Cardiology Flashcards
What are 2 clinical ethics analysis methods? They help you to look at what? Concept of connectivity and interdependence?
Seedhouse’s Ethical Grid
Four Quadrants Approach
Help you to look at things in a wider perspective
Behaviour of one individual may affect other or wider system
What is coevolution? What is being pushed away from equilibrium essential for?
Adaptation or changes by one organism altering other organisms i.e. doctor and patient
For survival and flourishing, pushing yourself away from the comfort zone, fundamental to learning and innovation, good for doctor-pt and GPR and trainer
Four inner sections of Seedhouse’s Ethical Grid? 4 sections of Four Quadrants Approach?
Respect persons equally, create autonomy, respect autonomy, serve needs first
Medical indications- beneficence and nonmalificence, patient preferences- respect for autonomy, quality of life- beneficence and nonmalificence, contextual features- loyalty and fairness
How does history affect the doctor and patient? Example of feedback on GPs?
Both the patient and doctor are influenced by their individual and collective histories, decision made in one consultation will affect those made in the next
Throwaway phrase by GP can have far reaching effects on patient
Features of self-organisation, emergence and creation of new order? What are conscientious objections of a patient? Core ethical beliefs?
Whole is more than sum of the parts, Gestalt principle, emergent properties arise from interaction of elements in the system
Moral claims thats based on an individual’s core beliefs, different from other kinds of objections in which persons may oppose certain acts but are willing to perform them anyway
Most important to person, constitute part of his/ her identity and are basis of his/ her moral integrity, also like refusal of healthcare professional to provide certain treatments
Healthcare professionals balance conscientious objections with what, respecting what also? 2 key requirements if refusing treatment?
Professional obligations, respect patient autonomy and informed consent
Advanced notification, public disclosure
What 3 things commonly develop atherosclerosis? Risk factors for atherosclerosis?
Circumflex, LAD and right coronary arteries
Age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history
Distribution of atherosclerotic plaques? Atherosclerotic plaque is a complex lesion consisting of what? Plaque will either do what or what?
Found within peripheral and coronary arteries, focal distribution along the artery length
Lipid, necrotic core, connective tissue, fibrous ‘cap’
Occlude the vessel lumen–> restriction of blood flow (angina) or may rupture (thrombus formation and subsequent death)
How do atherosclerotic plaques form? Inflammatory cytokines found in plaques?
Injury to endothelial cells–> endothelial dysfunction, chemoattractants released to attract leucocytes migrate into vessel wall, released from site of injury and conc-gradient produced
IL-1- key one, IL-6, IFN- gamma
Earliest lesion of atherosclerosis? Appear at what age? Consist of what?
Fatty streaks
Very early stage (less than 10)
Aggregations of lipid-laden macrophages and T lymphocytes within intimal layer of vessel wall
What are intermediate lesions composed of? Adhesion of what to vessel wall?
Lipid laden macrophages (foam cells- macrophages taken up lots of lipids), vascular smooth muscle cells, T lymphocytes
Platelets- aspirin inhibits this
Fibrous plaques/ advanced lesions do what and are prone to what? Covered by what may be what? Contain what and plaque filled with what?
Impeded blood flow, prone to rupture, covered by dense fibrous cap made of extracellular matrix proteins including collagen (strength) and elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris
Calcified
Smooth muscle, macrophages and foam cells, T lymphocytes, red cells
Fibrin
What needs to happen for fibrous cap to be maintained? When would the plaque rupture? What are within the plaque? What happens?
Needs to be resorbed and redeposited
If balance shifts i.e. in favour of inflammatory conditions, then cap becomes weak and plaque ruptures
Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel
Thrombus formation and subsequent vessel occlusion
What can ECGs identify? 3 pacemakers of heart and intrinsic rate values?
Arrythmias, myocardial ischaemia and infarction, pericarditis, chamber hypertrophy, electrolyte disturbances i.e. hyperkalaemia or hypokalaemia, drug toxicity i.e. digoxin and drugs which prolong the QT interval
SA node= dominant- IR of 60-100bpm
AV node- back-up- IR of 40-60 bpm
Ventricular cells- back-up with intrinsic rate of 20-45bpm
Standard calibration values? Electrical impulse that travels towards the electrode produces what? P wave is what? Seen in every lead apart from what?
25mm/s, 0.1mV/mm
An upright ‘positive deflection’
Atrial depolarisation- apart from aVR
PR interval is what? What is QRS complex? ST segment?
Time taken for atria to depolarise and electrical activation to get through AV node
Ventricular depolarisation
Interval between depolarisation and repolarisation
T wave? What is dextrocardia? One large box is how many seconds? Vertically one large box is what value mV? What do bipolar and unipolar leads have?
Ventricular depolarisation
Heart is on right side of chest instead of left
0.2s, 0.5mV
Bi= two different points on body, uni= one point on body and virtual reference with 0 electrical potential located in centre of heart
What are the 12 leads of an ECG? Where are standard limb leads put? QRS complex should not exceed what in augmented limb leads? Should be dominantly upright in what 2 leads? That and T waves tend to have?
3 standard limb leads, 3 augmented limb leads, 6 precordial leads I= right to left arm II= right arm to left leg III= left arm to left leg 110ms Leads I and II Same general direction in limb leads
3 augmented limb leads? All waves negative in what lead? Degrees of standard limb leads? Of augmented limb leads?
aVR, aVL, aVF
aVR
I= 0, II= +60, III= + 120
aVF= 90, aVL=-30, aVR= -150
PR interval should be how long? Width of QRS complex should not exceed what? Should dominantly upright in what 2 leads?
120-200ms
110ms
Leads I and II
What 2 waves tend to have same general direction in limb leads? All waves negative in what lead? r wave must grow from where to at least what? S wave from where to where and disappear where?
QRS and T waves
Lead aVR
From V1 to at least V4
V1 to V3 and disappear in V6
ST segment should start isoelectric except in what 2 where it may be elevated? P waves should be upright in what leads?
V1 and V2
I, II and V2 to V6
Should be no Q wave or only small q less than 0.04 secs in width in what leads? T wave must be upright in what leads? P wave always positive in what 2 leads? Always negative in what lead?
I,II, V2 to V6
I, II, V2 to V6
Lead I and II, always negative in lead aVR, best seen in leads II
Right atrial enlargement shown by what? Left atrial enlargement? What indicates P pulmonale? Also?
Tall, pointed P waves
Notched/ bifid P wave in limb leads
Pointed P wave taller than 2.5mm in limb leads
P mitrale
Short PR interval indicates what syndrome? What allows early activation of the ventricle? Long PR interval?
WPW syndrome, Accessory pathway
First degree heart block
Non-path Q waves may be present in what leads? R wave in lead V6 smaller than in what? Depth of S wave should not exceed what?
I,III, aVL- smaller than V5
30mm
ST segment is what? Elevation/ depression by what or more? What is J junction?
Flat
By 1mm or more
Point between QRS and ST segment
Normal T wave what shape? Should what fraction of R wave amplitude? Abnormal T waves are what shape?
Asymmetrical- first half having gradual slope than second
At least 1/8 but less than 2/3 of amplitude of R
Symmetrical, tall, peaked, biphasic or inverted
QT interval measured in what lead as it does not have prominent U waves? Decreases when what increases? Should be what length? Should not be more than half of interval between what waves?
In lead aVL
Heart rate
0.35-0.45 seconds
Adjacent R waves
Features of U wave? 2 methods of measuring heart rate?
Small, round, symmetrical and positive in lead II, direction same as T wave, more prominent at slow heart rates
Rule of 300/1500
10 second rule
Rule of 300 method? 10 second rule?
Number of big boxes between 2 QRS complexes and divide this into 300 for regular rhythms
Number of beats on ECG x6 for irregular rhythms
QRS axis represents what? Abnormalities hint at what? Normal QRS axis? -30 to -90 referred to as what? +90 to +180 referred to as what?
Overall direction of heart’s electrical activity
Ventricular enlargement, conduction blocks
LAD
RAD
2 approaches to determining QRS axis? 2 types?
Quadrant and equiphasic approach
Predominantly positive, predominantly negative, equiphasic
3 steps of quadrant approach?
QRS complex in leads I and aVF
Determine if predominantly positive or negative
Combination should place axis into one of 4 quadrants
3 steps of equiphasic approach?
Most equiphasic QRS complex
Identified lead lies 90 degrees away from lead
QRS in this second lead is positive or negative
Values for tachycardia and bradycardia? ST segments raised in what leads for acute anterolateral MI? What about acute inferior MI?
Tachy= above 100, Brady= below 60
Anterior (V3-V4) and lateral (V5-V6) leads
Inferior II, III, aVF leads
Normal systolic ejection fraction and weight of heart? Hypertrophic response triggered by what? Left-sided failure causes what? Right-sided? Diastolic? Hibernating myocardium?
60-65%, 300-400g
Angiotensin 2, ET-1 and insulin-like growth factor 1, TGF-Beta, activate mitogen-activated protein kinase
Pulmonary congestion and overload of right side
Venous congestion and hypertension
Stiffer heart
Vacuolated cardiac myocytes following injury (usually hypoxic) may enhance myocyte survival but poor contraction
Fetal embryogenesis of heart? Congenital heart disease results from what? E.g.? Multifactorial inheritance factors?
Single chamber until 5th week of gestation, divided by intra-ventricular and intra-atrial septa from endocardial cushions
Faulty embryonic development
VSD, ASD, PDA, Fallots
Single genes= trisomy 21= Downs, Turners, Di-George, infections- rubella, drugs, diabetes
Conditions with initial left-right shunt? Right-left shunt? No shunt?
VSD, ASD, PDA, trunks arteriosus
Tetralogy of Fallot, tricuspid atresia
Complete transposition of great vessels, coarctation, pulmonary stenosis, aortic stenosis, coronary artery origin from pulmonary artery, Ebstein malformation, endocardial fibroelastosis
Initial left to right shunting is fine, but progression to Eisenmenger’s complex involves what? Patent foramen oval eventually produces what?
Right side–> left side shunting associated with right cardiac failure and right site cardiac hypertrophy
Cardiac arrhythmia, pulmonary hypertension, right ventricular hypertrophy and cardiac failure, risk of infective endocarditis
Patent ductus arterioles (PDA) involves what shunting and therefore leads to what? Can be closed how?
Left to right shunting, meaning lung circulation is overloaded with pulmonary hypertension and right side cardiac failure
Risk of infective endocarditis
Surgically, by catheters or by prostaglandin inhibitors (indomethacin)
4 main features of tetralogy of Fallot? Shape on radiology and macroscopically? Result of pulmonary stenosis?
Pulmonary stenosis, ventricular septal defect, dextraposition/ over-riding septal defect, right ventricle hypertrophy
Boot-shape
Right ventricle shunted into left heart—> cyanosis from birth
Surgical correction during first 2 years of life, progressive cardiac debility and risk of cerebral thrombosis
What is complete transposition of the great arteries (TGA)? Bias to who, survival only possible if there is what? Tx?
The aorta coming off the right ventricle and pulmonary trunk off the left ventricle
Male bias, particular associated with diabetes, only if there is communication between the circuits and virtually all have an atrial septal defect allowing blood mixing
Arterial switch with less than 10% overall mortality
What is coarctation of the aorta? More common in who? Results? Associated with what?
Narrowing of the aorta at, or just distal to the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery)
Narrowing just after arch, excessive blood flow through carotid and subclavian vessels into systemic vascular shunts
Decreased renal perfusion after surgical correction even
Turner’s syndrome and berry aneurysms of the brain
What is secondary endocardial fibroelastosis a frequent complication of? Primary may follow a what?
Congenital aortic stenosis and coarctation
Profound dense collagen and elastic tissues deposited don endocardial aspect of left ventricle–> stiffening of heart
A familial pattern, both= rare
Ischaemic heart disease gives rise to main clinical presentations? Core problems?
Stable angina, acute coronary syndromes, myocardial infarction
Cardiac arrest/ sudden death, chest pain, shortness of breath
Risk factors for ischaemic heart disease? Reasons for imperfect blood supply to the heart?
Systemic hypertension, cigarette smoking, diabetes mellitus, elevated cholesterol
Atherosclerosis, thrombosis/ thromboembolism, artery spasm, collateral blood vessels, BP/HR/CO abnormalities, arteritis
Pathological complications of ischaemic damage?
Arrhythmias- supra ventricular and ventricular, left ventricular failure- cardiogenic shock, extension of infarction, rupture of myocardium, cerebral infarction, carotid atheroma, aortic aneurysm, PVD, gangrene
Where does stable angina result from?
Mismatch of supply of oxygen- due to anaemia, hyperaemia, polycythaemia and demand of myocardium- due to HTN, tachycarrhythmia, valvular heart disease, hyperthyroidism, hypertrophic cardiomyopathy
Cold weather, heavy meals and emotional stress= exacerbating factors
3 types of angina?
Stable- induced by effort and relieved by rest
Unstable (crescendo)- of recent onset or deterioration in previously stable angina with symptoms frequently occurring at rest, increasing frequency/ severity, on minimal exertion/ at rest, form of acute coronary syndrome
Prinzmetal’s angina- caused by coronary artery spasm (rare)
Clinical presentation of angina?
Central chest tightness or heaviness, provoked by exertion, provoked by exertion, especially after meal or in cold windy weather or by anger/ excitement
Relieved by rest/ GTN spray, pain may radiate to one/ both arms, neck, jaw or teeth
May be dyspnoea, nausea, sweatiness and faintness
Scoring of angina?
- Have central, tight, radiation to arms, jaw and neck
- Precipitated by exertion
- Relieved by rest or spray GTN
3/3= typical angina, 2/3= atypical, 1/3= non-anginal pain
Physics of stable angina?
Pouiseuille: as radius falls, pressure increases and so volume decreases- after radius falls below 75% it becomes noticeable- pt will not experience any symptoms until artery falls below 75%
Pain of angina (OPQRST)? Differential diagnosis of angina?
Onset, position, quality- nature/ character, relationship, radiation, relieving factors, severity, timing, treatment
Pericarditis, pulmonary embolism, chest infection, aorta dissection, gastro-oesophageal, musculoskeletal, psychological
ECG of someone with stable angina? Other forms of diagnosing?
May be normal/ show ST depression, flat/ inverted T waves, look for signs of past MI
ECG on patient, then make them run on treadmill uphill, monitor length of exercise, ST segment depression= sign of late-stage ischaemia, may patients= unsuitable
CT scan calciums scoring- CT heart, atherosclerosis- calcium= white
SPECT/ myoview- radio-labelled tracer injected into patient, taken up by coronary arteries where there is good blood supply- this will light up, no light after exercise= myocardial ischaemia
Lifestyle Tx of angina? Pharmacological?
Stop smoking, encourage exercise, weight loss, treat underlying conditions
Aspirin- anti platelet effect, COX inhibitor
Statins- HMG-CoA reductase inhibitors
Beta blockers- reduce heart contraction, B1 activation–> Gs–> cAMP to ATP–> contraction
GTN spray
Ca2+ channel blocker
Revascularisation- increase flow reserve: PCI and CABG
What is PCI? Pros and cons?
Dilating coronary atheromatous obstructions by inflating balloon within it, insert balloon and remove it, stent persists and keeps artery patent, expanding plaque= make artery bigger
Pros= less invasive, convenient, short recovery and repeatable
Cons= risk of stent thrombosis, not good for complex disease
What is CABG? Pros and cons?
Left internal mammary artery (LIMA) used to bypass proximal stenosis (narrowing) in LAD coronary artery
Pros: good prognosis, deals
with complex disease
Cons: invasive, risk of stroke/ bleeding, one time treatment, need to stay in hospital- long recovery
What do betablockers reduce? Side effects? Do not give in what conditions?
HR (negatively chronotropic,) left ventricle contractility (negatively inotropic,) cardiac output
Tiredness, nightmares, bradycardia, erectile dysfunction and cold hands and feet
Asthma, heart failure/ heart block, hypotension and bradyarrhythmias
What does GTN spray do and reduce? Side effect?
Venodilator- nitrate
Dilates systemic veins thereby reducing venous return to right heart
Reduces preload, work of heart and O2 demand, also dilates coronary arteries
Profuse headache immediatly after use
What do calcium channel blockers do and reduce?
Primary arterodilators
Dilates systemic arteries resulting in BP drop, reduces afterload on heart, less energy to produce same CO
Less work on heart and O2 demand e.g. verapamil
Acute coronary syndromes umbrella that includes what things? With a STEMI you develop what? Usually diagnosed with what? Produce what some time after MI?
STEMI, NSTEMI (acute myocardial infarction) and unstable angina
Complete occlusion of a major coronary artery, causes full thickness damage of heart muscle
Diagnosed on ECG at presentation–> Q wave some time after MI so also known as Q-wave infarction
What is unstable angina? When does an NSTEMI occur?
Angina of recent onset (less than 24 hours,) or cardiac chest pain with crescendo pattern, deterioration in previously stable angina, with symptoms frequently occurring at rest
Angina of increasing frequency or severity, on minimal exertion or even at rest
When developing a complete occlusion of a minor or partial occlusion of a major coronary artery previously affected by atherosclerosis
Causes partial thickness damage of heart muscle
Diagnosis after troponin results and sometimes other investigation results available
Also known as non-Q wave infarction–> myocardial necrosis and rise in serum troponin/ creatine kinase-MB (CK-MB)
5 types of MI?
Type 1= spontaneous MI with ischaemia due to primary coronary event e.g. plaque erosion/ rupture, fissuring or dissection
Type II= MI secondary to ischaemia due to increased O2 demand/ decreased supply such as in coronary spasm, coronary embolism, anaemia, arrythmias, hypertension or hypotension
Type 3,4,5: MI due to sudden cardiac death, related to PCI and related to CABG respectively
Risk factors of ACS? Pathophysiology?
Age, male, family history of IHD, smoking, hypertension, diabetes mellitus, hyperlipidaemia, obesity and sedentary lifestyle
Rupture/ erosion of fibrous cap of coronary artery plaque–> platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation
Platelets release serotonin and thromboxane A2–> myocardial ischaemia
Plaque and occlusion in unstable angina? In myocardial infarction?
Necrotic centre and ulcerated cap–> partial occlusion
Necrotic centre–> total occlusion
Clinical presentation of unstable angina?
Chest pain; new onset, at rest with crescendo pattern, breathlessness, pleuritic pain, indigestion, new onset angina
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily activities
Acute central chest pain, lasting more than 20 minutes, associated with:
sweating, nausea and vomiting, dyspnoea, fatigue, shortness of breath, palpitations
May present without chest pain e.g. in elderly/ diabetics
Distress and anxiety, pallor, increased pulse and reduced BP, reduced 4th heart sound, may be signs of heart failure, tachy/ bradycardia, peripheral oedema
Differential diagnosis of unstable angina? ACS on ECG?
Angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism, oesophageal reflux/ spasm
Can be normal, ST depression and T-wave inversion, hyperacute T waves
STEMI–> persistent ST-elevation, hyperacute T waves or new LBBB pattern, may see pathological Q waves few days after MI
Troponin T and I levels in ACS?
Most sensitive and specific markers of myocardial necrosis
Serum levels increase within 3-12 hours from onset of chest pain and peak at 24-48 hours, fall back to normal over 5-14 days
Prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation
CK-MB can be used as marker for what? Low accuracy why? Can be used to determine what? Myoglobin elevated when? Look for what on CXR?
Myocyte death- low accuracy= present in serum of normal individuals and in patients with significant skeletal muscle damage
Re-infarction as levels drop back to normal after 36-72 hours
Very early in MI, test= poor specificity since myoglobin present in skeletal muscle
Cardiomegaly, pulmonary oedema or widened mediastinum (aortic rupture)
Pain relief in ACS? Oxygen sats? Groups of anti-platelet therapy and method of taking?
Aspirin(oral)
P2Y12 inhibitors (oral)- inhibit ADP-dependent activation of IIb/IIIa glycoproteins, preventing amplification response of platelet aggregation, alongside aspirin in dual anti-platelet
Glycoprotein IIb/ IIIa antagonists- only IV
Beta blockers(IV and oral)
Statins (oral)- HMG- CoA reductase inhibitors
ACE inhibitors
Non-pharm treatment of ACS?
PCI and CABG
Risk factor modification- stop smoking, lose weight and exercise daily, healthy diet, treat hypertension and diabetes, low fat diet with statins
What is an acute MI and two types? Most common medical emergency? Risk factors?
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombus
STEMI- complete occlusion of major coronary artery, full thickness damage, diagnosed on ECG at presentation, tall T waves, ST elevation, pathological Q wave
NSTEMI- complete occlusion of minor/ partial occlusion of major coronary artery, partial thickness damage, retrospective diagnosis after troponin results, ST depression/ T wave inversion
STEMI
Age, male, history of prem coronary heart disease, premature menopause, diabetes mellitus, smoking, hypertension, hyperlipidaemia, obesity and sedentary lifestyle, family history of IHD
Pathophysiology of acute MI?
Rupture/ erosion of vulnerable fibrous cap of coronary artery atheromatous plaque–> platelet aggregation, adhesion, local thrombosis, vasoconstriction and distal thrombus embolisation–> prolonged complete arterial occlusion–> myocardial necrossi within 15-30 minutes in STEMI
STEMI= sub-endocardial myocardium initially affected but continuted ischaemia, infarct zone extends through sub-epicardial myocardium–> transmural Q wave MI, early reperfusion may salvage regions
Clinical presentation of acute MI?
Severe chest pain for more than 20 minutes
Pain radiate to left arm, jaw, neck
Does not usually response to sublingual GTN spray- opiate analgesia required
Pain described as substernal pressure, squeezing, aching, burning or sharp pain, with sweating, nausea, vomiting, dyspnoea, fatigue and/ or palpitations
Breathlessness, fatigue, distress and anxiety, pale, clammy and marked sweating, significant hypotension, bradycardia or tachycardia
Differential diagnosis of acute MI? Diagnosis of STEMI and NSTEMI?
Stable angina, unstable angina, NSTMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis, MSK chest pain
On presentation, ST elevation, tall T waves, LBBB, T wave inversion and pathological Q waves
NSTEMI= retrospective diagnosis, ST depression and T wave inversion
Infarct site anteriorly, leadings showing change? Inferior? Lateral? Posterior? Subendocardial?
ST elevation V1-V3 ST elevation II, III, AVF I, AVL, V5-V6 ST depression V1-V3, dominant R wave, ST elevation V5-V6 Any
Treatment of MI pre-hospital? In hospital? Coronary revascularisation?
Aspirin 300mg chewable, GTN (sublingual,) morphine
IV morphine, oxygen if their sats are below 95%/ breathless, beta-blocker- atenolol, P2Y12 inhibitor- clopidogrel
PCI: presented to all patients who present with acute STEMI who can be transferred–> primary PCI centre within 120mins of first medical contact, not possible- give fibrinolysis and transfer to PCI centre after infusion
CABG- fibrinolysis enhance breakdown of occlusive thromboses by activating plasminogen–> plasmin
Risk factor modification following MI? Secondary prevention?
Stop smoking, lose weight and exercise daily, healthy diet, treat hypertension and diabetes, low fat diet with statins
Statins, aspirin long term, warfarin if large MI, B blockers and ACE inhibitors
Complications of MI?
Sudden death- often due to VF, arrhythmias- in first few days, persistent pain- 12 hours to few days after due to necrosis
Heart failure- ventricular dysfunction and necrosis
Mitral incompetence- first few days or later
Pericarditis- transmural infarct–> inflammation of pericardium, more common in STEMI
Cardiac rupture- early= from shearing between mobile and immobile myocardium
Late= due to weakening of wall following muscle necrosis and acute inflammation
Ventricular aneurysm- due to stretching of newly formed collagenous scar tissue
What is type A coronary prone behaviour pattern described as? Methods of assessing behaviour?
Friedman and Rosenman- competitive, hostile, impatient
Questionnaires- MMPI, Jenkins Activity survey and Bortner Rating Scale, self-report= poorer predictors, structured clinical interview
Depression/ anxiety could share common what? Measurement instruments?
Antecedents e.g. social deprivation
MMPI, Beck depression inventory (BDI,) general health questionnaire, Spielbergers’ State anxiety inventory
Significant associations between MI and what? Research supports role of what in relation to stress and adverse coronary health outcomes? Association between social relationships and morbidity/ mortality?
Psychosocial job characteristics
Psychological demands, control and social support
Quantity and quality found to be related- helps coping with life events, motivation to engage in healthy behaviours
What can doctors do to improve psychosocial factors influencing CHD?
Observe/ explore behaviour patterns
Identify signs of depression/ anxiety, ask questions from assessment tools, ask patients about their job/occupation, available support and liaise with relevant services
What is race? Ethnicity/ ethnic group?
Classification based on physical characteristics into which humankind was divided- separate biological races no longer accepted as scientifically valid/ ethically useable, ethnic group= preferable
Group of people whose members identify with each other through common heritage- common language, culture of ideology which stresses common ancestry, superseded biological idea of ‘race’
3 forms of socioeconomic position and circumstance? What does vulnerable mean? Social exclusion?
Income, class- ownership of assets, status- hierarchy/ prestige
Indicates inability to cope with hostile environment, not lucky enough to have coping mechanisms needed for everyday living
Inability of individual group/ community to participate effectively in economic, political and cultural life: alienation and distance from mainstream society e.g. travellers, asylum seekers, refugees, from BME groups
Ethnic differences in health? Men in Caribbean risk of stroke and CHD? % White British in UK?
Genetic/ biological factors, individual behaviour/ cultural factors, material/ structural factors, migration and racism, inequalities in access to healthcare, artefact
50% more likely to die from stroke, but lower mortality from CHD
87%
Psychosis how many times in Afro-Caribbean than in White British? TB tends to impact heavily on who? Overall cancer rates lower in who? Lung cancer lower in who compared to who?
x7
Poorest and most marginalised groups including migrant communities- latent can be missed and extrapulmonary TB misunderstood, unstable living conditions can interfere with treatment and recovery
Lower in BME, lower in S Asia, Caribbean and Africa than Ireland and Scotland- smoking?
Thrombosis occurs in what 2 systems? Pressures and rich in what? Can cause what?
Arterial- high pressure: platelet rich, can lead to stroke/ MI, venous= low pressure, fibrin rich, cause PE/ DVT
Arterial thrombosis in coronary, cerebral and peripheral circulations can lead to what? Risk factors?
Coronary–> MI, cerebral–> CVA/ stroke, peripheral–> peripheral vascular disease (claudication, rest pain, gangrene)
Smoking, hypertension, diabetes, hyperlipidaemia, obesity/ sedentary lifestyle, stress/ type A personality
How is arterial thrombosis diagnosed?
If MI–> history, ECG, cardiac enzymes, if CVA–> history and examination, CT scan/ MRI, peripheral vascular disease–> history and examination, ultrasound, angiogram
Treatment for AT if coronary circulation/ MI? If cerebral circulation/ stroke?
Aspirin, thrombolytic therapy- streptokinase tissue plasminogen activator, degrades fibrin
Aspirin, clopidogrel, fibrinolytics IV (streptokinase, alteplase)
Treat risk factors- during window of opportunity
2 main forms of venous thrombosis? Causes?
Pulmonary embolism and DVT
Surgery, immobilisation, oestrogens, malignancy, long haul flights, inherited thrombophilia, acquired- anti-phospholipid syndrome, Lupus anticoagulant, hyperhomocysteinaemia
Prevention of VT?
Mechanical- hydration, early mobilisation, compression stockings, chemical- LMWH, lower dose, thromboprophylaxis: low risk= <40 yrs, high risk= hip, knee, pelvis surgery, malignancy, increased risk factors, prolonged immobility
Diagnosis of DVT?
1) D-dimer- negative= normal, positive= also in pregnancy, infection, malignancy and post-op
2) Compression ultrasound of proximal veins- can’t squash= DVT in femoral and popliteal veins
Treatment of DVT?
a) Anticoagulants- SC/IV e.g. heparin, Fondaparinux, enoxaparin, Dalteparin, LMWH for min 5 days
b) Warfarin- oral= prevent recurrence, short term, lifelong for mechanical valve replacement
Compression stockings, treat underlying cause
Spontaneous= more likely to recur than provoked
Symptoms of DVT?
Typically around calf and ankle, unilateral, difficulty walking, warmth, non-specific, diagnosis= unreliable, pain, swelling, signs= tenderness, swelling, warmth, discolouration
Formation of pulmonary embolism? Symptoms? Signs?
Clot starts in leg–> IVC into right side of heart–> pulmonary heart, big= blocks both, obstructs–> pulmonary hypertension, tachycardia, cyanosis, R heart strain, close to death
Breathlessness, pleuritic chest pain(could be infection, MSK, pneumothorax,) signs/ symptoms of DVT, no other likely diagnosis (could be asthma, COPD, pneumonia, MI, HF)
Tachycardia, tachypnoea, pleural rub
Diagnosis of PE?
CXR usually normal in PE, look for pneumonia, ECG- sinus tachy, exclude cardiac cause, mainly to exclude alternative causes
D-dimer- excludes diagnosis, ventilation/ perfusion scan- mismatch defects, better for pregnant- less radiation, CTPA spiral CT with contrast- visualise major segmental thrombi
Treatment for PE?
As for DVT- ensure normal Hb, platelets, renal function, baseline clotting, LMW heparin adjusted for 5 days, oral warfarin INR for 6 months
Treat cause if possible, IVC filter if cannot anticoagulate using unaffected groin
Structure of pericardium? What is within pericardium?
2 layers- visceral single cell layer adherent to epicardium, fibrous parietal layer 2mm thick, collagen and elastin fibres, 50ml serous fluid
Great vessels
Left atrium= mainly outside pericardium, parietal layer= fibrous attachments to fix heart to thorax
Function of pericardium?
Restrains filling volume of heart, stiff at higher tension, small reserve volume, if volume exceeded- pressure translated to cardiac chambers, small amount added to space has dramatic effect on filling but so does removal of small amount= tamponade physiology
What is acute pericarditis? Causes?
Inflammation of pericardium
Viral-flu, Epstein-Barr, varicella, HIV, bacterial- pneumonia- rheumatic fever, TB, staphs, streps, MAI in HIV
Fungi, autoimmune- Sjogrens syndrome, scleroderma, systemic vasculitides, neoplastic- secondary metastatic tumours, metabolic- uraemia, myxodema
Clinical features of pericarditis?
Central chest pain worse on inspiration or lying flat plus/ minus relief by sitting forward, friction rub may be heart, evidence of cardiac tamponade/ pericardial effusion, fever
Investigation of pericarditis?
ECG classically concave- saddle-shaped, ST segment elevation
Blood test- FBC, ESR, U and E, cardiac enzymes- troponin may be raised, viral serology, blood cultures
CXR- cardiomegaly
ECHO- if suspected pericardial effusion
Treatment of pericarditis?
Analgesia- ibuprofen, treat the cause, consider colchicine before steroids/ immunosuppressants if relapse or continuing symptoms occur
Differential diagnosis of pericarditis? Signs of constrictive pericarditis?
Pneumonia, pulmonary embolus, chosochondritis, gastro- oesophageal reflux, myocardial ischaemia/ infarction, aortic dissection, pneumothorax, pancreatitis, peritonitis, herpes zoster
Mainly of right heart failure w/JVP, Kussmaul’s sign, soft diffuse apex beat, quiet heart sounds, S3, diastolic pericardial knock, hepatosplenomegaly, ascites and oedema
Tests for constrictive pericarditis? Management?
CXR- small heart and/ not with pericardial calcification-if not, CT/MRI helps distinguish from other cardiomyopathies, ECHO–> cardiac catheterisation
Management: surgical excision
What is pericardial effusion? Causes? Clinical features?
Accumulation of fluid in pericardial sac
Any cause of pericarditis
Dyspnoea, raised JVP, bronchial breathing at left base, signs of cardiac tymponade
Diagnosis and management of pericardial effusion?
CXR- enlarged, globular heart
ECG- low-voltage QRS complex and alternating QRS morphologies, ECHO- echo-free zone surrounding heart
Treat cause, pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or therapeutic (cardiac tamponade)
Send fluid for culture, ZN stain/ TB culture and cytology
What is cardiac tamponade? Causes? Signs?
Accumulation of pericardial fluid- raises intrapericardial pressure, hence poor ventricular filling and fall in CO
Any pericarditis, aortic dissection, haemodialysis, warfarin, trans-septal puncture at cardiac catheterisation, post cardiac biopsy
Pulse, BP, pulsus paradoxus, JVP, Kussmaul’s sign, muffled S1 and S2
