Cardiology Flashcards
Name the 4 valves of the heart and their positions?
Tricuspid - between R atrium and R ventricle.
Pulmonary - between R ventricle and pulmonary artery
Mitral - between L atrium and L ventricle
Aortic - between L ventricle and aorta
Name the order of auscultation of the 4 heart valves? (from R to L side of body)
Aortic
Pulmonary
Tricuspid
Mitral
What two heart valve disorders are most common among the elderly?
aortic stenosis
mitral regurgitation
which murmur causes a crescendo-decrescendo ejection systolic murmur that radiates to the carotids?
aortic stenosis
what is the pathophysiology of aortic stenosis?
Atherosclerotic and calcium deposits on the aortic valve, causing the valve to harden and tighten.
This overall reduces the amount of blood which can flow through into the aorta from the left ventricle.
what are some common causes of aortic stenosis?
atherosclerotic disease (I.e CVD)
age
rheumatic fever
what are some clinical signs on examination of aortic stenosis?
ejection systolic murmur radiating to carotids
narrow pulse pressure
slow rising pulse
thrill
what are some symptoms of aortic stenosis?
dyspnoea
syncope/presyncope
chest pain
what are some of the physiological consequences of aortic stenosis?
leads to left ventricular hypertrophy, as the heart pumps harder in order to compensate for the stenosed valve, and this eventually can lead to congestive cardiac failure
what are some investigations to consider in patients presenting with dyspnoea, chest pain or syncope - and you are suspicious of aortic stenosis?
ECHO
BNP
ECG
What is the management of aortic stenosis?
surgical AVR is the treatment of choice for young, low/medium operative risk patients.
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty
what medications must be avoided in aortic stenosis?
antihypertensives - they will reduce peripheral vascular resistance and preload, which overall reduces the hearts ability to maintain adequate output. Generally, surgical intervention is required for aortic stenosis rather than antihypertensives.
what valve disorder causes a pan systolic murmur, best heard at the apex and radiating to the axilla?
mitral regurgitation
how does mitral regurgitation lead to heart failure?
Mitral regurgitation causes heart failure primarily through chronic volume overload on the left ventricle, leading to ventricular dilation, reduced contractility, and subsequent left ventricular failure. The increased pressure in the left atrium and pulmonary circulation leads to pulmonary congestion and potentially pulmonary hypertension. As the disease progresses, these changes culminate in symptomatic heart failure, with both systolic and diastolic dysfunction, and eventually right-sided heart failure in severe cases.
what are the consequences of untreated mitral regurgitation?
heart failure - initially L sided heart failure, then R sided heart failure.
pulmonary hypertension
atrial fibrillation
what are some symptoms of mitral regurgitation?
fatigue
dyspnoea
nocturnal paroxsymal dyspnoea
orthopnea
palpitations
what are some risk factors for mitral regurgtitation?
Female sex
Lower body mass
Age
Renal dysfunction
Prior myocardial infarction
Prior mitral stenosis or valve prolapse
Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome
what is the management of mitral regurgitation?
if clinically stable and MR is chronic - trial of diuretics to reduce the preload, and vasodilators such as ACE-I and ARB’s.
if clinically unstable, or severe - surgical MR replacement or repair.
what are the clinical signs of left heart failure?
dyspnoea
PND
orthopnea
breathlessness on exertion
fatigue
chest pain
what are the clinical signs of right heart failure?
peripheral oedema
breathlessness
abdominal discomfort
hepatomegaly / splenomegaly due to overload
JVD
weight gain
what investigations would you arrange for a patient in which you suspected heart failure?
First line - BNP blood test
Additional investigations to consider -
ECG
ECHO
24 hour BP monitoring
24 ECG - if suspecting AF
what actions should be carried out based on the BNP level?
BNP > 2000 -> urgent referral to cardiology in 2 weeks
BNP 400- 2000 -> referral to cardiology in 6 weeks, and ECHO
BNP < 400 -> watch and wait
what factors can affect the BNP level?
chronic kidney disease - reduced exertion of BNP
pregnancy
liver disease
diabetes
COPD
sepsis
what is the first line management of heart failure?
ACE-I , BB + diuretics (BAD)
what is BNP?
a hormone produced mostly by the cardiac tissue in response to L heart strain
what drugs reduce BNP?
ACE-I
ARB
diuretics
what raises the BNP?
CKD
liver disease
diabetes
COPD
heart failure
MI
what classification is used for severity of heart failure?
New York Heart Association Classification (NYHA)
NYHA I
No symptoms, no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
First line medical management of heart failure?
ACE-I and Beta Blocker + diuretic
How does an ACE-I work?
Reduce afterload, decrease blood pressure, and prevent remodeling of the heart.
By inhibiting the production of ACE which converts angiotensin I to angiotensin II. The role of angiotensin II is to vasoconstrict, and so ACE inhibitors reduce vasoconstriction, overall reducing the blood pressure and after load.
Additionally, angiotensin II is responsible for causing the release of aldosterone. Aldosterone causes retention of sodium and water vi the kidneys, increasing the overall blood volume and causing hypertension. ACE-I inhibit this, leading to overall reduction in preload, and hypertension.
ACE-I also prevent harmful cardiac remodeling, and reduce the workload on the heart.
What are some examples of ACE-I?
Ramipril
Lisinopril
What are contraindications to the use of ACE-I?
If there is confirmed valvulopathy that is causing haemodynamic instability
angio-oedema
renal artery stenosis
pregnancy
hyperkalaemia
hyponatraemia
how does a beta blocker work in heart failure?
Reduced Heart Rate: Slowing the heart rate reduces the heart’s workload and allows more time for the heart to fill with blood during each beat, improving cardiac output.
Decreased Myocardial Oxygen Demand: By reducing the force of the heart’s contractions and lowering blood pressure, beta blockers decrease the heart’s oxygen demand, which is beneficial in heart failure.
Inhibition of Harmful Remodeling: Chronic activation of the sympathetic nervous system can lead to harmful changes in the heart’s structure (remodeling).
Beta blockers help prevent or reverse this remodeling, improving heart function over time.
what are some contraindications to beta blockers?
Uncontrolled heart failure
Asthma/severe COPD
Sick sinus syndrome
Concurrent verapamil use - can cause severe bradycardia
what is second line treatment for heart failure?
add in an aldosterone receptor antagonist (also known as mineralocorticoid receptor antagonists)
what are some examples of aldosterone receptor antagonists?
spironolactone
eplernone
how do aldosterone receptor antagonists work in heart failure?
Reduction of Fluid Retention: By inhibiting aldosterone, ARAs reduce sodium and water reabsorption in the kidneys, decreasing fluid buildup and relieving symptoms like edema and pulmonary congestion.
Decreased Blood Pressure: Lowering fluid volume helps reduce blood pressure, which can decrease the heart’s workload.
Prevention of Cardiac Remodeling: ARAs help prevent harmful changes in the heart’s structure and function, such as fibrosis and hypertrophy, improving overall heart function and symptoms.
what are some contraindications to the use of aldosterone receptor antagonists?
hyperkalaemia
severe renal impairment
Addisons disease
hypersensitivity to ARA
what is the third line management of heart failure?
Third-line treatment should be initiated by a specialist.
Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy.
how does ivabradine work?
Ivabradine is typically used in heart failure patients with a resting heart rate of ≥70 beats per minute despite optimal treatment with other heart failure medications, particularly when beta-blockers are contraindicated or not tolerated.
It acts on the funny channels in the SA, to reduce heart rate thus reducing the strain on the heart.
what are some side effects of ACE-I?
dry cough
fatigue
dizziness
headaches
what are some side effects of beta blockers?
fatigue
dizziness
nausea
constipation
cool peripheries
MOA of digoxin?
Increases myocardial contractility
Decreases conduction within the AV node
Indications of digoxin?
Atrial flutter
AF
Heart failure
Side effects of digoxin?
GI upset
Arrhythmia
Confusion
Dizziness
Blurred vision
how does heart failure cause hypertension?
The heart’s reduced ability to pump blood effectively leads to decreased renal perfusion. This stimulates the kidneys to retain sodium and water to compensate for the reduced blood volume, increasing blood volume and contributing to higher blood pressure. This also activates the RAAS, which leads to vasoconstriction, and further elevates blood pressure.
Heart failure also stimulates the sympathetic nervous system, leading to further vasoconstriction.
HTN stage 1
clinic BP > 140/90
ABPM > 135/80
HTN stage 2
clinic BP > 160/100
ABPM > 150/95
HTN stage 3 / severe
clinic BP > 180/110
when to offer treatment in stage 1 HTN?
if < 80 years and has -
Target organ damage
Established cardiovasular disease
Established renal disease
Diabetes
10 year risk >10%
when should you admit in severe hypertension?
Signs of retinal haemorrhage or papilloedema (accelerated hypertension)
New onset confusion, chest pain, acute kidney injury, heart failure
what are some causes of HTN in younger patients? (i.e. <40 years)
essential HTN (likely genetic)
endocrine:
- phaechromocytoma
- primary hyperaldosteronism (conn’s)
- cushings disease (excessive cortisol causes HTN)
- renal disease (i.e. renal artery stenosis, polycystic kidney disease)
- thyroid (both hyperthyroidism and hypothyroidism)
Cardiac:
- coarctation of the aorta
- congenital cardiac disease (HOCM)
Meds:
- COCP
- stimulants
Lifestyle:
- severe obesity
- high salt intake
patient < 40 years with HTN?
Refer to secondary care to consider underlying causes
BP targets in T1DM?
<135/85
Unless have albuminuria or 2 features of metabolic syndrome, then it is <130/80
Step 1 HTN management: <55 years or T2DM
ACE-I/ARB
Step 1 HTN management: > 55 years or black/carribean?
CCB
Step 2 HTN management: <55 years or T2DM
ACE-I/ARB plus CCB OR thiazide like diuretic
Step 2 HTN management: >55 years or black/caribbean
CCB plus ACE-I/ARB OR thiazide like diuretic
Step 3 HTN management
ACE-I/ARB + CCB + thiazide like diuretic
Step 4 HTN management
K <4.5: low dose spironolactone
K >4.5: alpha or beta blocker
Name some examples of ARB
Losartan
Candesartan
Irbesartan
MOA of spironolactone?
Potassium sparing mineralcorticoid receptor antagonist - antaognises the effects of aldosterone, meaning Na and water are not retained in the kidney, and so causing diuresis.
what are the contraindications to spironolactone
Addison’s disease
Hyperkalaemia
Acute renal insufficiency, significant renal compromise, anuria (means it will be ineffective as no aldosterone produced)
what are the 3 different categories of angina?
stable angina
unstable angina
non-cardiac chest pain
what is the diagnostic criteria for stable angina?
Three of the features:
Precipitated by physical exertion.
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.
what is the diagnostic criteria for unstable angina?
Two of the features:
Precipitated by physical exertion
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw or arms.
Relieved by rest of GTN within about 5 minutes.
In addition, atypical symptoms include gastrointestinal discomfort, and/or breathlessness, and/or nausea.
Risk factors for angina?
Increasing age.
Male sex.
The presence of cardiovascular risk factors (i.e. CKD, HTN, T2DM, obesity, cholesterol, and chronic inflammatory conditions such as RA)
A history of established coronary artery disease (for example previous myocardial infarction, coronary revascularization).
Family history of early MI
Management of first presentation of stable typical angina?
Referral to rapid access chest pain clinic
Commence GTN sublingual spray
ECG
what advice should you give a patient with stable typical angina - whilst they are awaiting rapid access chest pain clinic?
Instruct the person that if they experience chest pain they should:
Stop what they are doing and rest.
Use their glyceryl trinitrate spray or tablets as instructed.
Take a second dose after 5 minutes if the pain has not eased.
Call 999 for an ambulance if the pain has not eased 5 minutes after the second dose, or earlier if the pain is intensifying or the person is unwell.
what is the pharmacological first line treatment of angina?
Prescribe a beta-blocker or a calcium-channel blocker (CCB) as first-line regular treatment to reduce the symptoms of stable angina, depending on the person’s comorbidities, contraindications, and preference
beta blocker - better if HR > 70
CCB - better if HR <70, or if has HTN
what is the pharmacological second line treatment of angina?
beta blocker + CCB together
what is the third line treatment of angina?
If both beta-blockers and CCBs are contraindicated or not tolerated, consider monotherapy with one of the following drugs.:
A long-acting nitrate (such as isosorbide mononitrate).
Nicorandil.
Ivabradine.
Ranolazine.
what drug treatment should be offered for secondary prevention of further CVD in angina?
Consider low dose antiplatelet therapy - i.e. aspirin 75mg OD
Consider ACE-I - especially in patients who have T2DM, HF, CKD and HTN.
Consider statin.
in which patients with angina should you consider early referral to cardiologist ?
Previous myocardial infarction, coronary artery bypass graft, or percutaneous transluminal coronary angioplasty and development of angina.
ECG (electrocardiographic) evidence of previous myocardial infarction or other significant abnormality.
Newly diagnosed atrial fibrillation and angina.
Heart failure and angina.
An ejection systolic murmur suggesting aortic stenosis.
Any suggestion of hypertrophic cardiomyopathy (for example by family history, physical examination, or ECG).
what are some causes of angina?
cardiac causes:
- atherosclerotic disease in the blood vessels supplying the heart
- left ventricular hypertrophy (this can happen in cardiomyopathies, HTN, aortic stenosis, AF)
non-cardiac causes:
- anaemia
- blood loss
how should a patient with angina who is considered high risk for CVD be managed?
optimise management of comorbidities i.e. heart failure, CKD, T2DM, HTN
advice to stop smoking
encourage eating a cardioprotective diet
encourage increase in physical activity - within the limits of what is comfortable for the patient
limit alcohol consumption
how often should patients with angina have a routine review with the GP?
Review the person every 6 months to 1 year depending on the stability of their angina and their comorbidities.
what should be covered during a routine angina review?
review symptoms - severity, frequency etc.
review CVD risk and any new modifiable risk factors
when should you refer a patient to hospital with HTN?
A clinic blood pressure of 180/120 mmHg and higher with:
Signs of retinal haemorrhage and/or papilloedema (accelerated hypertension), or
Life-threatening symptoms, such as new onset confusion, chest pain, signs of heart failure, or acute kidney injury.
Suspected phaeochromocytoma, for example labile or postural hypotension, headache, palpitations, pallor, abdominal pain, or diaphoresis.
what are the symptoms of infective endocarditis?
majority of patients present with fever, chills, poor appetite, weight loss, malaise, systemic illness
some present with heart failure symptoms
heart murmur
what is the pathophysiology of infective endocarditis?
all instances begin with a non-infective sterile thrombus which is the prequisite for bacterial adhesion and invasion.
following thrombus formation, there is invasion of the thrombus with bacteria.
what are the most common organisms involved in infective endocarditis?
staphylococcus aureus - most common with prosthetic valves, acute IE and IE relating to drug misuse
streptococci - S viridans for subacute cases
pseudomonas aeruginosa
which valves are most commonly affected by IE?
mitral valve - most common
aortic valve - second most common
tricuspid valve
pulmonary valve- rare
what is the first line medication for atrial fibrillation?
first line - rate control
beta blockers - bisoprolol
can also use CCB + digoxin
and calculate CHA2DS2 VASC score = start anticoagulation
what is dabigatran?
direct thrombin inhibitor - can be used as anticoagulant
when can dabigatran be used for anticoagulation?
non valvular AF AND -
- prx stroke
- EF <40%
- symptomatic HF
- age 75 years and older
- age 65 years or older with - DM, CAD or HTN
OR prophylaxis of VTE after hip or knee replacement
how do statins work?
inhibit HMC- CoA reductase, the rate limiting enzyme in hepatic cholesterol synthesis
what level of LFT derrangement would prompt discontinuation of statins?
if AST > 3x the upper limit of the reference range
what medications interact with statins?
MACROLIDES!!! - erythromycin/clarithromycin
what are common S/E of statins?
myopathy
liver impairement
when should statins be taken?
at night time - as overnight is when most cholesterol synthesis takes place
when should statins be increased?
if non-HDL not reduced by > 40%
what dose of atrovastatin is used for primary prevention?
20mg
what dose of statin is used for secondary prevention?
80mg
what are the side effects of ACE-I?
cough
angiodoema
hyperkalaemia
when are ACE-I contraindicated?
pregnancy
breast feeding
aortic stenosis - hypotension
renovascular disease i.e. renal artery stensosis
what are the contraindications to starting BB?
2nd/3rd degree heart block
uncontrolled HF
bradycardia < 60bpm
hypotension
arrythmias
bronchospasm / copd
severe PAD
what should be done before starting BB?
ECG
what are common SE of BB?
hypotension
bradycardia
cool peripheries
dizziness
nausea
headache
syncope
what are drug interactions for BB?
interacts with dihydropiridine CCB - hypotension
verapamil
anti-arrythmitic
digoxin
antipsychotics
what are the two classes of CCB?
non-dihydropiridine - verpamil/digoxin
dihydropiridine - amlodipine/lercanidipine/nifedipine
where do non-dihydropiridine CCB work?
on the SA node and AV node - reducing HR
on cardiac tissue - regulating arrhythmias
where do dihydropiridine CCB work?
peripheral vascular tissue - vasodilation, reducing BP and load on the heart
what are contraindications to CCB?
AF
HF
severe bradycardia
third degree heart block
sick sinus syndrome
what are SE of CCB?
flushing , headaches, postural hypotension, swelling - vasodilation SE
dizziness
GI disorders
malaise
fatigue
Management of acute MI in GP?
call 999
full set obs
stat dose aspirin 300mg
GTN sublingual if available
O2 if SpO2 < 94%
ECG if able - do not delay calling 999 for this
what are the shockable rhythms?
VT/VF
what are the non-shoackable rhythms?
asystole/PEA
what are the resus guidelines for BLS?
30:2 chest compressions
attach defib - if shockable - shock and resume CRP for 2 mins
if not shockable, cont for 2 mins then recheck
causes of acute onset chest pain?
ACS
pericarditis
aortic dissection
aortic aneurysm
PE
what are causes of heart failure?
High output - HTN, pagets disease, AV malformation
increased preload -
MR , fluid overload
increased after load -
AS, HTN
Decreased heart contracitility -
IHD, post MI, arrhythmias, cardiomyopathy, meds
when should specialist referral be made for heart failure?
if diagnosis unclear
severe
symptoms not managed with BAD
co-current angina/AF or arrhythmias
co-morbidities which may complicate the HF - COPD, renal failure, anaemia, thyroid disease, gout
women who are trying to get pregnant with heart failure
what treatments could specialists consider for heart failure?
SGLT-2 inhibitor
replace ACE with sacubitril valsartan
Ivabradine
hydralazaine
digoxin
what medications should be avoided in heart failure?
pioglitazone - can exacerbated fluid retention
NSAID’s / corticosteroids - can cause fluid retention
verapamil
flecanide - class 1 antiarrhytmics
what medications are used to manage hypertension in pregnancy?
oral labetalol first line
nefedipine is second line
what are the causes of high cholesterol?
primary - familial hypercholesterolaemia
secondary - lifestyle
when should hypercholesterol patients be referred for specialist care?
if total cholesterol > 9
non hdl > 7.5
what are the three different types of AF>
new onset < 7 days
permanent AF > 7 days
paroxysmal AF
who should be considered for rhthym control of AF?
haemodynamically unstable
new onset < 48 hours
have reversible causes
heart failure caused by AF
for whom cardio decide rhythm control more appropriate
what investigations should be done for AF in primary care?
ECG
bloods
ECHO
can do CXR if r/o underlying chest cause
ambulatory ECG if paroxsysmal
what is the management of AF in primary care if patients are stable?
calculate chads2vasc + ORBIT scores
start anticoagulation if needed
consider rate control - BB or CCB non-dihydropiridine
what is the chads2vasc score?
score to calculate persons risk of stroke
what is in the chads2vas score?
Congestive heart failure
Hypertension
Age > 75 yrs -2
DM
Stroke/TIA -2
vascular disease
age 64-75 -1
sex - female 1
what chads2vasc score indicates anticoagulation needed?
score of 1 or more for males
score of 2 or more for females
who should the chads2vasc be calculated for?
AF - paroxysmal or persistent
atrial flutter
what does the orbit score calculate?
risk of bleeding - can be used to decide whether to start anticoagulation
what is the orbit score made of?
Older age > 74 years
Reducing haemoglobin < 130 males / < 120 females
Bleeding hx (GI bleed/intracranial bleeding/stroke)
Impairement of kidneys eGFR <60
treatment with antiplatelets
which orbit score is low, medium or high?
low 0-2
medium 3
high 4-7
what is the MOA of DOAC’s?
apixiban , rivaroxaban and edoxaban inhibit factor Xa
dabigitran inhibits thrombin
what is the MOA of warfarin?
vitamin K antagonist
what is the recommendation for DOACS when someone is having minor surgery?
advised not to stop the anticoagulation
they can be performed 12-24 hours post last dose
what is the recommendation for DOACS when someone is having surgery with low bleeding risk?
DOAC should be stopped at least 24 hours prior to the surgery
If CrCL 15-29 then should be stopped at least 36 hours before
what is the recommendation for DOACS when someone is having high bleeding risk?
stop 72 hours prior to the surgery
what is the recommendation for DOAC for people who require low risk dental procedures?
treat without interrpting DOAC treatment
what is the recommendation for DOAC for people who require higher risk dental procedures?
delay morning dose of DOAC
then take the dose 4 hours after haemostasis achieved
then take next day dose as normal
what monitoring is needed for person taking DOAC?
at start of treatment - measure baseline clotting/FBC/renal/LFT
review after 1 month to assess SE/tolerance/adherance
check renal function + FBC yearly after that
what ECG changes are seen in RBBB?
QRS > 120m/s
MaRoW - M waves in V1-3
W wave (slurred S) - in V6
what is the pathophysiological cause of RBBB?
change in morphology of R ventricles - leading to delayed repolarisation
causes of RBBB?
most common age
R ventricular hypertrophy
chronically increased R ventricular pressure
PE/MI
cardiomyopathy
myocarditis
causes of LBBB?
always pathological
MI/HTN
AS
cardiomyopathy
what are the most common causes of palpitations?
atrial / ventricular ectopics
tachycardias - i.e. SVT
AF
atrial flutter
what causes SVT?
can be associated with exertion/caffeine/alcohol/drugs
usually in women - 75%
self-limiting but can persist acutely
management of acute SVT?
valsalva manouver
IV adenosine
electrical cardioversion
management of palpitations in GP (palpitations that are not currently occuring)?
arrange bloods - check TFT/anaemia
resting ECG -> if normal ambulatory
if SVT identified - refer to cardio
if normal but highly suspicious of SVT - refer to cardio
when should patients with palpitations be urgently referred to cardio?
history of syncope
palpitations precipitated by exercise
FHx of sudden cardiac death unnder 40 years
ECG - shows second or third degree heart block
when should patients with palpitations be referred routinely to cardio
abnormality on ECG other than 2nd/3rd degree heart block
hx of sustained SVT/AF/flutter
hx of associated HTN/heart failure
symptoms in keeping with paroxysmal SVT but not picked up on ambulatory readings
ventricular ectopics with underlying heart disease OR if they are frequent
when is referral to cardiology generally not needed for patients with palpitations?
if normal ECG and smyptoms are:
not provoked by exercise
not associated with light-headedness, syncope, breathlessness, chest pain
no structure heart disease/heart failure/hypertension
no FHx of sudden onset cardiac death
what are the ECG findings in first degree heart block?
PR interval > 300ms
what are the causes of first degree heart block?
genetic - normal variant
athletic training
medications - BB, CCB, digoxin, amiodarone
IHD/inferior MI/myocarditis - if symptoms suggestive of this
management of first degree heart block?
if no other symptoms and incidental finding - no management needed
what are the two different types of second degree heart block?
mobitz 1 and mobitz 11
what are the ECG findings of mobitz type I?
PR interval increases with each beat until QRS complex dropped
causes of mobitz type I?
increased vagal tone
athletes
can be normal
medications - BB/CCB/amiodarone/digoxin
myocarditis
MI
management of mobitz type 1?
if asymptomatic - does not need treatment
if symptomatic - usually responds well to atropine
all need ref to cardiology
rarely pacing
what are the ECG findings in mobitz II?
PR interval > 300 ms
QRS complex dropped at random
what are the causes of mobitz II?
usually due to structural damage ot the heart
myocarditis
autoimmune - SLE/systemic sclerosis
infiltrative disease - sarcoid, amyloidosis, haemochromatosis
anterior MI
medications
management of mobitz II?
needs immediate admission - much more likely to cause haemodynamic instability and sudden death , needs pacing
what is rheumatic fever?
autoimmune response following B haemolytic strep infection (i.e. usually occurs 2-4 weeks after sore throat)
what is the pathophysiology of rheumatic fever?
strep infecion (sore throat usually) -> activates immune system -> it is thought the antigen of strep infection is similar to the M protein and so they cross react and attack myosin and smooth muscle of arteries
what are the diagnostic features of rheumatic fever?
recent strep infection and either 2 major criteria or 1 major with 2 minor
what are the major criteria for rheumatic fever?
erythema marginatum
sydenhams chorea
polyarthritis
carditis and valvulitis
subcutaneous nodules
what is the minor criteria for rheumatic fever?
raised ESR/CRP
pyrexia
arthralgia
prolonged PR interval
management of rheumatic fever?
refer to cardio urgently
usually involves bed rest, penicillin abx, ECHO and ongoing monitoring
what causes sudden onset sharp constant sternal pain relieved by sitting forwards?
pericarditis
what are the symptoms of pericarditis?
sharp constant pain relieved by sitting forwards
radiates to L shoulder arm or into abdomen
worse lying on the L side
pleuritic
pericardial rub can be present
what are the causes of pericarditis?
viral infections
tuberculosis
uraemia
post MI
radiotherapy
connective tissue disease
hypothyroidism
malignancy
trauma
what ECG findings are seen in pericarditis?
saddle shaped ST elevation
PR depression
management of pericarditis?
refer for inpatient care
what is acute myocarditis?
acute inflammation of the myocardium of the heart, most typically caused by viral infections
how to acute myocarditis present?
similar to MI - chest pain + palpitations - referal for inpatient care needed
what is the inheritance pattern for HOCM if genetic?
autosomal dominant
if recurrance of DVT whilst on warfarin what should be done?
INR increased to 3.5
what investigations must be done before starting a patient on amiodarone?
TFT
LFT
U+E
CXR
what monitoring should be done for a patient on amiodarone/?
TFT + LFT every 6 months
what are the adver effects of amiodarone?
CHIPCHANGE
Cutaneous photosensitivty
Hepatic dysfunction
Increased LDL’s
Pulmonary fibrosis
CNS effects
Hyper/hypothyroidism
Asymptomatic corneal deposits
Neuropathy
GI dysfunction
Enahances effects of warfarin
Important to remember - pulmonary fibrosis, hyper/hypothyroidism, neuropahty, warfarin and liver
what are the DVLA rules for driving after ICD has been inserted?
off for 6 months if inserted for sustained ventricular arrhtyhmia
if implanted prophylactically off for 1 month
what are the DVLA rules for driving after pacemaker insertion?
off for 1 week
what are the DVLA rules for driving after CABG>
no driving for 4 weeks
what are the DVLA rules for driving after heart transplant?
no driving for 5 weeks
when should the DVLA be notified regarding an abdominal aneurysm?
if greater than 6cm - must be notified
what are the DVLA rules for driving re elevtice angioplasty?
1 week off
what is the BP target for patients on antihypertensives?
140/90
< 150/90 for those over 80 years
what are the ECG findings of WPW?
slurred delta wave
reduced PR interval
what anticoagulation is given for bioprosthetic heart valves?
warfarin for first 3 months then stopped
aspirin life long thereafter
no other anticoagulation needed
how long do you give anticoagulation in unprovoked DVT/PE?
6 months
how long do you give anticoagulation in provoked DVT/PE
3 months
what size aortic aneurysm disqualifies a patient from driving?
6.5cm
what should be done if pt on warfarin and INR 5-8 but no bleeding
Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
what should be done if INR 5-8 in pt on warfarin but having minimal bleeding?
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
what should be done if INR > 8 in pt on warfarin but having no bleeding?
Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
which ECG leads are inferior / R coronary artery?
II, III, aVF
which are the anteroseptal leads?
V1-V4
what artery supplies the anteroseptal leads?
LAD
which leads are the anterolateral leads?
V1-6, I, aVL
which artery supplies the anterolateral leads?
Proximal left anterior descending
which are the lateral leads ECG?
I, aVL +/- V5-6
which artery supplies the lateral leads?
circumflex
what is takayasu arteritis?
Takayasu’s arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse.
what are the symptoms of takayasu arteritis?
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)
what is microvascular angina?
angina - but normal coronary arteries on angiogram - no treatment needed unless symptomatic
what size of aortic anuerysm defines it as a aortic aneurysm?
3cm
when is elective surgery considered for aortic aneurysms?
size > 5.5cm
what tests would you do for a patient who has suspected familial hypercholesterolaemia?
LDL-C
DNA testing
how long must patients wait before returning to heavy lifting job after MI?
3 months
how long do patients have to wait before flying after an MI?
7-10 days
what is brugada syndrome?
a relatively common condition associated with sudden death in patients with structurally normal hearts and caused by a mutation in the cardiac sodium channel gene.
what are the typical findings of brugada syndrome on ECG?
‘Brugada sign’: coved ST segment elevation of at least 2mm in V1 and/or V2, followed by a negative T wave.
