Cardio Vascular System Flashcards
what is stenosis
where only a small amount of blood can get through the valve = heart has to work really hard at a higher pressure = doesn’t open properly
what is incompetence
is where the valve doesn’t shut properly or has a hole in it = backflow = extra work for the heart
what are the three major causes of heart valve pathology
Rheumatic Fever
Calcific Aortic Valve disease
Age related disease
how does rheumatic fever cause heart problems
Low prevalence
Yellow swollen tonsils
Strep. Pyogenes
Body fights it off and cross reaction with self antigens
inflammation in myocardium and causes fibrosis in heart valves and ruffled, white, damaged
(90% mitral, 40% aortic)
what is calcific aortic valve disease
Calcium in the aortic valve appearing age related
Sometimes amplified where the valve is abnormal
Knobbly yellow lumps, very hard calcifications
Causes problems closing and opening causing stenosis and incompetence
why is aortic valve disease a problem for heart health
coronary arteries that supply the heart branch off just after the aortic arch
less blood can get through, heart has to pump harder and gets stronger = left ventricular hypertrophy
same amount of blood gets to coronary arteries so heart muscle gets tired
what is age relate valve disease likely to effect and how
Degrading mitral valve
Easily seen on a echo mycogram
Floppy mitral valve, very thin
how would we detect a weak mitral valve
mycogram
what types of artificial heat valves can be provided
Synthetic = ball and cage, tilting disc, synthetically grown forom pericardium
Biological = porcine, human
what tissue are heart valves made from
pericardium
what complications can we get from valve replacements
haemolysis
Coagulation - anticoagulation therapy needed with metal or plastic
mechanical failure - cage can break and ball can be released from ball and cage
calcification
infective endocarditis as rough surface is retentive for bacteria
Stitches too tight in sewed
rejection e.g. porcine
how might rheumatic fever lead to risk of endocarditis
rheumatic fever is a Strep. Pyogenes infection
Body fights it off and cross reaction with self antigens
causes inflammation and damage/fibrosis of heart valves
This roughens the surface of the valves and forms retention for bacteria that cause infective endocarditis
in what case might a patient be at risk of infective endocarditis with healthy heart valves and which valve might it effect
if the patient is an intravenous drug user
staph aureus can cause tricuspid valve infective endocarditis
what valve would be affected if a patient with healthy valves was to get infective endocarditis from IV drug use
Tricuspid
what are the local (2) and systemic (3) effects of infective endocarditis
Local:
Valve stenosis/incompetence
myocarditis infection of the myocardium heart muscle
Systemic:
general effects of illness
embolisms = organ infarcts, black rashes, splinter haemorrhages
glomerulonephritis (immune complex deposition)
how can infective endocarditis cause major organ infarcts (4)
infarct is death of tissue due to loss of blood supply
Valves form ‘vegetations’ - fibrin and bacteria and fragile valves
This can dislodge and form embolisms in major organs
this can cut off blood supply leading to death of parts of organs
give three micro-organism that can cause infective endocarditis and their route
risk of EC = Strep. Viridians from oral cavity through transient bacteraemia
healthy = IV drug user, Staph. Aureus
immunocompromised = natural fungus e.g. aspergillus
Strep pyogenes- rheumatic fever?
what percent of deaths does coronary heart disease cause
30% in men
what is another name for coronary artery disease
ischaemic heart disease
what are the three pre-disposing factors for vessel injury and atherosclerosis
Change in blood flow laminar → turbulent (high BP)
Change in vessel wall e.g. injury
Change in blood constituents e.g. too many platelets
Also high blood pressure, smoking, high cholesterol, obesity
what are the three causes of ischaemic heart disease
atherosclerosis, myocardial hypertrophy and small vessel disease
what are some risk factors for atherosclerotic plaque formation (4)
smoking
uncontrolled diabetes (controlled diabetes = no risk at all)
hyperlipidaemia
Hypertension
why might we get left ventricular hypertrophy? and what can this cause
This occurs if there are constricted vessels or faulty valves where the heart has to work harder to pump the same amount of blood. This strengthens the ventricles and leads to left ventricular hypertrophy and however the blood supply to the heart muscle itself does not increase meaning bigger muscle gets the same blood supply, making it more likely to fatigue
causes ischaemic heart disease
what causes small vessel disease and what can cause it
non obstructed blood vessels can still cause pain, down to arteriole level
Nitric oxide is a vasodilator so if nitric oxide is either underproduced or over destructed, this causes smooth muscle constriction
this can contribute to ischaemic heart disease
testing blood for someone with chest pain, what would we be looking for
nitric oxide levels (small vessel disease)
lipid levels (hyperlipidaemia)
blood pressure
what are the three results of ischaemic heart disease
regional transmural myocardial infarction
subendocardial myocardial infarction
chronic ischaemia
what is the most common heart attack
regional transmural myocardial infarction
explain regional transmural myocardial infarction
Chunk of of heart tissue has died that is the full thickness of the heart
Due to blockage in coronary artery
acute occluding event in one of the three main coronary arteries
lack of collateral circulation from the other vessels
explain subendocardial myocardial infarction
Occurs more in hospitals
Just inner part of ventricle dies (furthest from blood supply)
Severe atherosclerosis in all three coronary arteries
Occurs when sudden reduction in blood flow e.g. hypotension in medical procedure or GA
Pale parts of heart are lack of blood supply
if a patient has a heart attack in a hospital and has severe coronary artery atherosclerosis, what type of heart failure is this likely to be
subendocardial myocardial infarction
explain chronic ischaemia
‘fixed’ atherosclerotic lesions
angina
myocardial fibrosis
hibernating myocardium
stunned myocardium
which type of ischaemia causes fibrosis
chronic ischaemia
what are some complications of infarctions
sudden death
Arrhythmias - fibrillation caused by muscle not completely contracting just doing random movements so not pumping blood around the body This is where basic life training comes in, After serious exercise
cardiac failure
If muscle has been degraded = Reduced pump function
mitral incompetence = rupture or necrosis of papillary muscles
pericarditis
cardiac rupture = weakening of wall due to muscle necrosis and acute inflammation, 3-7 days after infarction, rupture into pericardial sac, rupture of interventricular septum
mural thrombosis
ventricular aneurysm - Instead of rupturing it can stretch and form an aneurysm and fill with blood
pulmonary embolism
why can arrhythmias cause myocardial infarction
pumping in an irregular manor means no blood is getting efficiently pumped
heart and brain quickly deprived of blood and oxygen
what is ‘cardiac failure’
if muscle has been degraded, necrosed or infarcted
reduced pump function
<55% inject compared to normal 75%
what is a cardiac rupture and when is this likely
weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac
rupture of interventricular septum
what is an aneurism
a bulge that forms in the thinning wall of an artery that can bulge or it can rupture and form a bleed and swelling
what is the cause and sign of mitral valve incompetence
necrosis or damage to papillary muscles
causes a pan systolic murmur
a patient has pan systolic murmur, what does this indicate
mitral valve incompetence
what would a heart look like if it had had a rupture into the pericardial sac and what may cause this
black bulges full of blood
weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac
what would a heart look like if it had had a rupture into the pericardial sac and what may cause this
black bulges full of blood
weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac
what might happen 3-7 days after a heart attack
cardiac rupture into the pericardial sac
due to weakened/damaged muscle tissue
what is a mural thrombosis
thrombosis on the abnormal endothelial surface following infarction
7-14 days after infarction
embolization to any arterial site
what is a ventricular aneurism
stretching of newly-formed collagenous scar tissue
4 weeks or more after infraction
may be associated with cardiac failure
may contain thrombus or stretch
what is the clinical importance of hypertension (3)
commonest cause of heart failure in most countries
major risk factor for atherosclerosis
major risk factor for cerebral haemorrhage
what is systole and diastole
s = contraction
d = relaxation and filling with blood
in the heart, what does pressure go from and compare this to the aorta
In the heart the pressure goes from 0-120. In the aorta, since it stretches, it goes from 120-180 and this varies over the day.
what is seen as normal blood pressure
120-130 / 80-85 mmHg
what is seen as severe hypertension
> 180/110 mmHg
what are the 2 classifications of hypertension
primary and secondary
benign and malignant
what is primary hypertension and what is it affected by (3)
no definitely identified cause
affected by:
Balance between sodium and water
Adrenaline levels by adrenal gland
Renin angiotensin aldosterone system
what is secondary hypertension (3)
easy to identify and exclude
renal
-renin dependent
-salt and water overload
-Something wrong with kidneys increases BP
endocrine
-Cushing’s, Conn’s, pheochromocytoma
-Too many corticosteroids either from tumours or given
what can cause secondary hypertension (3)
renal: renin dependent, salt and water overload, Something wrong with kidneys increases BP
endocrine: Cushing’s, Conn’s, pheochromocytoma, Too many corticosteroids either from tumours or given
drug therapy: corticosteroids, NSAIDs
what is benign hypertension
long asymptomatic period
increased frequency of complications later
what is malignant hypertension
markedly raised diastolic pressure
symptomatic
rapidly fatal if untreated
haemorrhages in the retina with impairment is common
give 6 effects of hypertesnion
accelerated atherosclerosis
sclerosis of smaller vessels
microaneurysms and haemorrhages
heart failure
kidney failure
cerebral haemorrhages = ‘strokes
what are the 4 major components of the heart that can go wrong, with relative consequences
myocardium = ventricles = heart failure (ventricles weaker than needed)
valves = infective endocarditis, heart failure
conduction system = tachycardia, bradycardia
coronary artery supply = most problems = atherosclerotic plaque = angina, MI
what is heart failure and what causes it
when the heart is pumping in-effectively for the body and heart <55%
an be idiopathic, previous heart failure, high BP, drugs
what is the gold standard assessment for pump function of the heart
transthoracic echocardiography (ultra sound)
what are symptoms of heart failure and what causes these problems
Reduced cardiac output increases fluid pressure in lungs (left heart failure), reduces venous return to the heart via vena cava (right heart failure) and compensatory responses cause fluid retention and vasoconstriction. This causes;
Breathlessness (increased fluid pressure in lungs)
Swelling (increased fluid pressure in venous system)
Also; dizziness, tiredness, weight loss
what causes the symptoms of heart failure
Reduced cardiac output increases fluid pressure in lungs (left heart failure), reduces venous return to the heart via vena cava (right heart failure) and compensatory responses cause fluid retention and vasoconstriction.
what are crepitations and what are they a sign of
‘crackles’ in the lungs
heart failure
what are the sign of heart failure
low blood pressure
increased heart rate
Crepitations in lungs
haziness in lung radiograph = liquid = increased fluid pressure
Raised jugular venous pressure
Pitting ankle oedema / ascites
what are the causes of valve problems (5)
Degeneration (ie it just happens)
Rheumatic fever = increased risk of infective endocarditis
Congenitally abnormal valve
Endocarditis
Papillary muscle rupture after MI
how do we test for arrhythmias
Echocardiogram to test the electric signals in the heart
what classes as tachycardia or bradycardia
tac = >100bmp
brad = <60 bmp
what is an ectopic beat and are they a risk
extra occasional narrow or broad QRS complexes, feels like missed/skipped beat, type of tacchycardia
common in normal, healthy people but more common in heart disease
low risk
what is the most common ‘serious’ arrhythmia and how many people have it over 80
Atrial fibrillation
found in 1 in 4 people over 80
hat are risk factors for atrial fibrillation and what can it be a risk for
Hypertension, heart failure, valve disease, alcohol, age, obesity, lung disease, hyperthyroidism
Increases risk of stroke
compare atrial fibrillation and atrial flutter
similar symptoms, risks and treatment
fibrillation = No P waves, irregular QRS rate
flutter = Rapid abnormal P waves, often 2 per QRS
what are common symptoms and signs of atrial flutter/fibrillation
dizziness, tiredness, high heart rate (higher rate, higher risk of symptoms), palpitations, often asymptomatic
what is the second most common arrythmia after atrial fibrilation/flutter
Supraventricular tachycardia (SVT)
what is a Supraventricular tachycardia (SVT) and who is at risk of this
Narrow QRS complex tachycardia, often absent P waves
Can probably happen to anyone, few predisposing factors, can be born with accessory pathway that increases chances
what are the symptoms of supraventricular tachycardia SVT
many palpitations (dizziness and breathless )
rarely dangerous and if lasting a long time (more than minutes) then go to hospital
what is the most dangerous and 3rd most common arrhythmia group
ventricular tachycardia or fibrillation
what can cause ventricular tachycardia or fibrillation
any problem that affects the ventricles e.g. heart attack, drugs, idiopathic
compare ventricular tachycardia and ventricular fibrillation
tachycardia = Broad QRS tachycardia
Fibrillation = Coarse fibrillation waves with no organised QRS
compare 3rd and 2nd degree heart block
2nd = Intermittent failure to conduct between P wave and QRS
3rd = No relationship between P waves and QRS, slow QRS rate
how do we test for coronary artery disease
coronary angiogram
what is a ‘stable’ atherosclerotic plaque and what does this cause
a strong fibrous cap protects the blood from exposure to the lipid core of the lesion, preventing thrombosis
this causes angina
what is angina and what makes this worse
Angina is a recurrent feeling of chest pressure/heaviness/pain/indigestion, sometimes radiating to the arm, neck, or back
Angina is almost always precipitated by exertion or stress (circumstances where the heart needs a greater blood supply)
compare unstable angina and stable angina
Angina rarely lasts more than 10minutes, and rarely is at rest = stable = no increase in symptoms
Angina itself isn’t dangerous. However “Unstable angina” (increasing frequency, duration, or onset at rest) is a sign of risk and warrants immediate assessment
what is myocardial infarction
MI occurs when an atherosclerotic plaque in a coronary artery ruptures, opening up the lipid core triggering thrombus formation.
This causes permanent death of some myocardium (unlike angina)
compare angina and MI
both caused by constricted coronary arteries and atherosclerotic plaque
MI causes complete thrombosis and death of myocardium, angina does not
what is the time difference in angina and MI pain
angina = upt to 10 minutes
MI is more than 10 minutes usually but can activate instantly
what causes atherosclerotic plaque rupture
not know, can happen under stress, exercise, rest, sleep
why is an exercise ECG not a good way of measuring coronary heart disease
50% of women show the ‘positive’ change in ECG even without the disease
explain the myocardial perfusion test
test for coronary heart disease
injected with a radio-showing fluid that is picked up by herat tissue
under relaxation, all of heart is seen
under stress, a portion of heart may not be seen = this part of the heart is affected by coronary heart disease
what is the gold standard for diagnosing coronary heart disease
CT angiography and invasive angiography if CT positive
when do we use invasive over CT angiography
risk of MI or if we need to stent
give three ways to diagnose coronary heart disease
exercise ECG
myocardial perfusion test
invase/CT angiography
how do we treat coronary heart disease
better diet: low processed foods, fats and salts. more fruit and veg, oily fish, olive oil, nuts
exerise more
cholesterol lowering drugs e.g statins
lifestyle : control stress, anxiety, obesity, smoking, diabetes
how do we treat angina due to CAD
treat CAD which improves prognosis, not symptoms
no treat if no bother
medications: beta blockers, calcium channel blockers,
If medication not working/side effects; stenting or coronary artery bypass grafting
(these improve symptoms but not prognosis)
if someone has had a stent, why might this be and what effects does this have (prognosis/symptoms)
treat angina: improve symptoms but not prognosis
previous MI: improve prognosis- but not for long
what 2 investigations do we do if someone thinks they are having a heart attack
ECG imediately to see if the ST is raised = ST elevated MI
could be a non-elevated ST MI so also test:
Serum Troponin in blood - immediate and 6 hours after pain
if heart muscle is damaged, what substance would be found in the blood
serum Troponin
what is the immediate treatment for MI (3)
immediate dual action medications of antiplatelet e.g. Aspirin, clopidogrel, and pain releif e.g. morphine
Anticoagulation for 24-72hrs; Heparin, Fondapariux or similar
Both STEMI and NSTEMI should have angiography and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications
compare the treatment of STEMI and NSTEMI
Both STEMI and NSTEMI should have angiography (invasive) and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications
when should oxygen be given and what can it do if given at the wrong time
only if the patient is hypoxic
may constrict coronary arteries and cause MI
what should be given to a patient if they suddenly get chest pain and you are waiting for an ambulance
aspirin under the tongue
what is the secondary treatment for MI
DAPT (dual antiplatelet therapy) for a year then Aspirin alone, Statin, Betablocker for a year, ACE inhibitor, and treatment of any complication (heart failure, arrhythmia, etc).
Cardiac rehabilitation; exercise, education, diet, smoking cessation
how do we diagnose and test for heart failure
referring to the ventricles, so look at the ventricles
test blood for B-type Natriuretic Peptide (BNP)
if positive (as can be other things) do a transthoracic echocardiogram
best way is MRI
what is the gold standard to investigate ventricular function and heart failure
MRI
more accurate and higher resolution than ultrasound Transthoracic echocardiogram
if a patient describes a CT scan or a MRI scan for a heart diagnosis, what was the problem likely to be
CT = injected with fluid = angiography testing coronary arteries
MRI = dark tube = ventricular heart failure
what are ACE inhibitors
angiotensin-converting enzyme inhibitors
lowers blood pressure and used for treating heart failure
what is the function of steroid medication for heart failure
aldosterone antagonists
aldosterone seen as disadvantageous for the heart
what medications are given if a pt has heat failure
ACE inhibitors e.g. Ramipril - REMEBER
Beta blockers e.g. bisoprolol - REMEBER
Aldosterone antagoniosts
treatment of complications like anaemia and thyroid
what are the 4 valves of the heart
Aortic - aorta
Tricuspid = right atrium –> ventricle
Bicuspid/Pulmonary = to the lungs from right ventricle
Mitral = left atrium –> ventricle
which valves are more likely to be a cause of disruption in the heart (2)
mitral and Aortic
why do we rarely see mitral stenosis these days
this is primarily caused by rheumatic fever which we are vaccinated against
what investigation is good for valve movements in the heart (2)
transthoracic echocardiogram
transoesophageal is more accurate but unpleasant for patient
BE CAREFUL - this does not help diagnose coronary heart disease
why artery could be used for a less invase valve replacement for aortic stenosis
femoral artery - same as angiogram
what MUST a patient with metallic valve replacement be on and for how long
warfarin lifelong
nothing else, no DOACs or NOACs
if a patient with a metallic heart valve needed a high bleeding risk surgery, what would we have to do
pt would be on warfarin so would stop warfarin and bridge with heparin and this must be done in a specialist clinic
never stop warfarin without consulting and maybe never stop if metal
how can we diagnose and study arrhythmias
ECG but obviously cannot predict when arrhythmia occurs
can give smartphone app with watch to detect ECG at time
or small implanted loop ECG constantly recording
other than ECG, what can we investigate with Arrhythmic patients
Ventricular fibrillation and tachycardia usually due to the left ventricle so
echocardiogram for heart failure
angiogram for coronary artery disease
family screening for patients with possible genetic problems
what is the P wave on an ECG
small atrial depolarisation
what is the P wave on an ECG
small atrial depolarisation
what is QRS complex on an ECG
ventricular depolarisation
what is the T spike on an ECG
ventricular repolarisation
give the order of the ECG spikes
P wave = atrial depolarisation
QRS complex = ventricular depolarisation
T wave = Ventricular repolarisation
if we accidently injected intravenous lignocaine, what would we see on an ECG and how do we treat
wide QRS and very close complexes = ventricular tacchycardia
immediate defibrillation
if the P wave is irregular what is the patient likely to have and how do we treat
ventricular bradycardia
pacemaker
usually caused by old age
what does the CHADS-2Vasc score tell us and what score is significant
risk of stroke with Atrial fibrillation and flutter
weather or not to give warfarin or NOAC anticoagulant
score of 1 or over = give anticoagulant
how do we treat atrial fibrillation/flutter
reduce risk of stroke with anticoagulants
if tachycardia slow the rate with beta blockers or calcium ion channel blockers
how can we correct SVT
supraventricular tachycardia
can do a defibrillation or treat with adenosine or vasovagal maneouvors
to prevent happening again = ablation (surgical correction of electric current)
how do we treat ventricular fibrillation or arrhythmia
immediate defibrillation
prevent with beta blockers or implanted cardiovascular defibrillator under the skin
how and when do we provide a pacemaker
above skin of heart we place the pacemaker in with wires in the veins of right atrium and ventricle
when bradycardic
give three types of heart devices we can implant
dual chamber pacemaker box = only for bradycardia
Cardioverter/Defibrillator = Treats ventricular tachycardia or VF. Can also pace bradycardias
Cardiac Resynchronisation Therapy (CRT) = Treats heart failure + bradycardia (CRT-P) + CRT-D also has ICD
when should angina prevent dental treatment
stable angina is fine and well controlled
if the pain comes when they are at rest or pain worsening, they should get this seen an d prevent treatment
when a patient has heart failure, when should we defer dental treatment
well controlled heart failure is safe, if on beta blockers or calcium blockers, breathless on exertion or can lie flat at night
if cannot lie flat at night, getting more breathless or swollen ankles, refer to GP immediately
after a heart attack, how do we manage dental treatment
at high risk of another heart attack
Recent MI (within 6 weeks); defer until 3-6 months post MI, longer if possible.
what type of arrhythmia should defer a dental treatment
when there are frequent attacks of disabling tachycardia (few times a week)
if a patient is awaiting valve surgery, how does this affect treatment
if stable, continue with treatment
try do treatment before as when valve replaced = more likely infective endocarditis
what are 95% of hypertensions?
‘essential’ - no secondary cause
what effects can untreated hypertension cause around the body
• Brain: thrombotic, thromboembolic and haemorrhagic stroke, multiinfarct dementia, hypertensive encephalopathy
• Heart: LVH, LV failure, coronary artery disease
• Kidney: renal, failure
• Eyes: hypertensive, retinopathy
what is the main factor contributing to atherosclerotic plaque and then give 3 other factors
hypertension 5-10x
smoking 2x
diabetes 2x
hyperlipidaemia 1.5x
obesity 1.5x
what does prognosis of hypertension depend on (4)
level of systolic and diastolic blood pressure
age, sex other risk factors
evidence of end-organ damage
improved with antihypertensive therapy
what are some non-pharma logical treatment of hypertension
stop smoking
reduce salt fat and alcohol intake
exercise more
reduce weight
control diabetes
give some common anti=hypertensive drugs
Thiazide diuretics
ACE inhibitors
Beta blockers]calcium ion channel blockers
what do diuretics do
reduce the amount of water in the body
inhibit reabsorption of ions into the blood
in turn reducing osmosis of water back into the blood
what is the function of thiazide diuretics and hen do we use them
inhibit NaCL reabsorption in proximal and early distal tubules of nephron
First line treatment of hypertension
what are some common side effects of anti-hypertensive drugs
rash
electrolyte disturbance (kidney acting)
postural hypotension
how does angiotensin II act
direct vasoconstrictor
stimulates adrenal glands to produce aldosterone
what frequent (and why) and infrequent side effects do ACE inhibitors usually have
cough - alters bradykinin degradation
infrequent:
-hypotension
-rash
hyperkalaemia
renal failure especially in presence of renal artery stenosis
loss of tate/alteration
what do ace inhibitors do
inhibit conversion of angiotensin I to angiotensin II
what a
if a patient has loss of taste and has high BP, what are they likely taking
ACE inhibitors
what are losartan, valsartan, candesartan (suffix sartan)
Angiotensin II receptor antagonists ARBs
compare sympathetic and parasympathetic pathways in term of neurostramsitter and function
S:
-norepinephrine
-increased contractility of heart
-increase heart rate
-increase vasoconstriction
P:
-Acetyl Choline
-opposite
how do beta blockers act
act as antagonists for beta-adrenoreceptors
variable selectivity for cardiac beta 1 receptors
what is the most and least selective beta blocker
propranolol = least
bisoprolol = most
what function do beta blockers have
reduce heart rate, blood pressure, cardiac output
what are some contraindications for beta blockers
asthma, uncontrolled heart failure, bradycardia
what common side effects do we get with beta blockers
fatigue
hypotension
cold peripheries
bronchospasm
impotence
what is the effect of calcium channel blockers
vasodilators = reduce systematic vascular tone
give 2 types of calcium channel blockers with examples
e.. Verapamil = cause bradycardia, inhibit AV node conduction (atrial fibrillation)
e.g. Amlodipine = may cause reflex tachycardia
what are common side effects for calcium channel blockers
flushing
headache
dizziness
hypotension
oedema
give 4 drugs used for anti-anginal purposes
beta blocker (hypertension)
calcium channel (hypertension)
nitrates
potassium channel activators
how do beta blockers help angina
beta adrenal receptor blockers
reduce heart rate, blood pressure and myocardial contractility
lower oxygen demand
put less stress on coronary arteries
why must beta blockers be introduced slowly if cardiac failure
may exacerbate cardiac failure symptoms:
peripheral vascular disease (leg pain) - claudication
cause bronchospasm
if a patient is on beta blockers, why can we not suddenly take them off
cause arrhythmia
worsening angina
MI
how do nitrates help angina (3)
Produce nitric oxide at the endothelial surface leading to vascular smooth
muscle relaxation and arteriolar and venous dilatation
Reduce myocardial oxygen demand (lower preload and afterload) and
increase myocardial oxygen supply (coronary vasodilatation)
what type of medication is GTN spray
nitrate anti-angina
what are the side effects of nitrates
headache, flushing, postural hypotension
why is postural hypotension important to dentistry
if a patient e.g. takes GTN spray in dental chair
then stands up, they will get postural hypotension
may faint, be aware of cause
how do calcium antagonists work
Lower myocardial oxygen demand by reducing blood pressure and myocardial contractility and increase myocardial oxygen supply by
dilating coronary arteries
what type of drugs are Verapamil and diltiazem and when should they NOT be used
calcium antagonists - use for arrythmia and angina
never use with heart failure as reduce contractility of the myocardium and heart rate
what is the only potassium channel activator that we use and what is its function
Nicordandil
arterial and venous dilators
angina relief
what side effects are there with potassium channel activators
can cause mucocutaneous ulceration - relegated to second line therapy
a patient has angina treatment but cant remember their medication but also has white ulceration in the mouth. what is their likely medication
ulceration is mucocutaneous
Nicorandil = potassium channel activator
how do antiplatelets work
Inhibit platelet aggregation and arterial thrombus formation, thus
preventing heart attack, stroke and CV death
how does Aspirin work
irreversibly blocks platelet cyclo-oxygenase (COX1) and the
production of thromboxane A2, a platelet activating substance
how do Clopidogrel, prasugrel and ticagrelor work
platelet ADP (P2Y12) receptor inhibitors (Clopidogrel irreversible, ticagrelor reversible)
used alone or, more often, in combination with aspirin
reduces platelet activation
compare Clopidogrel and ticagrelor
Both anti-platelet inhibit platelet ADP (P2Y12) receptor
Clopidogrel - irreversible
Ticagrelor - reversible
how does aspirin work
Aspirin – blocks platelet cyclo-oxygenase (COX1) and the
production of thromboxane A2, a platelet activating substance
how to statins work
Hydroxymethyl-glutaryl (HMG) CoA reductase inhibitors
Lower LDL cholesterol and may increase HDL cholesterol
Reduce risks of myocardial infarction, stroke and CV death
what is heart failure
an imprecise term describing the state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure
Associated with activation of RAS axis and sympathetic nervous system
what 2 factors is heart failure associated with
Associated with activation of renin-angiotensin system RAS axis
sympathetic nervous system
give 7 symptoms of heart failure
swollen/tender abdomen and loss of appetite
swollen ankles
breathlessness
struggle to sleep due to breathlessness
chronic tiredness
cough with frothy sputum
increased urination at night
what are the 3 types of diuretics
K sparing
Thiazides
Loop Diuretics
where do loop diuretics work
ascending portion of the loop of Henle
how and where do K sparing diuretics act
Inhibit reabsorption of Na in the distal convoluted and collecting tubule
(aldosterone antagonists)
how does aldosterone effect heart function
Retention Na+ and Retention H2O = oedema
Excretion K+ and Excretion Mg2+ = arrythmia
what is digoxin used for
slows conduction in atrial fibrillation
increases vagal tone
what Acronym helps remeber the treatment of hypertension
ABC
Ace inhibitors (most important)
Beta blockers
Calcium ion channel antagonists
what is thrombosis
Inappropriate blood coagulation within a vessel
compare venous and arterial thrombosis
arterial:
high pressure system
Thrombosis is platelet rich bound in fibrin
venous:
low pressure
low pressure system
fibrin rich, very few platelets
Non return valves
what happens if a non-return venous valve is damaged
discoloration of skin
swelling
pain
what are the 2 results of arterial thrombosis
Myocardial infarction
Thrombotic stroke
what are th reuslts of a venous thrombosis
Leg deep vein thrombosis (MI)
Pulmonary embolism (PE)
Cerebral venous thrombosis in the venous sinuses = severe headache, pain, nausea, double vision
what are the signs and symptoms of a cerebral venous thrombosis vs a stroke
Cerebral venous thrombosis in the venous sinuses = severe headache, pain, nausea, double vision
stroke usually caused by thrombosis in the carotid artery
unilateral drop of face, loss of speech, cannot touch nose
how many people with a DVt also have a PE
75% of people with DVT will also have a pulmonary embolism so both must be treated
in general terms how do we treat arterial thrombosis
antiplateletes
how do we treat venpous thrombosis
anticoagulants
explain formation of arterial thrombosis
Initial fatty streak under the endothelium
Plaque enlargement
Turbulence due to protrusion into lumen
Loss of endothelium and collagen exposure and pro-coagulants (collagen = prothrombotic)
Platelet activation and adherence = cascade triggered
PLatelet = fibrinogen –> fibrin
Fibrin meshwork deposition and red cell entrapment
More turbulence, more platelet and fibrin deposition
Thrombus of layers of platelets, firbin and red cells
what are the main risk factors for arterial thrombosis
Family history = hypercholesterolaemia
Diabetes mellitus
Hypertension
Hyperlipidaemia
Smoking - irritates endothelium accelerating arterial disease + peripheral vascular disease
Atrial fibrillation for stroke
congenital high levels of clotting factors e.g. FVIII
male sex
how many people above 80 have AF
10%
explain atrial fibrillation
Left atrium becomes enlarged starting to fibrillate uncontrollably = turbulent due to no co-ordination = pro-thrombotic
Irregularly irregular heart rhythm
4% in >60years, 8% in >80years
Left atrial thrombus
Embolization leads to stroke or limb emboli
Impaired cardiac output
Antiplatelet drugs are ineffective for AF
we recommend anticoagulants for this as there is high fibrin in this blood
how do we treat AF (3)
atrial fibrillation
Anticoagulation first so that when put into correct rhythm we don’t get embolism and as embolism is the biggest danger
Heart rate control: Beta blockers, Ca channel blocker, Digoxin, AV junction ablation
DC cardioversion in sedation
compare aspirin and clopidogrel
both irreversible COX I inhibitors
aspirin has GI affects, clopidogrel doesn’t
clopidogrel is more expensive
clopidogrel is a stronger antiplatelete
how does aspirin work
COX1 inhibitor
prevents formation of thromboxane which is a pro-platelet factor
Inhibition lasts for the lifespan of platelet: ≈ 1 week.
Risk reduction of non fatal vascular event by 30%.
Risk reduction of fatal vascular event by 15%.
must we stop antiplatelet drugs during dental procedures
aspirin unlikely to be needed to stop
clopidogrel is stronger so consider removal for a week prior
how do we treat an arterial thrombosis
fibrinolytics e.g. streptokinase
how do we prevent aterial thrombosis
lifestyle - reduce factors, stop smoking, lose weight, dietary changes
drugs = antiplateletes e.g. aspirin
how do fibrinolytics work e.g. streptokinase
activates plasminogen –> plasmin
this factor breaks down fibrin coagulations
high risk of bleeding
what are some indications for use of fibrinolytics
MI,
stroke within 3 hours,
Life-threatening PE
how do we treat MI
Percutaneous coronary intervention (with possible cardiac stenting)
Combined with 3 – 12 months aspirin + clopidogrel
Coronary artery bypass grafting
Carotid endarterectomy - stent carotid artery and require anticoagulant therapy therafter
what is conoarary artery bypass grafting and when is it done
open heart surgery swapping a vein from the leg into the heart to make a new coronary connection
done where it is not possible to stent
what is a percutaneous coronary intervention, when is it done and what must it be done with
where we use a cannula in the arm to gain access to the coronary arteries to remove a clot
we may then place a stent
it is done when a pt experiences a MI
must be followed by 3-12 months of aspirin and clopidogrel dual therapy
how does diabetes increase risk of arterial thrombosis
High blood sugar is toxic to endothelium and damages endothelium, increases fatty streak deposit
a patient is on clopidogrel and aspirin, what is their likely status
recently had a stent placed following an MI
what is a newly licensed way of reducing recurrent vascular events
Rivaroxaban (anticoagulant) has recently be licensed to prevent recurrent vascular disease in addition to aspirin (anti-platelet) (in low doses)
how does AF lead to strokes
- Blood pools in atria
- Blood clot forms
- Blood clot breaks off
- Blood clot travels to brain and blocks a cerebral artery
causing a stroke
how might high fibrin in blood lead to leg ulcers
high fibrin = increased risk of venous thrombosis
= deep vein insufficency
post thrombotic syndrome
leg ulcer
what can result of DVT
pulmanory emboli –> death or pulmanory hypertension
deep vein insufficency –> post thrombotic syndrome
what three factors affect venous thrombosis
hypercoagulability (acquired and inherited)
stasis (acquired)
vascular damage (aquire)
what increases risk of stasis –> venous thrombosis
aeroplane travel
hospitalisation
disability
what increases risk of stasis –> venous thrombosis
aeroplane travel
hospitalisation
disability
what are some inherited risks for venous thrombosis
antithrombin deficiency (10-40 fold increase, biggest risk)
Protein C deficiency
protein S deficiency
Factor V Leiden
what is the function of protein C and S
prevent factor VIII formation
deficiency in this = increased risk of venous thrombosis
what is the risk increase of venous thrombosis under hospitalisation
150 fold
what is the risk increase of venous thrombosis when pregnant
15 fold
how do we prevent DVT
Adequate hydration - reduce pressure
Early mobilisation - reduce stasis
Graduated elastic compression hosiery stockings, tighter in calves
screening for Protein C, Protein S, Factor V andantithrombin deficency
thromboprophylaxis
assess any patients in hospital for thrombophilias
what chemical prophylaxis can we give to prevent venous thrombosis
Low molecular weight heparin
Direct oral anticoagulants
prevents 50 – 70% of VTE
how do we prevent recurrent DVTs (3)
anticoagulants for 3 months after a first event.
Provoked events (OCP) do not need anticoagulation >3 months
Distal DVT do not need anticoagulation >3 months
Consider long term anticoagulation after 1st unprovoked thrombosis or a risk factor that is permanent
how can we prevent DVTs going to PE
vena cava filters
anticoagulants
