Phase 2 - Cardio Flashcards
What is atrial fibrillation
An irregular heartbeat (often faster than usual) that occurs when the electrical signal in the atria are uncoordinated. - it is the most common arrhythmia.
It causes the atria to seem as though they are twitching. On an ecg instead of regular p waves, the atrial contraction looks like the baseline is a small scribble.
It isn’t usually life-threatening
What are the symptoms of atrial fibrillation
People may experience one or more of the following:
- IRREGULAR heartbeat
- Heart PALPITATIONS (rapid, fluttering, or pounding)
- Chest PAIN
- Extreme/General FATIGUE (blood delivered less effectively so less energy)
- SOB
- LIGHTHEADED/dizziness
- Weakness
Some people experience no symptoms
What are the risk factors for AFib
- HIGH BP (also increases with age - accounts for ~1 in 5 cases of AFib)
- other heart conditions like coronery heart disease or vavlvular disease which create an inflammatory state
- DIABETES
- Left ventricular hypertrophy
- HF
- Ischemic heart disease
- HYPERTHYROID
- CKD
- Advancing AGE
- OBESITY
- EUROPEAN ancestry - genetic component
- Moderate to heavy alcohol use
- Smoking
Complications of AFib
Associated with an increased risk of ischaemic stroke
- As the blood isn’t effectively pumped from the atria it can stagnate and form clots
Pathophysiology of AFib
Not well understood but it is believed that the risk factors (particularly things like hypertension that can stretch and wear out the myocytes) cause stress to the cells which can lead to tissue heterogeneity: the cells take on different electrical properties causing atrial conduction to become uncoordinated so various different parts of the atria are contracting at different times.
Multiple wavelet theory:
Forms multiple wavelets as opposed to a single wave front.
Automatic focus theory:
specific area initiates alternate electrical impulses and overrides sa node. Thought to originate in cells around pulmonary vein entry point.
Progression/Types of atrial fibrillation
Starts with paroxysmal AF - come and goes (<1 week)
Repeated paroxysmal events cause further stress (potentially through calcium overload) - get progressive fibrosis of cells.
Leads to Persistent AF - lasts >1 week without self-terminating (weeks to months)
When it has lasted for >12 months - Long-standing persistent AF
If the patient and clinician decide not to definitively treat the dysrhythmia - Permanent AF
Diagnosis/tests for AF
Persistent AF - ECG
Paroxysmal AF - may use holter monitor
- portable device that monitors rhythm over longer time period and records potential episodes of AF to check later
Treatments for AF
Medication to control heart rate and anticoagulents (wouldn’t give they have very high hypertension as there at more risk of dissections etc)
- Beta-blockers
- CCB (VERAPAMIL)
- Digoxin
- Warfarin
- direct-acting oral ANTICOAGs (DOACs)
- Dabigatran, Apixaban, Rivaroxaban, Edoxaban
** lower risk of brain haemorrhage
** need less frequent blood monitering (don’t need regular INR)
** fewer interactions
** don’t need to adjust dose frequently depending on blood results
- Dabigatran, Apixaban, Rivaroxaban, Edoxaban
Can get a RADIOFREQUENCY CATHETER ABLATION - some tissue is destroyed so the irregular electrical impulses aren’t conducted anymore
- Might do a MAZE PROCEDURE so the impulses are forced through a maze like direction to better control and coordinate impulses and contraction
- May put in an implantable PACEMAKER - contantly paces atrium
- May get AV NODE ABLATION so separates ventricular contraction from atrial contraction
** Needs a ventricular pacemaker!
What is a CHA2DS2-VASc score
It is a score that estimates the risk of stroke in people with non-rheumatic atrial fibrillation.
Used to determine if treatment with anticoagulants/anti-platelets is required
Stands for:
Congestive heart failure (left ventricular systolic dysfunction) (1 point)
Hypertension (1 point)
Age2 >= 75 (2 points)
DIabetes Mellitus (1 point)
S2 = prior stroke or TIA (transient ischaemic attack - mini self terminating stroke) or thromboembolism (2 points)
Vascular disease (1 point)
Age 65-74 years (1 point)
Sex (1 point) - female
If positive for 1 point (moderate risk) - oral anticoagulent should be considered
2 or more points (high risk) - oral anticoagulent recommended
What is an ORBIT score
estimates risk of major bleeding for patients on anticoagulents for AF
Older age: 75 or over (1 point)
Reduced Haemoglobin/Haemocrit/Anaemia (2 points)
Bleeding history (2 point)
Insufficient renal function (1 point)
Treatment with anti-platelet agents (1 point)
0-2 - low bleed risk
3 - medium bleed risk
4-7 - high bleed risk
think HARP B (Haematocrit, Age, Renal function, anti-Platlets, Bleeding history)
Differential diagnosis of palpitations
- ISCHAEMIC heart disease
- HF
- Cardiomyopathy
- VALVE disease
- Wolff-Parkinson-White syndrome (AVRT)
Drugs
Lifestyle factors:
- alcohol misuse
- caffine, nicotine, heroin, amphetamines, ecstasy, cannabis
Atrial flutter vs Atrial fibrillation
In atrial flutter the rhythm in the atria is more organised
ECG:
In atrial flutter there is a more organised saw-tooth pattern of p-waves
In AF the baseline is more scribbley and the ventricular rate is more irregular
Treatment:
Catheter ablation is the gold standard treatment for atrial flutter
Medicine is the first line treatment for AF
ECG variations for heart/AV block
1st degree is just elongated PR intervals (over 200ms - 5mm)
2nd degree:
- Mobitz type 1: complexes get closer together till a beat is missed then restarts pattern
- Mobitz type 2: complexes seem regularly spaced by one is missed ocassionally
3rd degree - p waves and qrs complex have different rhythms (individually they follow a rhythm but they don’t match each other)
What do the waves on ecg correlate to
p waves - atrial depolarization
qrs complex - ventricular depolarisation
t wave - ventricular repolarisation
(sometimes get a u wave - end of ventricular repolarisation - seen in hypokalaemia)
Normal conduction pathway of heart
- Starts at SA node
propagates through both atria - Depolarization spreads to AV node
- Passes through bundle of His
- left and right bundle branches
- Left = anterior and posterior fascicles
- Purkinje fibres
What is an ECG
A summation of electrical activity/events in the cardiac cycle
Pacemakers of the heart
SA node - dominant - intrinsic rate: 60-100 beats/min
AV node - back-up - intrinsic rate: 40-60 bpm
Ventricular cells - back-up - intrinsic rate: 20-45 bpm
Standard calibration of ECG
25 mm/s
-0.1 mV/mm
1mm = 40ms
5mm = 200ms (max length of normal PR interval)
In this setting work out heart rate:
300/no. of big sqares
What chemicals is mycocardial hypertrophy triggered by? When is this an adaptive response
Hyperthrophic response triggered by:
- angiotensin 2 (vasoconstrict)
- IGF-1 (insulin-like growth factor 1 - e.g. acromegaly)
- endothelin-1 (vasoconstrict)
- TGF beta (transforming growth factor - a cytokine - inflam)
They activate mitogen-activated protein kinase (growth)
Adaptive in athletes and temporarily during pregnancy
What occurs in fetal embryogenesis (in relation to heart formation)
Heart comprises of a SINGLE CHAMBER till 5TH WEEK of gestation
Devided by intra-ventricular and intra-atrial SEPTA from ENDOCARDIAL CUSHIONS (Lateral cushions form rest of atrio-ventricular septa and valves)
Muscular intra-ventricular septum grows upwards from apex producing 4 chambers and allowing valve development to occur
Types of congenital heart disease
Overall may only complicate up to 1% of all live births
- VENTRICULAR SEPTAL DEFECT (25-30%)
- ATRIAL SEPTAL DEFECT (10-15%)
- PATENT DUCTUS ARTERIOSUS (10-20%)
- FALLOTS
- (combination of VSD, right ventricular HYPERTROPHY, PULMONARY valve STENOSIS, shifting of AORTA so it LIES OVER the VSD and gets oxygen-rich and -poor blood) (4-10%)
(less important)
- Pulmonic stenosis (5-7%)
- Coarctation of aorta (narrower part) (5-7%)
- Aortic stenosis (4-6%)
- Transposition of great arteries (2 main arteries are reversed) (4-10%)
- Truncus arteriosus (2%)
- Tricuspid atresia (tricuspid doesn’t form) (1%)
Many die between 20-40 y/o
Risk factors for congenital heart disease
It has multifactorial inheritance
- particularly associated with HOMEOBOX GENES (DNA sequence that regulates large-scale anatomical features in early embryonic development)
Trisomy 21 (Downs)
Turners (X0)
di-George Syndrome (22q11 deletion)
Previous child with defect increases probability of second child with another defect
- INFECTIONS like rubella
- DRUGS:
- tahlidomide
- alcohol
- phenytoin
- amphetamines
- lithium
- oestrogenic steroids
- DIABETES
How are congenital heart defects classified
Cyanosis
Is it present or absent?
- Cyanotic
- tetralogy of Fallot,
- TGA (transposition of great arteries)
- truncus arteriosus (trunc of aorta/pulmon artery don’t seperate properly; mixed blood)
- tricuspid abnormalities,
- tapvr (total anomalous pulmonary venous return - oxygen rich blood from pulm vein goes into right heart instead of left; mixing with oxygen poor blood)
- acyanotic
- Ventral septal defect
If present, does it occur from birth or develop later?
Which heart defects cause left right shunt
- VSD,
- ASD,
- PDA,
- truncus arteriosus,
- Total anomalous pulmonary venous drainage (pulmonary veins rejoins a vein so it drains into right side)
- hypoplastic left heart syndrome
Which heart defects cause right-left shunt
Tetralogy of Fallot
Tricuspid atresia (abnormal narrowing)
Which heart defects have no shunt
- Complete transposition of great vessels
- Coarctation of aorta
- Pulmonary stenosis
- Aortic stenosis
- Coronary artery origin from pulmonary artery
- Ebstein malformation (tricuspid is lower + malformed)
- Endocardial fibroelastosis (connective tissue growth around myocardium -> restricting contractive ability)
Which are acute coronary syndromes
Unstable angina
NSTEMI
STEMI
(can be q-wave or non q-wave infarcts)
Clinical classification/presentation of unstable angina
Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
Usually new onset or abrupt deterioration in previously stable angina
Uncommon:
- marked sweating
- epigastric pain (more common in older patients, women, and patients with diabetes, chronic kidney disease, or dementia)
- dyspnoea (laboured breathing)
- syncope
- nausea + vom (esp in women)
Diagnosis of unstable angina
History (i.e. clinical symptoms, past history/family history, smoker)
ECG done within 10 mins (not usually much change, maybe st depression or t wave flattening or elevation)
Troponin (there is no significant rise in unstable angina)
Confirmed with further diagnostic imaging like invasive coronary angiography or functional (stress) testing
Treatments for unstable angina
Sublingual NITRATES to treat vasospasms
CALCIUM CHANNAL BLOCKERS e.g. AMLODIPINE
BETA BLOCKERS e.g. propanolol
((Clopidogrel (prodrug - can be unreliable as it can be rapidly inactivated by various metabolic processes)
Prasugrel (more reliable pro-drug - less susceptible to genetic variations in metabolism)
- typically use TICAGRELOR as alternative to clopidogrel
Possibly low dose aspirin
Basically antiplatelet and anticoagulent therapy done with cardiological advice))
STEMI vs NSTEMI
Main difference lies in the fact STEMI can be diagnosed ob ECG at presentation; NSTEMI looks more normal on ECG (some ST depression or T wave abnormalities which looks same as unstable angina) so
Risk factors for unstable angina (and cvd in general)
Diabetes mellitus
Hyperlipidaemia
Hypertension
Metabolic syndrome (diabetes, obesity + HTN)
Renal impairment
Peripheral arterial disease
History of ischaemic heart disease and any previous treatment
Family history (immediate relative getting coronary artery disease/ under 60 y/o)
Obesity
Advanced age
Smoking
Cocaine
Physical inactivity
Diagnosis of myocardial infarction
STEMI diagnosed via ST elevation on ECG (specifically ST elevation with RECIPROCAL DEPRESSION)
NSTEMI typically diagnosed retrospectively from troponin (will be high) and other test results
Can also be defined as Q-wave or non Q-wave retrospectively depending on whether new pathological Q waves develop on ECG because of it
What is the importance of Left bundle branch block
STEMI or MIs in general associated with LBBB are associated with larger infarcts unless effectively treated (more likely to lead to pathalogical Q wave formation, heart failure or death)
Q wave vs non Q wave MI on ecg
Non-Q wave has poor R wave progression, ST elevation and Biphasic T wave
Q wave MI has complete loss of R wave
Clinical presentation of MI
- Cardiac chest pain
- unremitting
- usually severe but may be mild or absent
- occurs at rest
- associated with sweating, breathlessness, nausea
and/or vomiting
*one third occur in bed at night
Risk of mortality associated with MI
- Early mortality
- 30% outside hospital
- 15% in hospital
- Late mortality
- 5-10% first year
- 2-5% annually thereafter
Higher risk associated with higher age, diabetes, renal
failure, left ventricular systolic dysfunction (elevated NT-proBNP level) and other risk factors
Immediate management of MIs
*Get in to hospital quickly – 999 call
*Paramedics – if ST elevation, contact primary PCI (percutaneous coronary intervention - ie coronary angioplasty) centre for transfer
- Need to be able to get to PCI unit within 2hr, otherwise give fibrinolysis
*Take aspirin 300mg immediately
*Pain relief
Hospital management of MI
*Make diagnosis
*Bed rest
*Oxygen therapy if hypoxic
*Pain relief – opiates/ nitrates
*Aspirin +/- platelet P2Y12 inhibitor
*Consider beta-blocker
*Consider other antianginal therapy
*Consider urgent coronary angiography e.g. if
troponin elevated or unstable angina refractory
to medical therapy
Causes of acute coronary syndromes
Usually from rupture of atherosclerotic plaque and subsequent arterial thrombosis
Uncommon:
- stress-induced (Tako-Tsubo) cardiomyopathy
- coronary vasospasm without plaque rupture
- drug abuse (ampethamines, cocaine)
- dissection of coronary artery related to deffects of vessel connective tissue
- thoracic aortic dissection
What is troponin? When is it positive
Protein complex which regulate actin-myosin contraction
Highly sensitive marker for cardiac muscle injury
- not specific for acute coronary syndrome
Also positive in:
* gram negative sepsis
* pulmonary embolism
* myocarditis
* heart failure
* arrhythmias
* cytotoxic drugs
* …………………and more (like exercising a lot!)
- doesn’t necessarily indicate permanent muscle damage but does indicate higher risk in people with suspected acute coronary syndrome
What is the physiological effect of aspirin
Causes irreversible inactivation of cyclo-oxygenase 1 (COX1)
- COX1 is needed for synthesis of Thromboxane A2 which stimulates platelt aggregation and vasoconstriction
- blocking this inhibits platelet aggregation
How does thrombin generation play a role in arterial thrombosis
thrombin itself increases platelet activation so when thrombin generation by platelets is a prcoagulent produced by the platelets that acts in a positive feedback loop and increases risk/speed of arterial thrombosis
Name some P2Y12 antagonists
Clopidogrel (easily inactivated by metabolic processes)
Prasugrel
Ticagrelor (oral, reversibly-binding P2Y12 antagonist - used as alternative to clopidogrel)
What is the role of P2Y12 inhibitors
P2Y12 amplifies platelet activation
P2Y12 inhibitors are platelet inhibitors
They are used in combination with aspirin for ACS as ‘DUAL ANTIPLATELET THERAPY’
Name 3 GPIIb/IIIa antagonists
Abciximab
Tirofiban
Eptifibatide
What is the role of GPIIb/IIIa antagonists
GPIIb/IIIa stimulates aggregation and amplifies platelet activation
GPIIb/IIIa antagonists are antiplatelets
Used in combination with aspirin and oral P2Y12 inhibitors in management of patients UNDERGOING PCI (angioplasty with stent)
Used selectively as increased RISK OF MAJOR BLEEDING but still useful in STEMI patients undergoing PCI to cover DELAYED ABSORPTION OF ORAL P2Y12 inhibitors (as opiates delay gastric emptying) as GPIIb/IIIa is the ONLY IV DRUG FOR ACS
What is the role of anticoagulants for ACS management
Used in addition to antiplatelets
Targets formation/activity of thrombin
Inhibits fibrin formation AND platelet activation
Typically used prior to angiography, for PCI or CABG (before surgery basically)
Which drug is used in NSTEMI before doing a coronary angiography
FONDAPARINUX
- safer than heparins as it is a lower level of anticoagulation
What drug is used during PCI for ACS treatment
Full-dose anticoagulents:
- HEPARIN (usually unfractioned but sometimes given as ENOXAPARIN, a low-molecular-weight heparin)
or
- BIVALIRUDIN (direct thrombin inhibitor - EXPENSIVE, not used in Sheffield)
When may fibrinolytic therapy be used in ACS
For an acute STEMI if primary PCI is not available
Which fibrinolytic drugs may be used for STEMI
STREPTOKINASE
alteplase, reteplase, and tenecteplase (not sure if relevant)
ONLY GIVEN IF PRIMARY PCI NOT AVAILABLE (in acute STEMI)
Which drugs are used in secondary prevention of ACS
STATINS
ACE inhibitors
Beta blockers
Aldosterone antagonist (SPIRONOLACTONE, EPLERONONE)
which factors affect response to clopidogrel
Dose
- Age
- Weight
- Disease states such as diabetes mellitus
- Drug-drug interactions e.g. omeprazole and strong CYP3A
inhibitors - Genetic variants: CYP2C19 loss-of-function alleles
What are the adverse effects of P2Y12 inhibitors
*Bleeding e.g. epistaxis, GI bleeds, haematuria
*Rash
*GI disturbance
What are the adverse effects of ticagrelor specifically
DYSPNOEA (laboured breathing) - usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel
VENTRICULAR PAUSES - usually sinoatrial pauses, may resolve with continued treatment
What is the significence of ticagrelor as opposed to other P2Y12 inhibitors
Has shown better evidence for longterm mortality reduction but causes more adverse effect
How long would you continue antiplatelet therapy after an MI
P2Y12 inhibitor may be continued for LONGER THAN 1 YEAR after ACS IF there is a HIGH RISK of further ischaemic events in aspirin-treated patients who DO NOT HAVE EXCESSIVE RISK of life-threatening BLEEDING
In patients WITHOUT HIGH LONGTERM RISK
- can drop aspirin after a few months
What is primary PCI
treatment of choice for STEMI
do angiogram to check for blockage
- predilatation of occluded artery
-position stent
- deploy stent
repeat angiogram 3 months later to check stent is staying in place
When is revascularisation done for NSTE ACS
Coronary angiography usually done for patients with RAISED TROPONIN or UNSTABLE ANGINA REFRACTORY TO MEDICAL THERAPY
NOT AMENABLE if patients have SEVERE DIFFUSE CORONARY ARTERY DISEASE
What are the types of revascularisation procedures
PCI - most common
CABG (coronary artery bypass graft) - used in ~10% of patients with NSTE ACS
When may patients have ACS without obstructive coronary artery disease
- If their actual diagnosis is not ACS
- If a plaque ruptured without significant stenosis and the obstructive thrombus resolved by the time of angiography
- If the cardiomyopathy was stress-induced (Tako-Tsubo)
General ACS management overview
DIagnosis: history, ECG (if ST elevation go straight to cath lab for PCI if possible), troponin +/- coronary angiography; consider other diagnoses if uncertain
Pain relief as necessary: opiates (but can delay absorption of P2Y12 inhibitor); nitrates for unstable angina/coronary vasospasm (may be ineffective for MI)
Check no active or recent life-threatening bleeding/severe anaemia (to check if anticoagulants can be given)
If STEMI go straight for primary PCI (need anticoagulation - heparin beforehand) if possible; otherwise give fibrinolytics (unusual)
Initial cardiac monitoring for arrhythmia
Initial antithrombotic therapy: dual antiplatelet therapy (DAPT) + anticoagulant;
- may use GPIIb/IIIa antagonist for PPCI (primary PCI)
Revascularisation if MI or refractory/high risk unstable angina and if feasible
Secondary prevention:
- DAPT duration individualised
- highdose statin (e.g. atorvastatin, 40-80mg daily) - high cholesterol is often inherited
- BP control:
* beta blocker if LV dysfunction, heart failure or ongoing ischaemia
* aldosterone antagonist is heart failure and hypokalaemia
In general terms what causes angina? What is the most common specific cause?
Angina is caused by a mismatch of oxygen demand and supply
The commonest cause is ischaemic heart disease
What are risk factors for ischaemic heart disease (IHD) and subsequently angina of ischaemic origin
Non-modifiable:
AGE
Family history
MALE sex (1.5:1 ratio)
Modifiable:
- CIGARETTE SMOKING
- DIABETES MELLITUS
- HYPERLIPIDAEMIA (tho this could be genetic to a degree)
- STRESS
- Kidney disease
- Hypertension (lower risk)
- Obesity (lower risk)
- Physical inactivity
What are the intrinsic exacerbating factors of angina/IHD?
Broadly related to either lack of supply or increased demand.
Supply related:
- ANAEMIA
- HYPOXAEMIA
- polychythemia (increased RBC conc - thicker blood, less able to travel through vessels)
- Hypothermia
-Hypovolaemia
- Hypervolaemia
Demand related:
- HYPERTENSION
- TACHYARRYTHMIA
- VALVULAR HEART DISEASE
- Hyperthyroidism
- Hypertrophic cardiomyopathy
What are environmental exacerbating factors for angina
Exercise
Cold weather
Heavy meals (blood diverted to stomach)
Emotional stress
Pathophysiology of angina/myocardial ischaemia
Myocardial ischemia occurs when there is an imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:
- Impairment of blood flow by proximal arterial stenosis, atherosclerotic plaques or thrombi narrowing arteries
- Increased distal resistance e.g. as in left ventricular hypertrophy
- Reduced oxygen-carrying capacity of blood
What physics equations relate to blood vessel function
Poiseuille’s law:
Change in pressure = 8 x viscosity x length x flow
/ pi x radius to the power of 4
Bascially means coronary flow changes to the 4th power of the radius: nothing much happens until the diameter stenosis reacher 70% - then rapid decline
ALSO! Ohm’s law:
V=IR ie.
CHANGE in P = FLOW x RESISTANCE
How does the body normally adapt to increased exertion
Uses the Coronary flow reserve (CFR) - how much coronary arteries can increase under stress
Body adapts to increasing pressure by lowering microvascular resistance
In CHD fixed stenosis prevents adaptation of coronary arteries so high resistance and high pressure
Aside from stable and unstable angina, what are other types of angina
Cresendo angina - getting progressively worse over a period of time
Prinzmetal’s angina - RARE coronary SPASM
Microvsacular angina (‘ANOCA’)
- angina with apparently normal main coronary arteries
- caused by microvessels being unable to adapt -> increased resistance
- mainly affects WOMEN
- Cause unknown
What is the relevance of the epidemiology of stable angina
Incidence
Men 35/100,000/y (especially in older people)
Women 20/100,000/y
Prevalence
Men 5% (5000/100,000)
Women 4% (4000/100,000)
Main takeaway is that prevalence is much higher than incidence indicating that many people are diagnosed and survive - i.e. good prognosis (1.7% died and 7% had non-fatal CV evens)
Symptoms of angina
CHEST PAIN (typically described as tightness/weight/discomfort)
- typically shows up after exertion or eating
- mainly in chest radiating to neck, jaw, teeth, arms, back
BREATHLESSNESS
NO fluid retention (unlike heart failure)
NOT USUALLY palpitations
RARELY syncope or pre-syncope
Can sometimes get pale and sweaty tho this typically indicates a more severe case
Differential diagnoses of chest pain
MYOCARDIAL ISCHAEMIA (what typically causes angina)
- Pericarditis/myocarditis
- AORTIC DISSECTION (severe tearing pain, front to back - typically will have many of risk factors esp hypertension - dangerous!)
- Pulmonary embolism/pleurisy
- Chest infection/pleurisy
- Gastro-oesophagal (reflux, spasm, ulceration)
- Musculo-skeletal problems
- Psychological causes
Typically if they say it is a severe pain it is probably not angina
Treatment of angina
- Reassure that it has good prognosis
- Lifestyle changes (1st LINE)
- Always try to get them to stop smoking first if they smoke
- Reduce weight
- Exercise
- Improve diet
- Give advice in cases of emergency
- MEDS:
- GTN SPRAY (sublingual glycerltrinitrate)
- maybe aspirin
- maybe beta-blockers
- statins
- Revascularisation if required/feasible
How do you diagnose angina
- Take history
- Examination for exacerbating causes
- INVESTIGATIONS:
- routine bloods, LIPIDS, ECG (abnormal during periods of pain - st-t segement (esp ST DEPRESSION) changes associated with CAD (worse prognosis))
- DIAGNOSTIC TESTS:
- CT cor angiogram (1st line test)
- Other non-invasive if they have known CHD and uncertain history e.g. EXERCISE TESTING, MRI perfusion, myoview scan, stress ecocardiogram etc
- Cor Angiogram - IF non-invasive INCONCLUSIVE or VERY HIGH RISK patient
Pros and cons of CT coronary angiography
- Non-invasive
-Good RULE-OUT TEST and for spotting severe disease - Poor resolution - not good at seeing moderate disease well
- Anatomical, not functional
Pros and cons of exercise testing (for heart issues)
Basically get patient to walk on treadmill while hooked to ECG
- Good functional test
- Relies on ability to exercise (not useful in elderly, obese, arthritic etc.)
What is a myoview scan
Uses pharmacological stressor (regadenoson) to
Increase HR and CO (to check for ischaemia)
Fuzzy pictures: imperfect sensitivity and specificity
What is a stress echo test for heart problems
Uses pharmacological stressor and seeks regional wall abnormality
Highly skilled operative required so not often used
Pros and cons of perfusion MRI for heart issues
BEST non invasive test
- good sensitivity and specificity
Not available everywhere
Pros and cons of cor angiography
- Good sensitivity
- Gold standard treatment for more serious CAD
- Invasive
- ANatomical, not functional
Drug treatment for angina (types of drugs and how they work)
NITRATE (GTN or longacting oral nitrates)
- dilates coronary arteries and reduces resistance
- arterial vesodilation reduces afterload
- also causes venous dilation so reduces venous pressure and ventricular preload/venous return
Beta-blocker
- reduces heart rate so lowers oxygen demand
- reduces LV contractility
- reduced cardiac output so less oxygen demand
Statins
- HMG-CoA reductase inhibitor (inhibits rate limiting step of cholesterol synthesis)
- lower cholesterol as most people with angina have CAD and need to lower ldl
ACE inhibitors:
- block RAAS to reduce blood volume and hypertension
- redcues production of Angiotensin 2 which is also a vasocontrictor so less vesoconstriction (reduced peripheral resistance)
Calcium channel blocker (2nd line)
- blocks entry of calcium thus reduces contraction (negative chronotropic and ionotropic effects) - heart has to do less work so lower oxygen demand
- reduced arterial contraction/constriction reduces peripheral resistance and afterload
Potentially potassium channal opener or Ivabradine (lowers heart rate)
Side effects and contraindications of beta blockers
Bradycardia
Cold peripherals
Erectile dysfunction
Tiredness
Nightmares
DO NOT USE IN SEVERE ASTHMA
Side effect of nitrates
The vasodilation can cause HEADACHES (usually for around 3 days) until body adjusts
Side effects of calcium channal blockers
Flushing (from vasodilation)
Postural hypotension
Swollen ankles (blood can collect in legs and feet so odoema)
Aspirin - function, side effects, when is it used
CYCLO-OXYGENASE 1 INHIBITOR
- REDUCES PROSTAGLANDIN SYNTHESIS including THROMBOXANE 2
- Reduces platelet aggregation (also antipyretic, ANTI-INFLAMMATORY, ANALGESIC)
Side effects: GASTRIC ULCERATION (it is an NSAID in higher conc.s)
Typically given after one MI or if they have stent
- not typically used for stable angina
What are ACE inhibitors usually used for
Hypertension and DM treatment
- esp if they also have IHD
Which blood vessels are used for CABG
internal mammary artery (typically for LAD bypass)
saphenous vein (typically for right CA)
or radial artery potentially
pros and cons of PCI
Pros:
Less invasive than CABG
Convenient
Repeatable
Acceptable
Cons:
Risk stent thrombosis
Risk restenosis
Can’t deal with complex disease
Dual antiplatelet therapy required
Pros and cons of CABG (coronary artery bypass graft)
Pros:
Prognosis better
Deals with complex disease
Cons:
Invasive (very)
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay (intensive care for 5 days normally)
Time for recovery (~ 3 months)
PCI vs CABG use for acute and chronic coronary syndromes
STEMI: PCI commonly used and CABG not used
NSETMI: PCI commonly used, CABG sometimes used
Stable angina: both can be used depending on need and availability
Physiology of the pericardium in relation to pathology
Mechanically restrains filling volume of heart - initially stretch but becomes stiff at high tension
~50ml of serous fluid - small reserve volume
If this volume is exceeded pressure is translated ro cardiac chambers
Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount – Tamponade physiology
How does a chronic pericardial effsuion occur
Chronic, slow accumulation of serous fluid allows adaptation of parietal pericardium and heart
This compliance reduces effect on diastolic filling of chambers
- slow accumulation effusions rarely cause tamponade
What is acute pericarditis
An inflammatory pericardial syndrome with or without effusion (quick onset)
Usually benign and self-limiting
How is acute pericarditis clinically diagnosed
If they have 2 of the following can diagnose as acute pericarditis
- CHEST PAIN
- ECG CHANGES (1% of cases with ST elevation have pericarditis)
- Friction rub - more COMMON in SUBACUTE (more progressed than acute)
- Pericardial effusion - usually mild
Epidemiology of pericarditis
Difficult to quantify
1% in autopsy series
5% of A&E attendances with chest pain
1% of cases with ST elevation
80-90% of all pericarditis IDIOPATHIC
- Seasonal with VIRAL TRENDS (management isn’t affected by which virus)
- HIGHER IN YOUNG, previously healthy patients
Clinical presentation of pericarditis
CHEST PAIN
- severe
- sharp and pleuritic (no constricting, crushing character of ischaemic pain)
- RAPID ONSET
- LEFT ANTERIOR CHEST OR EPIGASTRIUM
- radiate to trapezius ridge of arm (from co-inervation by phrenic)
- RELIEVED by SITTING FORWARD
- EXACERBATED by LYING DOWN
DYSPNOEA
Cough
Hiccups (phrenic irritation)
Systemic disturbance
- Viral prodrome, Antecedent fever
- Skin rash, joint pain, eye Sx, weight loss
Past medical history of:
- Cancer
- Rheumatological Dx
- Pneumonia
- Cardiac procedure (PCI, ablation)
- MI
Aetiology of pericarditis (causes) - infectious reasons
VIRAL (common):
- Enteroviruses (coxsackieviruses, echoviruses),
- herpesviruses (EBV, CMV, HHV-6),
- adenoviruses,
- parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis
Bacterial (uncommon in uk):
- mycobacterium TB (other bacteria rare) - TB effusion pericarditis
- Purulent bacterial pericarditis and effusion (rare <1%)
* staph, step and pneumococci (high mortality)
Non-infectious aetiology of pericarditis
AUTOIMMUNE (common):
- Sjögren syndrome,
- rheumatoid arthritis,
- scleroderma
- systemic vasculitides
NEOPLASTIC (most common non-infectious reason):
- secondary metastatic tumours esp from lung, breast cancer and lymphoma
Metabolic:
- uraemia (usually from end-stage kidney disease)
- myxoedema
TRAUMATIC/IATROGENIC
- Rare early onset of:
* Direct injury (penetrating thoracic injury, oesophageal perforation)
* Indirect injury (non-penetrating thoracic injury, radiation injury)
- COMMON delayed onset of:
* PERICARDIAL INJURY SYNDROMES (e.g. post-MI - damage to myocardium irritates pericardium)
* IATROGENIC TRAUMA (e.g. PCI, pacemaker, radiofrequency ablation)
Other:
- amyloidosis
- aortic dissection
- pulmonary arterial hypertension
- chronic heart failure
Differential diagnosis for pericarditis
- MI/MYOCARDIAL ISCHAEMIA
-AORTIC DISSECTION - Pneumonia
- Pleurisy
- Pulmonary Embolus
- Pneumothorax
- Costochondritis (inflammation at rib-sternum joint)
- Gastro-oesophageal reflux
- peritonitis
- Pancreatitis
- Herpes zoster (shingles)
Investigations/examination for pericarditis
Clinical examination:
- Pericardial rub - pathognomonic
- sinus tachycardia
- fever
- signs of effusion
ECG
Bloods
CXR (chest x-ray)
Echocardiogram
What does pericardial rub sound like
like crunching snow or scratching at left sternal edge
- can just sound like more common murmurs
What are the clinical signs of pericardial effusion
Pulsus paradoxus - can hear pulse but can’t feel it peripherally upon inspiration - pressure in heart lowering output
kussmaul sign - increased right atrial pressure -> increased jugular venous pressure on inspiration
What does the ECG look like in pericarditis
Diffuse ST elevation
Concave ST segment (sort of saddle shaped)
- may resemble STEMI pattern
NO RECIPROCAL ST DEPRESSION (unlike STEMI)
PR depression
- Mechanism: epicardial inflammation as adjacent to pericardium
- parietal is inert
Blood tests done for pericarditis
FBC:
- shows modest increase in WCC, mild lymphocytosis
ESR (erythrocyte sedimentation rate - reveals inflammatory activity) & CRP (C-reactive protein - also checks inflammation)
- high ESR may suggest aetiology
ANA (antineuclear antibody) in young females (to check for SLE: systemic lupus erythematosus - more common in females)
TROPONIN
- elevations suggest myopericarditis
What does CXR look like in pericarditis
- often normal in idiopathic
- pneumonia common if bacterial
- enlargement of cardiac silhouette can suggest effusion (only detectable at >300ml)
What is a complication of pericardial effusion
cardiac tamponade
What is cardiac tamponade
Rapid filling of pericardial space with blood or other fluid
- puts pressure on heart -> decreased diastolic filling -> reduced CO -> drop in blood pressure
- can go into shock, cardiovascular collapse or MI - life threatening
What can cause cardiac tamponade
haemorrhage
slower growing effusions which eventually develop into tamponade:
- TB, myocarditis
- autoimmune
- neoplasms
- uremia
- side effect of pericarditis
Signs of tamponade
Beck’s triad (signs of cardiac tamponade)
- hypotension (weak pulse/narrow pulse pressure)
- Raised jugular venous pressure/distension (related to sometimes getting Kussmaul sign)
- muffled heart sounds
- pulsus paradoxus
- With large effusion, irregular ecg as the heart is bobbing about
Why may pulsus paradoxus not be present in pericardial effusion
may be absent in ASD (atrial septal defect),
elevated diastolic pressures,
pulmonary hypertension,
aortic regurgiation
Management of pericarditis
Not a lot of evidence mainly consensus opinion
Sedentary activity until resolution of symptoms and ECG/CRP
(-Probably only applies to athletes - 3 months)
NSAID (Ibuprofen 600mg TDS PO 2/52) or Aspirin (750-1000mg BD PO 2/52) - very high doses
Colchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence
Prognosis of pericarditis
- mostly good long term prognosis
- cardiac tamponade rarely occurs in acute idiopathic pericarditis
- Constrictive pericarditis may occur in 1% with acute idiopathic - reason for giving COLCHICINE
15-30% with acute will get recirrence
How much does colchicine reduce recurrence rate
50%
How can risk of developing constriction in pericarditis be classified
Low (1%):
- for idiopathic and presumed viral
Intermediate (2-5%)
- autoimmune
- immune mediated
- neoplastic
high (20-30%)
- bacterial (esp TB and purulent)
What is a treatment given for Tuberculous effusion TB pericarditis
Pericardectomy (~50% 5 year survival)
What is the name of post cardiac injury syndromes
Dressler’s syndrome (can cause pericarditis)
- shows up ~1-2 weeks post MI
What is atherosclerosis?
The build up of plaque (consisting particularly of cholesterol) in/on artery walls
Starts gruel-like substance - becomes hard
Causes stenosis and narrowing of arteries - major cause of death (especially from plaque rupture -> thrombus formation -> arterial blockage -> MI)
Risk factors for atherosclerosis
Age
FAMILY HISTORY
HIGH SERUM CHOLESTEROL
TOBACCO SMOKING
HYPERTENSION
DIABETES
Obesity
Distribution of atherosclerotic plaques within body
Found within peripheral and coronary arteries
Focal distribution but can occur along the length of the artery
Can be affected by haemodynamic factors e.g.
May be more likely to form:
- at areas of turbulence/changed flow e.g. bifurcations
* turbulence causes altered endothelial function and cange in wall thickness leading to NEOINTIMA
- there is a link to altered gene expression in key cells
What is neointima
The formation of new/thickened arterial intima by the migration and proliferation of cells from the media
- typically around prosthesis or in atherosclerosis, esp in areas of turbulent flow
What does the structure of an atherosclerotic plaque consist of
Lipid
NECROTIC CORE
Connective tissue
FIBROUS CAP
What is the response to injury hypothesis of atherosclerosis
Injury to endothelial cells initiates endothelial dysfunction
Signals sent to circulating leukocytes -> they accumulate and migrate into vessel wall
Inflammation occurs
What 2 things primarily cause inflammation of arterial wall in atherosclerosis
LDL
- can pass in and out of arterial wall and in excess can ACCUMULATE in arterial wall
* Undergoes OXIDATION and GLYCATION (bonding of sugar to protein or lipid - without enzymatic regulation)
ENDOTHELIAL DYSFUNCTION
- response to injury
What stimulates the movement/adhesion of leukocytes at sites of inflammation
Chemoattractants (chemokines) released by the endothelial cells at the site of an injury which send signals to leukocytes.
They produce a concentration gradient causing leukocytes movement towards injured site and then extravasation (chemotaxis).
Integrins also help adhere leukocytes to endothelium before extravasation occurs.
Which inflammatory cytokines are found in plaques
IL-1 (canakinumab - IL-1 antibody drug)
IL-6 (tocilizumab - IL-6 receptor inhibitor)
IL-8 (works esp on neutrophils)
IFN-gamma
TGF-beta (transforming growth factor)
MCP-1 (monocyte chemoattractant protein-1)
(C reactive protein - produced by liver; increases during inflammation)
What are the stages of atherosclerosis
Fatty streaks
Intermediate lesions
Fibrous plaques OR Advanced lesions
Plaque rupture OR Plaque erosion
What do fatty streaks consist of and when do they appear
Aggregations of LIPID-LADEN MACROPHAGES (foam cells) and T LYMPHOCYTES within INTIMA
appear at early age (<10 years)
What are intermediate atherosclerotic lesions composed of
Lipid-laden macrophages (FOAM CELLS)
T LYMPHOCYTES
VASCULAR SMOOTH MUSCLE CELLS
Adhesion/aggregation of PLATELETS to wall
Isolated pools of extracellular lipid
What is the make-up of fibrous plaques/advanced lesions
Contains:
- FOAM CELLS
- T LYMPHOCYTES
- SMOOTH MUSCLE CELLS
- MACROPHAGES
Forms the LIPID CORE and NECROTIC DEBRIS
Covered by FIBROUS CAP
- may be calcified
Impedes blood flow and prone to rupture
What is the fibrous cap of an atherosclerotic plaque made of
Endoplasmic reticulum membrane proteins:
- COLLAGEN
- ELASTIN
laid down by smooth muscle cells
What occurs in plaque rupture
Normally fibrous caps are RESORBED and REDIPOSITED as plaques grow and recede
If balance shifts to more inflammatory conditions (increased enzyme activity) - weakens cap and plaque ruptures
Basement membrane, collagen and necrotic tissue are exposed and the vessels in the plaque haemorrhage.
-> Tissue factor triggers THROMBUS FORMATION and VESSEL OCCLUSION
When does plaque erosion occur
Typically caused by small ‘early lesions’
Thickened fibrous cap may lead to collagen triggering thrombosis rather than tissue factor (as in plaque rupture)
