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28 Cards in this Set

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Presenting symptoms in a cardiac hx

Chest pain


Dyspnoea


Fatigue


Palpitation


Presyncope/ syncope


Illnesses/ factors to rule rule out that are associated with heart disease

1. Thyroid diseases


2. Diabetes & dyslipidaemias


3. Rheumatic fever in childhood- valvular heart disease


4. Hypertension


5. Smoking ( in pack years)- major risk factor for coranary artery disease


6. Alcohol ( in units)


7. Use of injectable drugs ie. Cocaine - infective endocarditis


8. Drug hx - cardiotoxic drugs like betablockers & some calcium channel blockers


9. Family hx- cardiac disease ,sudden death


Causes of chest pain


1. MI


2. Pericarditis


3. Aortic dissection


4. Pulmonary embolism

Amplyfying MI

1.MIIschaemia of the heart that produces chest pain (angina) that is characterised by ; retrosternal pain, radiating to the arms, throat or jaws, has a constricting character, provoked by exertion & relieved within minutes by rest and worsens w time .MI is mainly caused by coronary artery disease that can be due to , artherosclerosis, arteritis, coronary disection, embolism, congenital CAD.


In Acute coronary syndromes, it's a cardiac emergency w pain similar to angina but more severe and not relieved by rest


Other associating signs are sweating, vomitting, tachycardia (anterior MI), bradycardia (inferior MI), 4th heart sound, pulmonary edema w large infarcts

Amplyfying pericarditis

Pain is sharp in nature, aggravated by inspiration, cough or postural changes, exacerbated by lying recumbent & reduced by sitting foward.

Amplyfying aortic dissection

Produces severe tearing painin either front or the back of the chest, the onset is abrupt unlike the crescendo quality of ischaemic cardiac pain.

Amplyfying pulmonary embolism

Sudden sharp pleuritic chest pain, breathlessness and haemoptysis and syncope..., there shpuld be a hx of recent surgery ,lower limb fx or long distance air travel, obese, heart failure, malignancy

Signs of congestive heart failure

1. Fluid retention,; raised jvp, peripheral edema, lung basal crackles


2. S3 sound


3. Reduced cardiac output, ; cool skin, peripheral cyanosis,




Symptoms


1. Exertional fatigue & dyspnoea w orthopnoea & PND, nocturnal cough

Ivestigations in left ventricular failure

1. Cheest x-ray- will show bilateral consolation w a perihilar distribution


2. Echocardiogram - confirms left v.disease


3. ECG- will show evidence of previous MI


4. ABG - hypoxaemia

Causes of angina

1. Impared myocardial oxygen supply


*Coronary artery disease- atherosclerosis, arteritis, DM


*coronary artery spasms


*congenital coronary artery disease


* severe anaemia or hypoxia


2. Increased myocardial oxygen demand


* left ventricular hypertrophy- hypertension, aortic valve disease, DCM


*tachyarrhythmias

Types of acute coronary syndromes

1. STEMI


2. NSTEMI

Causes of heart failure

1. Restricted filling


* mitral stenosis


* constrictive pericarditis


* restrictive cardiomyopathy


* hypertrophic cardiomyopathy



2. Contractile impairment


*coronary artery disease


* DCM


* myocarditis



3. Pressure loading


*Hypertension


*aortic stenosis


*coarctation of aorta



4. Volume loading


* mitral regurgitation


*aortic regurgitation



5.arrhythmia


* severe bradycardia


* severe tachycardia

Dyspnoea

Is a symptom of left ventricular failure due to increased pulmonary pressure. It can be


*exertional dyspnoea


Exercise causes a sharp increase in left atrial pressure & causes pulmonary congestion. Breathlessness in heart failure can be classified by new york heart association classification (NYHA) ; class1- asymptomatic, class2- symptoms on normal exertion, ie. Walking up a flight of stairs, class3- symptoms on minimal exertion ie. Getting dressed, class4- symptoms at rest


* orthopnoea,- pulmonary congestion on lying flat hence dib & the pt is forced to use extra pillows or sleep sitting


*paroxysmal nocturnal dyspnoea

Diagnosis of congestive heart failure

1. ECG- abnormal, often shows Q waves (previous MI), left ventricular hypertrophy (Hypertension), or left bundle branch block


2. Chest xray - cardiac enlargement, congested lung fields


3. Echo- left ventricular dilatation

Cause of radiofemoral delay

Coarctation of aorta

Types of valvular heart disease

1. Valvular stenosis (obstructing forward flow)


2. Valvular regurgitation (allowing backward flow or leaking)

Causes of valve disease?

1. Valve regurgitation


*acute rheumatic carditis


*chronic rheumatic carditis


* infective endocarditis


* syphilitic aortitis


* congenital


* traumatic valve rupture


* senile degeneration


3. Valve stenosis


* congenital


* rheumatic carditis


* senile degeneration

Pathogenesis of rheumatic heart disease

It starts w acute rheumatic fever which is a condition triggered by a delayed humoral immunity response to infection w specific strainsbof group A streptococci which have antigens that cross react w cardiac myosin & sarcolemmal membrane proteins. Antibodies produced against the strep antigens cause inflammation in the endocardium, myocardium &pericardium (all together called pancarditis) as well as joints & skin. Aschoff nodules are pathgnomic & occur only in the heart in the chronic phase of rheumatic carditis. Acute rheumatic fever is a mulyisystem disorder that presents w fever, anorexia, lethargy & joint paint 2-3wks post an episode of step pharyngitis. There may be no hx of sore throat however. diagnosis is made by using revised jones criteria ( 2 or more major criteria/ 1major + 2 or more minor)


Carditis, it's incidence decreases w increasing age, presents w dib due to HF and palpations ir chest pain, tachycardia, cardiac enlargement ,murmurs ( soft systolic murmur due to mitral regurgitation is very common or a soft mid-diastolic murmur due{the carey coombs murmur} is typical due to valvulitis w nodules forming on the mitral leaflets). ECG findings commonly include ST and T wave changes. When Conduction defects including AV block occur it causes syncope.


Treatment;


1.bed rest


2. Heart failure due to valve regurgitation- valve replacement. If AV block occurs ussually resolves but if it progresses pacemaker insertion may be required


3. Antibiotics-


4. Arthritis- aspirin/ steroids


Pathogenesis of Chronic rheumatic heart disease

Chronic valvular disease develop in atleast half of those that suffer rheumatic fever w carditis.


Mitral valvr is affected in about 90% of cases followed by aortic, tricuspid then pulmonary.


The pathological process in chronic rheumatic heart disease is progressive fibrosis leading to fusion and shortening of the valves that leads to stenosis w or w/o regurgitation

What is infective endocarditis?

Microbial infection of a heart valve, the lining of the heart chambers or blood vessels.


Most common causes are streptococci & sraphylococci. 50% of patients are over 60yrs, the underlying condition was rheumatic heart disease, congenital heart disease, calcified aortic valve or mitral prolapse.

Pathophysiology of infective endocarditis

Staph endocarditis of the tricuspid valve is a common complication of IV drug use. Infections tend occur at sites of endothelial damage because they attract deposits of platelets and fibrin that are vulnerable to colonisation of blood borne organisms. Presence of avascular valves, platelets and fibrin help proliferation of organisms. Vegetations composed of organisms, fibrin and platelets grow & may become large enough to cause obstruction or embolism. Adjacent tissues are destroyed & abscesses may form. Valve regurgitation may develop. Extracardiac manifestation s such as vasculitis and skin lesions may occur. Mycotic aneurysms may develop in arteries at site of infected emboli. In fatal cases infaction of the spleen & kidneys and sometimes an immune glomerulonephritis may be found in postmoterm.

Clinical features of infective endocarditis

*Petechial rash


*Osler's nodes, Splinter hemorrhages on fingers


*Hematuria


*Cardiac failure, varying murmurs, conduction disorder


*subconjustival hemorrhages, roth's spots in fundi of the eye


*cerebral emboli


*splenomegaly & finger clubbing in long standing endocarditis

What criteria is used for diagnosing infective endocarditis?

Dukes criteria


*2 major


* 1 major & 3minor


*5 minor


The above is definitive endocarditis


*1 major & 1 minor


*3 minor


Possible endocarditis

Indications for cardiac surgery in infective endocarditis

*heart failure due to valve damage


* large vegetations on left sided heart valves w echo appearance suggestive of high risk of emboli


*failure of antibiotic therapy


* abscess formation

Framingham diagnostic criteria for heart failure

Major criteria


1.cardiomegaly


2. Acute pulmonary edema


3. Pulmonary rales


4. PND/orthopnoea


5.hepatojugular reflux


6. Distended neck veins


7. Gallop (s3)


Minor criteria


1.hepatomegaly


2.ankle edema


3.pleural effusion


4. Nocturnal cough


5. Dyspnoea on exertion


6. Tachycardia >120

Investigations to be done when you suspect heart failire

1. Clinical hx & physical examination


2. ECG& ECHO


3. Chest xray


4. FBP, RFT, serum electrolytes


5. Natriuretic peptides - are hormones(Atrial type, Btype, Ctype, &Dtype) produced by the heart muscles that have natriuretic, diuretic & or kaliuretic properties from the ANP. And from BNP inhibition of RAAS, sympathetic outflow hence lowers BP.


*NT-proBNP > 125mg/ml. NT-proBNP, is secreted alongside BNP and has been documented to have important diagnostic value in heart failure. BNP is produced by direct synthesis in response to the degree of ventricular stretch, and also upregulated in failing ventricular myocardium. The messenger RNA for proBNP is unstable, so there is active regulation of BNP levels according to ventricular wall tension. Hence, it acts as a reliable biomarker of ventricular dilatation.[9]


*BNP>35mg/ml


Increased plasma levels of circulating NP have been described in patients with congestive heart failure, N-terminal proANP and BNP have been reported to be more sensitive indicators of systolic left ventricular (LV) dysfunction.


Physical signs, routine laboratory tests, electrocardiograms and chest films are not diagnostically consistent in differentiating heart failure from other diseases, such as pulmonary disease. Rapid testing of BNP and NT-proBNP has been reported to differentiate pulmonary etiologies from cardiac etiologies of dyspnea.However, some types of pulmonary disease, such as cor pulmonale, pulmonary embolism and lung cancer, are also associated with elevated NP levels.

What is finger/toe clubbing?

When there is loss of the sharmroth's sign due to hypertrophy of tissues in the nail bed giving rise to convexity of the nail and nail bed. Clubbing can occur rapidly w/in 2 to 3 weeks as in empyema/lung abscess or may develop over years as in congenital cyanotic heart disease, unilateral clubbing of the upper limbs may develop in aneurysm of the ipsilateral subclavian artery. Clubbing receds when the underlying lesion is cured.


There are 4 grades of finger clubbing


Other nail changes


*koilonychia-flattened ,brittle & in advanced cases spoon shaped & it's suggestive of severe iron deficiency state, the condition subsides when the deficiency is rectified. In early iron deficiency anaemia the nails are just flat (platonychia) , angular chelitisia another manifestation of iron deficiency anaemia


* leuconychia - white patches on the nails, can be seen in normal persons. white bands may indicate hypoalbuminemic states like chronic liver disease or nephrotic syndrome.


* splinter hemorrhages- infective endocarditis/vasculitis



Cause of generalised edema(anasarca)

1. Cardiac failure


Edema mostly in lower parts, it's worse during the end of the day and clears up w recumbency in ambulant individuals. In bedridden patients edema is most prominent over the sacrum


2. Renal causes


Due to acute nephritic & nephrotic syndrome( due to hypoalbuminemia). The edema is most prominent over the eyelids & face especially on waking up after sleep


3. Chronic liver disease


Leads to hypoalbuminemia. Normal level os albumin is 3.5-5g/dl. When albumin level falls to 2.5 fall in oncotic osmotic pressure happens hence edema.


4. Beriberi


Its a deficiency of viatamin B1(thiamine). There are 2 types, dry beriberi & wet beriberi. Wet beriberi is the one that affects the heart causing CCF . Dry beriberi affects nerves and can lead to paralysis


Alcohol abuse can lead to beriberi as it impares the body's ability to absorb and store thiamine.


Foods rich in thiamine are brown rice.