Cardiology Flashcards
what is the main problem with atherosclerosis
plaque rupture - thrombus formation and partial/complete arterial blockage leading to heart attack
what is the best known risk factor for coronary artery disease
age
risk factors for atherosclerosis
age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history
where are atherosclerotic plaques most commonly distributed
peripheral and coronary arteries
what factors might govern the distribution of atherosclerotic plaque
- changes in flow/turbulence (bifurcations)
- wall thickness
- altered gene expression
what is found within an atherosclerotic plaque
- lipid
- Necrotic core
- Connective tissue
- Fibrous cap
what are the outcomes of an atherosclerotic plaque
it will either occlude the vessel lumen or it could rupture
what inflammatory cytokines can be found in plaques
IL-1, IL-6, IL-8, IFN-y, TGF-b, MCP-1 and C reactive protein
what are the steps in leukocyte recruitment and movement through the vessel wall
Capture
Rolling
Slow Rolling
Firm adhesion
Transmigration
what are the features of a fatty streak
- the earliest lesion of atherosclerosis
- Appear at a very early age (<10 years)
- consist of aggregations of foam cells and T lymphocytes within the intimal layer of the vessel
what are intermediate lesions
they progress from the fatty streak, containing foam cells, vascular smooth muscle cells, T lymphocytes, and platelet adhesion. They also contain isolates pools of extracellular lipid
what are the features of a fibrous cap (or advanced lesions)
- impedes blood flow
- prone to rupture
- covered by a dense fibrous cap made from
extracellular matrix proteins or collagen and elastin - contains a lipid core and necrotic debris
- may be calcified
what does a fibrous cap contain
smooth muscle cells
macrophages
foam cells
T lymphocytes
what causes a plaque rupture
if the balance is shifted and there are high inflammatory conditions, and increased enzyme activity, the cap becomes weak and the plaque can rupture
what is plaque erosion
this is where lesions tend to be small early lesions. A thickened fibrous cap may lead to collagen triggering thrombosis. A platelet-rich clot may cover the luminal surface and there is a small lipid core
what is a red thrombus
where there are red blood cells and fibrin present
what is a white thrombus
when there are platelets and fibrinogen present
what are the clinical characteristics that predispose someone to a plaque rupture
dyslipidemia
hypertension
diabetes Mellitus
chronic kidney disease
multi vessel disease
what can be done when someone gets a ruptured plaque
- stent implantation
- distal embolisation
what are clinical characteristics which predispose someone to plaque erosion
smoking
being female
being younger than 50
having anterior ischemia
how is coronary artery disease treated
PCI - percutaneous coronary intervention
stent
what are coronary stents made of
stainless steel
what action does aspirin
it irreversibly inhibits platelet cyclo-oxygenase
what is the action of clopidogrel or ticagrelor
it inhibits P2Y12 ADP receptors on platelets and therefore has antiplatelet action
what are statins used for
to lower cholesterol
what is the action of statins
it inhibits HMG CoA reductase and therefore reduces cholesterol synthesis
what is a PCSK9 inhibitor
it is a monoclonal antibody that inhibits PCSK9 protein in the liver and leads to improved clearance of cholesterol from the blood
what are the major cell types involved in atherosclerosis
epithelium, macrophages, smooth muscle cells and platelets
what are examples of acute coronary syndromes
Q wave MI
ST elevation MI
Non Q wave MI
Non ST elevation MI
unstable angina
Non ECG changes
what are the characteristics of an unstable angina
pain at rest
crescendo pattern
how would you diagnose an unstable angina
- history
- ECG
- troponin test - not normally risen in angina
what is the management for a myocardial infarction
300mg of aspirin immediately
- blood test
- ECG
- oxygen therapy
- pain relief
- Aspirin +/- platelet P2Y12 inhibitor
- Consider beta blockers
- Consider antiangial therapy
- Consider urgent angiography
what are other reasons someone may have acute coronary syndrome other than MI
stress-induced cardiomyopathy
vasospasm
drug abuse
dissection
what is troponin C a marker of
its a biological marker of myocardial damage and is used as a diagnostic tool for cardiac injury
what does aspirin do
it prevents platelet clotting
what is the side effect of using aspirin and P2Y12 inhibitors (clopidogrel, prasugrel and ticagrelor) together
it increases the risk of bleeding
why are GP2b/3a blockers not used in clinical practice very often anymore
as they increase the risk of major bleeding
what medication is the most effective against angina
beta blockers
what is a major issue with using clopidogrel
it is a prodrug and it is unreliable as it can rapidly inactivate. therefore you can have different responses in different people and it is unpredictable
what factors can alter clopidogrel’s activity
- weight
- hight
- drug interactions
- genetic variations - CYP2C19 loss of function mutation
what is the process of Atherogenesis
There is damage to the endothelial cells which causes LDLs to move into the intima.
Due to the damage the endothelium secretes chemoattractants
leukocytes migrate and accumulate in the intima absorbing the LDLs and becoming foam cells
This forms a fatty streak
foam cells will rupture and release lipids
smooth muscle cells migrate from the media to the intima
a dense fibrous cap with a necrotic core is formed
this plaque can partially occlude the lumen and blood flow can be restricted.
this plaque can rupture ad a thrombus formed which can fully occlude the lumen
which cardiac arteries does atherogenesis affect most commonly
LAD, circumflex and RCA
what risk factors increase your chance of atheroma formation
age
smoking
obesity - high serum cholesterol
diabetes
hypertension
family history
male
put these in ascending order of severity
- stable angina, NSTEMI, STEMI, unstable angina
Stable angina> unstable angina > NSTEMI> STEMI
what are the main causes of cardiac myocyte damage
atheroma, valvular disease (stenosis) and anaemia
what is angina
Angina is the result of myocardial ischaemia, where blood supply < metabolic demand
what is stable angina
chest pain after cold/exercise and lasts about 1-5 minutes. it is relieved by rest or GTN spray
what is unstable angina/NSTEMI/STEMI
chest pain at rest and prolonged (longer than 20 minutes). there is no release at rest
what is seen on ECG during a STEMI
ST elevations
what does STEMI stand for
ST-elevation myocardial infarction
what is prinzmetal’s angina
it is caused by coronary artery spasms; occur at rest or at night
what are the symptoms of ischemic heart disease
chest pain - discomfort, heaviness
radiation - left arm, shoulder, jaw
NSFW - nausea, sweating, fatigue and weak breathing
what are atypical presentations of ischemic heart disease
no pain
low grade fever
pale, cool, clammy skin
hyper/hypotension
how do you diagnose ischemic heart disease
history taking and physical examination
- resting ECG
- exercise ECG
blood tests - HBA1C, full blood count, cholesterol profile
CT - coronary angiography
biological markers: troponin, myoglobulin, CK
what is heart contraction initiated by
depolarisation and changes intracellular calcium concentrations
what needs to occur for heart muscle relaxation to occur
removal of calcium - energy dependent
what are the two types of cardiac myocytes
- atrioventricular conduction system - slightly faster
- general cardiac myocytes
is blood flow through the myocardium from the aortic root diastolic or non-diastolic
diastolic
what is the normal systolic ejection fraction
about 60-65%
as venous return increases does cardiac/volume increase or decrease
it increases
what happens if you exceed the stretch capacity of the sarcomeres in the heart
then the cardiac contraction force diminishes
when can myocardial hypertrophy be an adaptive or physiological response
in athletes or in pregnancy
what is the myocardial hypertrophic response triggered by
angiotensin 2
ET-1
IGF-1
TGF - b
these activate mitogen-activated protein kinase
what happens in left sided cardiac failure
there is pulmonary congestion and then overload of the right side
what happens in right sided heart failure
there is venous hypertension and congestion
what is diastolic cardiac failure (HFpEF)
it is when the left ventricle of the heart becomes stiff and unable to fill properly
what happens in fetal embryogenesis of the heart
- the heart comprises a single chamber until week 5 of gestation
- it is then divided by intra-ventricular and intra-atrial septa from endocardial cushions
- the muscular intra-ventricular septum grows upward from the apex producing four chambers and allowing valves to develop
what does congenital heart disease result from
results from a faulty embryonic development
- misplaced structures or arrest of the progression of normal structure development
what percentage of live births can congenital heart disease complicate
may complicate up to 1% of live births
what are the four most common congenital heart defects
Ventricular septal defect -25-30%
Atrial septal defect - 10-15%
Patent ductus arteriosus - 10-20%
Fallots 4-10%
what single gene conditions are associated with an increased risk of congenital heart disease
- Trisomy 21
- Turners syndrome XO
- di-George syndrome
what infection in pregnancy is associated with an increased risk of congenital heart disease
rubella
What drugs in pregnancy increase the risk of congenital heart disease
thalidomide, alcohol, phenytoin, amphetamines, lithium, oestrogenic steroids
what classifications are used for congenital heart disease
- if cyanosis is present or absent
- whether it occurs from birth or whether it develops later
what types of congenital heart disease show an initial left to right shunt
Ventricular septal defect
atrial septal defect
patent ductus arteriosis
anonymous pulmonary venous drainage
hypoplastic left heart syndrome
what types of congenital heart disease show a right to left shunt
tetralogy of Fallot
tricuspid atresia
what types congenital heart disease show no shunt
complete transposition of great vessels
coarctation
pulmonary stenosis
aortic stenosis
coronary artery origin from pulmonary artery
Ebstein malformation
Endocardial fibroelastosis
what is patent foramen ovale
hole in the heart between the right and left atria that doesn’t close correctly after birth.
can be found in the central septum (90%) or in the lower part of the septum primum.
what can a patent foramen ovale lead to
cardiac arrhythmias, pulmonary hypertension, right ventricular hypertrophy, and cardiac failure. Also has a risk of infective endocarditis
what is patent ductus arteriosus
where the ductus arteriosus persists beyond birth
what can a patent ductus arteriosus lead to
the left-to-right shunting eventually means the lung circulation is overloaded with pulmonary hypertension and right-sided cardiac failure subsequently
can a patent ductus arteriosus be closed
yes can be closed surgically, by catheters or my prostaglandin inhibitors (idomethacin)
what is tetralogy of Fallot
It has four main features
1. Pulmonary stenosis
2. Ventricular septal defect
3. Dextraposition/over-riding ventricular septal defect
4. Right ventricle hypertrophy
what is the characteristic shape of Tetralogy of Fallot on radiology and macroscopically
boot shaped
What happens due to a Tetralogy of Fallot
As a result of the pulmonary stenosis, right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction usually is performed during the first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases
What is complete transposition of the great arteries (TGA)
it involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle.
does complete transposition of the great arteries have a male or female bias
male bias
is survival possible with complete transposition of the great vessels
only possible if there is communication between the circuits and virtually all have an atrial septal defect allowing for blood mixing
what is the treatment for complete transposition of the great vessels
arterial switch - less than 10% overall mortality
what is coarctation of the aorta
this is secondary to an excessive obliterating process that normally closes the ductus arteriosus, extending into the aortic wall. The net result is a narrowing of the aorta after the arch witch excessive blood flow diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body
What are the complications of coarctation of the aorta
- associated with berry aneurysms
- cardiac failure
- rupture of dissecting aneurysm
- infective endarteritis
- cerebral haemorrhage
- stenosis of the bicuspid aortic valve
what is the treatment for coarctation of the aorta
dilatation (stenting) of the stenosed segment
what is endocardial fibroelastosis
secondary -complication of congenital aortic stenosis and coarctation. Profound dense collagen and elastic tissues deposited on endocardial aspect of the left ventricle produces progressive stiffening of the heart and cardiac failure. Similar changes may affect the valves.
primary - may follow a familial pattern
what is Dextrocardia
the normal anatomy of the heart is versed with a rightward orientation
- often associated with severe cardiovascular abnormalities
what are the different types of angina
standard, prinzmetal/unstable, accelerated/Crescendo
what are risk factors for ischaemic heart disease
systemic hypertension
cigarette smoking
diabetes mellitus
elevated cholesterol
Sex
obesity
age
family history
sedentary life
what are some reasons for an imperfect blood supply to the heart
atherosclerosis
thrombosis
thromboemboli
artery spasm
collateral blood vessels
blood pressure/cardiac output/heart rate
arteritis
what conditions can limit coronary flow
Coronary arteritis
Dissecting aneurysm of aorta
Syphilitic aortitis, congenital abnormality of coronary artery origin
Myocardial bridge
what can occur upon reperfusion of ischaemic myocardium
reperfusion of completely infarcted tissue can produce significant haemorrhage. It can allow oxygen delivery and a further degree of injury as a result of generation of superoxide radicals
what are pathological complications of ischaemic damage of the heart
Arrhythmias (supraventricular and ventricular)
Left ventricular failure – cardiogenic shock.
Generally reflects >40% muscle damage
Extension of infarction, rupture of the myocardium (into pericardial space, between chambers, across papillary muscle insertion)
what is an aneurysm
it is a dilation of part of the myocardia wall, usually associated with fibrosis and atrophy of myocytes
what is pericarditis (dressler syndrome)
this is a delayed pericarditic reaction following infarction (2-10 weeks)
what is the WHO classification of hypertension
> 140/90mm Hg
what is hypertensive heart disease
it reflects cardiac enlargement due to hypertension and in the absence of other causes
there is compensatory hypertrophy of the heart with increased myocyte size. Eventually, the hypertrophy will no longer be able to compensate and oxygen delivery will start to fail
what is the most common reason for angina
ischemic heart disease
what are exacerbating factors of angina
supply - anaemia, hypoxia, polycythemia, hypothermia, hypovolaemia, hypervolaemia
demand - hypertension, tachyarrhythmia, hypertrophic cardiomyopathy, hyperthyroidism (should be treated)
what environmental factors can bring on angina
exercise
cold weather
heavy meals
emotional stress
what is ohms law in biology
pressure = flow X resistance
P=QR
what is poiseuilles law in biology
P = 8uLQ / pi r^4
essentially coronary flow falls off with the 4th power of the radius
what is microvascular angina
small blood vessels are affected, main coronary vessels mostly normal
what is the treatment for angina
lifestyle - stop smoking, weight, exercise, diet
advice for emergency
medication - GTN spray, aspirin and beta blocker
revascularisation
what is the gold standard non-invasive test for angina (IHD) diagnosis
a perfusion MRI
what is the gold standard (but invasive) test for angina (IHD) diagnosis
coronary angiography
what are beta blockers affect on the heart
bradycardia
reduce contractility
decrease cardiac output
what are contra-indications of beta blockers
in severe asthma will block beta receptors in the lungs and can cause bronchoconstriction
How do nitrates work
dilates veins, reducing the venous return and therefore preload. Can also dilate arterioles, reducing blood pressure and afterload
what are side effects of nitrates
headache due to venous dilation
what are side effects of beta blockers
tiredness
bradycardia
erectile dysfunction
cold hands and feet
what are the effects of calcium channel blockers
decreased contraction therefore work the heart has to do and its oxygen demand
decrease heart rate
cause arterial dilation, decreasing BP and afterload
what are side effects of calcium channel blockers
flushing
postural hypertension
swollen ankles
what is a major side effect of aspirin therapy
gastric ulceration
why would you give an ACE inhibitor to someone with IHD
inhibits the production of angiotensin 2 and therefore prevents vasoconstriction and increases sodium and water excretion. This will reduce blood pressure
when is bypass surgery used in cardiac disease
when there is multivessel disease
how is bypass surgery performed
there is internal mammary graft from the chest, to the right coronary artery past the blockage. Can use veins from your leg (long saphenous vein), if other coronary arteried have blockages as well
what are the pros and cons of Percutaneous Coronary Intervention (stent)
pros - less invasive, convenient, repeatable, acceptable
cons - risk stent thrombosis, risk restenosis, cant deal with complex disease, dual antiplatelet therapy
what are the pros and cons of coronary artery bypass graft
pros - prognosis is better, deals with complex disease
cons - invasive, risk of stroke/bleeding, can’t do if frail, one time treatment, long length of stay, long recovery time
what is acute pericarditis
it is an inflammatory pericardial syndrome
what is Cor pulmonale
it is right ventricular hypertrophy and dilation due to pulmonary hypertension
what can cause Cor pulmonale
- embolisation of material into the pulmonary circuit
- chronic bronchitis and emphysema
- pulmonary fibrosis
- cystic fibrosis
- recurrent emboli
- primary pulmonary hypertension
- peripheral pulmonary stenosis
- IV drug use
- high altitude
- abnormal movement of the thoracic cage
what are features of right sided heart failure
venous overload, peripheral oedema, and progressive hepatic congestion
what bacteria causes acute rheumatic fever
Group A b-haemolytic streptococcus infection
what remains a major factor with regard to heart disease in developing countries
acute rheumatic fever
why can acute rheumatic fever cause cardiac dysfunction
development of immunity against streptococcal pharyngitis produces antibodies that cross-react with cardiac myocytes and valvular glycoproteins. This produces localised inflammation and subsequent scarring
what are the clinical features of acute Rheumatic fever
Carditis (cardiomegaly, murmurs, pericarditis and cardiac failure)
Polyarthritis
chorea - sudden, uncontrolled jerky movement
erythema - redness of skin/mucus membranes
marginatum - rash
subcutaneous nodules
What are minor criteria for acute rheumatic fever diagnosis
previous history of rheumatic fever, arthralgia, raised CRP, ESR, and white cell count. Antibodies against group A strep antigens, anti-streptolysin O, anti-DNAsa B and anti-hyaluronidase
how long does it take for symptoms of acute rheumatic fever to diminish
3-6 months
what other disorders can affect cardiac valves
SLE, Rheumatoid arthritis, ankylosing and other connective tissue disorders
How can progressive cardiac dysfunction occur due to acute rheumatic fever
Chronically scarring and deformity produces contracture of the valve and chordae tendinae. These may subsequently calcify and distort blood flow allowing localised thrombosis. They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis.
what is infective endocarditis
Infective endocarditis, also called bacterial endocarditis, is an infection caused by bacteria that enter the bloodstream and settle in the heart lining, a heart valve or a blood vessel
what are characteristic microorganisms of infective endocarditis
strep. Viridans and Staph. Aures
Fungal and atypical bacteria are also recognised
what occurs in infective endocarditis
infection produces a rapidly increasing cardiac valve distortion and disruption, with an acute cardiac dysfunction
what are symptoms of infective endocarditis
sudden cardiac failure
septic problems
generation of infected thromboemboli
damage to kidneys
fever
anorexia
fatigue
splenomegaly
clubbing
neurological dysfunction
what is the mortality rate of infective endocarditis
30-40% mortality rate
what is the most common cause of infective endocarditis in children
congenital heart disease
what are the most common cause of infective endocarditis in adults
rheumatic valvular heart
mitral valve prolapse
intravenous drug abuse
prosthetic valves
diabetes
elderly
pregnancy
what is non bacterial thrombotic endocarditis/marantic endocarditis
- sterile thrombotic matter deposits on valves with variable degrees of valve dysfunction
- degenerative valve disease
what is calcific aortic stenosis
it is when there are nodular calcific deposits in the cusps with progressive distortion of valves.
what can nodular calcific stenosis lead to
obstruction of left ventricle outflow, leading to pressure overload and cardiac hypertrophy. There can be a risk of sudden cardiac death and MI
what type of valve accelerates development of calcific aortic stenosis
bicuspid aortic valves
what is mitral valve disease
when there is an issue with the mitral valve and can lead to regurgitation due to a lack of closure
what is one of the main causes of mitral valve stenosis
One of the main causes of mitral valve stenosis is rheumatic heart disease. This is where an infection causes the heart to become inflamed
what is mitral valve prolapse
it is the degeneration of the mitral valve such that the inner fibrosa becomes loose and fragment, with fragments of mucopolysaccharide material
what can occur in mitral valve prolapse
it can cause the valve cusp to bow upwards and may not close which can produce incompetence regurgitation.
what diseases are mitral valve prolapse associated with
underlying connective tissue disorders, Marfan’s syndrome and myotonic dystrophy
can mitral valve prolapse lead to sudden cardiac death
Yes
what is myocarditis
inflammation of the myocardium
usually associated with muscle cell necrosis and degeneration
what is the most common type of myocarditis
viral myocarditis
- viral toxicity with associated cell mediated cell damage
what is the most common type of myocarditis
viral myocarditis
- viral toxicity with associated cell mediated cell damagewhat are the causes of myocarditis
what is the most common type of myocarditis
viral myocarditis
- viral toxicity with associated cell mediated cell damagewhat are the causes of myocarditis
what are the causes of myocarditis
viruses - coxsacke, adeno, echo, influenza
Rickettsia
bacteria - Diptheria, staphylococcal, streptococci, borrelia, leptospira
fungi and protozoa parasites - toxoplasmosis and cryptococcus
metazoa - echinococcus
what are non infectious causes of myocarditis
hypersensitivity/immune-related diseases - rheumatic fever, SLE, scleroderma, drug reaction, RA
radiation
Miscellaneous - sarcoid and uraemia
what is myocarditis often associated with
a preceding upper respiratory tract infection
what is giant cell myocarditis
A very rare highly aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells. Often fatal.
Early treatment is transplantation but disease can often recur.
what metabolic diseases are associated with myocarditis
Hyperthyroidism, hypothyroidism
Thiamin deficiency (vitamin B1/thiamin)
Particularly association with poor diet
what is cardiomyopathy
primary cardiac disease with contractile dysfunction and atypical morphology
what are the different forms of cardiomyopathy
dilated cardiomyopathy
hypertrophic cardiomyopathy
arrhythmogenic right ventricular cardiomyopathy
secondary
rare forms
what is dilated cardiomyopathy
Dilated cardiomyopathy is a type of heart muscle disease that causes the ventricles to thin and stretch, growing larger. It typically starts in the left ventricle.
is there a genetic component to dilated cardiomyopathy
yes - 1/3 familial inheritance but could be more. It is mostly autosomal dominant inheritance.
what mutations are linked with dilated cardiomyopathy
dystrophin
troponin T
beta myosin heavy chain
actin
lamin A/C
desmin
what is clinical presentation of dilated cardiomyopathy
Shortness of breath, thromboemboli, cardiac failure, dysrhythmias and ultimately death
what are causes of secondary dilated cardiomyopathy
alcohol
cobalt toxicity
catecholamines
Micro-infarction
Anthracyclines - dose dependent toxicity
cocaine
pregnancy
what is hypertrophic cardiomyopathy
the heart muscle cells enlarge and the walls of the heart chambers thicken. The heart chambers are reduced in size so they cannot hold much blood, and the walls cannot relax properly and may stiffen. Also, the flow of blood through the heart may be obstructed.
what mutations are linked to hypertrophic cardiomyopathy
beta myosin
myosin binding protein c
troponin C
titin
what mutations found in hypertrophic cardiomyopathy are linked to clinical features
beta myosin - cardiac hypertrophic and dysrhythmias
troponin T - risk of sudden death
what changes occur in hypertrophic cardiomyopathy
asymmetric hypertrophy with distortion
increased fibrosis
ventricular outflow distortion
myocyte disarray
variation in small artery structure
at investigations are done for hypertrophic cardiomyopathy
echocardiology and other imaging modalities together with investigation of genetics and family history
what is arrhythmogenic right ventricular cardiomyopathy
a degenerative condition with progressive dilatation of right ventricle, with fibrosis, lymphoid infiltrate and fatty tissue replacement
what is restrictive cardiomyopathy
this is a group of diseases in which poor dilation of the heart restricts the ability of the heart to take on blood and pass it to the rest of the body.
what causes restrictive cardiomyopathy
amyloid - cardiac or amyloidosis AL/AA
deposits in the heart and stiffens it
what does restrictive cardiomyopathy show on an ECG
a low voltage ECG
what is endomyocardial disease
Endomyocardial fibrosis (EMF) is a disease of rural poverty that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.
clinical signs of endomyocardial disease
high grade eosinophilia
rash
progressive endocarditis
cardiac failure
what is glycogen storage disease
Glycogen storage disease (GSD) is a rare condition that changes the way the body uses and stores glycogen, a form of sugar. It is passed down from parents to children (inherited). For most GSDs, each parent must pass on one abnormal copy of the same gene. Most parents do not show any signs of GSD.
type 2, 3 and 4
what is hurler syndrome
Mucopolysaccharosis-glycosaminoglycans deposition in cells
what is hemochromotosis
multiorgan dysfunction with excess iron deposition in multiple tissues.
what is a sarcoidosis
A chronic granulomatous disease with numerous granulomas of non-caseating giant cell type. May involve the heart producing widespread areas of fibrosis and compensatory hypertrophy. It can produce a restrictive disorder. If it involves the conduction system then this may be the prime pathology of the patients with the risk of sudden death.
what is cardiac myxoma
cardiac tumour (75%) with bias towards the atria.
proliferation of myxoid cells with endothelial vascular channels and usually produces obstructive symptoms
what is rhabdomyoma
paediatric tumour with similarity to fetal cardiac cells
probably a hamartoma
what is a cardiac sarcoma
Cardiac sarcoma is a rare type of primary malignant (cancerous) tumor that occurs in the heart
These are rare and can show differentiation towards vascular, fibrous and muscle phenotypes. Almost invariably fatal.
what is the definition of haemopericardium
direct bleeding from the vascular wall through the ventricular wall fallowing a MI
what is the definition of haemopericardium
direct bleeding from the vascular wall through the ventricular wall fallowing a MI
what is cardiac tamponade
it is compression of the heart leading to acute cardiac failure following bleeding into the pericardial space direct bleeding from the vascular wall through the ventricular wall fallowing a MI
what is a cardiac tamponade
compression of the heart leading to acute cardiac failure following bleeding into the pericardial space
what is acute pericarditis
Acute pericarditis is an inflammatory process involving the pericardium that results in a clinical syndrome characterized by chest pain, pericardial friction rub, changes in the electrocardiogram (ECG) and occasionally, a pericardial effusion.2 Generally, the diagnosis requires 2 of these 3 features.
what are the signs and symptoms of acute pericarditis
Acute pericarditis typically presents with acute onset severe, sharp retrosternal chest pain, often radiating to the neck, shoulders, or back. Positional changes are characteristic with worsening of the pain in the supine position and with inspiration; and improvement with sitting upright and leaning forward.
Classically, a scratchy, grating, high-pitched friction rub is heard. This is felt to be caused by fibrinous deposits in the inflamed pericardial space.
where is the pericardial friction rub best heard
It is best heard during inspiration at the left lower sternal border, with the patient leaning forward. The rub may disappear with the development of an effusion and impending cardiac tamponade.
what are the features of elastic arteries
have two elastic laminae along with
tunica interna
tunica media
tunica adventitia
they also contain vasa vasorum
how does clot lysis occur
plasminogen is converted into plasmin. This then acts on fibrin to produce fibrin degradation products, and remove the fibrin cap on the clot.
what are complicated plaques
when there is calcification, mural thrombus or a vulnerable plaque
what are complications of plaque rupture
acute occlusion due to thrombus
chronic narrowing of vessel lumen with healing of the local thrombus
aneurysm change
embolism of thrombus +/- plaque lipid content
what is essential hypertension
Essential (primary) hypertension occurs when you have abnormally high blood pressure that’s not the result of a medical condition. This form of high blood pressure is often due to obesity, family history and an unhealthy diet. The condition is reversible with medications and lifestyle changes
what is the relationship between resistance and lumen size
resistance = 1/r^4
what are acquired causes of hypertension
chronic vascular disease - diabetes, primary elevation of aldosterone, cushings syndrome, pheochromocytoma, hyperthyroidism, coarctation or the aorta and rennin secreting tumours
what is arteriosclerosis
deposition of basement membrane like material and accumulation of plasma proteins within the vessel wall
in what conditions can arteriosclerosis be accelerated
diabetes and hypertension
what blood pressure indicates malignant or accelerated hypertension
> 160/110 mmHg
what is malignant or accelerated hypertension
Malignant/Accelerated hypertension is defined as a recent significant increase over baseline BP that is associated with target organ damage.
often seen in fundoscopic examination and is a medical emergency
what is raynaud’s phenomenon
Intermittent bilateral ischaemia of digits/extremities precipitated by motional cold temperature. Accelerated in cases of scleroderma and SLE. May produce distal atrophy and ulceration.
what is fibromuscular dysplasia
Abnormal architecture for the arteries producing variable lumen narrowing and distal poverty of circulation.
Particular importance in the renal arteries which produce renal vascular insufficiency and progressive hypertension due to renin-angiotensin stimulation.
what is vasculitis
an inflammatory and variably necrotic process centered on the blood vessels that can involve arteries veins and capillaries
how does vasculitis occur
it has an immune background of one of the following
- there is deposition of immune complexes
- there is direct attack on vessels by antibodies
- cell mediated immunity
viral infection
what viral antigens have been found in human vasculitis cases
HSV, CMV, parvovirus
what is polyarteritis nodosa
patchy necrotising arteries, affecting small and medium arteries. It is associated with neutrophils, lymphocytes, plasma cells and macrophages
what can polyarteritis nodosa lead to
can thrombose and cause a distal infarction, or heal with subsequent aneurysms. can cause widespread damage to the kidneys, cerebrocirculation and cardiac tissue. Can be rapidly fatal without treatment
what is hypersensitivity angiitis
it is a disease that involves deposition of immune complexesis causing inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura.
- can also be a feature of vascular disease
what is a diagnostic marker of hypersensitivity angiitis
palpable purpura
what drugs can cause hypersensitivity angiitis
aspirin
penicillin
phenytoin (Dilantin, an antiseizure medication)
allopurinol (used for gout)
what infections can cause hypersensitivity angiitis
streptococci
staphylococci
viral hepatitis
TB
bacterial endocarditis
what is Churg -Strauss syndrome
Churg-Strauss syndrome is a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA).
what organs can Churg -Strauss syndrome affect
lungs, spleen, kidney, heart, liver, CAN
what drug can be used to improve Churg-Strauss syndrome
steroids
what are features of Churg - Strauss syndrome
granulomatous inflammation with intense eosinophilic infiltrates
what is giant cell arteritis
an inflammation of the lining of your arteries. Most often, it affects the arteries in your head, especially those in your temples
what is the commonest type of vasculitis
giant cell vasculitis
what are risk factors for giant cell arteritis
Age. Giant cell arteritis affects adults only, and rarely those under 50
Sex. Women are about two times more likely to develop the condition than men are
Race and geographic region
Polymyalgia rheumatica
Family history.
What happens to vessels during giant cell arteritis
blood vessel is often thickened
there is granulomatous inflammation involving the full thickness of the wall - macrophages, lymphocytes, plasma cells, neutrophils involved.
variable necrosis
giant cells congregate in internal elastic lamina
thrombosis may occur
what can giant cell arteritis lead to
tends to be self-limiting but it can lead to blindness if it affects the ocular artery
what is Wegener’s granulomatosis
this is vasculitis of the respiratory tract and the kidney
what can Wegener’s granulomatosis cause in the lungs
bilateral pneumonitis with nodular infiltrates that can undergo cavitation mimics TB. Chronic sinusitis and ulcers of the nasal tissues are also common
what can Wegener’s granulomatosis cause in the kidney
focal necrotizing glomerulonephritis which progresses to crescentic glomerulonephritis
what are common symptoms of Wegener’s granulomatosis
pneumonitis
sinusitis
haematuria
proteinuria
skin rash
joint pains
neurological changes
what gender bias does Wegener’s granulomatosis have
male bias
what is Buerger disease
this is an inflammatory disease of medium and small arteries affecting the distal limbs
what does Buergers disease have a strong association risk with
tobacco smoking
what is the pathophysiology of Beurger disease
there is cell-mediated hypersensitivity to collagen type 2 and 3 with impaired endothelium - can have thrombotic and micro-abscess change
this can cause distal ischaemic symptoms and necrosis
stopping what can lead to remission of beurgers disease
stopping smoking
what is kawasaki disease
it is mucocutaneous lymph node syndrome - generation of antigens that bind to MHCII receptors
what arteries does Kawasaki syndrome principally effect
the coronary arteries
what pathogens is Kawasaki disease associated with
parvovirus B19
Coronovirus
staphylococci
streptococci
chlamydia infection
what is an aneurysm
dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels
what are aneurysms described as
fusiform
saccular
dissecting
arterio-venous
what is an abdominal aortic aneurysm
it is when there is over 50% dilation of the aortic diameter
are the majority of abdominal aortic aneurysms found
below the renal arteries
what is the major problem with abdominal aortic aneurysms
aneurysm rupture - those greater than 5-6 cm at increased risk
what are different treatment options for abdominal aortic aneurysms
waiting for rupture - higher mortality risk
prophylactic replacement with Dacron graft
endoluminal prosthesis - stent with prosthetic cover
what is a berry aneurysm
vascular dilation found in the cerebral circulation
what is a berry aneurism a consequence of
longstanding hypertension and/or focal area of weakness within the artery
where in the cerebrum are berry aneurysms commonly found
circle of Willis leading to a subarachnoid haemorrhage
what is a dissecting aneurysm
a tear occurs in the inner layer of the body’s main artery (aorta). Blood rushes through the tear, causing the inner and middle layers of the aorta to split (dissect)
where do the majority of dissecting aneurysms occur
just above the aortic ring
what disorders can predispose someone to getting a dissecting aneurysm
Marfans syndrome and other connective tissue disorders
what is syphilitic aortitis
an inflammatory disease affecting the vasa vasorum in the late stages of syphilis
what is the pathophysiology of syphilitic aortitis
Syphilitic aortitis begins as inflammation of the outermost layer of the blood vessel, including the blood vessels that supply the aorta itself with blood, the vasa vasorum
As it worsens, the vasa vasorum undergo hyperplastic thickening of their walls thereby restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall.
Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm
what are varicose veins
an enlarged and torturous vein, principally affecting the superficial leg veins
what are risk factors for varicose veins
age
female
hereditary
posture
obesity
wht causes varicose veins
progressive incompetence of valves with back pressure on venous circuit. This can cause thinning and dilation of the vascular wall with patchy calcification
what is lymphatic vessel obstruction
Lymphatic obstruction is a blockage of the lymph vessels that drain fluid from tissues throughout the body and allow immune cells to travel where they are needed. Lymphatic obstruction may cause lymphedema, which means swelling due to a blockage of the lymph passages.
what can cause lymphatic vessel obstruction
Infections with parasites, such as filariasis
Injury
Radiation therapy
Skin infections, such as cellulitis (more common in obese people)
Surgery
Tumors
at is the common surgical cause of lymphatic vessel obstruction
A common cause of lymphedema is removal of the breast (mastectomy) and underarm lymph tissue for breast cancer treatment. This causes lymphedema of the arm in some people, because the lymphatic drainage of the arm passes through the armpit (axilla)
what is a haemangioma
this is a benign proliferation of blood vessel tissue - name varies on the site and age of the patient
what are the different classifications of a haemangioma
capillary haemangioma
juvenile haemangioma
cavernous haemangioma
what is a glomus tumour
a benign neoplasm involving the glomus body (component of the dermis layer of the skin, involved in body temperature regulation)
what is mainly affected in a glomus tumour
the hands - painful
what is a haemangioendothelioma
a vascular tumour of endothelial cells of low grade malignancy (can metastasise)
what is an angiosarcoma
it is a highly aggressive malignant neoplasm of endothelial cells
where is angiosarcoma commonly found
skin, soft tissue, breast, bone, liver and spleen
what environmental carcinogens can cause angiosarcoma
arsenic and vinyl chloride
what infection does karposi’s sarcoma have a link with
HIV and AIDS
what virus causes karposi’s sarcoma
human herpes virus 8
is karposi’s sarcoma often seen
on the skin
what are risk factors for developing a deep vein thrombosis
venous flow stasis
injury - trauma, surgery, childbirth
hypercoagulability - pregnancy, cancer, inherited disorders
advanced age
sickle cell disease
what are outcomes of DVT
lysis
organisation
provocation
embolism
what symptoms may reflect a DVT
painful or tender calves - Homan sign
what is the treatment for DVT
anticoagulants mainly
what is an embolism
it is the passage of material (often thrombus) through the venous or arterial circulations.
what is a paradoxical embolism
an embolus that travels through the venous circuit and then across from the right to left side of the heart through patent foramen ovale
what are sources of embolism
atherosclerotic plaques
mural thrombus in heart or vasculature
infective endocarditis
what are sites particularly vulnerable of an emboli
brain, intestine, distal limb, kidneys and coronary circulation
what are other types of emboli (other than thrombus) are there
air embolism
acute decompression sickness
amniotic fluid embolism
fat embolism
bone marrow embolism
talc/cotton or other materials from intravascular injection
how do you treat ischemic heart disease
- statin: simvastatin
- nitrate: GTN spray
- Dual antiplatelet: aspirin and clopidogrel
In acute NSTEMI - beta blockers, morphine, oxygen, aspirin and nitrate
Acute STEMI - PCI (stent) if not fibrinolysis (streptokinase)
surgical interventions - PCI and CABG
what is pericarditis
inflammation of the pericardium with/without effusion
what are causes of acute pericarditis
infectious - viral (common), coxsackievirus
Bacterial (mycobacterium tuberculosis
Non infectious - Trauma (common), uraemia, myocardial infarction
what are signs of pericarditis
Chest pain, relieved by sitting forward/worsened by lying down and inspiration
- fever
- shortness of breath
- pericardial friction rub (high-pitched scratchy sound heard loudest on midline during inspiration)
what investigations are done with suspected pericarditis
- ECG (diagnostic) - saddle-shaped ST elevation with PR depression
- do an echo/chest X-ray if suspect effusion
how do you manage pericarditis
NSAIDS (ibuprofen) and colchicine
limit exercise
what are complications of pericarditis
cardiac tamponade
what is a cardiac tamponade
it is a life threatening condition whereby there is an accumulation of fluid in the pericardial space
what is the pathophysiology of a cardiac tamponade
fluid in the pericardial space causes compression of the heart chambers and a decrease in venous return. Therefore decreases in filling of the heart and therefore cardiac output
what are signs/symptoms of cardiac tamponade
Becks triad
- falling BP
- rising JVP
- muffled heart sounds
Pulsus paradoxus
what is pulsus paradoxus
large decrease in stroke volume - where the systolic blood pressure drops by over 10mmHg on inspiration
- eventually unable to feel distal pulse
what is the gold standard investigation for cardiac tamponade
Echo
what is the management of cardiac tamponade
pericardiocentesis - removal of the fluids from the pericardial space
what is kaussmaul’s sign
an increase in jugular venous pressure rather than a fall that you would expect.
what are the major risks when someone has hypertension
- stroke
- MI
- renal disease
- cognitive decline -dementia
- premature death
what part of the cardiovascular system impact hypertension the most
peripheral resistance
what can impact peripheral resistance
the renin-angiotensin-ldosterone system
sympathetic nervous system
when is hypertension suspected in clinic
when BP is 140/90mmHg or higher
what are people with suspected hypertension offered to confirm diagnosis of hypertension
ambulatory blood pressure monitoring
what is stage 1 hypertension
clinic BP = 140/90
ABMP = 135/85
what is stage 2 hypertension
clinic BP = 160/100
ABMP = 150/95
what is severe hypertension
SBP = 180
DBP = 110
what is the treatment for primary (essential) hypertension
- lifestyle modification
- antihypertensive drug therapy
when do you offer antihypertensive drug treatment for someone with stage 1 hypertension
someone under 80 who has one of the following
target organ damage
established cardiovascular disease
renal disease
diabetes
10 year cardiovascular disease of 20% or greater
when do you offer antihypertensive drug treatment in stage 2 hypertension
start them on treatment at any age
what are the targets for antihypertensive therapy
- peripheral resistance (and cardiac output)
- RAAS
- Sympathetic nervous system
- Local vascular vasocontrictor and dilator mediator
what is the action of angiotensin II in the body
vascular hyperplasia and hypertrophy
aldosterone release
tubular sodium reabsorption
also acts as a vasoconstrictor and increases cardiac output
what is the action of noradrenaline in the cardiovascular system
peripheral resistance increase
increase cardiac output
(also increases renin release)
What are the main uses of ace inhibitors
used in hypertension, heart failure, diabetic nephropathy
give examples of ACE inhibitors
Ramipril
Enalapril
Perindopril
Trandolapril
What are the main adverse effects of ACE inhibitors
- Related to reduced angiotensin II formation: hypotension, Acute renal failure, Hyperkalaemia, teratogenic effects in pregnancy
- Related to increased kinin production: cough, Rash, anaphylactoid reactions
why does kinin production increase with ACE inhibitors
ACE also converts bradykinin to inactive peptides. With ACE inhibitors you increase bradykinin production, getting side effects like cough and rash.
what diseases do you use angiotensin II receptor blockers in
hypertension
diabetic nephropathy
Heart failure (when you cant use ACE inhibitors)
what examples of angiotensin II receptor blockers
Candesartan
Losartan
Valsartan
Irbesartan
Telmisartan
what are the main adverse effects of angiotensin II receptor blockers
systemic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angioedema
are angiotensin II receptor blockers contraindicated in pregnancy
YES
what conditions are calcium channel blockers used in
hypertension
arrhythmia (tachycardia)
ischemic heart disease
What are examples of calcium channel blockers
Amlodipine
Nifedipine
Felodipine
Lacidipine
Diltiazem
Verapamil
what are the three subtypes of calcium channel blockers
- Dihydropyridines
- Phenylalkylamines
- Benzothiazepines
what is the action of dihydropyridines (CCB)
Preferentially affects vascular smooth muscle - peripheral arterial vasodilators
what are examples of dihydropyridines (CCB)
Amlodipine
Nifedipine
Felodipine
what is the action of phenylalkylamines
the main effect is on the heart
- Negatively chronotropic (reduced heartbeat)
- Negatively inotropic (reduced contractility)
what is an example of phenylalkylamines
Verapamil
what is the action of benzothiazepines
intermediate heart/peripheral vascular effects
what is an example of benzothiazepine
diltiazem
what are the adverse effects of calcium channel blockers
- due to peripheral vasodilation: flushing, headache, oedema, palpitations
- Due to negative chronotropic effects: bradycardia, AV block
- Negative ionotropic effects: worsening of cardiac failure
- verapamil causes constipation
what calcium channel blockers cause adverse effects due to negative chronotropic effects
verapamil
diltiazem
what calcium channel clocker causes adverse effects due to peripheral vasodilation
mainly dihydropyridines
what calcium channel blocker causes adverse effects due to inotropic effects
verapamil
what are the uses of beta - adrenoceptor blockers
ischaemic heart disease
heart failure
arrhythmia
hypertension
what are examples of beta blockers
bisoprolol
propranolol
carvedilol
metoprolol
atenolol
nadolol
what does the word cardioselective mean
often used to imply B-1 selectivity
- this is a misnomer since up to 40% of cardiac beta adrenoceptors are B2
what beta blockers are beta 1 selective
metoprolol
Bisoprolol
what beta blockers are non selective
propranolol
Nadolol
Carvedilol
(atenolol is slightly B 1 selective but not very)
what are the main adverse effects of beta blockers
fatigue
headache
sleep disturbance/nightmares
bradycardia
hypotension
cold peripheries
erectile dysfunction
what can beta blockers cause worsening of
asthma, or COPD
PERIPHERAL VASCULAR DISEASE - claudication or Raynaud’s
heart failure - given standard dose or acutely (need to start dose small and slowly up the dose)
what are diuretics used for (CVD)
hypertension
heart failure
what are the different classes of diuretics
- thiazides and related drugs (distal tubule)
- Loop diuretics
- Potassium-sparing diuretics
- aldosterone antagonists
what are examples of thiazides
bendroflumethiazide
hydrochlorothiazide
chlorthalidone
what are examples of loop diuretics
furosemide
bumetanide
what are examples of potassium sparing diuretics
amiloride
triamterine
spironolactone - also aldosterone agonist
eplerenone - also aldosterone agonist
what are the main adverse effects of diuretics
hypovolaemia
hypotension
low serum potassium, sodium, magnesium and calcium
raised uric acid (gout)
erectile dysfunction - thiazides
impaired glucose tolerance
what are other examples of antihypertensives
alpha 1 adrenoceptor blockers
centrally acting antihypertensives
direct renin inhibitor
what is an example of an alpha 1 adrenoceptor blocker
doxazosin
at is an example of a centrally-acting antihypertensive
moxonidinl
methyldopa
what is an example of a direct renin inhibitor
aliskiren
according to NICE what is the hypertensive treatment for those over 55 or Afro-Caribbean of any age
Calcium channel blocker
according to NICE what antihypertenside treatment do you give an under 55 patient
ACE - inhibitor or Angiotensin II receptor blocker
what happens when someone doesnt respond to first like hypertension drugs
you combine ACE-inhibitor or angiotensin II receptor blocker PLUS calcium channel blocker
what happens when someone doesnt respond to second-line hypertension drugs
you combine ACE-I/ARB + CCB
+ thiazide - like - diuretic
How do you treat acute UA/NSTEMI
BMOAN
- Beta blocker
- morphine
- oxygen
- aspirin
- nitrate
how do you treat acute STEMI
- if available within 120 minutes of medical contact then PCI
- if not then fibrinolysis (streptokinase/alteplase)
what surgical interventions do you use to treat IHD
- PCI (stent)
- CABG (preferred in patients with diabetes and over 65)
what is the definition of heart failure
the inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body
what can heart failure result from
can result from structural or functional cardiac disorder that impairs the hearts ability to function
what compensatory mechanisms occur when the heart starts to fail
BP falls which is detected by baroreceptors causing an increase in sympathetic activation. This leads to positive inotropic and chronotropic effects thus increasing the cardiac output
Activation of the RAAS system
what are causes of heart failure
- ischemic heart disease
- cardiomyopathy
- valvular heart disease (AS/MR)
- hypertension
- alcohol excess
- Cor pulmonale
- anemia, arrhythmia, hyperthyroidism
- congestive heart failure (both sided)
what is cor pulmonale
it is a disease of the lungs/pulmonary vessels causing pulmonary hypertension and therefore right ventricular hypertrophy. This can cause right sided heart failure with venous overload, peripheral oedema and hepatic congestion
what are the different types of heart failure
systolic heart failure
diastolic heart failure
acute/chronic
heart failure reserved ejection fraction
heart failure preserved ejection fraction
what is systolic heart failure
the inability of the ventricle to contract properly
what is diastolic heart failure
the inability of the ventricle to relax and fill properly
what is HF reserved ejection fraction
systolic where the ejection fraction is lower than 40%
what is HF preserved ejection fraction
diastolic where the ejection fraction is larger than 40%
what are risk factors of heart failure
over 65
male
obese
previous MI
African descent
what are the symptoms/signs of heart failure
SOFA PC
- shortness of breath
- orthopnea
- fatigue
- ankle swelling
- pulmonary oedema
- cold peripheries
Raised JVP
End respiratory crackles
what blood test can you do to diagnose heart failure
Brain (B type) natriuretic peptide (BNP)
What will heart failure look like on an ECG
The ECG may reveal abnormalities such as atrial fibrillation, abnormal Q waves, LV hypertrophy (LVH), and a widened QRS complex
what would a transthoracic ECG show in heart failure
- wall motion abnormalities
- valvular disease
- cardiomyopathies
what could a chest X ray show when someone is heart failure
- Alveolar oedema
- B-lines
- Cardiomegaly
- Dilated upper lobe vessels
- Effusion (pleural)
how can you diagnose heart failure
Blood test
ECG
Transthoracic ECG
Chest X-ray
how do you treat acute heart failure
- oxygen
- morphine
- furosemide
- GTN spray
What lifestyle changed can you make to treat chronic heart failure
- stop smoking!
- eat less salt, optimise weight and nutrition
- avoid NSAIDs/verapamil
How can you medically treat chronic heart failure
AABCDD
1st line: ACE-I and beta blockers
2nd line: ARB and nitrate
3rd line: Cardiac resynchronisation or digoxin
Diuretics: furosemide as a symptom relief
What are primary causes of hypertension
often primary cause is unknown
what are secondary causes of hypertension
renal disease
pregnancy
endocrine disease
coarctation
drugs
toxins
what signs/symptoms of hypertension
Usually asymptomatic
When malignant hypertension look for damage to brain, eye, heart and kidney
what head (brain) symptoms can you get in hypertension
central oedema, hemorrhage, headache
what eye symptoms can you get in hypertension
papilledema, cotton wool spots
what pecs/heart symptoms do you get in hypertension
AF, aortic dissection, chest pain, dysponoea (acute HF)
what renal symptoms do you get in hypertension
haematuria, proteinuria (acute kidney infarction)
how do you diagnose hypertension
Recheck patients BP on 2-3 occasions over few weeks/months
if high offer ABPM
what happens if stage 1 hypertension is diagnosed
Do a QRISK to decide on treatment pathway
what happens if stage 2 hypertension is diagnosed
start antihypertensive treatment
what happens if a patient has malignant hypertension and signs of a papilloedema/and signs of renal haemorrhage
they will get same day admission
start antihypertensive drug treatment immediately
for diabetics with hypertension what is always the first line treatment
ACE-I
what antihypertensive treatment is contraindicated in pregnancy (or if patient is on general anesthesia)
ACE-I
what organisms can cause infective endocarditis
staphylococcus aureus (most common for IV drug use)
Streptococcus viridians (mouth/oral surgery and most common for non IV drug users)
Staphylococcus epidermis (prosthetic valves)
what are symptoms of infective endocarditis
signs of infection - fever, fatigue, loss of appetite)
what are the clinical manifestations of infective endocarditis
splinter haemorrhages
osler nodes
janeway lesions
roth spots
what are Osler nodes
tender nodules in fingers
what are Janeway lesions
nodules on the palms of the hands
What are Roth spots
haemorrhage with a clear centre on fundoscopy (eye)
how do you diagnose infective endocarditis
modified dukes criteria
Echo - GOLD STANDARD
ECG - prolonged PR interval
what is the Modified dukes criteria - the major criteria
- blood cultures positive for endocarditis - needs to be from two separate blood cultures or bloods coming in are persistently positive (i.e taken 3 - 12 hours apart)
- Evidence of endocardial movement - echocardiogram positive such as abscess, or a new valvular regurgitation
what is the minor criteria for the modified duke’s criteria
- predisposing heart condition or IV drug use
- fever
- vascular/immunological signs
- positive blood culture (doesnt meet major criteria)
- positive echocardiogram (doesnt meet major criteria)
How do you use the modified dukes criteria to diagnose infective endocarditis
Definite IE = 2 major/1 major with 3 minor/all 5 minor
what is the treatment for infective endocarditis
antibiotics for 4-6 weeks
What antibiotic would you use for staphylococcus induced infective endocarditis
Flucloxacilin and rifampicin and gentamicin
IF MRSA use vancomycin, rifampicin and gentamicin
what antibiotic would you use for a non staphylococcus infective endocarditis
benzylpenicillin plus gentamicin
what antibiotics would you use for an unknown organism infective endocarditis
Flucloxacillin, plus ampilicin and gentamicin
what murmur is heard with mitral valve stenosis
rumbling mid-diastolic murmur with an opening snap (best heart on expiration and patient on their left side)
- diastolic decrescendo, presystolic crescendo
what murmur is heard for mitral regurgitation
pansystolic murmur radiating to the left axilla
- systolic holo or pan
what murmur is heard for aortic stenosis
an ejection systolic murmur which radiates to the carotids and apex
- systolic crescendo/-decrescendo
what murmur is heard for aortic regurgitation
an early diastolic murmur (best heard on expiration with patient sat forward)
- diastolic decrescendo
what are the symptoms of a mitral valve stenosis
- exertional dyspnoea
- haemoptysis (coughing of blood due to pulmonary oedema)
- palpitations (AF)
- chest pain
what are the symptoms of mitral valve regurgitation
- palpitations
- exertional dyspnoea
- fatigue
- weakness
what are the symptoms of an aortic valve stenosis
Triad of
- syncope
- angina
- dyspnoea
what are the symptoms of aortic valve regurgitation
palpitations
angina
dyspnoea
what are the signs of mitral valve stenosis
malar flush - plum red discolourisation of high cheeks
atrial fibrillation
tapping apex beat
low volume pulse
loud S1
what are the signs of mitral valve regurgitation
atrial fibrillation
displaced thrusting apex
soft or absent S1
what are the signs of aortic valve stenosis
sustained heaving apex
slow rising pulse
narrow pulse pressure
soft S2 if severe
what are the signs of aortic valve regurgitation
water hammer pulse
wide pulse pressure
displaced apex
carotid pulsation (Corrigan’s sign)
Head nodding with heartbeat (De Musset’s)
Capillary pulsation in nail bed (Quincke’s)
what are causes of mitral valve stenosis
Rheumatic heart disease - most common
annular calcification
congenital
mucopolysaccharidosis
what are causes of mitral valve regurgitation
papillary muscle rupture/dysfunction (post MI)
mitral valve prolapse
rheumatic heart disease
infective endocarditis
connective tissue disorders
Myxomatosis mitral valve
what are causes of aortic valve stenosis
senile calcification of valve
congenital bicuspid valve
rheumatic heart disease
what are causes of aortic valve regurgitation
acute - aortic dissection and infective endocarditis
chronic - connective tissue disorders, rheumatic heart disease, RA, AS and takayasu’s
Congenital bicuspid valve
what is the key complication in the first 24h of an MI
Arrhythmia
what hypertension medication can cause a dry cough
lisinopril
how do you work out pulse pressure
systolic - diastolic pressure
how do you work out the mean arterial pressure
diastolic pressure + 1/3 pulse pressure
what is the afterload
Force against which the ventricles must contract to expel the blood out of the ventricles
what vascular changes are seen in hypertension
- accelerated hypertension
- causes thickening of media of muscular arteries
what can happen to the heart in hypertension
major risk factor for developing ischemic heart disease
what nervous system pathology is seen in hypertension
intracerebral haemorrhage
what kidney pathology is seen in hypertension
can cause or develop from renal disease
kidney size is reduced and small vessels show intimal thickening and hypertrophy
what tests do you do to check for end organ damage in hypertension
urinalysis - check albumin: creatinine ratio and haematuria
ECG/echo
Fundoscopy
Bloods - look for serum creatinine, eGFR and glucose
what is the treatment for malignant hypertension
sodium nitroprusside
what does lead I on an ECG measure
the lateral side of the heart
- supplied by circumflex artery
what does lead II on an ECG measure
The inferior side of the heart
- supplied by the right coronary artery
what does lead III on an ECG measure
The inferior side of the heart
- supplied by the right coronary artery
what does lead aVL on an ECG measure
the lateral side of the heart
- supplied by the circumflex artery
what does lead aVF on an ECG measure
the inferior boarder of the heart
- supplied by the right coronary artery
what does lead V1 on an ECG measure
the septal portion of heart
- supplied by the left anterior descending artery
what does lead V2 on an ECG measure
the septal portion of the heart
- supplied by the left anterior descending artery
what does lead V3 measure on an ECG
the anterior boarder of the heart
what does lead V3 measure on an ECG
the anterior boarder of the heart
- supplied by the right coronary artery
what does lead V4 measure on an ECG
the anterior boarder of the heart
- supplied by the right coronary artery
what does lead V5 measure on an ECG
the lateral boarder of the heart
- supplied by the circumflex artery
what does lead V6 measure on an ECG
the lateral boarder of the heart
- supplied by the circumflex artery
in what ECG lead are all waves negative
in lead avR !!!
what are the ten rules of ECG
- PR = 120-200 ms (3-5 small squares)
- QRS not wider than 110ms (3 little squares)
- QRS upright in leads I and II
- QRS and T waves have same direction in leads I, II and III
- ALL waves negative in aVR lead
- R wave increases in size from V1-V4, S wave grows from V1 to 3 and is absent in V6
- ST segment is isoelectric in all leads except V1 and V2 where it may be slightly raised (very raised is bad)
- P waves upright in I and II and V2-V6
- There should be no Q waves larger than 0,04s in I, II, V2-V6
- T wave upright in I, II, V2-V6
what does right atrial enlargement look like on ECG
Tal (>2.5mm) and pointed P waves in limb leads
what does left atrial enlargement look like on an ECG
Notched/bifid M shaped P waves in the limb leads
what disorders causes short PR intervals
Wolff-Parkinson-white syndrome
Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave and short PR interval)
what disorders cause a long PR interval
first degree heart block
what is a pathological Q wave
when its more than 2mm deep and over 1mm wide, OR, over 25% amplitude of the subsequent R wave
what is the J point
it is the junction point between QRs and ST segment
what are U waves on an ECG
U wave related to after depolarisations which follow repolarisations
U waves are small, round, symmetrical and positive in lead II, with amplitude < 2 mm
U wave direction is the same as T wave
More prominent at slow heart rates
what percent of births have a congenital heart defect
1%
how percentage of congenital heart defects are tetralogy of fallot
10%
how can you resolve a tetralogy of fallot
surgical intervention
what are the common structural heart defects
ventricular septal defect
atrial septal defect
atrioventricular septal defect
patent ductus arteriosus
coarctaction of the aorta
bicuspid aortic valve and aortopathy
pulmonary stenosis
tetralogy of fallot
eisenmenger syndrome
what is ventricular septal defect
an abnormal connection between the two ventricles
what is the outcomes of having a ventricular septal defect
high pressure in the left ventricle
low pressure in the right ventricle
blood flows from the high pressure to low, flowing back into the right ventricle and increasing blood flow through the lungs
what does a large ventricular septal defect lead to
a very high pulmonary blood flow in infancy
breathlessness
poor feeding
failure to thrive
what can a large ventricular septal defect lead to
Eisenmenger’s syndrome and right ventricle hypertrophy
How do you fix a large ventricular septal defect
PA band, complete repair
what happens when you have a small ventricular septal defect
there is a small increase in pulmonary blood flow only
- often asymptomatic
what do you have an increased risk of if you have a small ventricular septal defect
endocarditis
How do you fix a small ventricular septal defect
no intervention is needed
what are the clinical signs of a large ventricular septal defect
small breathless skinny baby
increased respiratory rate
tachycardia
big heart on chest X ray
murmur varies in intensity
what are the clinical signs of a small ventricular septal defect
loud systolic murmur
thrill (buzzing sensation)
will have a normal heart rate and size
What is Eisenmengers syndrome
In Eisenmenger syndrome, there is irregular blood flow in the heart and lungs. This causes the blood vessels in the lungs to become stiff and narrow causing pulmonary arterial hypertension. Eisenmenger syndrome permanently damages the blood vessels in the lungs.
what is the pathophysiology behind Eisenmengers syndrome
There is a high pressure pulmonary blood flow (due to irregular connection in heart), which damages the pulmonary vasculature. This leads to an increased resistance through the lungs, increasing the right ventricular pressure.
This causes the shunt to reverse and the patient becomes BLUE
what is an atrial septal defect
an abnormal connection between the two atria (premium, secundum and sinus venosus)
at what age does atrial septal defects normally present
often present in adulthood
what is the physiology of an arterial septal defect
there is a sightly higher pressure in the left atria than the right and therefore the shunt is from the left to the right. This causes an increased flow into the right hear and therefore the lungs
what occurs in a large atrial septal defect
there is a significant increase in flow through the right heart and lungs during childhood which leads to a right heart dilation.
shortness of breath on exertion
increased chest infections
if there is any stretch on the right side of the heart, the shunt should be closed
what occurs in a small arterial septal defect
there is a small increase in flow
no right heart dilation
no symptoms
leave this alone
what are the the clinical signs of an arterial septal defect
pulmonary flow murmur
fixed split second heart sound - delayed closure of PV because more blood)
big pulmonary arteries on chest X ray
big heart on chest X ray
how do you close an arterial septal defect
- surgical intervention
- key hole technique
what is an atrio-ventricular septal defect
hole in the middle of the heart - involves the ventricular and atrial septum, the mitral and tricuspid valves (can be complete or partial)
what genetic condition do you often see atrio-ventricular septal defects
Downs syndrome
What is the pathophysiology of atrio-ventricular septal defect
instead of two separate AV valves there is one large malformed one
what happens when there is a complete AVSD defect
breathlessness as neonate
poor weight gain
poor feeding
torrential pulmonary blood flow
how do you repair complete AVSD
PA band in infancy (surgery)
what happens in a partial AVSD defect
can present like a small ventricular or arterial septal defect - can be left along if there is no right heart dilation
what are clinical signs of a patent ductus arteriosus
a continuous ‘machinery’ murmur
if its large you can have heart hypertrophy and breathlessness
can lead to Eisenmengers syndrome
how do you close a patent ductus arteriosus
surgical or percutaneous
what are the clinical signs of coarctation of the aorta
right arm hypertension
bruits of the scapulae and back from collateral vessels
murmur
what is a bicuspid AV
when you only have two cusps rather than three in the aortic valve
what is pulmonary stenosis
narrowing of the outflow of the right ventricle
what can severe pulmonary stenosis lead to
right ventricular failure as neonate
collapse
poor pulmonary blood flow
right ventricular hypertension
tricuspid valve regurgitation
what is the treatment for pulmonary stenosis
balloon valvuloplasty
open valvotomy
open trans-annular patch
shunt
What do you give someone who has resistant hypertension
ACE-I/ARB + CCB + thiazide - like diuretic
with the addition of spironolactone, high dose thiazide, alpha blocker, beta blocker
What is a NSTEMI (subendocardial infarct )
an unstable plaque with a thrombus occluding over 90% of the vessel. Blood flow is restricted enough that cells start to die. This patient often has pain at rest.
What is a STEMI (transmural infarct)
an unstable plaque and a thrombus occluding 100% of the lumen - Infarction
How would you diagnose prinzmetals angina
ST elevation on ECG
Troponin C is negative
The spasm can be reproduced by Ach
What patients may have a silent MI (no pain)
Diabetics
Elderly
Post heart transplant patients
What are signs of a right ventricular MI
Jugular venous distension
lower leg oedema
hypotension
bradycardia
what are signs of left ventricular MI
pulmonary oedema
hypotension
S4 heart sound
Tachycardia (reflex)
what do you need to watch out for in the first 24 hours after an MI
patient can go into premature ventricular contraction which can lead to ventricular fibrillation if it was a significant infarct.
- have cold extremities
- can cause flash pulmonary oedema
what can happen 24hrs to 3 days after a MI
- can get rupture syndromes due to ventricular septal defect, leading to a free wall rupture and blood can leak into the pericardial cavity. This can lead to cardiac tamponade
- can get mitral regurgitation due to papillary rupture (murmur)
what can happen 3-14 days after an MI
pericarditis due to inflammation
patient has an increased risk of left ventricular aneurysm causing clots and an increased chance of embolism
How would you diagnose an NSTEMI
ST depression
T wave inversion
Troponin positive
how would you diagnose an unstable angina
ST depression
T wave inversion
Troponin negative
What is the stress test for IHD
make someone exercise and you look for any flow limiting stenosis
- Perform an ECG looking for a reduction in ST or T wave inversion
- Echo looking at wall motion anomalies
- MPI looking for cod spots
you can also do a drug induced stress test using dobutamine
what leads to you see an inferior STEMI in
leads II III and avF
what do you think when you see a hyperacute T wave
ischemia that is progressing to infarction
why would you give someone nitroglycerine after a MI
it causes dilation of the cardiovascular system which causes a reduction in the preload. This reduces stroke volume and therefore the oxygen demand of the heart
what type of patient would you not give nitroglycerin to
those who are preload dependent - Right ventricular MI
what is the definition of a tachyarrhythmia
an abnormal rate of above 100bpm
what is the definition of a bradyarrhythmia
an abnormal rate of below 60bpm
what arrythmias are defined as supraventricular tachyarrhythmias
sinus tachycardia
atrial tachycardia (focal and multifocal)
atrial fibrillation
atrial flutter
AVN re-entral tachycardia
AVRT
what arrythmias are defined as ventricular tachyarrhythmias
ventricular tachycardia (monomorphic and polymorphic)
Polymorphic V.T with prolonged QT
Torsades de pointes
Ventricular fibrillation
what is sick sinus syndrome
The SAN is dysfunctional and produces a sinus bradycardia, From this you can develop SVT
what are the different types of bradyarrhythmias
sinus bradycardia
first degree heart block
second decree heart block (Mobitz 1 and 2)
third degree heart block
What is cushings triad
decreased heart rate
increased blood pressure
irregular respiratory rate
what metabolic reasons could cause an increase in vagal tone (bradycardia)
Hypothyroidism
hyperkalaemia
increase in intercranial pressure (cushings triad)
what can cause early after depolerisation
Electrolyte imbalance (low potassium, calcium and magnesium)
Drugs such as antibiotics, anti arrhythmia or antipsychotic drugs
what is an early after depolerisation
Early afterdepolarizations (EADs) are secondary voltage depolarizations during the repolarizing phase of the action potential
what can cause a delayed after depolerisation
ischemia causing irritation, hypoxia, inflammation, increased sympathetic tone or digoxin toxicity
what is delayed after depolerisation
The delayed afterdepolarization (DAD) arises from the resting potential after full repolarization of an action potential and it may reach threshold for activation.
what would you see on an ECG for early after depolerisation
polymorphic V.T with a long QT (torsardes)
What would you see on an ECG for delayed after depolerisation
Multifocal atrial tachycardia
Focal atrial tachycardia
VT with a normal QT
What arrythmias have re-entrance circuits
AVN re-entrance tachycardia
Atrioventricular re-entrance tachycardia
Atrial fibrillation
Atrial flutter
Ventricular fibrillation
Ventricular tachycardia
what is an AVRT
(wolf-Parkinson-White syndrome)
an accessory pathway (bundle of Kent) means electrical impulses can travel between the atria and ventricle without needing to go through the AVN
What is AVNRT
abnormal pathway within the AV node
- alpha = slow conduction and a short refractory period
- beta = fast conduction and long refractory period
most common is the slow fast pathway
what are the two types of AVRT
Orthodromic - ventricle back to atria (narrow QRS)
Antidromic - atria to ventricle (depol bottom up) ( wide QRS)
why might you get a conduction block
inferior wall MI
Fibrosis
Hyperkalaemia
Beta blockers
calcium channel blockers
digoxin
amyloidosis and sarcoidosis
What is seen on a sinus tachycardia ECG
P waves are present, narrow QRS complex and T wave is present - rapid rate
What is seen in a focal atrial tachycardia ECG
Inverted P wave (in lead II and upright in avR), narrow QRS
What is seen in atrial flutter ECG
Saw tooth P waves (II, III, avF)
What is seen in an AVRT/AVNRT ECG
No P waves seen (can have retrograde P waves) and you will have an narrow QRS
what is seen on an atrial fibrillation ECG
No P waves
Fibrillation waves in P1
irregular PR intervals
IRREGULARLY IRREGULAR
what is seen in multifocal atrial tachycardia ECG
morphologically different P waves
what is seen in ventricular tachycardia ECG
QRS is wider than 0.14 seconds (with atrioventricular dissociation)/ Extreme right axis deviation
what is seen in supraventricular tachycardia with a bundle branch block ECG
QRS is less than 0.4 seconds and there is no AV dissociation
what is seen in atrial fibrillation with bundle branch bock
QRS is the same morphology but it is irregular
what is seen in a sinus bradycardia ECG
normal morphology but it is slower than your normal rate
what does a first degree heart block look like on ECG
P wave with a prolonged PR interval (over 200ms)
what does a second degree heart block look like on ECG
There is not a QRS complex for every P wave with a prolonged PR interval
what does a mobitz type 2 heart block look like on ECG
Not every P wave has a QRS following it but there is a normal PR interval
What does a type 3 heart block look like on an ECG
Complete AV dissociation, beating independently to eachother
What does hypocalcaemia present on an ECG
Prolonged QT interval (secondary to a prolonged ST segment)
what does hypercalcaemia present on an ECG
short QT interval, ST segment shortening with an increased amplitude in the QRS complex. T wave is prolonged and you may have a prominent U wave
how does hypokalaemia present on ECG
small or inverted T waves, prominent U waves, a long PR interval and depressed ST elevations
how does hyperkalaemia present on an ECG
tall tented T waves, small P waves, wide QRS, ventricular fibrillations, sine wave
what is the most likely cause of sudden cardiac death
hypertrophic obstructive cardiomyopathy
how long is the bleeding time
3-5 minutes (how long it takes to clot)
what is the S3 heart sound
it shows rapid ventricular filling in early diastole
What is the S4 heart sound
Pathological gallop - due to blood forced into a stiff hypertrophic ventricle
what is the definition of angina pain
- central crushing chest pain radiating to the neck or jaw
- brought on with exertion
- relieved by rest or GTN spray
what is decubitus angina
it is induced when lying flat
what is the GRACE score
it is a predictor of mortality from MI in the next 6 months to 3 years in patients
What is the QRISK score
it predicts the risk of CVD in 10 upcoming years. Includes age, blood pressure, socioeconomic status, ethnicity etc.
a score of over 10 (10% increased risk in the next 10 years) starts the patient on lipid lowering therapy
when do symptoms start to occur in angina
then 70-80% of the lumen is occluded
what is acute coronary syndromes
It is the umbrella term for unstable angina, NSTEMI and STEMI
what ECG changes occur after an MI
Hyperacute T wave
pathologially deep Q waves
Left bundle branch block
what is seen in ECG for unstable angina
Normal - may show some ST depression or T wave inversion
What is seen in ECG for NSTEMI
ST depression and T wave inversion
- no Q waves
What is seen in ECG for STEMI
ST segment elevation in local leads (2+)
Q waves - pathological
what is a type 1 and type 2 MI
type 1 = ischemic heart disease
type 2 = increased demand or cavospasm
why might diabetics have silent MIs
diabetic neuropathy dont feel the pain and therefore you can miss the diagnosis
how do you acutely treat acute coronary syndrome
MONAC
- morphine
- O2
- Nitrates
- Aspirin
- Clopidogrel
what is the initial loading dose of aspirin
300mg
What is the long term dose of aspirin
75mg
what are the acute complications of acute coronary syndromes
Heart failure due to ventricular fibrillation, mitral incompetence, left ventricular free wall rupture, cardiogenic shock
what are complications that can occur 2 weeks post acute coronary syndromes
Dressler syndrome - autoimmune pericarditis
Heart failure
Left ventricular aneurysm
what is heart failure with a preserved ejection fraction
when ejection fraction is over 50%
- diastolic failure with a preserved pump function so there is filling issues
what is heart failure with reduced ejection fraction
When ejection fraction is lower than 40%
there is systolic failure and the pump fails, decreasing CO
what are three cardinal non specific signs of heart failure
- shortness of breath
- ankle swelling
- fatigue
what is the new york heart association classes of heart failure severity
- No limit on physical activity
- slight limit on moderate activity
- marked limit on moderate and gentle activity
- symptoms present at rest
what is inactive BNP
this is NT proBNP and has levels 5X higher than BNP
- can also be measured in MI diagnosis according to NICE
what is seen on a chest X-ray in people with heart failure
ABCDE
Alveolar bat wing oedema
Keley B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural Effusion
what is the definition of an abdominal aortic aneurysm
Permanent aortic dilation exceeding 50%, where the diameter is over 3cm
- typically infrarenal
what is the pathophysiology of an abdominal aortic aneurysm
smooth muscle, elastic and structural degeneration in all three layers of the vascular tunica with leukocyte infiltrate
when can abdominal aortic aneurysms occur in the thoracic aorta
during marfans or chlers danlos as well as atherogenesis
- monitor these closely
where are the most common locations for an aortic dissection
- Sinotubular junction - where aortic root becomes tubular near the aortic valve
- Just distal to the left subclavian artery
What is the stanford classification of aortic dissection location
A = proximal to left subclavian 2/3
B = distal to left subclavian 1/3
what is the pathophysiology of aortic dissection
Blood dissects the media and intima and pools in the false lumen which can propagate forwards or backwards = leads to reduced perfusion of end organs, organ failure and shock
what are the symptoms of aortic dissection
sudden onset of ripping or tearing chest pain
- shock/hypotension
- new aortic insufficiency murmur
- neurological symptoms
- dicreased peripheral left arm pulse
- cardiac tamponade
how do you diagnose aortic dissection
widened mediastinum on chest X ray - over 8cm
CT angiogram
TOE - sensitive
how do you treat aortic dissection
surgical - open repair or EVAR
Medication - Beta blocker Esmolol or labetolol, pluss a partial alpha blocker to prevent reflex tachycardia
Vasodilator sodium nitroprusside
what are complications of aortic dissection
Cardiac tamponade
Aortic insufficiency - regurgitation
Pre-renal AKI
Stroke
what are secondary causes of hypertension
- phaeochromocytoma
- cushings
What is a DVT
it is a thrombus in the deep leg vein
- if below calf it is less concerning
- if above calf it is life threatening
what can pulmonary embolism cause
Cor pulmonale
what are patient symptoms of pulmonary embolism
Sudden onset of pleuric chest pain
Dyspnoea
Evidence of DVT - swollen leg
Tachycardia, hypertensive, increased JVP
What are symptoms of a deep vein thrombosis
unilateral swollen calf with engorged leg veins, typically warm
how do you diagnose a pulmonary embolism
ECG - sinus tachycardia S1Q3T3
T wave inversion of anterior and inferior leads
New right bundle branch block
how do you diagnose a deep vein thrombosis
Use the wells DVT score
if its less than 1 check D dimer, if its not raised there is no pulmonary embolism
if DVT score is over 1 or D dimer is raised then do a duplex ultrasound which is diagnostic
what does the D dimer measure
it is a measure of clot burden
- if its sensitive it rules in a PE
what is a differential diagnosis for DVT
CELLULITIS - skin infection typically caused by staph aureus and strep pyogenes
- can cause tender, inflamed and swollen calf
what is the pathophysiology of peripheral vascular disease
Acute to acute on chronic
Intermittent claudication due to atherosclerotic partial lumen occlusion. This can progress to total limb ischemia
what are the 6Ps to remember in acute limb ischemia
Pulselessness
Pallar
Pain
Perishingly cold
Paralysis
Parasthesia
what happens when the blood vessel to a region becomes occluded
irreversible nerve damage - within 6hrs
Irreversible muscle damage - 6-10rhs
Skin symptoms last to appear
what are the symptoms of peripheral vascular disease
- Ankle-brachial pressure index is less than 0.9
- lack of lower leg pulse
- skin on leg is cooler, colour change
- Bruits - pulsitile regions
- Buerger test positive
what is the Fontaine classification
- asymptomatic
- intermittent claudication
- chronic limb ischemia
- ischemic ulcers - gangrene
How do you diagnose peripheral vascular disease
ABPI
- 0.5-0.9 intermittent claudication
- less than 0.5 = ischemia
color duplex or ultrasound
what is the treatment for peripheral vascular disease - intermittent claudication
risk factor management
- smoking cessation
- change dies
- loose weight
What is the treatment for peripheral vascular disease - chronic limb ischemia
revascularisation surgery - PCI
amputation if severe
what is the treatment for peripheral vascular disease - acute limb threatening ischemia
SURGICAL EMERGENCY
Revascularisation within 4-6hrs
what are complications of peripheral vascular disease
Amputation
Permanent limb weakness
rhabdomyolysis
increased risk of cerebrovascular accidents and CVD
what are causes of pericarditis
Idiopathic
Viral - coxsackie
Bacterial - TB
Fungal
Autoimmune - SLE
Dressler’s syndrome
Neoplastic
WHat is the pathophysiology of pericarditis
Inflamed pericardial layers rub against each other exacerbating the inflammation. THis can remain dry or become effusive (extra fluid)
what are the symptoms of cardiac tamponade
Becks triad - Hypotension, increased JVP, muffled S1+2 sounds
Pulsus paradoxicus
what are risk factors of infective endocarditis
Male
Elderly
Prosthetic valves
IV drug user
Congenital heart defects
Rheumatic heart disease
what is the consequence of regurgitation
insufficiency and proximal chamber dilation
- Loss of structural chamber integrity and strength
what is the consequence of valve stenosis
increase in upstream pressure and proximal chamber hypertrophy
- heart becomes huge and rigid; poorly compliant
When are right sided valve defects heard
Inspiration
What are right sided valve defects
defects with pulmonary or tricuspid valves
When are left sided defects heard best
expiration
what are the two types of left sided valve defects
aortic valve or mitral valve defects
what is tachycardia
Any beat higher than 100 bpm
what is atrial fibrillation
an irregularly irregular heart rhythm
What are causes of atrial fibrillation
Heart failure
Hypertension
Secondary to mistral stenosis
sometimes idiopathic
what are risk factors for developing atrial fibrillation
60+
DM (T2)
Hypertension
valve defects
history of MI
What is the pathophysiology behind atrial fibrillation
Rapid reentrant ectopic foci cause atrial spasm which causes atrial blood to pool instead of pump efficiently to ventricles
what are the different types of atrial fibrillation
Paroxysmal - episodic
Persistent - longer than 7 days
Permanent
how do you diagnose atrial fibrillation
ECG diagnostic - narrow QRS (<120ms) and irregularly irregular. No P wave
how do you treat atrial fibrillation
Beta blockers or CCBs and oral anticoagulants
Cardioversion and warfarin
what is important to do when assessing anticoagulation for atrial fibrillation
the CHA2DS2 VASc score - stroke risk to determine if someone should start anticoagulation therapy
What is the HASBLED score
it assesses the risk of major bleeds in AF patients on anticoagulation
what is atrial flutter
irregular organised atrial firing
- there is atrial spasm but is still coordinated
how do you treat atrial flutter
If unstable cardiovert
If stable then rhythm or rate control via BBs and oral anticoagulation
how do you diagnose Wolff-Parkinson White syndrome
ECG
1. Slurred delta waves
2. Short PR interval
3. Wide QRS
how do you treat Wolff-Parkinson White
- Vasalva carotid massage
- IV adenosine, 6mg then 12mg then another 12mg
- Consider surgical radiofrequency ablation of bundle of kent
what is long QT syndrome
Ventricular tachyarrhythmia normally caused by a congenital channel disorder affecting cardiac calcium channels
what are causes of long QT
Romano Ward syndrome
Jerrel lange neilsen syndrome
Hypokalaemia
Hypocalcaemia
What is Torsades de pointes
Polymorphic ventricular tachycardia in patients with prolonged QT. There are rapid irregular QRS complexes which are round baseline and can cease or develop into ventricular fibrillation
what happens during ventricular fibrillation
Shapeless rapid oscillations on the ECG
- patient becomes pulseless and goes into cardiac arrest
- need defibrillation
what can cause a right bundle branch block
Pulmonary emboli, ischemic heart disease, VSD
What is seen on EGC in right bundle branch block
MaRRoW
M seen in V1 (RSR wave)
W seen in V6 (deep S wave)
What are causes of left bundle branch block
IHD, valvular disease
What is seen on ECG on left bundle branch block
WiLLiaM
W seen in V1
M seen in V6
what are symptoms of hypertrophic cardiomyopathy
May present with sudden death
Others: chest pain, palpitations, shortness of breath, syncope
what are symptoms of rheumatic fever
New murmur
Uncoordinated jerky movement
arthritis
erythema nodosum
pyrexia
how do you diagnose rheumatic fever
chest X ray - cardiomegaly
ECHO - look for valvular damage
How do you treat rheumatic fever
IV benzypenicillin
then phenoxypenecillin for 10 days
Haloperidol for jerky movements
what can arial septal defect lead to
overloading of the right heart circulation which can lead to hypertrophy and in worse case Eisenmenger syndrome
what is atrioventricular septal defect associated with
Downs syndrome
what is shock
Medical emergency - hypoperfusion, life threatening due to acute circulation failure
how does shock present
- Confusion
- Skin - pale cold sweaty
- Prolonged hypotension
- Decreased urine output
- Reduced GCS
- Weak pulse
what is hypovolemic shock
due to blood loss/ fluid loss
treat with ABCDE plus IV fluid
What is septic shock
Uncontrolled bacteria infection
- warm, tachycardic
Treat with ABCDE and broad spectrum antibiotics
What is cardiogenic shock
Due to heart pump failure
Treat with ABCDE and treat underlying cause
what is anaphylactic shock
Due to IgE mediated type 1 reaction
Treat with ABCDE and IM adrenaline
What is neutrogenic shock
Due to spinal cord trauma
Treat with ABCDE with IV atropine (blocks vagal tone)
what organs are most at risk of failure during shock
Kidney
Lung
Heart
Brain
what medication is given in infants who have patents ductus arteriosus
Indomethacin - prostaglandin synthase inhibitor
What is seen on a chest X Ray in heart failure
ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural effusion
what are risk factors for mitral stenosis
female
older
decreased BMI
post MI
Connective tissue disorder
what can cause mitral regurgitation
Myxomatoses mitral valve - progressive disarray of the valve where mass of cells in valve connective tissue makes the leaflets heaver and prolapse
papillary muscle rupture
what are symptoms of mitral regurgitation
excisional dyspnoea
pan systolic murmur radiating to the axilla
S1 soft
how do you threat a type three heart block
IV atropine and a permanent pacemaker
