cardiovascular system Flashcards
atherosclerosis definition
pathology of arteries in which there is deposition of lipids in the arterial wall, with surrounding fibrosis and chronic inflammation
risk factors for atherosclerosis
age tobacco smoking high serum cholesterol obesity diabetes hypertension family history
distribution of atherosclerosis
found within peripheral and coronary arteries
focal distribution along artery length
structure of atherosclerotic plaque
contains lipid, necrotic core, connective tissue, fibrous cap
eventually plaque occludes the vessel lumen causing ischaemia or ruptures, forming a thrombus
inflammation and atherosclerosis
LDL’s pass in and out of arterial endothelial cells
in excess they accumulate in the arterial wall and undergo oxidation and glycation
damage to endothelial cells leads to endothelial dysfunction
adhesion of leukocytes in atherosclerosis
chemoattractants are released from the endothelium and send signals to leukocytes
progression of atherosclerosis
fatty streaks intermediate lesions fibrous plaques plaque rupture plaque erosion
fatty streaks
appear at early age (<10)
consist of aggregations of lipid-laden macrophages and T cells in the intimal layer of the vessel wall
intermediate lesions
layers:
- lipid laden macrophages (Foam cells)
- vascular smooth muscle cells
- T lymphocytes
- adhesion and aggregation of platelets to vessel wall
- isolated pools of extracellular lipid
fibrous plaques
impedes blood flow
prone to rupture
covered by dense fibrous cap (collagen and elastin) laid down by smooth muscle cells that overlies lipid core and necrotic debris
may be calcified
smooth muscle cells, macrophages, foam cells, T cells
plaque rupture
constantly growing and receding
the cap is resorbed and redeposited
if balance is shifted in favour or inflammatory conditions it becomes weak and it ruptures
highly thrombotic plaque constituents are exposed (basement membrane, collagen, necrotic tissue)
thrombus formation
plaque erosion
fibrous cap does not disrupt
luminal surface under the clot may not have endothelium present but is smooth muscle cell rich
exposed thrombogenic subendothelial basement membrane to blood
treatment for coronary artery disease
percutaneous coronary intervention- stent implantation
restenosis was a limitation
restenosis
recurrence of abnormal narrowing of an artery or valve after corrective surgery
drug elution
anti-proliferative and inhibits healing
works by reducing smooth muscle cell proliferation so reduced the regrowth after placement of a stent
other useful drugs in atherosclerosis
aspirin- inhibits platelet cyclo-oxygenase but can cause excessive bleeding
statins- reduce cholesterol synthesis
clopidogrel- inhibitor of receptor on platelets
ECG
electrocardiogram is a representation of the electrical events of the cardiac cycle
ECGs can identify:
arrhythmias MIs pericarditis chamber hypertrophy electrolyte disturbances drug toxicity
pacemakers of the heart
SA node
AV node
ventricular cells
pacemakers of the heart: SA node
dominant pacemaker
intrinsic rate is 60-100 beats/min
pacemakers of the heart: AV node
back up pacemaker
intrinsic rate of 40-60 beats/min
pacemakers of the heart: ventricular cells
back up pacemaker
intrinsic rate of 20-45 beats/min
ECG: impulse conduction
sinoatrial node -> AV node-> bundle of His -> bundle branches -> purkinje fibres
ECG: calibration
25mm/s
0.1mV/mm
ECG: PQRST
p wave= atrial depolarisation
QRS= ventricular depolarisation
T wave= ventricular repolarisation
ECG: PR interval
atrial depolarisation and delay in AV junction (AV node to bundle of His)
ECG paper
horizontally:
- one small box= 0.04 seconds
- one large box= 0.2 s
vertically:
-one large box= 0.5mV
ECG leads
measure difference in electrical potential between two points
ECG: bipolar leads
two different points on the body
ECG: unipolar leads
one point in the body and a virtual reference point with zero electrical potential, located in the centre of the heart
12 lead ECG, type of leads
3 standard limb leads
3 augmented limb leads\6 precordial leads
ECG: Rule 1 (PR interval length)
PR interval should be 120-200 milliseconds (3-5 small squares)
ECG: Rule 2 (QRS width)
width of QRS complex should not exceed 110ms ( or 3 small squares)
ECG: Rule 3 (QRS in leads I and II)
QRS complex should be dominantly upright in leads I and II
ECG: Rule 4 ( QRS and T)
QRS and T waves tend to have same general direction in the limb leads
ECG: Rule 5 (waves in aVR)
all waves are negative in lead aVR
ECG: Rule 6 (R and S waves growing)
R wave must grow from v1 to at least V4
S wave must grow from V1 to at least V3 and disappear in V6
ECG: Rule 7 (ST segment)
ST segment should start isoelectric except in V1 and V2, where it may be elevated
ECG: Rule 8 (P waves)
P waves should be upright in I,II and V2-V6
ECG: Rule 9 (Q waves)
should be no Q wave (or only a small Q , less than 0.04s in I,II and V2-6
ECG: Rule 10 ( T waves)
T wave must be upright in I,II and V2-6
ECG: P wave
- always positive in I and II but negative in aVR
- <3 small squares in duration
- <2.5 squares in amplitude
- commonly biphasic in V1
- best seen in II
ECG: right atrial enlargement
tall (>2.5), pointed P waves
ECG: left atrial enlargement
notched, bifid P wave in limb leads
M for mitrale
ECG: short PR interval
wolff-parkinson-white syndrome
accessory pathway allows early activation of the ventricle
ECG: long PR interval
first degree heart block
ECG: QRS complex
- non-pathological Q waves present in I,II aVL, V5 and V6
- pathological >25% amplitude of subsequent R wave
- R waves in V6
ECG: ST segment
flat- isoelectric
elevation or depression by 1mm or more is considered normal
ECG: T wave
- normal is asymmetrical, first half having a more gradual slope than the second
- should be at least 1/8, but less than 2/3 of the amplitude of R wave
- abnormal= symmetrical, tall, peaked, biphasic or inverted
ECG: QT interval
- measured in lead aVL as it doesn’t have prominent U waves
- 0.35-0.45s
- decreased when heart rate increases
- HR=70bpm, QT <0.4s
ECG: U wave
- related to after depolarisations, which follow repolarisations
- small, round, symmetrical and positive in lead II
- same direction as T wave
ECG: rule of 300 or 1500, for determining heart hate
count number of large boxes between QRS complexes and divide this into 300 (smaller boxes with 1500)
e.g. 300/4= 75bpm
ECG: 10 second rule for determining heart hate
ECGs record 10 seconds of rhythm per page
count number of beats present on ECG
multiply by 6
better for irregular rhythms
ECG: the QRS axis
represents overall direction of the hearts electrical activity
ECG: abnormalities in the QRS axis
ventricular enlargement
conduction blocks
ECG: determining the axis
quadrant approach
equiphasic approach
ECG: quadrant approach
QRS complex in leads I and aVF
determine if they are positive or negative
combination should place the axis into one of the 4 quadrants
ECG: equiphasic approach
most equiphasic QRS complex
identified lead lies 90 degrees away from the lead
QRS in this second lead is positive or negative
ECG: right bundle branch block
- RBB is blocked so septal depolarisation from left to right (what normally occurs)
- left ventricular depolarisation down LBB, no RV depolarisation yet
- RV depolarisation from the LV
ECG: left bundle branch block
- LBB is blocked to septal depolarisation from right to left
- RV depolarisation, no LV depolarisation yet
- LV depolarisation from RV
angina definition
a symptom which occurs as a consequence of restricted coronary blood flow
almost exclusively secondary to atherosclerosis
angina and coronary arteries
epicardial= main exterior arteries e.g. LAD, circumflex etc.
small vessels= microvessels
symptoms occur when diameter falls below 75%
angina pathophysiology
Oxygen supply/demand mismatch:
- impairment of blood flow by proximal stenosis
- increased distal resistance
- reduced oxygen carrying capacity of blood- anaemia
electro-hydraulic analogy: healthy, rest
resistance of the epicardial arteries is negligible and so the flow through the system is determined by the resistance of the microvascular vessels
flow around 3ml/s
electro-hydraulic analogy: healthy, exercise
more flow is needed to meet metabolic demand so microvascular resistance falls so flow increases
flow is increased 5 fold (15ml/s)
electro-hydraulic analogy: disease, rest
compensated
epicardial disease causes the resistance of the epicardial vessel to increase
compensation occurs by reduction of microvascular resistance, maintaining flow @ 3ml/s
electro-hydraulic analogy: diseased, exercise
decompensated
microvascular resistance falls to try to increase flow, however it will ‘max out’
flow can therefore not meet metabolic demand- myocardium is ischaemic
types of angina
stable angina
unstable angina
crescendo angina
microvascular angina
angina non-modifiable risk factors
gender
family history
personal history
age
angina modifiable risk factors
smoking diabetes hypertension hypercholesterolaemia sedentary lifestyle stress
angina precipitants (supply)
anaemia hypoxaemia polycythaemia hypothermia hypovolaemia hypervolaemia
angina precipitants (demand)
hypertension tachyarrhythmia hyperthyroidism hypertrophic cardiomyopathy cold weather emotional stress
angina incidence
men= 35/100,00/year women= 20/100,000/year
angina prevalence
men= 5% (5000/100,000) women= 4% (4000/100,000)
angina mortality
annual= 1.2-2.4%
cardiac death= 0.6-1.4%
MI=0.6-2.7%
angina history taking
chest pain/discomfort: -heavy, central, tight, radiation to arms/jaw/neck -precipitated by exertion -relieved by rest/GTN (from above): -3/3= typical angina -2/3= atypical angina -1/3 or 0/3= non-anginal pain
angina differential diagnosis (*=important)
*pericarditis/myocarditis
*pulmonary embolism
chest infection
*aortic dissection
*gastro-oesophageal (reflux/spasm/ulceration)
*MSK
*psychological
MI??
angina examination
often seem normal or near normal signs of risk factors: -smoking -diabetes -hypertension -high cholesterol signs of complications
angina basic investigations: 12 lead ECG
often appear normal
can be signs of ischaemic heart disease
angina basic investigations: echo
will seem normal
can be signs of previous infarcts or give alternative diagnoses
angina basic investigations: pre test probability
calculates probabilities of obstructive coronary disease by categorising patients according to their gender, age and typical pain
angina diagnosis: treadmill test
induce ischaemia while walking uphill at a fast pace
look for ST segment depression
detects a late stage of ischaemia
unsuitable if:
- can’t walk
- unfit
- BBB
- young female
angina diagnosis: CT angiogram
- high negative predictive value
- ideal for excluding CAD in younger, low risk individuals
- limited in tachycardia, AF or calcified disease
angina diagnosis: invasive angiogram
traditionally purely anatomical
some modern functional testing techniques such as FFR (pressure gradient across stenosis)
angina diagnosis: stress echo
functional test
dynamic imaging with and without pharmacological stress, looking for regional wall motion abnormalities
angina diagnosis: SPECT/myoview
radio-labelled tracer taken up by metabolising tissues
1st scan under stress, if perfusion defect bring back for a 2nd
a rest scan to see if its fixed defect (scar) or reversible (ischaemia)
angina diagnosis: cardiac MRI
same principle as stress echo
choosing an angina diagnosis test
- pre test probability of CAD
- invasive vs non-invasive
- allergies
- sensitivity/specificity
- radiation
- patient choice
angina primary prevention
reducing the risk of CAD and it's complications antihypertensives statins and lipid modulating therapies diabetic therapy smoking cessation general diet advice plenty of exercise
angina secondary prevention
risk factor modification
lifestyle changes similar to primary
pharmacological to reduce symptoms and risk of cardiovascular events
interventional such as surgery and PCI
angina treatment: beta blockers
1st line anti-anginal
beta 1 specific
reduce heart rate and contractility by antagonising the sympathetic nervous system
angina treatment: beta blocker side effects
bradycardia
tiredness
erectile dysfunction
cold hands and feet
angina treatment: beta blocker contraindications
excess bradycardia severe heart block severe bronchospasm asthma coronary spasm
angina treatment: nitrates
1st line anti-anginal
primary venodilators (systemic veins)
reduce preload of the heart and therefore the work of the heart and O2 demand
angina treatment: calcium channel antagonists
1st line anti-anginal
arterodilators (systemic arteries) decreasing BP and afterload of the heart
so reduce energy needed for same CO
dilating coronary arteries antagonises spasm
angina treatment: antiplatelets
e.g. aspirin reduce events cyclo-oxygenase inhibitor: -decrease prostaglandin synthesis (thromboxane) -decrease platelet aggregation
causes gastric ulceration
angina treatment: statins
HMGCoA reductase inhibitors
reduces events
reduces LDL cholesterol
revascularisation
restore coronary artery and increase the flow
performed when medication fails or when risk of disease is high
types of revascularisation
percutaneous coronary intervention (PCI- stenting)
coronary artery bypass graft (CABG- surgery)
PCI pros
less invasive
convenient
repeatable
acceptable
PCI cons
stent thrombosis
restenosis
disease is complex
dual anti-platelet therapy
CABG pros
prognosis
deals with complex disease
CABG cons
invasive risk of stroke or bleeding can't do it if frail one-time treatment length of stay time of recovery
When to use PCI or CABG
STEMI- PCI
NSTEMI_ mainly PCI but also CABG
stable-PCI or CABG
acute coronary syndromes
a spectrum of acute cardiac conditions from unstable angina to MI
all associated with sudden reduced blood flow to the heart
acute coronary syndromes: the big five risk factors
smoking hypertension diabetes mellitus hypercholesterolaemia family history
acute coronary syndromes: other risk factors (not the big five)
CKD peripheral arterial disease (PAD) inflammatory conditions ethnicity stress
unstable angina clinical classification
cardiac chest pain at rest
cardiac chest pain with crescendo pattern
new onset angina
unstable angina diagnosis
history
ECG
troponin (no significant rise)
acute MI
supply of blood to the heart is suddenly blocked
usually causes permanent cardiac muscle damage, although this may not be detectable in small MIs
ST elevation MI (STEMI)
sudden complete blockage of a coronary artery
can usually be diagnosed on ECG at presentation
non ST elevation MI (NSTEMI)
severely narrowed coronary artery but it isn’t 100% blocked
retrospective diagnosis made after troponin results are available
Q wave MI vs non-Q wave MI
a way of defining MI on the basis of whether pathological Q waves develop on the ECG
non-Q wave MI
no new Q waves
poor W wave progression
ST elevation
biphasic T wave
Q wave MI
large Q waves
STEMI (or MIs associated with left bundle branch block) are larger infarcts so more likely to lead to pathological Q wave formation
MI: symptoms
cardiac chest pain:
- unremitting
- severe (can be mild or absent)
- occurs at rest
- sweating, shortness of breath, nausea/vomiting
- 1/3 occur in bed at night
MI: mortality
early:
- 30% outside hospital
- 15% inside hospital
late:
- 5-10% in first year
- 2-5% annually thereafter
MI: risk factors
higher age diabetes renal failure left ventricular systolic dysfunction smoking obesity high cholesterol etc.
acute coronary syndromes: causes
majority= rupture of atherosclerotic plaque and consequent arterial thrombosis
uncommon= coronary vasospasm, drug abuse, artery dissection
formation of a thrombus
endothelial injury (exposes subendothelial collagen),
initial adhesion of platelets (GPIb on platelets binds to VWF, assisting binding to collagen),
stable adhesion and aggregation (GPIIb/IIIa, soluble platelet agonists)
troponin as an investigation
highly sensitive marker for cardiac muscle injury but not specific as it is a protein released in other forms of muscle injury (regulates actin-myosin contraction)
when is troponin also tested positive
gram negative sepsis pulmonary embolism myocarditis heart failure arrhythmias cytotoxic drugs
after MI troponin
rises for 4-8 hours, peaking at 12-18 hours
back to normal in 10-14 days
troponin: hsTnT, Rohe assay
make sure one measurement taken at least 6 hours after pain,
if not elevated 6 hours after pain- no MI
if it is elevated, repeat after 3 hours
if significant rise or fall (alongside other diagnostic factors) MI confirmed
acute coronary syndromes: initial management
999- to get to hospital fast
paramedics- look for ST elevation (contact primary PCI centre)
take aspirin 300mg immediately
pain relief
initial management of an MI
MONA
Morphine
Oxygen
Nitrates
Aspirin
acute coronary syndromes: hospital management
diagnosis bed rest oxygen therapy if hypoxic pain relief aspirin beta blocker
acute coronary syndromes: pharmacological treatment
P2Y12 inhibitors
GPIIb/IIIa antagonists
anticoagulants
acute coronary syndromes: P2Y12 inhibitors
P2Y12 causes amplification of platelet activation
so inhibitors used in combination with aspirin as dual anti-platelet therapy
acute coronary syndromes: GPIIb/IIIa antagonists
GPIIb/IIIa causes amplification of platelet activation
used in combination with aspirin and P2Y12 inhibitors in patients undergoing PCI
acute coronary syndromes: anticoagulants
target formation and/or activity of thrombin
inhibit both fibrin formation and platelet activation
acute coronary syndromes: pharmacological secondary prevention
lifelong aspirin P2Y12 inhibitors for one year or longer in high risk patients lifelong statins ACE inhibitors beta blockers
acute coronary syndromes: complications to treat after
heart failure
diuretics
implantable defibrillator
heart transplant
thrombosis
blood coagulation inside a vessel
arterial thrombosis
thrombus formed inside an artery
high pressure system, platelet rich
arterial thrombosis: risks in coronary circulation
can cause an MI
arterial thrombosis: risks in cerebral circulation
cerebrovascular accident
stroke
arterial thrombosis: risks in peripheral circulation
peripheral vascular disease
gangrene
venous thrombosis
thrombus formed in a vein
low pressure system, fibrin rich
venous thrombosis: DVT
thrombosis in vein lying deep below the skin
venous thrombosis: pulmonary embolus
dislodged thrombus occluding pulmonary vasculature
venous thrombosis: circumstantial causes
surgery immobilisation oestrogen (combined pill, HRT) malignancy long haul flights
venous thrombosis: genetic causes
factor V leiden (5%)
PT20210A (3%)
antithrombin deficiency
protein C or S deficiency
venous thrombosis: acquired causes
anti-phospholipid syndrome
lupus anticoagulant
hyperhomocysteinaemia
venous thrombosis: DVT investigations
compression ultrasound
doppler
d dimer
venous thrombosis: pulmonary embolus investigations
CT scan
CT pulmonary angiogram
V/Q perfusion scan
venous thrombosis: treatment
initially: low molecular weight heparin
after: oral warfarin for 3-6 months OR DOAC for 3-6 months
venous thrombosis: prevention
thromboprophylaxis: any measure taken to prevent thrombosis such as low molecular weight heparin or early mobilisation and good hydration
anticoagulant pharmacology
heparin low molecular weight heparin aspirin warfarin new oral anticoagulant drugs
anticoagulant pharmacology: heparin
glycosaminoglycan
binds directly to antithrombin and increases its activity
indirect thrombin inhibitor
anticoagulant pharmacology: low molecular weight heparin
smaller molecule, less variation in dose and renally excreted
once daily, weight adjusted dose given subcutaneously
anticoagulant pharmacology: aspirin
inhibits cyclo-oxygenase irreversibly
inhibits thromboxane formation and hence platelet aggregation
anticoagulant pharmacology: warfarin
orally active prevents synthesis of active factors II, VII, IX and X antagonist of vitamin K prolongs prothrombin time long half life (36 hours)
anticoagulant pharmacology: new oral anticoagulant drugs
NOAC/DOAC orally active like aspirin and warfarin directly acting on factor II or X shorter half life no blood tests or monitoring
deep vein thrombosis and pulmonary embolism prevalence
25,000 a year die from these in the uk
50% preventable
premature mortality
deep vein thrombosis: symptoms
non-specific
pain and swelling in the leg
deep vein thrombosis: signs
tenderness
warmth
discolouration
oedema
pulmonary embolism: symptoms
breathlessness
pleuritic chest pain
rapid breathing
hypotension
pulmonary embolism: signs
tachycardia tachypnoea pleural rub cyanosis right heart strain
inherited cardiac conditions: cardiomyopathies
refers to primary heart muscle disease and is often genetic
inherited cardiac conditions: hypertrophic cardiomyopathy
constriction of ventricles due to hypertrophy of the cardiac muscle- this can also block small coronary arteries
caused by sarcomere protein gene mutations
1 in 500 people
the fibrosis is non conduction so electrical impulses travel around, causing arrhythmias
inherited cardiac conditions: dilated cardiomyopathy
dilated ventricles due to thinner walls
cytoskeletal gene mutation
systole is ineffective
presents with heart failure symptoms
inherited cardiac conditions: arrhythmogenic cardiomyopathy
significant rhythm disturbance
desmosome gene mutations
myocardium replaced with fibrous and fatty tissue- causing arrhythmias
inherited cardiac conditions: channelopathy
inherited arrhythmia
caused by ion channel protein gene mutations (K+, Na+ or Ca2+)
structurally normal heart
recurrent syncope
inherited cardiac conditions: channelopathy ECG
long QT
short QT
brugada (ST elevation)
tachycardia triggered by adrenaline
inherited cardiac conditions: sudden arrhythmic death syndrome (SADS)
usually refers to normal heart and arrhythmia
inherited cardiac conditions: familial hypercholesterolaemia
inherited abnormality of cholesterol metabolism
leads to serious premature coronary and other vascular disease
inherited cardiac conditions: aortic aneurysm
aortovascular syndromes include marfan, loeys-dietz and vascular ehler danlos
inherited cardiac conditions: family testing
ICCs are usually dominantly inherited- 50% risk of inheritance
risk needs to be assessed for each individual
tamponade
compression of the heart by an accumulation of fluid in the pericardial sac
causes hypotension
pericardial effusion
too much fluid within the pericardium
chronic pericardial effusion
allows adaption of the parietal pericardium
compliance reduces the effect on diastolic filling of the chambers- rarely causes tamponade
acute pericardial effusion
effusion onset is quick and parietal pericardium can’t adapt
volume needed to cause cardiac tamponade is lower
acute pericarditis
inflammatory pericardial syndrome with or without effusion
acute pericarditis: clinical diagnosis
2/4 at least of the following:
- chest pain (85-90%)
- friction rub(33%)
- ECG changes(60%)
- pericardial effusion (up to 60%)
pericarditis: epidemiology
80-90% is idiopathic
5% of A&E attendances with chest pain
pericarditis: aetiology
viral bacterial autoimmune neoplastic metabolic traumatic and iatrogenic other
pericarditis: viral cause
most common cause in developed world
enterovirus, herpes virus, adenovirus
pericarditis: caused by TB
90% HIV +ve in developed countries
17-40% constrictive pericarditis
pericarditis: clinical presentation
severe, sharp pleuritic chest pain, with rapid onset- relieved by sitting forward, exacerbated by lying down
dyspnoea
cough
pericarditis: differential diagnosis
pneumonia pulmonary embolus gastro-oesophageal reflux MI aortic dissection pneumothorax
pericarditis: investigations
clinical examination ECG bloods chest xray echo
pericarditis: clinical examination
pericardial rub
sinus tachycardia
fever
beck’s triad: hypotension, muffled heart sounds, raised jugular venous pressure
pericarditis: ECG
diffuse ST segment
concave ST segment
no reciprocal ST depression
PR depression
pericarditis: bloods
FBC- modest WBC increase
ESR
troponin
pericarditis: chest xray
often normal in idiopathic
pneumonia
modest enlargement of cardiac silhouette
pericarditis: management
sedentary activity until resolution of symptoms
NSAIDs
aspirin
colchicine
pericarditis: prognosis
have good long term prognosis
15-30% develop recurrence
colchicine reduced recurrence rate by 50%
pericarditis: major complications
fever >38 degrees subacute onset large pericardial effusion cardiac tamponade lack of response to aspirin or NSAIDs after a week of therapy
pericarditis: minor complications
myopericarditis
immunosuppression
trauma
oral anticoagulant therapy
heart failure
- a state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
- a syndrome and not a diagnosis on its own
heart failure incidence/prevalence
incidence= 63,000 cases/year (29,000 females, 34,000 males)
prevalence= 878,000 total ( 405,000 female, 473,000 male)
mean age= 71-76 years
heart failure aetiology
most common cause= myocardial dysfunction
others= hypertension, cardiomyopathy, valvular
heart failure risk factors
old age african decent men before women reach menopause obesity people who previously have had an MI
heart failure pathophysiology
when the heart begins to fail RAAS and sympathetic nervous system try to compensate to maintain cardiac output
However when heart failure progresses these mechanisms are overwhelmed- decompensation
heart failure pathophysiology mechanisms
venous return- preload
outflow resistance- afterload
sympathetic system activation
RAAS
systolic failure
reduced ejection fraction
inability of the left ventricle to contract normally, resulting in a decrease in cardiac output
caused by ischaemic heart disease, MI and cardiomyopathy
diastolic failure
preserved ejection fraction
inability of the ventricles to relax and fill fully, decreasing stroke volume and so decreasing CO
caused by chronic hypertension which increases afterload so heart pumps against more resistance
acute heart failure
new onset or decompensation of chronic heart failure
characterised by pulmonary and/or peripheral oedema
w/ or w/o signs of peripheral hypotension
chronic heart failure
develops slowly
venous congestion is common
arterial pressure well maintained until quite late
heart failure symptoms
three cardinal symptoms= shortness of breath, fatigue ankle oedema
cold peripheries
increased weight
dyspnoea especially when lying flat
heart failure signs
tachycardia displaced apex beat added heart sounds and murmurs cyanosis hypertension
new york heart association classification for heart failure
class I: no limitation, asymptomatic class II: slight limitation, mild heart failure class III: marked limitation, moderate HF class IV: inability to carry out physical activity without discomfort, severe HF
heart failure treatment
lifestyle changes diuretics ACE inhibitors beta blockers digoxin revascularisation surgery heart transplant
causes of acute decompression of chronic heart failure
uncorrected hypertension obesity infection arrhythmias excess alcohol NSAIDS
heart failure complications
renal dysfunction rhythm disturbances DVT/PE LBBB and bradycardia hepatic dysfunction
heart failure investigations:
blood tests
chest xray
ECG
echo
heart failure investigations: blood tests
brain natriuretic peptide- secreted by myocardium in stress
FBC
U&E
epinephrine, vasopressin and renin= high
heart failure investigations: chest xray
alveolar oedema
cardiomegaly
dilated upper lobe vessels of lungs
pleural effusions
heart failure investigations: ECG
shows underlying causes
if ECG and BNP are normal then heart failure is unlikely
if both abnormal then do an echo
heart failure investigations: echo
assess cardiac chamber dimension
look for wall motion abnormalities
infective endocarditis
infection of heart valves or other endocardial lined structures w/i the heart (septal defects, pacemaker leads)
infective endocarditis: types
left sided native (mitral, aortic)
left sided prosthetic
Right sided, rarely prosthetic as rare to have those valves replaced
infective endocarditis: pathogenesis
have an abnormal valve
regurgitant or prosthetic valves are more likely to get infected
introduce infectious material into blood stream
infective endocarditis: epidemiology
young= rheumatic heart disease or drug abusers elderly= weakened immune system congenital heart disease anyone with prosthetic heart valves M:F= 2:1-9:1
infective endocarditis: incidence
0.6-6/100,000 people/year
10 year survival= 60-90%
infective endocarditis: presentation
signs of systemic infection (fever, sweats)
embolisation (stroke,pulmonary embolus, bone infections, MI)
valve dysfunction (heart failure)
infective endocarditis: diagnosing criteria
definite IE= 2 major, 1 major+3minor or 5 minor
possible IE= 1 major, 1 major+3minor or 5 minor
major= bugs grown from culture, evidence of endocarditis on echo minor= predisposing factors, fever, vascular or immune phenomena and equivocal blood cultures
infective endocarditis: echos
TTE= transthoracic echo, safe, non invasive, no discomfort, but poor images so lower sensitivity
TOE=transoesophageal echo, excellent pictures, uncomfortable, risk of perforation or aspiration
infective endocarditis: peripheral signs of spread and embolism
bruises, infarcts (10-15%)
splinter haemorrhages
osler’s nodes (small, tender, purple nodules on the pulp of digits)
roth spots on fundoscopy
infective endocarditis: diagnosis
bloods
ECG
TTE/TOE
infective endocarditis: blood tests
cultures can be negative in 2-5% of patients
certain organisms require longer incubation
WBC rarely helpful
C-reactive protein (inflammation marker) is almost always present
infective endocarditis: diagnosis with TTE/TOE
TTE is crucial for detecting vegetation but sensitivity is still only 60%
TOE sensitivity is 90-95%
infective endocarditis: treatment
antimicrobials for 6 weeks depending on the culture
treat complications such as heart failure, abscess drainage, stroke rehab
surgery
infective endocarditis: surgery
- when the infection cannot be cured with antimicrobials
- to fix complications such as aortic root abscess or valve damage
- remove infected devices
- remove large vegetations before they embolise
infective endocarditis: prevention
NICE recommends not to give prophylaxis
ESC consider prophylaxis in high risk patients
talk to patient and dentist
tetralogy of Fallot
ventricular septal defect
pulmonary stenosis
hypertrophy of right ventricle
overriding aorta
tetralogy of Fallot: physiology
the stenosis of RV outflow leads to RV being higher pressure than the left
blue blood passes from RV to LV so patients are blue
tetralogy of Fallot: epidemiology
10% of all congenital heart defects
1/1000 live births
15% have associated genetic abnormality
tetralogy of Fallot: treatment
surgical repair
a shunt between R subclavian artery and R pulmonary artery to increase pulmonary blood flow
often get pulmonary valve regurgitation in adult life so redo surgery required
ventricular septal defects
abnormal connection between the two ventricles
common- 20% of all congenital heart defects
1-4/1000 of live births
large ventricular septal defects: physiology
very high pulmonary blood flow in infancy
breathless, poor feeding, failure to thrive
require fixing in infancy
can lead to eisenmengers syndrome
small ventricular septal defects: physiology
small increase in pulmonary blood flow only
asymptomatic
endocarditis risk
need no intervention
large ventricular septal defects: clinical signs
small breathless skinny baby increased respiratory rate tachycardia big heart on chest xray murmur varies in intensity
small ventricular septal defects: clinical signs
loud systolic murmur thrill well grown normal heart rate normal heart size
eisenmenger’s syndrome
pathophysiology:
- high pressure pulmonary blood flow
- damages delicate pulmonary vasculature
- RV pressure increases
- shunt direction reverses and patient becomes blue
high mortality rate
atrial septal defects
abnormal connection between the two atria
common
often present in adulthood
atrial septal defects: physiology
slightly higher pressure in LA than RA
shunt left to right
therefore not blue
increase flow into right heart and lungs
large atrial septal defects: physiology
significant increased flow through the right heart and lungs in childhood
right heart dilation
SOB on exertion
increased chest infections
small atrial septal defects: physiology
small increase in flow
no right heart dilation
no symptoms
leave alone
atrial septal defects: clinical signs
pulmonary flow murmur
fixed split-second heart sound
big pulmonary arteries big heart on chest xray
atrial septal defects: treatment
surgical closure
percutaneous (key hole) closure
atrioventricular septal defects
2/10,000 live births
common in Down’s syndrome
hole in the centre of the heart
interatrial and/or interventricular
complete atrioventricular septal defects: physiology
breathless neonate poor weight gain poor feeding torrential pulmonary blood flow needs repair or PA band in infancy repair is surgically challenging
partial atrioventricular septal defects: physiology
can present in late adulthood
presents like a small VSD/ ASD
may be left alone if there is no right heart dilation
patent ductus arteriosus: signs
continuous machinery murmur
if large, big heart breathless
eisenmenger’s syndrome
large patent ductus arteriosus: physiology
torrential flow from aorta to pulmonary arteries in infancy
breathless, poor feeding, failure to thrive
common in prem babies
need surgical closure
small patent ductus arteriosus: physiology
little flow from the aorta to Pas
usually asymptomatic
murmur found incidentally
endocarditis risk
patent ductus arteriosus: treatment
surgical or percutaneous
local anaesthetic
venous approach
low risk of complications
coarctation of the aorta
narrowing of the aorta at the site of insertion of the ductus arteriosus
perfusion to lower body is reduced
severe coarctation of the aorta
complete or almost complete obstruction to aortic flow
collapse with heart failure
needs urgent repair
mild coarctation of the aorta
presents with hypertension
incidental murmur
should be repaired to prevent problems long term
coarctation of the aorta: clinical signs
right arm hypertension
bruits over scapulae and back from collateral vessels
murmur
coarctation of the aorta: long term problems
hypertension
re-corarctation requiring repeat intervention
aneurysm formation
coarctation of the aorta: treatment
surgical vs. percutaneous repair
bicuspid AV
has 2 cusps instead of the typical 3 1-2% of population M>F severely stenotic in infancy or childhood degenerate quicker than normal valves
pulmonary stenosis
narrowing of the outflow of the right ventricle
8-12% of all congenital heart defects
valvar, sub valvar, supra valvar, branch
severe pulmonary stenosis
right ventricular failure as neonate collapse poor pulmonary blood flow RV hypertrophy tricuspid regurgitation
mild pulmonary stenosis
well tolerated for many years
right ventricular hypertrophy
pulmonary stenosis: treatment
balloon valvuloplasty
open valvotomy
open trans-annular patch
shunt
atrial septal defects: primum
defect level of tricuspid and mitral valves
atrial septal defects: secundum
enlarged foramen ovale, inadequate growth of septum secundum, or excessive absorption of septum primum
atrial septal defects: sinus venosus
defect involves venous inflow of either SVC or IVC
hypertension: prevalence
> 75 year olds have 50% risk of hypertension
middle age have 10-30% risk
young have 5% risk
hypertension: main causes
85% of cases caused by genetics and lifestyle (obesity, excessive salt, alcohol)
hypertension: Conn’s syndrome
overproduction of aldosterone due to unilateral adrenal adenoma
results in sodium and water retention which increases BP
drugs causing hypertension
NSAIDS combined oral contraceptive corticosteroids ciclosporin cold cures SNRI antidepressants
other causes of hypertension
renal parenchymal disease renovascular disease endocrine coarctation or aorta pregnancy sleep apnoea
hypertension: investigation
eye exam- only area where blood vessels visible so can see damage caused by hypertension
hypertension: calcium channel blockers
inhibit the opening of voltage-gated calcium channels in vascular smooth muscle, reducing calcium entry and thereby calcium available for muscle contraction
hypertension: ACE inhibitors
prevents the generation of angiotensin II from angiotensin I
angiotensin II is vasoconstrictor that stimulates aldosterone release enhancing reabsorption of sodium
hypertension: angiotensin receptor blockers
blocks the action of angiotensin II at peripheral receptors
hypertension: thiazide diuretics
inhibit sodium reabsorption at distal tubule, reducing extracellular fluid volume which is elevated in hypertension
hypertension: beta-blockers
resistant hypertension may also be treated using alpha or beta adrenoceptor antagonists
BP response expected from 50mg atenolol
decrease in systolic or 10mmHg
white coat hypertension
anxiety when seeing a doctor so BP increases
95% of population BP is higher when in a clinical setting
how to measure BP at home
ambulatory BP monitoring: patient wears for 24 hours and measure every 20 mins
semi-automated device:
patients measures twice in morning and evening for a week
hypertension thresholds
clinical= 140/90
home=135/85
stages of hypertension
stage 1= low risk
clinical=140-160/90-100
home=135-150/85-95
stage 2=high risk
clinical >160/100
home= >150/95
illnesses caused by hypertension
heart failure stroke MI renal failure retinopathy
lifestyle changes to lower blood pressure
weight loss alcohol intake reduction salt intake reduction smoking cessation medication review stress reduction
aortic stenosis
normal valve area= 3-4cm2
symptoms occur when valve area is 1/4 of normal
congenital aortic stenosis
occur with unicuspid, bicuspid or tricuspid valves
acquired aortic stenosis
degenerative calcification
rheumatic heart disease
aortic stenosis: pathology
pressure gradient develops between the left ventricle and the aorta
LV function initially maintained by compensation but when these mechanisms are exhausted the function declines
aortic stenosis: presentation
syncope
angina
dyspnoea on exertion
aortic stenosis: signs
slow rising carotid pulse
soft or absent second heart sound
ejection systolic murmur
aortic stenosis: natural history
onset of symptoms is poor prognostic indicator mild to sever: 8% in 10 years 22% in 22 years 38% in 25 years
aortic stenosis: prognosis
angina and AS= 50% survive 5 years
syncope+AS= 50% survive 3 years
HF+AS mean survival <2 years
aortic stenosis: investigations
echo- measures left ventricular size and function and valve area
mild aortic stenosis: area and velocity
area >1.5cm2
velocity= 2.6-3 m/s
moderate aortic stenosis: area and velocity
1-1.5cm2
3-4m/s
severe aortic stenosis: area and velocity
<1cm2
>4m/s
aortic stenosis: management
dental hygiene
IE prophylaxis
surgical replacement
transcatheter aortic valve implantation
aortic stenosis: indications for intervention
symptomatic patients
any patient with decreasing EF
patients undergoing CABG with severe AS
mitral regurgitation
back flow from LV to LA during systole
mitral regurgitation: aetiology
myxomatous degeneration
ischaemic MR
rheumatic heart disease
infective endocarditis
mitral regurgitation: pathophysiology
pure volume overloads
compensation= left atrial enlargement, increased contractility
RV dysfunction due to pulmonary hypertension
mitral regurgitation: signs and symptoms
soft s1 and pan-systolic murmur (auscultation)
exertion dyspnoea
heart failure
mitral regurgitation: natural history
compensatory phase= 10-15 years
patients with asymptomatic sever MR have 5%/year mortality rate
mitral regurgitation: investigations
ECG
CXR
ECHO
mitral regurgitation: management
medication
serial echo
IE prophylaxis
surgery
aortic regurgitation
leakage of blood from aorta into LV during diastole
aortic regurgitation: aetiology
bicuspid aortic valve
rheumatic
infective endocarditis
aortic regurgitation: pathophysiology
combined pressure and volume overload
compensatory mechanisms
aortic regurgitation: physical examination
wide pulse pressure
hyperdynamic and displaced apical pulse
aortic regurgitation: natural history
asymptomatic until 4th/5th decade
rate of progression= 4-6% a year
aortic regurgitation: investigations
CXR
echo
aortic regurgitation: management
IE prophylaxis
vasodilators
serial echos
surgical treatment
mitral stenosis
obstruction of LV inflow that prevents proper filling during diastole
normal area=4.6cm2
symptoms begin at areas <2cm2
aetiology
rheumatic heart disease=77-99% of all cases
IE=3.3%
mitral annular calcification =2.7%
mitral stenosis: pathophysiology
progressive dyspnoea (70%)
increased transmitral pressures
right heart failure symptoms
mitral stenosis: natural history
disease of plateaus:
mild= 10 years after initial RHD
moderate= 10 years later
severe= 10 years later
mitral stenosis: signs
right sided heart failure
pinkish-purple patches on cheeks due to vasoconstriction- mitral facies
mitral stenosis: heart sounds
diastolic murmur
loud opening S1 snap
mitral stenosis: investigations
ecg
cxr
echo
mild mitral stenosis: valve area
> 1.5cm2
moderate mitral stenosis: valve area
1-1.5cm2
severe mitral stenosis: valve area
<1cm2
mitral stenosis: management
serial echos
beta-blockers and diuretics
IE prophylaxis
surgery