Hamzah's cardio pathology Flashcards
Define angina
recurrent transient episodes of chest pain due to myocardial ischaemia
Types of angina
classic/stable - induced by effort, relieved by rest
unstable (crescendo) - increases rapidly in severity, occurs at rest. Massive risk of MI
Decubitus - occurs when lying down
Prinzmetal - occurs at rest = coronary artery spasm
Aetiology of angina
atheroma = main cause others = anaemia, coronary artery spasm, aortic stenosis
Pathogenesis of angina
myocardial ischaemia occurs when demand outstrips supply. stenosis of a coronary artery impairs coronary blood flow when myocardial oxygen demand increases.
Risk factors for angina
diabetes, smoking, hyperlipidaemia, hypertension, family history, lack of exercise
Clinical presentation of angina
central crushing chest pain
comes on exertion and relieved by rest
exacerbated by cold weather, heavy meals, anger
radiates to arms and neck
other symptoms = dyspnoea, nausea, sweating, faintness
Differential diagnosis of angina
ACS, pericarditis, myocarditis, aortic dissection, GORD
Diagnostic tests for angina
ECG - normal but may show ST depression and flat/inverted T waves
Exercise ECG tests
coronary artery angiography
Treatment of angina
modify risk factors - stop smoking, weight loss, control hypertension
secondary treatment to prevent MI, stroke = low dose aspirin
symptomatic treatment = sublingual GTN spray, beta blockers, calcium channel blockers
surgery = PCI, CABG
What do acute coronary syndromes include?
unstable angina - no infarction
NSTEMI - subendocardial infarction
STEMI - transmural infarction
Pathophysiology of ACS
rupture, erosion of the fibrous cap leads to platelet aggregation and the formation of a platelet rich clot. Vasoconstriction occurs due to serotonin and thromboxane A2 release by platelets. This leads to ischaemia of myocardium
Symptoms of ACS
acute central chest pain (20 mins+)
sweating, dyspnoea, palpitations
Signs of ACS
Distress, Pallor/sweatiness, high/low pulse, hyper/hypotension. 4th heart sound
Differential diagnosis of ACS
angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism, oesophageal reflux/spasm
Diagnostic tests for ACS
Blood - FBC, U&Es, lipids
ECG - pathological Q waves
Cardiac enzymes - cardiac troponin T and I - peak at 24-48 hrs
Treatment of ACS
=MONA
morphine, oxygen, nitrates, aspirin (300mg).
High risk STEMI/NSTEMI = MONAT
morphine, oxygen, nitrates, aspirin, T-clopidogrel/Ticagrelor
beta blockers, anti-coagulant (FONDAPARINUX)
PCI if high risk
secondary treatment = ACEi, statins
Acute STEMI treatment
aspirin, pain relief, antiemetic, oxygen, restore coronary perfusion - PCI or CABG, thrombolysis
Complications of MI
Heart failure, rupture of IV septum, mitral regurgitation, arrhythmias, pericarditis - Dressler’s syndrome
When is hypertension clinically treated?
sustained BP>160/100
>140/90 on 2 separate occasions - treat if at increased risk of coronary events, have DM or end-organ damage
Aetiology of hypertension
Essential hypertension = primary hypertension - hypertension with no underlying cause - genetics, obesity, high salt intake
Secondary hypertension = hypertension that is the result of a specific and potentially treatable cause - renal disease, endocrine disease (Conn’s, Cushing’s, pheochromocytoma, acromegaly), coarctation of aorta, steroids, pregnancy
Risk factors for hypertension
age, family history, male gender, African or Carribean origin, high salt intake, obesity, smoking
Pathogenesis of hypertension
Complex - multiple factors interact to produce hypertension
sustained hypertension promotes atherosclerosis, increases the work of the LV (–> LV hypertrophy) and increases the risk of LV failure, intracerebral haemorrhage and chronic kidney disease
Clinical presentation of hypertension
check for retinopathy, check for end organ damage, signs of underlying disease (renal disease, Cushing’s, low femoral pulse=coarctation)
What is malignant or ‘accelerated’ hypertension?
Rapid rise in BP leading to vascular damage.
Fibrinoid necrosis of vessel wall results in end organ damage in kidneys, retina and cardiovascular system.
Diagnostic tests for hypertension
ABPM - excludes white coat effect and is 24hrs
Home BP monitoring.
To quantify overall risk –> fasting glucose, cholesterol
ECG –> look for end organ damage
U&Es –> exclude secondary causes
24hr urinary metanephrines
Treatment of hypertension
treat underlying cause
target BP = 140/85 and for diabetics = 130/80
non-pharmacological = reduce weight, low-fat diet, low-salt diet, stop smoking, exercise
pharmacological = ACEi, thiazide diuretics (Bendroflumethiazide), beta-blockers, ARBs, Calcium channel blockers
Define heart failure
Where cardiac output is inadequate for the body’s demands
Aetiology of heart failure
systolic = IHD, MI, cardiomyopathy
diastolic = tamponade, constrictive pericarditis, systemic hypertension
valvular disease, anaemia, ventricular septal defect
Define acute heart failure
new onset acute characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion
Define chronic heart failure
develops or progresses slowly. venous congestion is common but arterial pressure is well maintained until very late
What is low output heart failure?
cardiac output is low and fails to rise with exertion. Causes = pump failure and excessive afterload
What is high output heart failure?
rare. the heart is pumping the right amount of blood but this is not enough to meet the demands of the body. causes = anaemia, pregnancy, hyperthyroidism
New York Classification of HF
- Heart disease present but no undue dyspnoea from ordinary activity
- Comfortable at rest; dyspnoea during ordinary activities
- Less than ordinary activity causes dyspnoea - limiting
- Dyspnoea present at rest; all activity causes discomfort
What is systolic heart failure?
the ventricles can’t pump hard enough. <40% of ejection fraction
What is diastolic heart failure?
not enough blood fills into ventricles during diastole (same ejection fraction but lower SV and total volume)
Aetiology of left sided heart failure
IHD
hypertensive heart disease - increased afterload - LV hypertrophy
dilated cardiomyopathy - chamber grows and muscle gets weaker over time
diastolic
- LV hypertrophy - less room for blood to fill
- aortic stenosis
- hypertrophic cardiomyopathy
- restrictive cardiomyopathy = LV can’t stretch and fill
Pathogenesis of left sided heart failure
low cardiac output = low BP
low BP stimulates baroreceptors and reduces renal blood flow
sympathetic overdrive + RAAS
In the short term, BP is restored as well as afterload and preload
In the long term, the heart has to work harder and so LV hypertrophy occurs
LV hypertrophy reduces the volume of the ventricular cavity - reduced stroke volume
Clinical presentation of LHF
symptoms = dyspnoea, poor exercise tolerance, fatigue, orthopnoea, PND, cold peripheries, weight loss, muscle wasting
signs = pulmonary oedema, frothy pink sputum, cyanosis
Diagnostic tests for LHF
FBC, U&Es, ECG, echocardiogram
Causes of RHF
left ventricle failure - high pressure in pulmonary artery makes it harder for right ventricle to pump blood –> biventricular heart failure
left-right cardiac shunt - septal defect causes blood shunt from left to right. increases fluid volume of right side of the heart causes hypertrophy and becomes susceptible to ischaemia (systolic dysfunction) and smaller volume (diastolic dysfunction)
Chronic lung disease and cor pulmonale - in response to hypoxia the PA constrict which raises PBM. This makes it harder for the right ventricle to pump blood out - RV hypertrophy
Effects of RHF
systemic vein congestion - jugular venous distension
blood backs up to spleen and liver. can causes ascites and cardiac cirrhosis
pitting oedema in legs
Clinical presentation of RHF
peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis
Management of heart failure
Acute HF = medical emergency - oxygen, diamorphine, furosemide, GTN spray
Chronic HF = healthy lifestyle changes
treat underlying cause
treat exacerbating factors (infection, anaemia, high BP)
drugs = diuretics, ACEi, Beta-blockers, Mineralocorticoid receptor antagonists (spironolactone), digoxin, vasodilators
surgical intervention = revascularisation in IHD (PCI or CABG), valvular replacement, heart transplant, implanted autonomic cardiac defibrillator or pacemaker
What is an abdominal aortic aneurysm?
a permanent dilation of the abdominal aorta of more than 3cm in diameter
Causes of AAA
most = aortic atherosclerosis,
can also be caused by CT disorders (Marfans), trauma
Pathogenesis of AAA
proteolytic enzymes weaken the media of the aorta leading to aneurysmal change
Clinical presentation of AAA
unruptured aneurysms are often asymptomatic but may cause abdominal or back pain
ruptured AAA present as a surgical emergency with abdominal pain and shock
Diagnostic tests of AAA
ultrasound scan or CT scan
Treatment of AAA
elective surgical repair considered for aneurysms with a diameter greater than 5.5cm
surgical replacement of the aneurysmal section with prosthetic graft
endovascular repair with stent insertion if surgery not possible
What is an aortic dissection?
a tear in the tunica intima leading to blood flow into the tunica media. This forms a false lumen in the diseased media
Aetiology of aortic dissection
most are related to hypertension
Types of aortic dissection
Type A - 75% - involves the ascending aorta or aortic arch
Type B - 25% - involves the descending aorta
Pathogenesis of aortic dissection
caused by hypertension - tears the tunica intima
dissections may propagate in the blood flow direction (=anterograde) or against the normal flow of blood (=retrograde)
Dissections may re-enter the aortic lumen at a distant site (- creating a double-barrelled aorta) or rupture externally into the pericardial cavity, pleural cavity or peritoneal cavity
Presentation of aortic dissection
- abrupt onset of severe, tearing chest pain
- involvement of branch arteries may involve unequal arm pulses and blood blood pressures
Investigation of aortic dissection
Chest x-ray = widened mediastinum
CT scan
TOE - transoesophageal echo
MRI scan
Treatment of aortic dissection
surgical repair
urgent control of BP = IV esmolol
What is acute pericarditis?
inflammation of the pericardium
Aetiology of pericarditis
idiopathic viruses - coxsackie, echovirus bacteria - TB, staphs, streps, Lyme disease autoimmune - SLE Dressler syndrome metabolic - uremic pericarditis
Clinical presentation of pericarditis
central chest pain. Worse on inspiration or lying flat. Relieved by sitting forward
Diagnostic tests for pericarditis
ECG - concave (saddle shaped) ST segment elevation and PR depression
Blood tests - FBC, ESR, U&Es, cardiac enzymes, echocardiogram
pericardial friction rub heard on auscultation
Treatment of pericarditis
NSAIDs or aspirin with gastric protection for 1-2 weeks
colchicine - inhibits neutrophil migration
treat underlying cause
What is a pericardial effusion?
The accumulation of fluid in the pericardial sac
Causes of pericardial effusion
pericarditis, myocardial rupture
Clinical features of pericardial effusion
dyspnoea, chest pain, signs of local structures being compressed, nausea (diaphragm), cardiac tamponade signs
Diagnostic tests for pericardial effusion
Chest X-ray
ECG changes - low voltage QRS complexes
Echocardiography
Treatment of pericardial effusion
Treat underlying cause
Pericardiocentesis
- diagnostic –> send bacteria to labs
Therapeutic –> cardiac tamponade
What is constrictive pericarditis?
the heart is encased in a rigid and stiff pericardium.
If inflammation persists, immune cells cause fibrosis of serous pericardium
Clinical features of constrictive pericarditis
RVHF signs = hepatomegaly, increased JVP, ascites, oedema
Diagnostic tests for constrictive pericarditis
chest X-ray - small heart and pericardial calcification
CT/MRI scan
Management of constrictive pericarditis
surgical excision
What is cardiac tamponade?
A pericardial effusion that raises intrapericardial pressure. This reduces ventricular filling and thus leads to a drop in cardiac output.
Cardiac tamponade signs
increased pulse, decreased BP, pulsus paradoxus (abnormally large decrease in SV and BP during inspiration), increased JVP
Diagnostic tests for cardiac tamponade
Beck’s triad = falling BP, rising JVP, muffled heart sounds
ECG - low voltage QRS complex
Echocardiogram
Management of cardiac tamponade
pericardial effusion needs urgent drainage
send fluid for culture, ZN stain/TB culture
What is infective endocarditis?
infection of the heart valves or other endocardial lined structures within the heart
Where does infective endocarditis infection occur?
mitral or aortic valves, prosthetic valves, right sided is more common in IVDU, pacemakers
Aetiology of infective endocarditis
usual cause = prior antibiotic therapy
strep viridans, staph aureus, rarely=candida(fungi)
Risk factors for infective endocarditis
prosthetic valves, congenital valve defects, IVDU
Pathophysiology of infective endocarditis
mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valves. the valves are destroyed by virulent organisms –> regurgitation.
vegetations are a source of embolus
Epidemiology of IE
disease of the elderly, IVDU, young with congenital heart disease, anyone with prosthetic heart valves
Clinical presentation of IE
- systemic fever signs = fever, night sweats, weight loss, malaise
- valve destruction –> heart murmurs and HF
- splinter haemorrhages under nails
- Roth’s spots in retina
Diagnostic tests for IE
blood cultures may remain negative due to prior antimicrobial therapy
Blood tests - high ESR/CRP
TOE - identifies vegetations and valvular dysfunctions
What is the Duke Criteria for IE?
Diagnosis requires 2 major or 1 major and 3 minor or 5 minor criteria
Major criteria for IE
positive blood culture, vegetation on endocardium, new murmur
Minor criteria for IE
predisposing factors - IVDU fever - more than 38C vascular signs immunological signs equivocal blood cultures
Treatment for IE
Anti-microbial
Treat complications - emboli, HF, arrhythmias
surgery if infection cannot be treated with antibiotics or severe complications.
Drug order for hypertension
<55 = ACEi/ARB –> CCBs/thiazide diuretics/
> 55/Black = CCBs –> ACEi/ARB/thiazide diuretic
Peripheral vascular disease
occurs due to atherosclerosis causing stenosis of arteries.
Chief feature in peripheral vascular disease
intermittent claudication
Modifiable risk factors of peripheral vascular disease
hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia
Non-modifiable risk factors of peripheral vascular disease
age, male gender FH
What is intermittent claudication?
pain in a muscle or group of muscles due to ischaemia which is exacerbated by exercise and relieved by rest
What is critical ischaemia?
severe obstruction of the arteries which markedly reduces blood flow to extremities and has progressed to the point of pain
Fontaine classification of peripheral vascular disease
- Asymptomatic
- Intermittent claudication
- Ischaemic rest pain
- Ulceration/gangrene (critical ischaemia)
Symptoms of peripheral vascular disease
Cramping pain in calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest.
ulceration, gangrene and foot pain at rest = critical ischaemia
burning foot pain at night relieved by hanging legs over side of bed
Signs of peripheral vascular disease
- Absent femoral, popliteal or foot pulses
- Cold white legs
- Atrophic skin
- Punched out ulcers
- Postural colour change
- Capillary refill time >12 seconds = sever ischaemia
Diagnostic tests for peripheral vascular disease
Exclude DM and artheritis (C-reactive protein, ESR, CRP)
FBC, U&Es, ECG, lipids, ankle-brachial pressure index
Imaging in peripheral vascular disease
Colour duplex USS - non-invasive and easily available
MR/CT angiography - provides location and extent of stenosis
Risk factor modification of peripheral vascular disease
Smoking cessation, BP control, cholesterol control, clopidogrel (reduces cardiovascular risk)
How is claudication managed?
- Supervised exercise programmes - reduce symptoms by improving collateral blood flow (2hrs/week for 3 months) - patient to exercise to point of maximum pain
- Vasoactive drugs - naftidrofuryl oxalate - only if revascularization is not an option
Revascularization in peripheral vascular disease
- Percutaneous transluminal angioplasty (PTA) - balloon inflated in narrowed segment and stent inserted
- Surgical reconstruction - arterial bypass graft (autologous vein grafts are superior to prosthetic grafts)
Causes of mitral stenosis
Majority = rheumatic heart disease
congenital, malignant carcinoid
Pathophysiology of mitral stenosis
narrowing of mitral valve prevents free flow of blood from the left atrium to the left ventricle during ventricular diastole
Complications of mitral stenosis
left atrial hypertrophy, pulmonary hypertension, RVHF, pulmonary oedema, breathlessness, AF
Symptoms of mitral stenosis
Begin when mitral valve orifice is less than 2cm squared (normal=4-6cm)
- dyspnoea, fatigue, palpitations, chest pain, systemic emboli, coughing up blood
Signs of mitral stenosis
malar flush on cheeks
low volume pulse
AF
mid-diastolic murmur
Diagnostic tests in mitral stenosis
ECG - AF, P-mitrale 0 broad bifid P waves
CXR - LA enlargement, PO, Mitral valve calcification
Echocardiogram = diagnostic
Treatment of mitral stenosis
- treat complications
- beta blockers in AF
- anticoagulate with warfarin to prevent embolus
- diuretics - decrease preload
- balloon valvuloplasty
- mitral valve replacement
What is mitral valve regurgitation?
mitral valve doesn’t close properly
Aetiology of mitral regurgitation
developed world = prolapsing mitral valve
developing wall = rheumatic heart disease
infective endocarditis, LV dilatation, annular calcification, CT disorders, ischaemic heart disease
Pathophysiology of mitral regurgitation
mitral valve prolapse –> abnormal valve leaflets balloon into LA during ventricular systole
IHD –> ischaemic papillary dysfunction and widening of mitral valve annulus to to LV dilatation
Eventually there is development of LVHF
Symptoms of mitral valve regurgitation
dyspnoea, fatigue, palpitation, IE symptoms (if this is the cause)
Signs of mitral valve regurgitation
AF, displaced apex beat, RV heave, soft S1
Diagnostic tests for mitral valve regurgitation
ECG - AF and p mitrale (bifid P waves)
CXR - enlarged LA, pulmonary oedema
Echocardiogram –> assess LV size and site using doppler echo
Cardiac catheterization ==> confirms diagnosis
Treatment of mitral valve regurgitation
control pulse - AF - beta blockers diuretics surgery - MV replacement or repair anticoagulant if AF Mild disease = serial echo every 1-5 years
Aortic stenosis
narrowing of aortic valve - most common valve disease
Causes of aortic stenosis
most = calcification of norml valve - elderly
calcification of bicuspid aortic valve - middle aged
rheumatic heart disease
Pathophysiology of aortic stenosis
Obstruction to LV emptying results in LV hypertrophy
This can lead to angina, arrhythmias and LV failure
Symptoms of aortic stenosis
classic triad = angina, syncope, HF
symptoms = dyspnoea, dizziness, faints, systemic emboli (if IE present)
Signs of aortic stenosis
SYSTOLIC EJECTION MURMUR
slow rising pulse with narrow pulse pressure, LV heave, aortic thrill, ejection click
Differential diagnosis of aortic stenosis
hypertrophic cardiomyopathy, aortic sclerosis
Diagnostic tests in aortic stenosis
- ECG - p mitral, depressed ST and T wave inversion
- CXR - LVH, calcified aortic valve, post stenotic dilation of ascending aorta
- Doppler echocardiography - assesses pressure gradient across the valve
- cardiac catheter - assesses LV function (risk = emboli)
Treatment of aortic stenosis
valve replacement
What is aortic regurgitation
The diastolic flow of blood from the aorta into the LV
Causes of aortic regurgitation
diseases which dilate the aortic root = Marfan’s, IE, rheumatic fever
Acute = IE, aortic dissection, chest trauma Chronic = rheumatic heart disease, Marfan's, bicuspid aortic valve, hypertension
Pathophysiology of aortic regurgitation
dilatation of the aortic root pulls the annulus of the aortic valve and prevents the tight closure of the valve leaflets
chronic regurgitation –> LV hypertrophy –> LVHF
Symptoms of aortic regurgitation
exertional dyspnoea, orthopnoea, PND, palpitations, angina, syncope, CHF
Signs of aortic regurgitation
HIGH PITCH EARLY DIASTOLIC PULSE
collapsing (water hammer) pulse, wide pulse pressure, displaced apex beat
Diagnostic tests for aortic regurgitation
ECG –> LVH
CXR –> cardiomegaly and dilatation of ascending aorta, PO
Echocardiogram = diagnostic
Cardiac catheterization
Treatment of aortic regurgitation
- reduce systolic hypertension - ACEi
- monitor –> echo every 6-12 months
- valve replacement
