Cardiology Flashcards
What does the P wave represent on ECG
What does the PR interval represent electrically and physiologically and how long is this?
Atrial depolarisation
The atria contracts during the PR interval, the PR interval is the time taken for electrical activity to spread from the SA node to the AV node
This is from the start of the P wave to the start of the QRS complex
120-220ms, 3-5 small squares
What does the QRS complex on the ECG represent?
How long does this take?
ventricular depolarisation
120ms 3 small squares
What does the ST segment on the ECG represent?
end of the S wave to the start of the T wave
ventricular contraction
What does the T wave represent?
Venticular repolarisation
what is the QT interval and how long should this be?
start of the Q wave to the end of the T wave
400-440ms prolonged is more than 450
What causes the first heart sound (S1)
-what would cause this to be loud
-what would cause this to be soft
• Closure of mitral and tricuspid valves
• Soft if long PR or mitral regurgitation
• Loud in mitral stenosis
• Variable intensity in complete heart block
What causes the second heart sound S2?
caused by the closure of the aortic valve (A2) closely followed by that of the pulmonary valve
(P2)
What would cause a loud S2?
Causes of a loud S2
• Hypertension: systemic (loud A2) or pulmonary (loud P2)
• Hyperdynamic states
• Atrial septal defect without pulmonary hypertension
What would cause a soft S2?
Causes of a soft S2
• Aortic stenosis
What would cause a fixed split S2?
What would cause a widely split s2?
Causes of fixed split S2
• Atrial septal defect
Causes of a widely split S2
• Deep inspiration
• RBBB
• Pulmonary stenosis
• Severe mitral regurgitation
what would Cause a reversed (paradoxical) split S2 (P2 occurs before A2)?
Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)
• LBBB
• Severe aortic stenosis
• Right ventricular pacing
• WPW type B (causes early P2)
• Patent ductus arteriosus
What is S3? what is this caused by?
• Caused by diastolic filling of the ventricle
• Considered normal if < 30 years old (may persist in women up to 50 years old)
• Heard in left ventricular failure, constrictive pericarditis
• Gallop rhythm (S3) is an early sign of LVF
What is S4? what is this caused by?
• may be heard in aortic stenosis, HOCM, hypertension
• caused by atrial contraction against a stiff ventricle
• in HOCM a double apical impulse may be felt as a result of a palpable S4
what is pulsus parodoxus?
-when is this seen?
Pulsus parodoxus
• Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or
absent pulse in inspiration
• Severe asthma, cardiac tamponade
when is a slow rising pulse seen?
Slow-rising/plateau
• Aortic stenosis
when is a collapsing pulse seen?
Collapsing
• Aortic regurgitation
• Patent ductus arteriosus
• Hyperkinetic (anemia, thyrotoxic, fever, exercise/pregnancy)
what is pulsus alterans? when is this seen?
Pulsus alternans
• Regular alternation of the force of the arterial pulse
• Severe LVF
what is a bisferiens pulse? when is this seen?
Bisferiens pulse
• ‘Double pulse’ - two systolic peaks
• Mixed aortic valve disease
*HOCM may occasionally be associated with a bisferiens pulse
when is a jerky pulse felt?
‘Jerky’ pulse
• Hypertrophic obstructive cardiomyopathy
What does the ‘a’ wave in JVP represent?
-when is this large?
-what are cannon ‘a’ waves? when is this seen?
‘a’ wave = atrial contraction
• Large if high atrial pressure e.g. Tricuspid stenosis, pulmonary stenosis, pulmonary
hypertension
• Absent if in atrial fibrillation
Cannon ‘a’ waves
• Caused by atrial contractions against a closed tricuspid valve
• Are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm,
single chamber ventricular pacing
what causes the ‘c’ wave in jvp?
-is this normally visible?
• Closure of tricuspid valve
• Not normally visible
when are giant ‘v’ waves seen in JVP?
• Giant v waves in tricuspid regurgitation
what is the ‘x’ descent in JVP?
Fall in atrial pressure during ventricular systole
what is the ‘y’ descent in JVP?
Opening of tricuspid valve
what happens to blood pressure during exercise?
Blood pressure
• Systolic ↑, diastolic ↓
• Leads to ↑ pulse pressure
• In healthy young people the ↑ in MABP is only slight
what happens to cardiac output in exercise?
-what does this result from?
-what happens to heart rate and stroke volume?
• ↑ in cardiac output may be 3-5 fold
• Results from venous constriction, vasodilation and ↑ myocardial contractibility, as well as from
the maintenance of right atrial pressure by an ↑ in venous return
• Heart rate up to 3-fold ↑
• Stroke volume up to 1.5-fold ↑
how is the left ventricular ejection fraction worked out?
how is stroke volume worked out?
Left ventricular ejection fraction = (stroke volume / end diastolic LV volume) * 100%
Stroke volume = end diastolic LV volume - end systolic LV volume
what are normal ECG variants seen in an athlete?
In an athlete:
• Sinus bradycardia
• Junctional rhythm
• First degree heart block
• Wenckebach phenomenon
what are ECG changes seen in hypothermia?
• Bradycardia
• ‘J’ wave - small hump at the end of the QRS complex
• First degree heart block
• Long QT interval
• Atrial and ventricular arrhythmias
what are the ECG changes seen in digoxin toxicity?
• Down-sloping ST depression (‘reverse tick’)
• Flattened/inverted T waves
• Short QT interval
• Arrhythmias e.g. AV block, bradycardia
what are causes of ST depression on the ECG?
• Normal if upward sloping
• Ischemia
• Digoxin
• Hypokalemia
• Syndrome X
what is seen on the ECG in LBBB?
what are the causes?
W in V1 and M in V6
Causes:
• Ischemic heart disease
• Hypertension
• Cardiomyopathy
• Idiopathic fibrosis
what is first degree heart block? what causes this?
PR interval is lengthened beyond 0.20 seconds (>5small squares)
Also named: 1st degree heart block
Causes:
• Idiopathic
• Ischemic heart disease
• Digoxin toxicity
• Hypokalemia*
• Rheumatic fever
• Aortic root pathology e.g. Abscess secondary to endocarditis
• Lyme disease
• Sarcoidosis
• Myotonic dystrophy
what causes LAD?
left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
what are causes of RAD?
• Right ventricular hypertrophy
• Left posterior hemiblock
• Chronic lung disease
• Pulmonary embolism
• Ostium SECUNDUM ASD
• Wolff-parkinson-white syndrome* - left-
sided accessory pathway
• Normal in infant < 1 years old
• Minor RAD in tall people
Who does isolated systolic hypertension affect?
Isolated systolic hypertension (ISH) is common in the elderly, affecting around 10% of
people older than 70 years old.
How can you group secondary causes of hypertension?
Renal disease - 80%
Endocrine disorders
Others
o Pregnancy
o Coarctation of the aorta
o The combined oral contraceptive pill
o Steroids
o Maoi
What are the renal causes of secondary hypertension?
o Glomerulonephritis
o Pyelonephritis
o Adult polycystic kidney disease
o Renal artery stenosis
what are the endocrine disorders that can causes secondary hypertension?
o Cushing’s syndrome
o Primary hyperaldosteronism including Conn’s syndrome
o Liddle’s syndrome
o Congenital adrenal hyperplasia (11-β hydroxylase deficiency)
o Pheochromocytoma
o Acromegaly
what are direct renin inhibitors?
-how does this work?
-what have trials looked into?
-adverse effects?
-what does this have a role in?
• e.g. Aliskiren (branded as Rasilez)
• By inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
• No trials have looked at mortality data yet. Trials have only investigated fall in blood pressure.
Initial trials suggest aliskiren ↓ blood pressure to a similar extent as angiotensin converting
enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
• Adverse effects were uncommon in trials although diarrhea was occasionally seen
• Only current role would seem to be in patients who are intolerant of more established
antihypertensive drugs
what are three centrally acting antihypertensives?
• Methyldopa: used in the management of hypertension during pregnancy
• Moxonidine: used in the management of essential hypertension when conventional
antihypertensives have failed to control blood pressure
• Clonidine: the antihypertensive effect is mediated through stimulating α-2 adrenoceptors in the
vasomotor center.
what is the blood pressure target in DM?
what drugs are used first line?
which drugs should be avoided?
Hypertension and DM is an added cardiovascular risk factor for diabetics and should therefore by
actively looked for and treated. It is also a risk factor for the development of diabetic nephropathy.
Selected points
• The blood pressure target for diabetics is 140/80 mmHg. If there is end-organ damage the target
is 130/80 mmHg
• ACE inhibitors are first-line*. Otherwise managed according to standard NICE hypertension
guidelines
• BNF advises to avoid the routine use of beta-blockers in uncomplicated hypertension, particularly when given in combination with thiazides, as they may cause insulin resistance,
impair insulin secretion and alter the autonomic response to hypoglycemia
*increase insulin sensitivity and can therefore theoretically cause hypoglycemia - rarely clinically
relevant
what are the clinical features of pericarditis?
• Chest pain: may be pleuritic. Is often relieved by sitting forwards
• Other symptoms include non-productive cough, dyspnea and flu-like symptoms
• Pericardial rub
• Tachypnea
• Tachycardia
what are the causes of pericarditis?
• Viral infections (Coxsackie)
• TB
• Uremia (causes ‘fibrinous’ pericarditis)
• Trauma
• Post MI, Dressler’s syndrome
• Connective tissue disease
• Hypothyroidism
what ECG changes are seen in pericarditis?
ECG changes
• Widespread ‘saddle-shaped’ ST elevation
• PR depression
what are the causes of myocarditis?
Causes
• Viral: coxsackie, HIV
• Bacteria: diphtheria, clostridia
• Spirochetes: Lyme disease
• Protozoa: Chagas’ disease, toxoplasmosis
• Autoimmune
• Drugs
what is the clinical presentation of myocarditis?
• Usually young patient with acute history
• Chest pain, SOB
what are risk factors for endocarditis? which is the strongest one?
the strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. Other factors include:
• Previously normal valves (50%, typically acute presentation)
• Rheumatic valve disease (30%)
• Prosthetic valves
• Congenital heart defects
• Intravenous drug users (IVDUS, e.g. Typically causing tricuspid lesion)
what are the causes for endocarditis?
-most common
-seen in prosthetic valves
-seen in IVDUs
-seen in colorectal ca
-which is a complication of colonic resection?
-culture -ve causes?
Causes
• Streptococcus viridans (prev. Most common cause)→ has good prognosis, poor dental hygiene
• Staphylococcus epidermidis (especially prosthetic valves)
• Staphylococcus aureus (especially acute presentation, IVDUS most common cause)
• Streptococcus bovis is associated with colorectal cancer
• Bacteroides fragilis endocarditis is very rare complication of colonic resection, bacteria reaches
heart via venous return, this is why it affects right > left side → Treat with Metronidazole
• Non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic
endocarditis
Culture negative causes (BP-CHB)
• Brucella
• Prior antibiotic therapy
• Coxiella burnetii
• HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
• Bartonella
Following prosthetic valve surgery Staphylococcus epidermidis is the most common organism in the
first 2 months and is usually the result of perioperative contamination. After 2 months the spectrum of
organisms which cause endocarditis return to normal, except with a slight ↑ in Staph aureus infections
what are 4 poor prognostic factors in endocarditis?
• Staph aureus infection (see below)
• Prosthetic valve (especially ‘early’, acquired during surgery)
• Culture negative endocarditis
• Low complement levels
what is the mortalitis according to organism in endocarditis
-staphylococci
-bowel organism
-streptococci
Mortality according to organism
• Staphylococci - 30%
• Bowel organisms - 15%
• Streptococci - 5%
how is endocarditis diagnosed?
• Pathological criteria positive, or
• 2 major criteria, or
• 1 major and 3 minor criteria, or
• 5 minor criteria
what are pathological criteria in the diagnosis of endocarditis?
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
(valve tissue, vegetations, embolic fragments or intracardiac abscess content)
what are the major criteria in the diagnosis of endocarditis?
- Positive blood cultures
• Two positive blood cultures showing typical organisms consistent with infective endocarditis,
such as Streptococcus viridans and the HACEK group.
• Persistent bacteremia from two blood cultures taken > 12 hours apart or three or more positive
blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis.
• Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci.
• Positive molecular assays for specific gene targets - Evidence of endocardial involvement
• Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation
or dehiscence of prosthetic valves), or
• New valvular regurgitation
what are the minor criteria in the diagnosis of endocarditis?
• Predisposing heart disease
• Microbiological evidence does not meet major criteria
• Fever > 38oc
• Vascular phenomena: major emboli, splenomegaly, clubbing, splinter hemorrhages, petechiae
or purpura
• Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots (boat shaped
hemorrhages in retina)
• Elevated CRP or ESR
what is the current management for endocarditis?
-inital blind therapy with and without prosthetic valve
-in staphyloccal endocarditis
-in streptococcal endocarditis
• Initial blind therapy - flucloxacillin + gentamicin (benzylpenicillin + gentamicin if symptoms
less severe)
• Initial blind therapy if prosthetic valve is present or patient is penicillin allergic - vancomycin
+ rifampicin + gentamicin
• Endocarditis caused by staphylococci - flucloxacillin (vancomycin + rifampicin if penicillin
allergic or MRSA)
• Endocarditis caused by streptococci → benzylpenicillin + gentamicin (vancomycin +
gentamicin if penicillin allergic)
what are the 7 indications for surgery in endocarditis?
Indications for surgery
• Severe valvular incompetence (both native and prosthetic)
• Early prosthetic valve endocarditis
• Aortic abscess (often indicated by a lengthening PR interval)
• Infections resistant to antibiotics/fungal infections
• Cardiac failure refractory to standard medical treatment
• Recurrent emboli after antibiotic therapy
• HACK group, brucella, coxilla, pseudo- aeruginosa and vancomycin resistant enterococci
when should patients be given antibiotic prophylaxis for endocarditis?
• If a person at risk of infective endocarditis is receiving antimicrobial therapy because they are
undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected
infection they should be given an antibiotic that covers organisms that cause infective
endocarditis
What did SAVE, SOLVD, CONSENSUS trials show with regards to heart failure?
ACE inhibitors improve mortality in heart failure
what did RALES trial show with regards to heart failure?
Spironalactone improves mortality in heart failure
what did CIBIS trial show with regards to heart failure?
β-blockers improve mortality in heart failure
what did the VHEFT-1 trial show with regards to heart failure?
Hydralazine with nitrates improve mortality in heart failure
what is the management of heart failure?
-what vaccines should be given?
-does digoxin have a role?
• All patients should be given an ACE inhibitor unless contradictions exist
• Once an ACE inhibitor has been introduced a β-blocker should be started regardless of whether
the patient is still symptomatic
• Offer annual influenza vaccine
• Offer pneumococcal vaccine
Digoxin has also not been proven to ↓ mortality in patients with heart failure. It may however improve
symptoms due to its inotropic properties. Digoxin is strongly indicated if there is coexistent atrial
fibrillation
what is used to classify severity of heart failure?
(NYHA) The New York Heart Association (NYHA) classification is widely used to classify the
severity of heart failure:
describe the stages of heart failure with NYHA
NYHA Class I
• No symptoms
• No limitation: ordinary physical exercise does not cause undue fatigue, dyspnea or palpitations
NYHA Class II
• Mild symptoms
• Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue,
palpitations or dyspnea
NYHA Class III
• Moderate symptoms
• Marked limitation of physical activity: comfortable at rest but less than ordinary activity results
in symptoms
NYHA Class IV
• Severe symptoms
• Unable to carry out any physical activity without discomfort: symptoms of heart failure are
present even at rest with ↑ discomfort with any physical activity
describe the treatment of acute pulmonary oedema
• High-flow oxygen
• Furosemide 0.5-1 mg/kg IV
• Morphine 2-4 mg IV
• Sublingual nitroglycerine (GTN).
• Steps then are dictated by the systolic BP after initial treatment:
o If the BP is >100 mmHg, start IV nitroglycerine 10-20 μg/min
o BP of 70-100 mmHg, with no shock start IV dobutamine 2-20 μg/min
o If the BP is 70-100 mmHg with shock, start IV dopamine 5-15 μg/min
o If the BP is < 70 mmHg with shock, start IV noradrenaline 0.5-30 μg/min.
what amount of heart failure is diastolic? what is the mortality?
• 1/3 of heart failure is diastolic (normal Left Ventricular Systolic Function-LVSF)
• Mortality in Diastolic HF is 5-8% (lower than Systolic HF: 10-15%)
what is the diagnosis of diastolic heart failure?
Diagnosis:
• Echo is the golden diagnostic tool
• CXR and ECG cannot differentiate Diastolic vs. Systolic HF.
what is the management of diastolic heart failure?
Management:
• Initially, reduction of pulmonary venous pressure (PVP) and congestion, using diuretics
• ARBs are superior to ACE inhibitors
describe the features of cardiac tamponade
-JVP
-HR and BP
-heart sounds
-pulse
-ECG
• Raised JVP, with an absent Y descent - this is due to the limited right ventricular filling
• Tachycardia
• Hypotension
• Muffled heart sounds
• Pulsus paradoxus (which occurs also in Asthma)
• Kussmaul’s sign (much debate about this) (more in constrictive pericarditis)
• ECG: electrical alternans (QRS complex amplitude alternates)
what is kussmauls sign?
Kussmaul’s sign is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration.
describe the differences between constrictive pericarditis and cardiac tamponade
-JVP
-pulses paradoxus
-Kussmauls sign
-CXR
JVP
-Absent Y descent in cardiac tamponade
-X + Y present in constrictive pericarditis
Pulses paradoxus present in cardiac tamponade
Kussmauls sign seen more in constrictive pericarditis
Pericardial calcification on CXR in constrictive pericarditis
DVLA rules in driving with:
-elective angioplasty
-ACS
-angina
-pacemaker insertion
-ICD
-successful catheter ablation
-Aortic aneurysm
-heart transplant
• Angioplasty (elective) - 1 week off driving
• CABG - 4 weeks off driving
• Acute coronary syndrome- 4 weeks off driving, 1 week if successfully treated by angioplasty
• Angina - driving must cease if symptoms occur at rest/at the wheel
• Pacemaker insertion - 1 week off driving
• Implantable cardioverter-defibrillator: if implanted for sustained ventricular arrhythmia: cease
driving for 6 months. If implanted prophylatically then cease driving for 1 month
• Successful catheter ablation - 2 days off driving
• Aortic aneurysm > 6cm - notify DVLA. Licensing will be permitted subject to annual review.
An aortic diameter of 6.5 cm or more disqualifies patients from driving
• Heart transplant: DVLA do not need to be notified
name 3 examples of nuclear imaging of the heart
• Thallium
• ‘MIBI’ or (SPECT) scans: Cardiac Single Photon Emission Computed Tomography uses
Technetium (99mTc) sestamibi, a coordination complex of the radioisotope technetium-99m
with the ligand methoxyisobutylisonitrile (MIBI).
• Positron Emission Tomography (PET) scans: Fluordeoxyglucose (FDG) is used.
what is the role of SPECT scanning of the heart?
The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of
images are usually acquired. First the myocardium at rest followed by images of the myocardium
during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress
images any areas of ischemia can be classified as reversible or fixed (e.g. following a myocardial
infarction). Cardiac PET is predominately a research tool at the current time
what is MUGA and what is this used for in scanning the heart?
MUGA
• Multi Gated Acquisition Scan, also known as radionuclide angiography
• Radionuclide (technetium-99m) is injected intravenously
• The patient is placed under a gamma camera
• May be performed as a stress test
• Can accurately measure left ventricular ejection fraction. Typically used before and after
cardiotoxic drugs are used
what is cardiac CT used for?
Cardiac Computed Tomography (CT): useful for assessing suspected IHD, using two main methods:
• Calcium score: there is known to be a correlation between the amount of atherosclerotic plaque
calcium and the risk of future ischemic events. Cardiac CT can quantify the amount of calcium
producing a ‘calcium score’
• Contrast enhanced CT: allows visualization of the coronary artery lumen
If these two techniques are combined cardiac CT has a very high negative predictive value for ischemic
heart disease.
what is cardiac MRI used for?
Cardiac MRI: (commonly termed CMR) has become the gold standard for providing structural images
of the heart. It is particularly useful when assessing congenital heart disease, determining right and
left ventricular mass and differentiating forms of cardiomyopathy. Myocardial perfusion can also be
assessed following the administration of gadolinium. Currently CMR provides limited data on the
extent of coronary artery disease.
when is exercise ECG not used and what is used instead?
Exercise ECG:
USELESS in patients with:
• Conduction abnormalities
• resting (ECG) abnormalities like ST segment depression of >1mm
• WPW
• Digoxin
• Ventricular paced rhythm
In such patients myocardial perfusion imaging is the preferred modality for evaluation of CAD.
in patients with chest pain
-what warrants emergency admission
-what warrants same day assessment
-what if the chest pain has been ongoing more than 72 hours
• Current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency
admission
• Chest pain 12-72 hours ago: refer to hospital the same-day for assessment
• Chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement
before deciding upon further action
describe 3 features that NICE describe as anginal chest pain
-what is typical angina
-what is atypical angina
-what is non-anginal chest pain
NICE define anginal pain as the following:
o Constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
o Precipitated by physical exertion
o Relieved by rest or GTN in about 5 minutes
• Patients with all 3 features have typical angina
• Patients with 2 of the above features have atypical angina
• Patients with 1 or none of the above features have non-anginal chest pain
if patients have typical angina - who of these need further investigation?
If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further
diagnostic testing is required. It should be noted that all men over the age of 70 years who have typical
anginal symptoms fall into this category.
For patients with an estimated risk of 10-90% further investigations are needed
what investigation is used for patients who have typical angina and a risk of 61-90
61-90% Coronary angiography
what investigation is used for patients who have typical angina and a risk of 30-60%
Functional imaging, for example:
• Myocardial perfusion scan with SPECT
• Stress echocardiography
• First-pass contrast-enhanced magnetic resonance (MR) perfusion
• MR imaging for stress-induced wall motion abnormalities.
what investigation is used for patients who have typical angina and a risk of 10-29%
10-29% CT calcium scoring
management of angina
-in stable angina with good exercise tolerance
-if pain is worsening
NICE 2011 Guidelines:
• In good exercise tolerance, consider medical therapy before angiography (β-
blocker is the most important)
• If pain is worsening, no need for exercise test, directly do angiography (Cath)
describe the medical management of angina
-what should all patients recieve
-what is the preferred initial treatment
• All patients should receive aspirin and a statin in the absence of any contraindication
• Sublingual glyceryl trinitrate to abort angina attacks
• β-blocker is the preferred initial treatment. For patients unable to take a β-blocker there is no
clear guidelines on the best alternative. Options include a rate-limiting calcium-channel blocker
(verapamil or diltiazem); a long-acting dihydropyridine calcium-channel blocker (e.g. modified-
release nifedipine); a nitrate; or a potassium-channel activator
• If there is a poor response to initial treatment then the β-blocker should be ↑ to the maximum
tolerated dose (e.g. atenolol 100mg od)
• Again, there are no clear guidelines on the next step treatment. CKS advise adding a long-acting
dihydropyridine (e.g. nifedipine, amlodepine, felodipine) although other options include
isosorbide mononitrate and nicorandil
what is the treatment of prinzmetal angina
Prinzmetal angina - treatment = dihydropyridine calcium channel blocker
what to do with patients who develop nitrate tolerance?
Nitrate tolerance
• Many patients who take nitrates develop tolerance and experience ↓ efficacy
• BNF advises that patients who develop tolerance should take the second dose of isosorbide
mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for
4 hours and maintains effectiveness
• This effect is not seen in patients who take modified release isosorbide mononitrate
what is ivabradine?
-how does it work?
-adverse effects?
Ivabradine (Procoralan)
• A new class of anti-anginal drug which works by reducing the heart rate
• Acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity
• Adverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due
to the mechanism of action, may also be seen
• There is no evidence currently of superiority over existing treatments of stable angina
when should fondaparinux not be used in ACS, what is used instead?
Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patient’s creatinine is > 265 μmol/l unfractionated heparin should be given.
if a patient is using clopidogrel what should omeprazole be switched to?
lansoprazole
when should tirofiban be used in ACS
Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to
patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month
mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital
admission.
when should coronary angiography be considered in ACS
Coronary angiography should be considered within 96 hours of first admission to hospital to patients
who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in
patients who are clinically unstable.
how does aspirin work?
Aspirin Antiplatelet - inhibits the production of thromboxane A2
how does clopidogrel/ticagrelor work?
Clopidogrel Antiplatelet - inhibits ADP binding to its platelet receptor
how does enoxaparin/fondaparinux work?
Enoxaparin Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
how does bivalirudin work?
Bivalirudin Reversible direct thrombin inhibitor
what are poor prognostic factors for ACS?
Poor prognostic factors:
• Age
• Development (or history) of heart failure, Killip class*
• Peripheral vascular disease
• ↓ systolic blood pressure
• Initial serum creatinine concentration
• Elevated initial cardiac markers
• Cardiac arrest on admission
• ST segment deviation
describe Killip classification
I No clinical signs heart failure 6%
II Lung crackles, S3 17%
III Frank pulmonary edema 38%
IV Cardiogenic shock 81%
describe the arterial supply of the heart
left aortic sinus → left coronary artery (LCA)
right aortic sinus → right coronary artery (RCA)
LCA → LAD + circumflex
RCA → posterior descending
RCA supplies SA node in 60%, AV node in 90%
describe the venous drainage of the heart
Venous drainage of the heart: coronary sinus drains into the right atrium
describe the ECG leads affected in:
anteroseptal
inferior
anterolateral
lateral
posterior
Myocardial infarction and the associated vessels.
Anteroseptal: V1-V4: Left anterior descending
Inferior: II, III, aVF: Right coronary
Anterolateral: V4-6, I, aVL: Left anterior descending or left circumflex
Lateral: I, aVL +/- V5-6: Left circumflex
Posterior: Tall R waves V1-2: Usually left circumflex, also right coronary
Post MI, what drugs should be offered
• ACE inhibitor
• β-blocker
• Aspirin
• Statin
when should an aldosterone antagonist be used post MI
Aldosterone antagonists:
patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy
How long is DAPT given for post ACS
Most patients who’ve had an acute coronary syndrome are now given dual antiplatelet therapy (DAPT). Clopidogrel was previously the second antiplatelet of choice. Now ticagrelor and prasugrel (also ADP-receptor inhibitors) are more widely used. The NICE Clinical Knowledge Summaries now recommend:
post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events
what are contraindications to thrombolysis?
• Active internal bleeding
• Recent hemorrhage, trauma or surgery (including dental extraction)
• Coagulation and bleeding disorders
• Intracranial neoplasm
• Stroke < 2 months
• Aortic dissection
• Recent head injury
• Pregnancy
• Severe hypertension
when does dresslers syndrome usually occur?
This usually occurs 1 to 8 weeks after MI.
what is the presentation of dresslers syndrome?
Presentation:
• Malaise, fever, pericardial pain
• Elevated erythrocyte count
• Sometimes may also have pleuritis and pneumonitis.
what is dresslers syndrome caused by?
It has been postulated that the syndrome results from release of cardiac antigens which then stimulate
antibody production. The immune complexes are then deposited in the pericardium, pleura and lung.
There may be accompanying pleural and pericardial effusion and therefore echocardiography should be
done.
