Cardio Flashcards
SA node intrinsic rate?
60-100 bpm
AV node intrinsic rate?
40-60 bpm
ventricular cells intrinsic rate?
20-45 bpm
what is p wave?
atrial depolarisation - in every lead par aVR
PR interval?
time taken for atria to depolarise and electrical activation to get
through AV node
QRS complex?
ventricular depolarisation
ST segment
interval between depolarisation and repolarisation
t wave
ventricular reporlarisation
Acute anterolateral myocardial infarction
ST segments are raised in
anterior (V3 - V4) and lateral (V5-V6) leads
ECG paper, horizontal measurements?
One small box = 0.04s/40ms
• One large box = 0.20s
ECG paper, vertical measurements
One large box = 0.5mV
where is left ventricle palpated?
palpated in the 5th left intercostal space and mid-clavicular
line, responsible for the apex beat
cardiac output equation?
Cardiac output (L/min) = Stroke volume (L) x Heart rate (BPM)
preload?
the volume of blood in the left ventricle which stretches the cardiac
myocytes before left ventricular contraction - how much blood is in the
ventricles before it pumps (end-diastolic volume). When veins dilate it results in
a decrease in preload (since by dilating veins the venous return decreases).
afterload?
the pressure the left ventricle must overcome to eject blood during
contraction - dilate arteries = decrease in afterload
s3 heart sound?
- in early diastole during rapid ventricular filling, normal in children and
pregnant women, associated with mitral regurgitation and heart failure
s4 heart sound?
‘Gallop’, in late diastole, produced by blood being forced into a stiff
hypertrophic ventricle - associated with left ventricular hypertrophy
what does atherosclerotic plaque contain?
lipid, necrotic core, connective tissue and fibrous cap
atherosclerosis formation? - inanition
Initiated by an injury to the endothelial cells which leads to endothelial
dysfunction
- Once initiated, chemoattractants (chemicals that attract leukocytes) are
released from endothelium to attract leukocytes which then accumulate and
migrate into the vessel wall
- Chemoattractants are released from site of injury and a concentration-
gradient is produced
– leukocytes then allow migration of monocytes and T-helper cells - monocyte → macrophage within the intima layer of vessel wall
inflammatory cytokines found in plaque?
- IL-1 - KEY ONE
- IL-6
- IFN - gamma
atherosclerosis formation? intermediate lesion?
- macrophages ingest oxidised LDL then become foam cells
- foam cells promote smooth muscle migration from tunica media to intima and proliferation of SMC
- there is also adhesion and aggregation of platelets to vessel wall
atherosclerosis formation? fibrous plaque>?
- SMC allows synthesis of ECM eg collagen and elastin → this hardens and forms fibrous cap
- death of foam cells releasing lipid content → causing the plaque to grow, build pressure and rupture.
- foam cells release IL1, IL6 and IFN gamma
atherosclerosis formation? plaque rupture?
- plaque is still growing
- The fibrous cap needs to be resorbed and redeposited in order to be maintained
- If balance shifts e.g. in favour of inflammatory conditions (increased
enzyme activity) then the cap becomes weak and the plaque ruptures - Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel within the plaque
- thrombosis → plaque ruptures, blood coagulation and impedes blood flow
what is angina?
chest pain or discomfort as a result of reversible MI
types of angina?
Stable angina: • Induced by effort and relieved by rest Unstable (crescendo) angina: • Angina of recent onset (less than 24hrs) or deterioration in previously stable angina prinzemnatal angina - caused by coronary artery spasm
epidemiology of angina?
- more common in men
- can be due to; stenosis, valvular disease, atheroma, arrhythmia and anaemia
risk factors for angina?
- smoking
- sedentary lifestyle
- T2DM
- genetics
- hypercholesterolaemia
pathophysiology of angina? initiation?
Endothelial dysfunction and injury around sites of sheer and damage
with subsequent lipid accumulation at sites of impaired endothelial
barrier
• Local cellular proliferation and incorporation of oxidise lipoproteins
occurs
• Mural thrombi on surface and subsequent healing and repeat of cycle
pathophysiology of angina? adaption?
As plaque progresses to 50% of vascular lumen size the vessel can no
longer compensate by re-modelling and becomes narrowed
• This drives variable cell turnover within the plaque with new matrix
surfaces and degradation of matrix
• May progress to unstable plaque
pathophysiology of angina? clinical stage
The plaque continues to encroach upon the lumen and runs the risk of
haemorrhage or exposure of tissue HLA-DR antigens which might
stimulate T cell accumulation
• This drives an inflammatory reaction against part of the plaque contents
• Complications develop including ulceration, fissuring, calcification and
aneurysm change
pathological stages of angina?
Fatty streak:
- These show macrophages filled with abundant lipid (foam cells)
- Also smooth muscle cells with fat
Intimal cell mass:
- These are collections of muscle cells and connective tissue
without lipid - “cushions”
The atheromatous plaque:
- Characterised by distorted endothelial surface containing
lymphocytes, macrophages, smooth muscle cells and a variably
complete endothelial surface
- There is local necrotic and fatty matter with scattered lipid rich
macrophages
- Evidence of local haemorrhage may be seen with iron deposition
and calcification
- Complicated plaques are those which show calcification and mural
thrombus - making them vulnerable to rupture
clinical presentations of angina?
- central chest tightness
- worse on exertion
- relieved by rest/GTN spray
- pain radiate to arm, neck, jaw, teeth
- sweating, SOB, nausea
scoring presentation of angina?
- Have, central, tight, radiation to arms, jaw & neck
- Precipitated by exertion
- Relieved by rest or spray GTN
• 3/3 = Typical angina
• 2/3 = Atypical pain
• 1/3 = Non-anginal pain
differential diagnosis to angina?
- pericarditis
- PE
- chest infection
- dissection of aorta
- GORD
ECG would show what in angina?
- may show ST depression
- flat or inverted t waves
angina testing?
- treadmill test/ ECG exercise
- CT scan calcium scoring
- SPECT/myoview -> radio-labelled tracer
- cardiac catheterisation
treatment of angina?
- modifiable risk factors
- aspirin (antiplatlet)
- statin (HMG-CoA reductase inhibitor)
- beta blockers
- GTN spray (nitrate - vasodilator)
- CCB (reduce after load)
- revascularisation (PCI and CABG)
PCI and CABG?
PCI
-Dilating coronary atheromatous obstructions by inflating balloon
within it
- Insert balloon and stent, inflate balloon and remove it, stent
persists and keeps artery patent
- Expanding plaque = make artery bigger
- PRO; less invasive
- CON; risk of stent thrombosis
CABG
- Left Internal Mammary Artery (LIMA) used to bypass proximal
stenosis (narrowing) in Left Anterior Descending (LAD) coronary
artery
- PRO; good prognosis
- CON; invasive
acute coronary syndrome?
umbrella term that includes STEMI, unstable angina, NSTEMI
STEMI?
ST-elevation myocardial infarction (STEMI):
• Develop a complete occlusion of a MAJOR coronary artery
previously affected by atherosclerosis
• This causes full thickness damage of heart muscle
• Can usually be diagnosed on ECG at presentation
• Will produce a pathological Q wave some time after MI so also
known as Q-wave infarction
NSTEMI?
Non-ST-elevation myocardial infarction (NSTEMI):
• Occurs by developing a complete occlusion of a MINOR or a partial
occlusion of a major coronary artery previously affected by
atherosclerosis
• Is a retrospective diagnosis made after troponin results and
sometimes other investigation results are available
• This causes partial thickness damage of heart muscle
• Also known as a Non-Q wave infarction will see ST depression and/
or T wave inversion
difference between NSTEMI and angina?
- NSTEMI has rise in serum troponin or creatine kinase-MB
5 types of MI?
Type 1:
- Spontaneous MI with ischaemia due to a primary coronary
event e.g. plaque erosion/rupture, fissuring or dissection
Type 2:
- MI secondary to ischaemia due to increased O2 demand or
decreased supply such as in coronary spasm, coronary
embolism, anaemia, arrhythmias, hypertension or
hypotension
Type 3,4,5:
- MI due to sudden cardiac death, related to PCI and related to
CABG respectively
unstable angina risk factors?
- family history of IHD
- smoking
- hypertension, T2DM
- obesity
pathophysiology of unstable angina?
Rupture or erosion of the fibrous cap of a coronary artery plaque
- Leading to platelet aggregation and adhesion, localised thrombosis,
vasoconstriction and distal thrombus embolisation
- The presence of a rich lipid pool within the plaque and a thin, fibrous cap is
associated with an increased risk of rupture
- Thrombus formation and the vasoconstriction produced by platelet release
of serotonin and thromboxane A2 result in myocardial ischaemia due to
reduction of coronary blood flow
- Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/
fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia
or Sudden CVS death
- In unstable angina the plaque has a necrotic centre and ulcerated cap and
the thrombus results in PARTIAL OCCLUSION
- In myocardial infarction the plaque also has a necrotic centre but the
thrombus results in TOTAL OCCLUSION
presentations of unstable angina?
- Pallor
- Increased pulse and reduced BP
- Reduced 4th heart sound
- chest pain
- sweating
differential diagnosis of unstable angina?
- angina
- pericarditis
- myocarditis
- aortic dissection
- PE
- GORD
ECG, unstable angina?
- can be normal
- ST depression and T wave inversion
- can get tall T waves
biochemical markers for MI?
Troponin (T & I):
- T & I are the most sensitive and specific markers of myocardial
necrosis
- Serum levels increase within 3-12 hours from the onset of chest
pain and peak at 24-48 hours
- They then fall back to normal over 5-14 days
- Can act as prognostic indicator to determine mortality risk and
define which patients may benefit from aggressive medical therapy
and early coronary revascularisation
CK-MB:
- CK-MB can be used as a marker for myocyte death - but has low
accuracy since it can be present in the serum of normal
individuals and in patients with significant skeletal muscle damage
- However it can be used to determine re-infarction as levels drop
back to normal after 36-72 hours
Myoglobin:
- Becomes elevated very early in MI but the test has poor specificity
since myoglobin is present in skeletal muscle
treatment of unstable angina?
- pain relief; GTN spray, IV opiods
- antiemetics
- oxygen (94-98% sat, lower for those with COPD)
atheroma and platelets?
Atheromatous plaque rupture results in platelets being exposed to ADP/
Thromboxane A2/adrenaline/thrombin/collagen tissue factor
• This results in platelet activation/aggregation via IIb/IIIa glycoproteins
binding to fibrinogen (enables platelets to adhere to each other =
aggregation)
• Then thrombin (already present in surroundings) is able to enzymatically
convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin
mesh over platelet plug and the formation of a thrombotic clot
aspirin function?
blocks formation of thromboxane A2 thus
prevents platelet aggregation
P2Y12 inhibitor function?
Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby
preventing amplification response of platelet aggregation
glycoprotein 2b/3a antagonists?
Used in combination with aspirin and oral P2Y12 inhibitors in
patients with ACS undergoing Percutaneous Coronary Intervention
(PCI)
which is more common; STEMI or NSTEMI?
STEMI?
risk factor STEMI?
- male
- premature menopause
pathophysiology of STEMI?
Rupture or erosion of vulnerable fibrous cap of coronary artery
atheromatous plaque
- This results in platelet aggregation, adhesion, local thrombosis,
vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in
PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial
necrosis within 15-30 minutes in a STEMI (since major artery occluded fully)
clinical presentation of STEMI?
- chest pain that is severe >20 mins
- SOB
- pale, clammy
Ddx for STEMI?
stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, GORD
ECG STEMI?
- ST elevation
- Tall t-waves
- LBBB
ECG NSTEMI?
- ST depression
- T wave inversion
- diagnosis retrospective after troponin result
treatment for STEMI?
- 300mg chewable aspirin ASAP
- GTN
- morphine
- o2 if <95%
- beta blocker
- p2y12 inhibitor
- PCI
- CABG
- risk factor modifications
what can occur after MI?
- mitral incompetence
- pericarditis
- cardiac rupture; early and late
what is cardiac failure?
The inability of the heart to deliver blood and thus O2 at a rate that is
commensurate with the requirement of metabolising tissue of the body
epidemiology of HF?
- 10% in elderly
- African descent
- men
aetiology of HF?
- Ischaemic heart disease (IHD) - MAIN CAUSE
• Cardiomyopathy (disease of heart muscles, where the walls have
become thickened, stiff or stretched)
• Valvular heart disease e.g. aortic stenosis, aortic and mitral
regurgitation
• Cor pulmonale
• Hypertension
• Alcohol excess
• Any factor that increases myocardial work e.g. anaemia, arrhythmias,
hyperthyroidism, pregnancy and obesity
pathophysiology of HF?
When the heart begins to fail, there are many systems involved that initiate
physiological COMPENSATORY CHANGES that try to maintain cardiac
output and peripheral perfusion in order to negate the effects of the heart
failure
- However as heart failure progresses, these mechanisms are overwhelmed
and become pathophysiological also known as DECOMPENSATION
- mechanisms are preload, after load, sympathetic activation and RAAS.
preload In HF?
Venous return (preload):
- Myocardial failure leads to a reduction of the volume of blood
ejected with each heart beat, and an increase in the volume of blood
remaining after systole
- This increased diastolic (or preload - the volume of blood in the
ventricle before contraction) volume stretches the myocardial fibres
and, as Starling’s law of the heart says, myocardial contraction is
restored since the stretching of myocardial fibres will increase its
force of contraction
- However, in heart failure, the failing myocardium actually doesn’t
contract as much in response to increased preload meaning
cardiac output cannot be maintained and may decrease
after load in HF?
Outflow resistance (afterload) is the load or resistance against
which the ventricle contracts
- It is made up of:
• Pulmonary and systemic resistance
• Physical characteristics of the vessel walls
• The volume of blood that is ejected
- When there is an increase in afterload there is a increase in end-
diastolic volume and a decrease in stroke volume and thus a
DECREASE in cardiac output
- This results in a increase of end-diastolic volume and dilatation of
the ventricle itself (the more the ventricle is dilated the harder it
must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload
sympathetic system activation in HF?
When baroreceptors (located in the arterial wall of the aorta,
carotid and in the heart walls and major veins) detect a drop in
arterial pressure or an increase in venous pressure (due to back
flow of blood) they stimulate sympathetic activation
- This increases the force of contraction (positively inotropic) of the
heart (which increases stroke volume) as well as heart rate - both
resulting in an increase in cardiac output
- However in heart failure there is chronic sympathetic activation
which results in the receptors being acted on by the sympathetic
system to down regulate resulting in their being less receptor to act
on meaning the effect of sympathetic activation is diminished and
cardiac output stops increasing in response to sympathetic
activation
RAAS in HF?
Reduced cardiac output leads to diminished renal perfusion,
thereby activating the renin-angiotensin system whereby;
angiotensinogen is converted to angiotensin I under the action of
renin, angiotensin I is then converted to angiotensin II under the act
of angiotensin converting enzyme (ACE), angiotensin II then
stimulates the release of aldosterone from the adrenal cortex
above the kidneys
- This results in increased Na+ reabsorption and thus water
reabsorption as well as the release of ADH which stimulates water
retention
- This results in the increased volume of the blood which in turn
increases blood pressure and thus venous pressure which in turn
increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus
cardiac output
- However, with increased force of contraction the cardiac
myocytes require more energy and thus more blood however in
heart failure (which is most commonly caused by ischaemic heart
disease) there will be no increase in blood and thus the cardiac
myocytes will die resulting in a decrease in force of contraction
and thus a decrease in stroke volume and a decrease in cardiac
output
systolic HF?
Inability of the ventricle to contract normally resulting in a
decrease in cardiac output
• Caused by ischaemic heart disease, myocardial infarction
and cardiomyopathy (disease of heart muscle thus impairing
function)
diastolic HF?
Inability of the ventricles to relax and fill fully thereby
decreasing stroke volume and decreasing cardiac output
• Caused by hypertrophy (due to chronic hypertension which
results in increased blood pressure thereby increasing
afterload so heart pumps against more resistance and thus
cardiac myocytes grow bigger to compensate for this) of
ventricles resulting in there being less space for blood to fill in
and thus decreased cardiac output
• Also caused by aortic stenosis (the narrowing of the aortic
valve) which also increases afterload and thus decreases
cardiac output
acute v chronic HF?
Acute:
• Often used exclusively to mean new onset or decompensation
of chromic heart failure characterised by pulmonary and/or
peripheral oedema with or without signs of peripheral
hypotension
Chronic
- Develops slowly
• Venous congestion is common but arterial pressure is well
maintained until very late
clinical presentation of HF?
- SOB
- fatigue
- ankle swelling
- raised JVP
- murmurs
- ascites
- hypotension
- bi-basal crackles
investigation for HF?
blood tests; BNP (brain natuertic peptide) which is secreted by ventricles in response to increased myocardial wall stress
- CXR; ACDE (alveolar oedema, cardiomegaly, dilated upper lobe vessels of lungs and effusions)
- ECG
- echocardiography
treatment for HF?
- lifestyle changes
- diuretics; promote sodium and this water loss, reducing vernacular filling pressure (preload)
- ACE inhibitors
- Beta-blocker
- digoxin
- revascularisation
- surgery
- heart transplant
- cardiac resynchronisation
what is mitral valve disease?
Mitral valve is on the left side and is also known as the tricuspid valve, it
separates the left atrium from the left ventricle
mitral stenosis?
Obstruction of left ventricle inflow that prevents proper filling during diastole
• Mitral valve has 2 cusps
epidemiology of mitral stenosis
more men than women
history of rheumatic fever
untreated strep. infections
aetiology of mitral valve stenosis
Most common cause of mitral stenosis is rheumatic heart disease
secondary to rheumatic fever due to infection with group A beta-haemolytic
streptococcus e.g. Streptococcus Pyogenes
- or IE
- Or mitral annular calcification
pathophysiology of mitral stenosis?
Thickening and immobility of the valve leads to obstruction of blood flow
from the left atrium to the left ventricle
- In order for sufficient cardiac output to be maintained, the left atrial pressure
increases and left atrial hypertrophy and dilatation occur
- Consequently pulmonary venous, pulmonary arterial and right heart
pressures also increase
- The increase in pulmonary capillary pressure is followed by the development
of pulmonary oedema - this is seen particularly when atrial fibrillation occurs,
due to the elevation of left atrial pressure and dilatation, with tachycardia
and loss of coordinated atrial contraction
- This is partially countered by alveolar and capillary thickening and
pulmonary arterial vasoconstriction (reactive pulmonary hypertension)
- Pulmonary hypertension leads to right ventricular hypertrophy, dilatation
and failure with subsequent tricuspid regurgitation
clinical presentations of mitral stenosis?
- usually no symptoms until stenosis <2cm
- progressive SOB
- haemoptysis - due to rupture of bronchial vessels due to elevated pulmonary pressure
- signs of RHF
- atrial fibrillation
- malar flush
- loud S1 snap
investigations for mitral stenosis?
- gold standard -> echocardiogram
- ECG
- CXR
treatment for mitral stenosis?
- stenosis is mechanical problem so meds don’t prevent progression
- treat symptoms with beta blockers and diuretics
- percuataneous mitral balloon valvvotomy
- mitral valve replacement
mitral regurgitation?
Backflow of blood from the left ventricle to the left atrium during systole
• Mild physiological mitral regurgitation (MR) is seen in 80% of normal
individuals
epidemiology of mitral regurgitation
- females
- lower BMI
- advancing age
- renal dysfunction
- prior MI
aetiology of mitral regurgitation
Occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle - Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse) - Other causes include: • Ischaemic mitral valve • Rheumatic heart disease • Infective endocarditis • Papillary muscle dysfunction/rupture • Dilated cardiomyopathy
pathophysiology of mitral regurgitation
Regurgitation into the left atrium produces left atrial dilatation but little
increase in left atrial pressure if the regurgitation is longstanding, since the
regurgitant flow is accommodated by the large left atrium
- Pure volume overload due to leakage of blood into left atrium during systole
- Compensatory mechanisms: Left arterial enlargement, left ventricle
hypertrophy (since left ventricle must put in same effort to pump less blood(due to regurgitation) so needs to pump harder to maintain cardiac output and
thus hypertrophy to increase stroke volume) and increases contractility:
• Progressive left atrial dilatation and right ventricular dysfunction due to
pulmonary hypertension
• Progressive left ventricular volume overload leads to dilatation and
progressive heart failure
clinical presentation of mitral regurgitation?
- auscultation - soft S1 and prominent third extra heart sound S3
- exertion dyspnoea
- fatigue
- palpitation
- signs of right HF
investigations for mitral regurgitation
- ECG
- CXR
- echocardiogram
treatment for mitral regulation?
- vasodilators, beta blockers, anticoagulants, diuretics
- serial echocardiography to check for improvement
- surgery; if symptoms is at rest or ejection fraction <60%
aortic stenosis?
Narrowing of the aortic valve resulting in obstruction to the left ventricular
stroke volume, leading to symptoms of chest pain, breathlessness, syncope
and fatigue
epidemiology of aortic stenosis?
Congenital bicuspid aortic valve (BAV) predisposes to stenosis and
regurgitation - bicuspid valves are more likely to develop stenosis
- Congenital BAV is predominant in males
aetiology of aortic stenosis?
- Calcific aortic valvular disease (CAVD) - essentially calcification of the
aortic valve resulting in stenosis, most commonly seen in elderly
• Calcification of a congenital bicuspid aortic valve (BAV) (valve has 2
leaflets instead of 3 due to genetic disease - this is the most common
congenital heart disease) resulting in stenosis - Rheumatic heart disease - rare now due to eradication
types of aortic stenosis?
• Supravalvular (above valve) e.g congenital
fibrous diaphragm above the aortic valve
• Subvalvular (below valve) e.g congenital
condition in which a fibrous ridge or
diaphragm is situated immediately below
the aortic valve
• Valvular - most common
pathophysiology of aortic stenosis?
Due to the narrowing there is obstructed left ventricular emptying and a
pressure gradient develops between the left ventricle and the aorta resulting
in an increased afterload
- This results in increased left ventricular pressure and compensatory left
ventricular hypertrophy
- In turn, this results in relative ischaemia of the left ventricular myocardium
(since hypertrophy results in increased blood demand), and consequent
angina, arrhythmias and left ventricular failure
- The obstruction to left ventricular emptying is relatively more severe on
exercise - since exercise causes a many-fold increase in cardiac output,
however due to the severe narrowing of the aortic valve, the cardiac output
can hardly increase - thus, the blood pressure falls, coronary ischaemia
worsens, the myocardium fails and cardiac arrhythmias develop
- When this compensatory mechanism is exhausted left ventricular function
decline rapidly
clinical presentation of aortic stenosis?
- syncope - usually exertional
- angina
- heart failure
- dyspnoea
- absence of second heart sound
Ddx of aortic stenosis?
aortic regurgitation and subacute bacterial endocarditis
investigations for aortic stenosis
- echocardiogram; left ventricular size&function and doppler derived gradient and valve area
- ECG
- CXR
treatment for aortic stenosis?
- IE prophylaxis in dental procedures
- surgery
- TAVI - transcutaneous aortic valve implant
treatment for aortic stenosis?
- IE prophylaxis in dental procedures
- surgery
- TAVI - transcutaneous aortic valve implant
aortic regurgitation?
Leakage of blood into the left ventricle from aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps, of which there are three
aortic regurgitation, epidemiology?
SLE, marfans and Ehlers Danlos syndrome, aortic dilation and IE
aetiology of aortic regurgitation?
- Congenital bicuspid aortic valve (BAV) - chronic
• Rheumatic fever - chronic
• Infective endocarditis - acute
pathophysiology of aortic regurgitation
Aortic regurgitation is reflux of blood from the aorta through the aortic valve
into the left ventricle during diastole
- If net cardiac output is to be maintained, the total volume of blood pumped
into the aorta must increase and, consequently, the left ventricular size must
enlarge resulting in left ventricle dilation and hypertrophy
- Progressive dilation leads to heart failure
- Furthermore due to the fact that the remaining blood in the root of the aorta
supplies the coronary arteries via the coronary sinus during diastole -
regurgitation causes diastolic blood pressure to fall and thus coronary
perfusion decreases
- Also the large left ventricular size is mechanically less efficient, so that the
demand for oxygen is greater and cardiac ischaemia develops
presentation of aortic regurgitation?
In chronic regurgitation, patients remain asymptomatic for many years
before symptoms develop
- Exertional dysponea
- Palpitations
- Angina
- Syncope
-Quincke’s sign - capillary pulsation in the nail beds
- de Musset’s sign - head nodding with each heart beat
- Pistol shot femoral - a sharp bang heard on auscultation
Ddx for aortic regurgitation?
- HF
- IE
- mitral reguitation
investigation of aortic regurgitation?
- echocardiogram
- CXR
- ECG
treatment for aortic regurgitation?
- vasodilators
- surgery
IE?
An infection of the endocardium or vascular endothelium of the heart
• Known as subacute bacterial endocarditis
• Infection occurs on the following:
- Valves with congenital or acquired defects (usually on the left side of
the heart). Right sided endocarditis is more common in IV drug addicts
- Normal valves with virulent organisms such as Streptococcus
pneumoniae or Staphylococcus aureus
- Prosthetic valves and pacemakers
epidemiology of IE?
- more common in developing countries
- elderly with prosthetic valves
- IV drug user
- young with congenial heart disease
aetiology of IE?
- Staphylococcus aureus (IVDU, diabetes and surgery) - most common
cause
• Pseudomonas aeruginosa - Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha
haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep.
milleri & strep. oralis)
pathophysiology of IE?
Usually the consequence of two factors; the presence of organisms in the
bloodstream and abnormal cardiac endothelium that facilitates their
adherence and growth
- Bacteraemia may arise for patient-specific reasons:
• Poor dental hygiene - bacteria in tooth plaque can cause gum disease
which results in bleeding and inflammation of gums meaning when
brushing/in dental procedure this bacteria can enter the bloodstream
and reach the heart
• IV drug use
• Soft tissue infections
- Damaged endocardium promotes platelet and fibrin deposition, which allows
organisms to adhere and grow, leading to an infected vegetation
- Aortic and mitral valves are most commonly involved - IV drug users are
the exception since right-sided lesions are more common in them
- Virulent organisms destroy the valve they are on resulting in regurgitation
and worsening heart failure
clinical presentation of IE?
- regurgitant murmur
- embolic event
- sepsis
- renal infarction
- fever
- headache
- finger clubbing
- HF signs
- splinter haemorrhages
- embolic skin lesions
- osler nodes
- janeway lesion
- roth spots
- petechiae
investigations for IE?
- blood cultures
- blood tests; CRP and ESR raised
- urinalysis
- CXR
- ECG; long PR intervals
- echocardiogram; transthoraic or thransoesphageal (better)
treatment for IE?
- if staph. -> vancomycin and rifampicin
- if not staph. -> benzylpenicillin and getamyicin
- surgery to remove valve and replace prosthetic
- good oral health!
what are cardiomyopathies?
Group of diseases of the myocardium that affect the mechanical or electrical function of the heart
epidemiology of cardiomyopathy?
- All carry an arrhythmic risk
- Can occur at younger ages
- Restrictive cardiomyopathy is rare in childhood and has a poor outcome
once symptoms develop - In general they are inherited genetic conditions although there are some
acquired ones
