angina pectoris vs ACS symptoms:
Angina pectoris: Crushing pain on exercise, relieved by rest. May radiate to jaw or arms
ACS Similar in character to angina but more severe, occurs at rest, lasts longer
reasons for undertaking an echocardiogram is to assess ventricular function
The most common reasons for
undertaking an echocardiogram are to assess ventricular function in patients with symptoms suggestive of heart failure, or to assess valvular disease.
AV block:
So,
First-degree AV block This is the result of delayed atrioventricular conduction and is reflected by a prolonged PR interval (>0.22 s) on the ECG. No
change in heart rate occurs and treatment is unnecessary.
Second-degree AV block This occurs when some atrial impulses fail to reach the ventricles.
.
Third-degree AV block Complete heart block occurs when there is complete dissociation between atrial and ventricular activity; P waves and QRS
complexes occur independently of one another and ventricular contractions
AF management:
So,
in haemodynamically unstable patient - immediate heparinisation and attempt cardioversion with a synchronised DC shock
if cardioversion fails then IV amiodarone.
Stable patient:
to control the rate: Beta blockers or verapamil
scoring system: CHADs2 and CHAD-VAS score:
A scoring system known as CHADS2:
(Congestive heart failure, Hypertension, Age 75,
Diabetes mellitus and previous Stroke or transient ischaemic attack [TIA]) is used to determine the need for anticoagulation.
Each factor scores 1 except previous stroke or TIA, which scores 2. A total score of 2 implies that oral
anticoagulation is needed.
When the score is <2 the CHADS2VASc scoring
system is applied:
which adds Vascular disease (aorta, coronary or peripheral arteries)
Age 65–74
female Sex category.
Each factor scores 1, except previous age >75 and stroke or TIA, which score 2. A CHADS2VASc score of 2 requires oral anticoagulation and a score of 1 merits consideration for oral anticoagulation or aspirin.
Acute heart failure;
So,
Acute heart failure is a medical emergency, with left or right heart failure developing over minutes or hours.
initial investigations are similar (ECG, chest X-ray, blood tests, transthoracic echocardiogram) with additional blood tests of serum troponin (for myocardial necrosis) and D-dimer (for evidence of pulmonary embolism).
What does atheroma consist off?
Atheroma consists of atherosclerotic plaques (an
accumulation of lipid, macrophages and smooth muscle cells in the intima of arteries) which narrow the lumen of the artery.
Coronary artery disease:
Age CAD rate increases with age. It rarely presents in the young, except in familial hyperlipidaemia.
Gender - Men are more often affected than pre-menopausal women, although the incidence in women after the menopause is similar to that in
men, possible due to the loss of the protective effect of oestrogen.
Family history CAD is often present in several members of the same family.
risk factors for CAD
So,
Hyperlipidaemia - The risk of CAD is directly related to serum cholesterol levels,
High triglyceride levels are also independently linked with coronary atheroma. Lowering serum cholesterol slows the progression of coronary atherosclerosis
and causes regression of the disease.
Cigarette smoking increases the risk of CAD, more so in men.
Hypertension (systolic and diastolic) is linked to an increased incidence of CAD.
Metabolic factors- Diabetes mellitus, an abnormal glucose tolerance, raised fasting glucose, lack of exercise and obesity have all been linked to
an increased incidence of atheroma.
Diets high in fats (particularly saturated fat intake) and low in antioxidant
intake (fruit and vegetables) are associated with CAD.
Other risk factors Lack of exercise, psychosocial factors (work stress, lack of social support, depression), elevated serum C-reactive protein (CRP) levels (as an inflammatory marker), high alcohol intake and coagulation factors (high levels of fibrinogen, factor VII and homocysteine) are also associated with CAD,
Angina clinical feature:
Clinical features:
Angina is usually described as a central, crushing, retrosternal chest pain, coming on with exertion and relieved by rest within a few minutes. It is often
exacerbated by cold weather, anger and excitement, and it frequently radiates to the arms and neck.
Myocardial infarction: STEMI
MI is the most common cause of death in developed countries. It is almost always the result of rupture of an atherosclerotic plaque, with the development
of thrombosis and total occlusion of the artery.
clinical features of STEMI:
Central chest pain similar to that occurring in angina is the most common presenting symptom. Unlike angina, it usually occurs at rest, is more severe and lasts for some hours. The pain may radiate to the left arm, neck or jaw and is often associated with sweating, breathlessness, nausea, vomiting
and restlessness.
immediate management for STEMI:
Immediate management
• Reperfusion therapy: preferred therapy for patients presenting within 90 minutes of onset is primary angioplasty with dual antiplatelet therapy.
If presenting after 90 minutes and within 12 hours (preferably 6 hours), treat with thrombolysis, e.g. double-bolus reteplase or single-bolus tenecteplase.
• Metoprolol (5 mg slow i.v. injection) if heart rate>100 beats/min.
Repeat every 15 minutes, titrated against heart rate and BP. Do not give if hypotension, heart failure, bradycardia, asthma.
• Insulin infusion if blood glucose>11 mmol/L; aim for blood glucose of 7–10 mmol/L.
mitral stenosis:
Thickening and immobility of the valve leaflets leads to obstruction of blood flow from the left atrium to left ventricle.
As a result there is an increase in left atrial
pressure, pulmonary hypertension and right heart dysfunction. Atrial fibrillation is common due to the elevation of left atrial pressure and dilatation.
signs of mitral stenosis:
Mitral facies or malar flush occurs with severe stenosis. This is a cyanotic or dusky-pink discoloration on the upper cheeks.
• The pulse is low volume and may become irregular if atrial fibrillation develops.
• The apex beat is ‘tapping’ in quality as a result of a combination of a palpable first heart sound and left ventricular backward displacement produced by an
enlarging right ventricle.
• Auscultation at the apex reveals a loud first heart sound, an opening snap (when the mitral valve opens) in early diastole, followed by a rumbling mid-diastolic murmur. If the patient is in sinus rhythm the murmur becomes louder when atrial systole occurs (presystolic accentuation), as a result of
increased flow across the narrowed valve.
The presence of a loud second heart sound, parasternal heave, elevated JVP, ascites and peripheral oedema indicate that pulmonary hypertension producing right ventricular overload has developed.
How to assess severity of mitral stenosis :
Echocardiography confirms the diagnosis and assesses severity.
A valve area of <2 cm indicates moderate mitral stenosis while an area <1 cm indicates severe stenosis.
There are three main causes of aortic valve stenosis:
- Degeneration and calcification of a normal valve – presenting in the elderly
- Calcification of a congenital bicuspid valve – presenting in middle age
- Rheumatic heart disease.
aortic stenosis ECG:
ECG shows evidence of left ventricular hypertrophy and a left ventricular strain pattern when the disease is severe (depressed ST segment and T-wave
inversion in the leads orientated to the left ventricle,
aortic regurgitation pathophysiology:
Chronic regurgitation volume loads the left ventricle and results in hypertrophy and dilatation.
The stroke volume is increased, which results in an increased impulse pressure and the myriad of clinical signs described below.
Eventually, contraction of the ventricle deteriorates, resulting in left ventricular failure.
The adaptations to the volume load entering the left ventricle do not occur with acute regurgitation and patients may present with pulmonary oedema and
a reduced stroke volume (hence many of the signs of chronic regurgitation are absent)
aortic regurgitation signs:
A ‘collapsing’ (water-hammer) pulse with wide pulse pressure is pathognomonic.
• The apex beat is displaced laterally and is thrusting in quality.
• A blowing early diastolic murmur is heard at the left sternal edge in the fourth intercostal space. It is accentuated when the patient sits forward with
the breath held in expiration. Increased stroke volume produces turbulent flow across the aortic valve, heard as a mid-systolic murmur.
• A mid-diastolic murmur (Austin Flint murmur) may be heard over the cardiac apex and is thought to be produced as a result of the aortic jet impinging on the mitral valve, producing premature closure of the valve and physiological stenosis.
Infective endocarditis
Infective endocarditis is an infection of the endocardium or vascular endothelium of the heart. It may occur as a fulminating or acute infection, but more commonly runs an insidious course and is known as subacute (bacterial) endocarditis (SBE).
Infection occurs in the following:
• On valves which have a congenital or acquired defect (usually on the left side
of the heart). Right-sided endocarditis is more common in intravenous drug
addicts.
• On normal valves with virulent organisms such as Streptococcus
pneumoniae or Staphylococcus aureus.
• On prosthetic valves, when infection may be ‘early’ (within 60 days of valve
surgery and acquired in perioperative period) or ‘late’ (following
bacteraemia). Infected prosthetic valves often need to be replaced.
• In association with a ventricular septal defect or persistent ductus
arteriosus.
main causes of infective endocarditis
Staphylococcus aureus and enterococci are common
causes of
minor criteria for infective endocarditis:
Predisposition, e.g. prosthetic valve, intravenous drug use
Fever – 38°C
Vascular phenomena (e.g. major arterial emboli, septic pulmonary infarcts)
Immunological phenomena (e.g. Osler’s nodes, glomerulonephritis)
Echocardiogram – findings consistent with infective endocarditis but not meeting major criteria
Microbiological evidence – positive blood culture but not meeting major criteria
major criteria for infective endocarditis:
Typical microorganism for infective endocarditis from two separate blood cultures in the absence of a primary focus: e.g. Streptococcus viridans, Streptococcus bovis, community-acquired Staphylococcus aureus or enterococci
Persistently positive blood cultures, defined as recovery of a microorganism consistent with infective endocarditis from blood cultures drawn more than
12 hours apart or all of three or the majority of four or more separate blood cultures, with first and last drawn at least 1 hour apart
Single positive blood culture for Coxiella burnetii or antiphase IgG antibody titre>1:800
Evidence for endocardial involvement
TTE (TOE in prosthetic valve) showing oscillating intracardiac mass on a valve or supporting structures, in the path of regurgitant jet or on implanted material, in the absence of an alternative anatomic explanation, or
Abscess
New partial dehiscence of prosthetic valve
New valvular regurgitation
