Cardiology Flashcards
Atherosclerosis
Plaque rupture
Thrombus formation
Partial/complete arterial blockage
Heart attack, stroke or gangrene
RFs for atherosclerosis
Increasing age Smoking Raised cholesterol Obesity Diabetes Hptn Fx
Distribution of atherosclerotic plaques
Peripheral and coronary arteries
Focal distribution along artery length
Distribution governed by haemodynamic factors - Changes in blood flow/turbulence (such as bifurcations) cause the artery to alter endothelial cell function
Structure of an atherosclerotic plaque
Lipid
Necrotic core
Connective tissue
Fibrous cap
Plaque
Occlusion - Angina
Rupture - Thrombus formation (and death)
Causes of inflammation in arterial wall
LDL - Accumulates in arterial wall
Endothelial dysfunction due to injury
Stimulus for adhesion of leukocytes
Once inflammation is initiated, chemoattractants (chemicals that attract leukocytes) are released from endothelium and send signals to leukocytes
Chemoattractants are released from site of injury and a conc grad is produced
Stimulus = Chemoattractants
Inflammatory cytokines found in plaques
IL-1,6,8
IFN Gamma
CRP
Leukocyte recruitment to vessel walls
Mediated by selectins, integrins and chemoattractants
Cause leukocytes to roll, adhere and transmigrate
Progression of atherosclerosis - Stage 1
Fatty streaks - earliest lesion of AS
Early ages - less than 10 y.o
Progression of atherosclerosis - Stage 2
Intermediate lesions
Composed of foam cells (lipid laden macrophages), vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall, isolated pools of extracellular lipid
Progression of atherosclerosis - Stage 3
Advanced lesion - Fibrous plaque
Impedes blood flow
Prone to rupture
Dense fibrous cap made of collagen (strength) and elastin (flexibility) laid down by smooth muscle cells
May be calcified
Contains smooth muscle cells, macrophages, foam cells and T lymphocytes
Progression of atherosclerosis - Stage 4
Plaque rupture
Plaque is constantly growing and receding (resorbed and redeposited)
Cap becomes weak and plaque ruptures
Thrombus formation and vessel occlusion
Progression of atherosclerosis - Stage 5
Plaque erosion
Lesions tend to be early lesions
Fibrous cap thick may
Treating coronary artery disease
PCI - Percutaneous coronary intervention
Stent implantation
Restenosis
Narrowing/blocking of vessel lumen after surgical correction
Drug elution
Anti-proliferative and inhibits healing
Reduce restenosis
Useful drugs in atherosclerosis
Aspirin
Clopidogrel
Statins
ECG and drug toxicity
Digoxin prolong the QT interval
Depolarisation
Contraction of a muscle
Pacemakers of the heart
SAN (Dominant) - 60-100bpm
AVN (Back-up) - 40-60bpm
Ventricular cells (Back-up) - 20-45bpm
Standard calibration of an ECG
25mm/s (speed)
0.1mV/mm (voltage)
Impulse conduction
SAN AVN Bundle of his Bundle branches Purkinje fibres
PQRST
P - Atrial depolarisation
QRS - Ventricular depolarisation
T - Ventricular repolarisation
PR interval - allows time for atria to contract before ventricles
1st degree heart block
Long PR interval
QRS abnormalities
Ventricular enlargement
Conduction blocks
Angina types
Prinzmetal’s angina (coronary spasm)
Microvascular angina
Crescendo angina
Unstable angina (Critical ischaemia - plaques severely occluding artery)
IHD history
Personal details Presenting complaint Past med history Drug history, allergies Fx (only first degree relatives) Social history (smoking) Systematic enquiry
Cardiac symptoms
Chest pain Breathlessness Fluid retention (HF) Palpitation Syncope or pre-syncope
Pain
OPQRST Onset Position (site) Quality (nature/character) Relationship (exertion, posture, meals, breathing, etc) Radiation (Throat, arm, upper body) Relieving/aggravating factors Severity Timing Treatment (does it work immediately)
Chest pain - Differential diagnosis
MI Pericarditis/myocarditis Pulmonary embolism/pleurisy Chest infection/pleurisy Dissection of aorta Gastro-oesophageal (reflux, ulceration, spasm) MSK - Arthritis Psychological - Anxiety
Treatment
Lifestyle - Smoking, weight, exercise, diet
Advice for an emergency - 999
Medication
Revascularisation
NICE guidelines for angina - GP
History - typical/atypical angina?
Exam - exacerbating causes
Investigations - Routine bloods, lipids, ECG
Angina? - Refer to cardio
Treat - Smoking cessation, aspirin, BB, statin, GTN spray
NICE guidelines for angina - Cardiologist
Diagnostic test - CTCA (CT coronary angiogram)
High risk/CTCA shows stenoses - Refer to cath lab
Exercise testing
The patient runs on treadmill whilst ECG records
Myoview scan
Perfusion scan
Stress echo
Echocardiogram
Perfusion MRI scan
Gold standard
Indicates the structure and function of the heart - any ischaemic areas are highlighted
Invasive coronary angiography
Through radial artery
Not diagnostic, more about treatment planning (what interventions are appropriate)
Angina - 1st line drug - BB
BB - Lowers HR, Lowers LV contractility which together lower cardiac output and demand
SEs of BB - Tiredness, bradycardia, cold hands and feet, erectile dysfunction
CIs of BB - Asthma patients
Angina - 2nd line drug - Nitrates
Dilate vessels and reduce preload on the heart
Dilate coronary vessels
SE - Headache
Angina - 3rd line drug - CCB
Reduce afterload on the heart
Dilate arterial vessels
SE - Flushing, swollen ankles, postural hypotension
Angina - 4th line drug - Aspirin
Antiplatelet and anti-inflammatory
Cyclo-oxygenase inhibitor
SE - Gastric
Angina - 5th line drug - Statins
HMG CoA reductase inhibitors
Angina - 6th line drug - ACEi
Ramipril
Revascularisation
PCI/CABG
MDT meeting
Coronary angioplasty/Stenting -
PCI - Percutaneous coronary intervention
Risks - stent thrombosis, restenosis
CABG
If a stent is not appropriate then bypass is next step
Coronary artery bypass graft
Risks - v invasive, stroke risk, chest bleeding risk
PCI and CABG use
STEMI - PCI
NSTEMI - PCI>CABG
Stable angina - PCI/CABG
Unstable angina
Cardiac chest pain at rest
Diagnosis - Troponin level is not increased
Acute MI
ST elevation
Non ST elevation - retrospective diagnosis
MI - ECG features
ST elevation - can be inverse which confirm MI
Q waves - broad and deep indicate pathology
Poor R wave progression
Biphasic T wave
MI
Cardiac chest pain - persistent, severe but can be mild, occurs at rest, sweating, breathlessness, N/V
Causes permanent heart muscle damage
Higher risk - higher age, diabetes, renal failure, left ventricular systolic dysfunction
MI - Initial management
999
If ST elevated - transfer to PCI
Aspirin immediately
Pain relief
MI - hospital management
Oxygen therapy - if hypoxic
Pain relief - Narcotics/nitrates
Antiplatelets - Aspirin +/- P2Y12 inhibitor
BB
Coronary angiography - If troponin elevated
MI - Causes
Atherogenesis/atherothrombosis
Troponin
Protein complex regulates actin/myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for ACS
Antiplatelet drugs
Aspirin
Streptokinase
P2Y12 inhibitors
Clopidogrel
Used in combo with aspirin to manage ACS (Dual antiplatelet therapy)
Clopidogrel is a prodrug - activated by CYP450 enzymes
Drug interactions - Omeprazole
Tricagelor (rapid onset and offset) is preferred over clopidogrel (much more irreversibly bound to CYP450 which makes offset delayed)
Adverse effects - Bleeding (GI), haematuria, rash
Anticoagulants
Target thrombin
Inhibit fibrin formation and platelet activation
Heparin used during PCI/CABG
ACS - Order of medication
Initial pain relief - Morphine/nitrates Antiplatelet - Aspirin + clopidogrel Anticoag - Heparin BB, CCB Statins, ACEi
Heart weight
Heavier in males than females
Heart is composed of these proteins
Sarcomere proteins
Protein conformational change = contraction
Heart contraction
2 stage electrical generated contraction
Contractioon initiated by depolarisation and changes to calcium conc
Heart relaxation
Removal of calcium mediates relaxation
Types of cardiac myocytes
AV conduction system (fast conduction)
General cardiac myocyte
Heart failure
Failure to transport blood out of heart
Cardiogenic shock - severe failure
Myocardial hypertrophy
Athletes
Pregnancy
Diabetic complications
Stroke CVD (leading cause of mortality) Peripheral vascular disease Diabetic retinopathy, Blindness Diabetic neuropathy
Diabetic neuropathy - Consequences
Pain - burning, paraesthesia, nocturnal exacerbation, sharp and shoots up legs
Autonomic - Diarrhoea, urinary incontinence, erectile dysfunction
Insensitivity - Foot ulceration, infection, falls (lead to amputation)
Diabetic peripheral neuropathy
Typical ‘glove and stocking’ sensory loss
DN - Risk factors
Hptn
Smoking
Hba1c
DN - Treatment
Glycaemic control
SSRIs
Anticonvulsants - Carbamezapine, gabapentin)
Opioids - Tramadol, oxycodone
Diabetic foot ulceration
15% of people with DM
Diabetic amputation - pathophysiology
Neuropathy or vascular cause Trauma Ulcer Failure to heal Infection Amputation
Neuropathy
Painless nature of diabetic foot disease
DN - Complications
Motor nerve damage
Localised callus (hard skin)
Autonomic nerve damage - dry skin which leads to cracks/fissures and makes feet susceptible to infection. Treat by moisturising twice a day
DPN - Screening tests
Test sensation - Monofilament, neurotip, tuning fork
Peripheral vascular disease
Decreased perfusion due to macrovascaular disease
More distal sites
Ischaemia in legs
High rates of amputation
PVD - Symptoms
Intermittent claudication - pain and cramping (ischaemic legs)
PVD - Signs
Absent pedal pulses
Coolness of deet
Poor skin and nails
PVD - Investigation
Doppler
Duplex arterial imaging
PVD - Treatment
Smoking cessation
Surgery
MDT foot clinic (for ulcers)
Pressure-relieving footwear, podiatry
Diabetic retinopathy
The commonest cause of blindness in adults
DR - RFs
Diabetes (chronic)
Poor glycaemic control - Hba1c raised
Hptn
Pregnancy
DR - Eye screening
Retinal photographs
DR - Pathogenesis
Leakage of blood vessels
Occlusion of blood vessels
Micro-aneurysms - Pericyte loss and smooth muscle cell loss
Basement membrane thickens
Reduces junctional contact with endothelial cells
Glial cells grow down capillaries - Ischaemia and occlusion due to proliferation
These lead to changes in the retina and then blindness occurs as a result
DR - Treatment
Laser therapy - burns off abnormal blood vessels to prevent leakage etc
Not curative, just stabilises disease to prevent progression to blindness
Photocoagulation - burns as much of retina as possible, which unfortunately leads to tunnel vision with only central vision surviving
Diabetic nephropathy
Diabetes is main cause of end stage renal disease
Diabetic nephropathy
Hallmark is proteinuria
Progressive decline in renal function
RFs - Poor BP and BG control
Major RF for CVD
Diabetic nephropathy - Pathogenesis
Glomerulus changes - Thickening of BM
Glomerular injury
Filtration of proteins
DN occurs
End-stage renal disease
Stage 5 CKD
Nephropathy in T1DM and T2DM
T1DM - Microalbuminuria develops 5-10 years after diagnosis
T2DM - Microalbuminuria present at time of diagnosis
Diabetic nephropathy - Treatment
ACEi
Statins - Cholesterol control
Diabetes screening
Urine dip - Albumin:Creatinine ratio
Retinal photography
Foot exam (10g monofilament)
T2DM meds - Insulin sensitisers (first line)
Metformin
Pioglitazone
T2DM meds - Increase beta-cell function (second line)
Sulphonylureas
DDP4i
GLP1 receptor agonists
Diabetes lab tests
Fasting plasmaa glucose Hba1c Na, K, Ur, Crt Urine - Alb:Crt ratio LFTs - AST, ALT Lipids - T Chol, HDL, Trig
Diabetes - Lifestyle interventions
Local education programmes - In sheffield = Desmond and xpert
Exercise - 30mins a day
Dietician
T2DM - Pharmacotherapy regimen
1st line - Metformin (reduces insulin resistance) - Weight neutral/loss
2nd line - Sulphonylurea - Weight gain occurs
3rd line - DPP4i - Prolongs action of GLP1 (no weight change with DPP4i). GLP1 induce weight loss
4th line - SGLT2i (Reduce reabsorption of glucose in kidneys in proximal tubules from going back into the bloodstream) - Weight loss
5th line - Insulin - Weight gain
Bariatric surgery
Surgical weight loss in T2DM
BMI above 35
Reduce stomach size (gastric bypass) so patients appetite is reduced and weight loss occurs
Improves glycaemic control
DVT - Symptoms
Pain
Swelling
DVT - Signs
Tenderness
Swelling
Warmth
Discolouration
Proximal DVT
More problematic
Between hip and knee
DVT - Investigations
Ultrasound compression test for proximal veins (popliteal fossa) - if vein squashes flat then no DVT, if can’t squash flat then DVT possible
D-dimer blood test - Normal result excludes diagnosis, Raised result is not specific for thrombosis (cannot confirm diagnosis)
D-dimer is used after ultrasound to confirm diagnosis
Infection and inflmmation can raise D-dimer level which is why it’s not specific for DVT
Raised D-dimer is common
Low Hb =
Anaemia
DVT - Treatment
1st line - LMW Heparin (anticoag) - minimum 5 days
2nd line - Oral Warfarin (anticoag) - 3-6 months
DOAC - Direct-acting oral coag
Compression stockings - Decrease swelling and risk of long term post-thrombotic syndrome
DVT - Causes
Thrombophilia
Malignancy
DVT - RFs
Surgery Immbolity Leg fracture Pregnancy (Oestrogen raised) Long haul flights/travel (rare though) Inherited thrombophilia (genetic predisposition) - Caucasians
DVT - Prevention
Compression stockings Early mobilisation Hydration Mechanical foot pumps Chemical thromboprophylaxis - LMW Heparin
Thromboprophylaxis
Not required in young patients having short duration surgery
Required in high risk, long duration surgery
Pulmonary embolism
DVT which has broken off from vein and gone through heart and blocking up pulmonary artery
A big clot will block up both./bifurcation of pulmonary aeries and results in death
Pulmonary embolism
Hypotension
Cyanosis
Severe dyspnoea
Right heart failure
Pulmonary embolism - Removal
Embolectomy
Thrombolysis - mechanical or chemical (tPA)
Pulmonary embolism - Presentation
Chest pain - pleuritic SOB/breathlessness Haemoptysis - if pulmonary infarct Signs of DVT in legs Signs - Tachycardia, tachypnoea
PE - Investigations
CXR - Usually normal
ECG - May show sinus tachycardia, ECG to rule out cardiac causes
D-dimer - raised then do imaging, if normal then no pulmonary embolus (not specific though)
CTPA - Spiral CT with contrast, visualise major segmental thrombi - major diagnostic tool
Ventilation/perfusion scan - Mismatch defects
PE - Treatment
Same as DVT - LMW Heparin then warfarin/Or DOAC (Only in outpatients with minor PE)
If cannot anti-coag, consider IVC filter insertion to prevent further PE, however, legs may embolise as a result
PE - Prevention
Same as DVT
Warfarin
Oral Works on liver Prevents synthesis of active factors - 2,7,9,10 (still synthesised but do not work, does this by interfering with VitK pathway) VitK antagonist Long half-life Prolongs prothrombin time Narrow therapeutic range - have to keep monitoring INR Lots of drug interactions
INR
International normalised ratio
Derived from prothrombin time
DOAC
New oral anticoag drugs Oral Directly act on factors 2,10 (not via liver, more direct) No blood tests or monitoring required Short half life Not used in pregnancy Used for treatment/thromboprophylaxis Only used for INR target ranges of 2-3 (small targets)
DVT vs PE mortality
PE kills as opposed to DVT
Thrombosis
Blood coag inside a vessel
Thrombosis
Arterial - High pressure, platelet-rich - use antiplatelets (aspirin)
Venous - Low pressure, fibrin rich - anticoag (DOACs)
Arterial thrombosis - Consequences
MI
Stroke
Gangrene
MI diagnosis
ECG
Cardiac enzymes
Peripheral vascular disease diagnosis
Ultrasound
Angiogram
Arterial thrombosis - Treatment
Aspirin Clopidogrel Prasugrel Tiglacor Anti-platelet
Venous thrombosis - Causes
Genetic - Antithrombin deficiency, Factor 5 Leiden
Acquired - Anti-phospholipid syndrome (autoimmune)
Haemophilia
Lack of clotting factors
Heparin
Glycoaminoglycan Binds to antithrombin and increases its activity Indirectly inhibits prothrombin Injected Protamine reverses effects of heparin
LMW Heparin
Smaller molecule
Less variation in dose
Aspirin
Inhibits cyclo-oxygenase irreversibility
Inhibits thromboxane formation and hence platelet aggregation
Used in arterial thrombosis
Clopidogrel
Similar to aspirin
Irreversible platelet inhibitor
Target ADP receptor of platelet
Pericarditis
Cause of acute chest pain
Cardiac biomarkers
Troponin and CK
Pericardial sac
lubricates the heart
50ml of fluid
Cardiac tamponade - alteration of fluid level in pericardial sac
Acute pericarditis
Inflammation of pericardium
With or without pericardial effusion
Features - Chest pain, friction rub, ECG changes, pericardial effusion
Pericarditis - Causes
Infectious) Viral - common - Enteroviruses Bacterial - uncommon - TB Non-infectious) Autoimmune - RA, Sjogrens syndrome Neoplastic - Secondary metastatic tumours Trauma/iatrogenic - Direct injury
Pericarditis - Presentation
Chest pain - Severe, sharp, pleuritic, rapid onset, radiates to arm//trapezius ridge, relieved by sitting forward, exacerbated by lying down
Dyspnoea
Cough
Pericarditis - Examination
Pericardial rub - crunching snow
Sinus tachycardia
Fever
Effusion (pulsus paradoxus)
Pericarditis - Investigations
ECG - Saddle shaped, ST elevation, PR depression, concave ST segment
Bloods - Raised ESR/CRP, raised troponin, raised WBC
CXR
Echocardiogram
Cardiac tamponade - Signs
Pulsus paradoxus - Fall in systolic BP of >10mmHg
Pericarditis - Management
NSAIDs - Aspirin (high dose)
Pericarditis - Complications
Cardiac tamponade
Constrictive pericarditis
Calcified pericardium
Treatment - Pericardectomy (surgical removal of pericardium)
Pericarditis
Bacterial worse than viral
Dresslers syndrome
Secondary pericarditis with or without pericardial effusion, occurs as a result of injury to the heart
Cardiomyopathies
Hypertrophic - muscle thickens
Dilated - Heart chambers dilated
Arrhythmogenic - Structural abnormality leading to rhythm disturbances
Diseased desmosomes (adhesion molecules)
Hypertrophic cardiomyopathy
Diastolic dysfunction
Fibrosis scar tissue
ECG abnormality - Repolarisational T wave inversion, ventricular tachycardia
Dilated cardiomyopathy
Chamber dilation
Contraction impaired - heart failure
Arrhythmogenic cardiomyopathy
Arrhythmias Myocyte death - replaced by fibrous fatty tissue Ventricular Epsilon waves Diseased desmosomes (adhesion molecules)
Naxos disease
Palmar plantar caratiderma (hand and foot skin thickened)
Wooly hair
Abnormal ECG - Ventricular arrhythmias
Recessive disease
Ion channels abnormalities
Voltage-gated
Protein based
Normal heart (asymptomatic) with ECG abnormalities (electrical problem) - Long QT syndrome, brugada syndrome
Brugada syndrome
Ion channel abnormality
Ajamline test - diagnostic
CPVT
Catecholaminergic polymorphic ventricular tachycardia
Adrenaline driven - Stress, activity
Marfan syndrome
Fibrillin disorder
Genetic disorder of connective tissue - tall and thin figure, long arms, legs, fingers and toes
Aortic aneurysms
Familial hypercholesterolemia
LDL receptor genetic mutation - not taking up LDL Vascular disease is a complication Heart attack risk increased Lipid deposition in hands, tendons, eyes Raised cholesterol
Hypertension
Treat to reduce risk, not symptoms
Major risk factor for - Stroke, MI, HF, chronic renal disease, AF
Asymptomatic by itself
140/90
ABPM
Ambulatory blood pressure monitoring
Slightly lower than clinical BP
Hypertension - Diagnosis
Stage 1 - 140/90
Stage 2 - 160/100
Severe - 180/110
Hptn - Treatment
Lifestyle
Antihypertensive drug therapy
Secondary hptn - Underlying causes
Renal
Adrenal
Only treat hptn if patient has
Target organ damage
CV disease
Renal disease
Diabetes
BP targets
Under 80 years - 140/90
Over 80 years - 150/90
Mechanisms of BP control - Targets for therapy
Cardiac output and peripheral resistance
Interplay between RAAS (angiotensin 2) and sympathetic NS (noradrenaline)
Local vascular mediators (constrictors)
Vasoconstrictors
Angiotensin 2
Noradrenaline
ACEi
Inhibits ACE, stops production of angiotensin 2
Hptn
Ramipril
Enalapril
Adverse effects - Hypotension, hyperkalaemia, acute renal failure, cough, rash, anaphylaxis
CI - Preg
CCB
Calcium channel blockers (L type calcium channel blockers)
Hptn, arrhythmias
Amlodipine (dihydropyridine) - Peripheral arterial vasodilators
Verapamil (phenylalkylamines) - Works on heart
Diltiazem (benzothiazepines) - peripheral and heart
Adverse effects (peripheral) - Flushing, headache, oedema, palpitations
Adverse effects (heart) - Bradycardia, AV block
BB
Hptn
Bisoprolol
Propanolol
Atenolol
Adverse effects - Fatigue, headache, sleep disturbances, bradycardia, hypotension, cold peripheries, erectile dysfunction
Worsens conditions such as asthma, COPD, raynaud’s
Aldosterone antagonist
Spironolactone
ARB
Angiotensin 2 receptor blockers (AT1 receptor blocker)
Hptn
Losartan
Valsartan
Adverse effects - Hypotension, hyperkalaemia, renal dysfunction, rash
CI - Preg
Beta adrenoreceptor selectivity
B1 - Heart (bisoprolol)
B2 - Lungs/airways (propanolol)
Diuretics
Hptn, HF
Thiazides - distal tubule - Bendroflumethiazide
Loop diuretics - loop of henle - Furosemide
Aldosterone antagonists (Potassium-sparing) - Spironaloctone
Adverse effects - Hypovolaemia, hypotension, metabolic disturbances (low levels of Na, K, Mg, Ca), raised uric acid (lead to gout), erectile dysfunction
Alpha-1 adrenoceptor blockers
Doxazosin
Treats hptn
Hypertension - Treatment order (gold standard)
Under 55 - 1) ACEi, 2) CCB, 3)Thiazide, 4) BB/AB/Spironaloctone
Over 55/afro-carib - 1) CCB, 2) ACEi, 3) Thiazide, 4) BB/AB/Spironaloctone
Heart failure types
LVSD - Left ventricular systolic dysfunction
HFPEP - Diastolic failure
Acute/chronic
HF
Syndrome of symptoms that suggest impaired efficiency of the heart as a pump
Caused by structural or functional abnormalities of the heart
Common cause - Coronary artery disease
HF - drugs
ACEi ARB BB Diuretics (loop) Aldosterone antagonists
HF - Order of treatment
1) ACEi + BB (Low doses)
2) Aldosterone antagonists - Spironaloctone
3) ARB (if ACEi is not tolerated)
4) ARNI - Sacubitril/Valsartan
5) Digoxin
If ACEi is not tolerated then use an
ARB
If ACEi + ARB not tolerated then use
Hydralazine
Nitrates
Arterial and venous dilators
Lower BP
Reduce preload+afterload
Used for IHD (Angina) and HF
GTN spray (short-acting) - SE = Syncopy, headache
Isosorbide mononitrate tablets (longer-acting)
Chronic stable angina
Anginal chest pain Predictable Exertional, goes away when stop/take GTN Infrequent Stable
Unstable angina/NSTEMI
Unpredictable
Can be at rest
Frequent
Unstable
STEMI
Complete occlusion of artery Unpredictable Rest pain Persistent Unstable
Chronic stable angina - Treatment
1st line - BB/CCB (either)
2nd line - BB+CCB (both)
3rd line - Long acting nitrate (Isosorbide mononitrate)
Antiplatelets - Aspirin/clopidogrel(if aspirin intolerant)
Statins - Simvastatin/atorvastatin
NSTEMI/STEMI - Treatment
Pain relief - GTN spray, diamorphine Dual antiplatelets - Aspirin+clopidogrel Antithrombin - Fondaparinux Background therapy - BB, ACEi, etc Surgical - Angioplasty, CABG
Antiarrhythmic drugs
Na, Ca, K channel targets
Vaughan Williams classification - Antiarrhythmic drugs
Class 1 - Na channel blockers - Lidocaine
Class 2 - BB - Bisoprolol
Class 3 - Prolong action potential - Amiodarone
Class 4 - CCB - Verapamil
Digoxin
Cardiac glycoside - Treats HF Antiarrhythmic drug - Most commonly used in AF Inhibits Na/K pump Bradycardia, slows AVN SE - N/V, diarrhoea, confusion
HF
The inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
Syndrome of breathlessness, tiredness and fluid overload (systemic/pulmonary oedema) caused by a form of cardiac dysfunction
Ejection fraction
Percentage of blood leaving your heart each time it contracts
HF - Aetiology
MI Hptn Cardiomyopathy Valvular Endocardial
HF - Signs and symptoms
Signs - Tachycardia, raised JVP, heart sounds/murmurs, hepatomegaly (pulsatile/tender), peripheral/sacral oedema, ascites
Symptoms - SOB, fatigue, ankle swelling
NYHA
Class 1-4
Higher class = Severe symptoms
HF - Diagnosis
Raised NTproBNP - important biomarker in cardiac disease
Echocardiography - to assess structural/functional abnormalities
Raised NTproBNP - Causes
HF
Plus many other cardiac and non-cardiac conditions
Acute HF - Causes
Rhythmic disturbances
Viral stress
In patients with HF, increased plasma hormone levels of (RAN)
Renin
Noradrenaline
Arginine
HF with reduced ejection fraction (HFREF) - Gold standard treatments
ACEi (k-sparing)
BB - Low dose - Bisoprolol
Aldosterone antagonist - Spironaloctone (K-sparing)
ACEi
Is not as effective on afro-carib pop as others
Blacks with HF - Alternative
Isosorbide dinitrate and hydralazine
ACEi vs ARB
ACEi - dry cough, lower mortality
ARB - no dry cough, greater mortality
Ivabradine
HF with sinus rhythm
NTproBNP - Functions
Dilates blood vessel
Opposes Na diuresis
Digoxin
Slows heart
Cardiac resynchronisation therapy (CRT)
Multi-site pacing (stimulates ventricles to contract at the same rate)
Treats bundle branch blocks
Amiodarone
Treats arrhythmias
ICD
Implanted defibrillators
Raised aldosterone
Retains Na from blood
Removes K from blood (hypokalaemic)
Commonly due to tumour in adrenals
High BP, firstly examine
Eyes
White coat effect
The difference in BP measurement between home and clinical environment
Stage 1 hptn - Treatment
140 - Only high risk patients
160 - Low risk patients
Hypertension treatment effects
Reduced headaches and migraines
Otherwise, nothing else is improved
BP treatment target ranges
140/90
Doxazosin
Alpha-blocker
Hptn - Lifestyle changes
1) Weight loss - Diet (salt)
2) Smoking
3) Alcohol
Drugs which increase BP
SNRI (Selective noradrenaline reuptake inhibitors)
NSAIDs
Oral contraceptive pills
Corticosteroids
Stop BP-lowering agents during
Surgery
ECG provides information on
Arrhythmias
Ischaemia
Infarction
Electrolyte disturbances
Indications for an ECG
Chest pain
Palpitations
Breathlessness
Blackout
ECG - Principles
Positive deflection is towards the lead/vector
Width of deflection reflects speed of conduction
The amplitude of deflection is related to the mass of myocardium
Limb leads - 6
1-3
aVR
aVL
AVF
Chest leads - 6
V1-V6 (Anterior-left lateral)
Sinus rhythm
P wave: Positive) Inferior leads, lead 1 Negative) aVR, biphasic in V1 S wave: Negative S wave in V1 R wave: Positive R wave in V6
P wave - Abnormalities
Low amplitude (Hyperkalaemia, atrial fibrosis)
High amplitude - Tall (Right atrial enlargement)
Wandering pacemaker/focal atrial tachycardia
PR interval - Abnormalities
Prolonged in AV node disorders
Shorter in young patients
QRS complex - Abnormalities
Broad - BBB
Small - Pericardial effusion, obesity
Tall - Left ventricular hypertrophy, thin patients
QT interval - Abnormalities
Long - Low HR
Short - High HR
ST segment - Abnormalities
Elevated - MI, pericarditis
T wave - Abnormalities
Inversion - MI
Tachycardias
Atrial fib (Irregularly irregular) Atrial flutter (Rapid, sawtooth atrial pattern) Supraventricular tachy Ventricular tachy Ventricular fib
Ventricular tachy vs ventricular fib
Tachy is broader than fib
Bradycardia - Causes
Conduction tissue fibrosis
Ischaemia
Inflammation
Drugs
AV conduction problems
1st degree AV block - 1:1 AV ratio
2nd degree AV block 2:1 AV ratio
3rd degree AV block 3+:1 AV ratio
As degree of AV block increases, intervals become longer
LBBB
Broad QRS
LBBB vs RBBB
wiLLiam - LBBB
maRRow - RBBB
Ischaemia/Infarction
T wave flattening inversion
ST depression
ST elevation
Q waves
LAD
Anterior changes - V2,3,4
Circumflex
Lateral - 5,6
Lateral
2,3,5avf (inFERIOR
Electrolyte disturbances
Hyperkalaemia - Tall T waves, flattened P waves, broad QRS
Hypokalaemia - Flattened T wave, QT prolongation
Hypercalcaemia - Shortened QT
Hypocalcaemia - QT prolongation
Electrolyte disturbances
Hyperkalaemia - Tall T waves, flattened P waves, broad QRS
Hypokalaemia - Flattened T wave, QT prolongation
Hypercalcaemia - Shortened QT
Hypocalcaemia - QT prolongation
Pericarditis
Saddle shaped PR depression
ST elevation
Ectopic beats
Extra beats outside of sinus rhythm
Atrial or ventricular
AF - Treatment
1st line) BB, CCB, Digoxin
2nd line) Cardioversion (electrical - DC or pharma - Amiodarone)
AF increases
Stroke risk
CHADS-VASC score measures
Stroke risk
SVT - Treatment
Adenosine
Catheter ablation
Accessory pathways
Pre-excitation (delta waves on ECG)
VT - Treatment
Catheter ablation
BLackout - Treatment
Pacemaker
Complete heart block - Treatment
Pacemaker
Diabetes and NSTEMI/STEMI
Tend to be without chest pain (silent attack)
Biventricular ICD
Resynchronises left and right ventricles
Also treats VT episodes
PE - ECG changes
T wave inversion
Valvular heart diseases
Aortic stenosis
Mitral regurg
Aortic regurg
Mitral stenosis
Aortic stenosis - Types
Supravalvular
Subvalvular
Valvular
Aortic stenosis - Causes
Age-related degenerative calcification
Rheumatic heart disease
IE
Bicuspid aortic valve
Congenital
Aortic stenosis - Pathophysiology
Left ventricle becomes exhausted and function declines rapidly
Aortic stenosis - Presentation
Syncope (extertional)
Angina (increased myocardial oxygen demand - demand/supply mismatch)
Dyspnoea - Breathlessness on exertion
Aortic stenosis - Signs
Pulsus tardus - slowly rising carotid pulse
Pulsus parvus - decreased carotid pulse amplitude
Heart sounds - S4 gallop due to LVH
Ejection systolic murmur - crescendo-decrescendo character
Valvular diseases - Investigations
Echocardiography
AS - Management
Dental hygeine/care - Reduce bacteraemia + IE risk, IE prophylaxis
Surgical replacement
TAVI - Transcatheter aortic valve implantation
Mitral regurgitation - Causes
IE
Rheumatic heart disease
Mitral valve prolapse
MR - Causes
Auscultation - Pansystolic murmur
MR - Investigations
ECG - AF
CXR - LA enlargement
Echo -
MR - Management
ACEi - vasodilator
IE prophylaxis
Surgical
Systolic vs diastolic murmurs
Systolic murmurs easier to hear than diastolic murmurs
Aortic regurg - Causes
Bicuspid aortic valve
Rheumatic
IE
AR - Investigations
Auscultation - Diastolic blowing murmur,
Wide pulse pressure - High systolic pressure, low diastolic pressure
Mitral stenosis
V uncommon
MS - Causes
Rheumatic
IE
Age-related calcification
MS - Causes
Rheumatic
IE
Age-related calcification
IE
Infection of heart valve or other endocardial lined structures within the heart (septal defects, pacemaker leads, surgical patches)
IE - Types
Left-sided native - (mitral/aortic) Left-sided prosthetic Right-sided native Device related Prosthetic
IE - Causes
Blood infection
Prosthetic heart valve op
Drug abusers (IV)
IE - Presentation
Signs of systemic infection - Fever, sweats
Embolisation - stroke, pulmonary embolism, MI
Valve dysfunction - HF, arrhythmia
IE - Diagnosis
Modified dukes criteria Major criteria (2) - Blood cultures, echocardiography - endocarditis, valve leaks Minor criteria (5) - Predisposing factors, fever, vascular phenomena, immune phenomena, ambiguous blood cultures
IE - Peripheral signs
Splinter hemorrhages (nails)
Osler’s nodes (tender nodules in fingers)
Embolic skin lesions on hands (from the heart)
Roth spot in eyes
IE - Echocardiography
TTE - Transthoracic echo (lower quality, non-invasive)
TOE - Transoesophageal echo (better quality, invasive)
IE - Diagnosis
Blood cultures
Raised CRP
Raised WBC
TTE
IE = Treatment
IV antimicrobials
Surgical - remove large materials before they embolise, to remove infected devices
Antibiotic prophylaxis
IE - Management
Blood cultures
Echo
IE - most common bacterial cause
Strep viridans
Right-sided IE - Typical history
IV drug abusers, HIV positive
Staph aureus
Tetralogy of Fallot - 4 things
Ventricular septal defect Pulmonary artery stenosis Hypertrophy of right ventricle Overriding aorta Stenosis of the RV outflow leads to RV being at a higher pressure than the left Hypoxia episodes can then cause death Treatment - surgical
