excess VLDL, triglycerides. 3- Chronic renal failure VLDL, HDL, triglycerides. 4- Thiazides VLDL, triglycerides. 5- Non selective BB VLDL, triglycerides. 6- Hypothyroidism LDL , cholesterol. 7- Nephrotic $ LDL , cholesterol.

Drugs used in the management of hyperlipidaemia

Fibrates e.g. bezafibcate ciprofibrate. Their action mainly is lowering
triglycesides and increase HDL. Statins e.g. fluvastatin, Atorastin. Their main action is lowering of LDL cholesterol. Resins, they are cholesterol binding drugs and lower LDL . Nicotinic acid, it reduces LDL and triglycerides.

Atherosclerosis
Athogenesis (sequences of events)
(1) (2) (3)
(4) Endothelial injury adherence of blood macrophage or moncytes which imbibe LDL and actively enter the intima and become (foam cells). Active macrophages release free radical that oxidize the LDL, the oxidized LDL is toxic to endothelium causing endothelial loss and exposure of the subendothelial C.T. platelets aggregation. Platelets will release mitogenic factors migration of smooth muscles into the intima and its proliferation. Also activated macrophage secretes cytokines e.g. plat growth factors, T.N.F, fibroblast growth. F and ILI. The smooth mus cell & macropohags accumulate LDL from the plasma this is enhanced by LDL in blood.

13 9

CARDIOLOGY

(5)

Pathologic feature of atherosclerosis A- The fatty streak

Thin, flat, yellow streaks in the intima they consists of macrophages and smooth muscles cells whose cytoplasm distended with lipids (foam cells). They are present very early in life, they in number until about 20 yrs and then remain static or

N.B. There is controversy about whether some fatty streaks progress

into fibrous atheromatous plaque or whether they are independent of atherosclerosis.

B- Fibrous atheromatous plaque

It consists of fibrous cap under the endothelium & lipid zone consists of lipid laden macrophages.

C- Complicated plaque
Ulceration of plaque + calcification will lead to thrombosis.

N.B.

Risk factors of atherosclerosis & C.Hr.D. LDL : HDL > 5: 1 liable to atherosclerosis. Level of HDL seem to be protective. HDL may allow elution of cholesterol out of coronary Vs. Other risk factors see before in coronary heart disease.

14 0

CARDIOLOGY

Atherosclerosis and Peripheral Vascular Disease

male > female, strongly associated with smoking and affects the leg more than the arm. Patients are usually over 50 yrs. Sympt * Intermittent claudicating. * Cold feet or legs. * Peripheral cyanosis. * Late rest pain. Signs * Peripheral pulses. * leg ulcers, absenceof hair * finally frank gangrene.

Investig

ttt

X-ray calcification of Arteries. Doppler ultrasound. Angiography for revascularisation.

Medication has a little role. Balloon angioplasty for iliac or femoral stenosis. Calcium channel blockers. Amputation. Management of P. Vas. Disease G. measures Indicat for revascular Stop smoking. Acute ischaemia embolectomy Lose wt if obese. or amputation Stop vasoconstrictors. Chronic ischaemia with impaired Control D.M & hypertension.

 Exercise (collateral). Avoid infection, trauma. Vasodill and anticoagulant unhelpful.

skin and tissue viability. Disabling symptoms due to severe stenosis. are

14 1

CARDIOLOGY

N.B. Atherosclerosis is also presented with coronary heart disease and cerebrovascular disease.