Cardiology Flashcards
Break down the word atherosclerosis
Atheroma= fatty deposits in artery walls Sclerosis= process of hardening or stiffening of blood vessels
What is atherosclerosis caused by?
Chronic inflammation and activation of the immune system in the artery wall which causes deposition of lipids
What three things do fibrous atheromous plaques lead to?
- Stiffening - leads to hypertension and strain of heart pumping against resistance 2. Stenosis - leads to reduce blood flow (eg. Angina) 3. Plaque rupture- giving off a thrombus that blocks a distal vessel leading to ischaemia (eg. Acute conorary syndrome)
Atherosclerosis non-modifiable risk factors
- Older age 2. Family history 3. Male
Atherosclerosis modifiable risk factors
- Smoking 2. Alcohol consumption 3. Poor diet (High sugar and trans-fat and reduced fruit and vegetable and omega 3 consumption) 4. Low exercise 5. Obesity 6. Poor sleep 7. Stress
Medical co-morbidities that increase the risk of atherosclerosis
- Diabetes 2. Hypertension 3. Chronic kidney disease 4. Inflammatory conditions (rheumatoid arthritis) 5. Atypical antipsychotic medications
End result of atherosclerosis?
- Angina 2. Myocardial infarction 3. Transient ischaemic attacks 4. Stroke 5. Peripheral vascular disease 6. Messenteric ischaemia
Two types of prevention of cardiovascular disease?
- Primary prevention - for patients that have never had cardiovascular disease in the past 2. Secondary prevention - for patient that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease
How to optimise modifiable risk factors?
- Advice on diet, exercise and weight loss 2. Stop smoking 3. Stop drinking alcohol 4. Tightly treat co-morbities (diabetes)
Primary prevention of cardiovascular disease?
- Perform a Q-risk 3 score 2. Over 10% risk of having heart attack or stroke in the next ten years? Offer a statin (Current NICE = atorvastatin 20mg at night) 3. All patients with CKD or type 1 diabetes for more than ten years should also be offered atorvastatin 20mg
Nice guidelines to statin prescription?
- check lipids at 3 months- aim for increasing dose to aim for 40% reduction in non-HDL Cholesterol- always check adherence first! 2. Check LFTs within 3 months and at 12 months, don’t need to be checked again if normal 3. Statins can cause a transient and mild raise in ALT and AST in first few weeks of use and don’t need stopping if rise is less than 3 times the upper limit of normal
Secondary prevention of cardiovascular disease?
4 As: Aspirin (plus second anti platelet like clopidogrel for 12months) Atorvastatin 80mg Atenolol (or other beta-blocked - commonly bispropol - titrated to maximum tolerated dose) ACE inhibitor (commonly ramipril) (tritated to max tolerated dose)
Notable side effects of statins
- Myopathy (check creative kinase in patients with muscle pain or weakness) 2. T2DM 3. Haemorrhagic strokes (very rarely) Usually benefits far outweigh risks and newer statins are mostly very wel tolerated
What’s a Q-risk 3 score?
-Predicts risk of CVD in 10 upcoming years -Factors include: Age SBP BMI Socieconomic status Ethnicity -Score of ten plus (10% + risk in the next ten years) is an indication to start 1° lipid lowering therapy (statins)
What is atorvastatin an example of?
Lipid lowering therapy
Which arteries does atherogenesis affect most commonly?
LAD Circumflex RCA
Risk factors for IHD
Age Smoking Obesity, high serum cholesterol Diabetes Hypertension Family history M>F Cocaine use Stress Physical inactivity
Symptoms of stable angina pain?
- Central crushing chest pain radiating to neck/jaw 2. Brought on with exertion 3. Relieved with 5mins rest or GTN spray
Four types of angina?
- Stable - normal three point definition 2. Unstable - pain at rest, not relieved by inactivity or GTN spray + no ECG CHANGES 3. Prinzmetal’s - due to coronary vasospasm (not due to cv vessel atherogenesis) Seen increasingly in cocaine users ECG shows ST elevation 4. Decubitus - induced when lying flat (usually complication of cardiac failure)
Patholophysiology of ischaemic heart disease?
Atherogenesis: Endothelial injury attracts cells to site via chemokines (IL1, IL6, IFN-Y) 1. Fatty streak = Foam cells (lipid laden macrophages) and T-cells 2. Intermediate lesions = foam cells (bigger as taken up more lipid), t- cells and smooth muscle cells Platelets also aggregate and adhere to site inside vessel lumen 3. Fibrous plaques (advanced) = large lesions (foam cells, t-cells, smooth muscle, fibroblasts, lipids with a necrotic core) Develops a fibrous cap over lesion
Fibrous cap in stable angina?
Fibrous cap is strong and less rupture prone
What happens if plaque is prone to rupture?
Prothrombotic state, platelet adhesion and accumulation leads to progressive luminal narrowing
Difference between ischaemia and infarction?
Ischaemia= blood flow restricted Infarction= lumen fully occluded
When do symptoms for stable angina start?
When 70 to 80% lumen occluded Due to poiseulle’s law, nothing much happens until the diameter stenosis reaches 70% and then there is rapid decline
Symptoms of IHD?
Central crushing chest pain radiating to jaw/neck, worsens with time (doesn’t peak straight away ) NSFD: Nausea Sweating Fatigue Dyspnoeic weak breathing + hypotensive/tachycardic in ACS and “impending sense of doom” and palpitations
How to diagnose stable angina?
1st line= ECG- resting and with exercise (to induce ischaemia) Coronary angiography- looks for stenoses and atherosclerotic arteries (~70-80% occluded) Gold standard but invasive so not first line
Treatment for stable angina?
-Symptomatic= GTN sublingual spray -Lifestyle modifying (decrease weight, stop smoking, exercise, diet etc) -Pharmacological (all patients=1st line) 1. CCB (CI heart failure) or B-b (CI Asthma) Switch if either is not tolerated If both are contraindicated or not tolerated, other drugs to consider as monotherapy: - a long acting nitrate (isorbide monitrate) - nicorandil - ivabradine - ranolazine Secondary anti platelet treatment is recommended (75mg aspirin) (eg if they have a stent but not necessarily for stable angina) Potentially Revascularisation: PCI/CABG with an MDT meeting or coronary angiogram if symptoms not controlled
What does acute coronary syndromes cover?
Umbrella term for unstable angina, NSTEMI and STEMI
How to define different acute coronary syndromes?
Unstable angina- severe ischaemia NSTEMI- partial infarction + Q wave infarction STEMI- transmural infarct and ST elevation in local ECG leads +Non-Q infarction
Different acute coronary syndromes pathologies? (Chart)
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What does an ECG after MI look like?
hyperacute t wave -pathologically deep q waves - ST segment elevation
What’s the difference between types of MI?
T1 = traditional MI due to an acute coronary event (athermatous plaque rupture) T2 = secondary to ischaemia due to either increased oxygen demand or decreased supply (vasopasm, anaemia and sepsis)
Is troponin or creatine kinase mb a better indicator of cardiac damage long term?
Troponin has a shorter half life so CKMB is a better biomarker after a few days
Pathophysiology of ACS (angina)?
ACS is usually the result of a thrombus—> atherosclerotic plaque formation due to damage to arterial walls causing myocardial ischaemia When a thrombus forms in a fast flowing artery it is made up mostly of platelets. - why anti-platelet medications= key
Making a diagnosis of ACS? (Step by step) (primary investigations)
1) when patient presents with symptoms (eg chest pain) perform ECG 2) ST elevation or new left bundle branch block = STEMI 3) no ST elevation—-> troponin blood tests: - increased troponin + changes (ST depression, t wave inversion or path Q waves) = NSTEMI -normal troponin + no ECG changes then unstable angina or another cause (musculoskeletal chest pain)
Symptoms of ACS?
Same as stable angina but pain @ rest prolonged with no relief “impending doom” palpitations and Symptoms more severe
Alternative causes of raised troponin?
Gram negative sepsis Myocarditis Aortic dissection Pulmonary embolism Arrhythmias
Other investigations when considering ACS?
Those normally arranged for stable angina: - physical examination (heart sounds, signs of heart failure, BMI) - FBC (anaemia) - U&Es (check for electrolyte imbalances prior to ACEi and other meds) -LFTs (prior to statins) -Lipid profile -Thyroid function tests (hypo/hyperthyroid) -HbA1c and fasting glucose (for diabetes) Plus: -chest x ray to investigate other causes of chest pain and pulmonary oedema -Echocardiogram after event to assess for functional damage -Ct coronary angiogram to assess for coronary artery disease
Acute management of ACS generally?
MONAC Morphine + anti-emetic (metoclopramide) O2 (if stats <94% or 88-92% if COPD) Nitrates (GTN) Aspirin (300mg) Clopidogrel/Ticagrelor (75mg dual antiplatelet) or pasugrel if undergoing PCI (PY12 inhibitor) Anticoagulant: fondaparinux or heparin *not all patients require oxygen
What does GRACE score assess?
Mortality risk of patients with ACS from MI within the next 6 months to 3 years
Treatment for low risk NSTEMI/unstable angina
Monitor
Treatment for high risk NSTEMI/ unstable angina?
Immediate angiogram and consider PCI
Treatment for STEMI if presenting <12h of Sx and <2h of first medical contact?
PCI (percutaneous intervention) (Insertion of a catheter via radial or femoral artery to open up blocked vessels using an inflated balloon (angioplasty) and a stent may also be inserted) -unfractionated heparin and glycoprotein IIb/IIIa inhibitor
Treatment for STEMI if presenting <12h Sx and more than 2h of first management?
Ineligible for PCI:-Fibrinolysis/ thrombolysis - IV administered alteplase or tenecteplase -antithrombin agent eg unfractionated heparin (bivalirudin and/or glycoproteins IIB/IIIa may also be considered) Offer ECG 60-90 mins after If shows residual ST elevation offer immediate angiography and PCI
Why are diabetics major culprits of Silent MIs?
diabetic neuropathy -don’t feel the anginal pain and therefore may miss diagnosis and die from sudden collapse
Long term and secondary prevention after ACS?
6 As -Atenolol (or other Beta blocker titrated to toleration) (life) -Aspirin (initial dose 300mg -> 75mg life) -Atorvastatin (80mg life) -ACEi (eg ramipril titrated to 10mg) (life) -Another antiplatelet (eg. clopidogrel (75mg for 12months) -Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily) Can add an opiate or GTN spray for pain relief Dual antiplatelet duration will vary following PCI procedures (due to higher risk of thrombus formation in diff stents)
Acute complications of ACS (2 >= wk)
Heart failure due to vent fibrillation Mitral incompetence Left ventricle free wall rupture Cardiogenic Shock
Other complications of ACS (2< weeks)
Dressler syndrome (autoimmune pericarditis) Heart failure LV aneurysm-heart literally becomes saggy :(
How to interpret GRACE score
<5% low risk 5-10% medium risk >10% high risk
Complications of MI
DREAD -Death -Rupture of heart septum or Papillary muscles -Edema (Heart failure) -Arrhythmia and Aneurysm -Dressler syndrome
Define heart failure
Inability for heart to deliver O2 blood to tissues at a satisfactory rate for the tissues metabolic requirements * a syndrome not a diagnosis
Cause of heart failure?
IHD Cardiomyopathy Valvular disease Cor pulmonale Anything that increases cardiac work: -obesity -htn -pregnancy -hyperthyroid -arrhythmias
Risk factors for heart failure
Age (65+) Smoking Obesity Previous MI Male
Pathophysiology for Cor pulmonale?
RH failure due to disease of lungs +/ pulmonary vessels Increased pressure and resistance in pulmonary arteries results in right ventricle being unable to pump blood out Leads to back pressure of blood into right atrium, the vena cava and the systemic venous system
Pathophysiology of heart failure
-Failing hearts = decreased CO due to dysfunctional frank starling law 1- compensatory mechanism activation —Raas + sns initially works (=increase BP) Increases aldosterone + ADH Increases ADR / NaD 2- soon compensation fails and heart undergoes cardiac remodelling (decreased CO) in response to compensation * heart less adapted to function so increase in RAAS + SNS will exacerbate fluid overload * heart failure affecting both L+R circuits = congestive heart failure
Normal physiology of heart
Normally- increased preload= increased afterload= increased cardiac output (frank starling law)
Three ways heart failure can be classified?
1) Time classified 2) Acute or chronic 3) Ejection fraction classified
How is heart failure ejection fraction classified?
Normal = 50–70% > 50% = preserved Diastolic failure (filling issues) Eg. Hypertrophic cardiomyopathy, LVH (aortic stenosis) < 40% = reduced Systolic failure (pump issues) Eg. IHD - ischaemic tissue
What does LHS failure result in?
Pulmonary vessel backlog —> pulmonary oedema
What does RHS failure result in?
Systemic venous backlog —> peripheral oedema
3 cardinal non specific symptoms of heart failure
SOBASFAT 1 Shortness of breath 2 Ankle swelling 3 Fatigue
Other symptoms of heart failure
orthopnoea (dyspnoea worse lying flat) -increased JVP -bibasal crackles (pul oedema) -hypotensive -tachycardic
NY heart association class 1-4 of HF severity
1 no limit on physical activity 2 slight limit on moderate activity 3 marked limit on moderate + gentle activity 4 symptoms even at rest
Methods of diagnosing of heart failure?
Bloods ECG Chest X-ray ECHOcardiogram - gold standard
Blood results with heart failure?
BNP (brain natriuretic peptide) = key marker High >400ug/ml Level correlates with extent of damage So more severe heart failure = higher bnp It is released from stressed ventricles in response to increase mechanical stress *might also measure NT ProBNP (inactive BNP) and levels are 5x higher so increase of >2000 ug/ml
ECG results with heart failure?
Abnormal Eg evidence of LVH
Chest x ray results with heart failure
ABCDE Alveolar bat wing oedema B-lines Cardiomegaly Dilated upper lobe vessels Effusion (pleural)
Purpose of echocardiogram?
Assess heart chamber dimensions
Conservative treatment for heart failure
Lifestyle changes: Decrease bmi Exercise Stop smoking + alcohol
First line treatment for chronic heart failure
ABAL First line: -ACEi (eg ramipril titrated up to tolerated dose of 10mg) -Beta blocker (eg bisoprolol titrated up to 10mg) Add in: -Aldosterone antagonist when symptoms not controlled with A and B (eg spironactone or eplerenone) -Loop diuretic improves symptoms (eg. Furosemide 40mg once daily) *consider desynchronisation therapy (improves A-V coordination) - low dose and slow uptitration is key with ACEi and Bb
Surgical treatments for heart failure?
Revascularisation Valve surgery Heart transplant (last resort)
What if ace inhibitors are not tolerated?
ARB like candersartan titrated go 32mg can be used instead
What should patients have monitored when on diuretics, ace inhibitors and aldosterone antagonists?
U&E All three medications cause electrolyte disturbances
Patients with valvular heart disease should avoid which drug?
Ace inhibitors unless indicated by a specialist
Respiratory causes of cor pulmonale?
COPD is most common cause -pulmonary embolism -interstitial lung disease -cystic fibrosis -primary pulmonary hypertension
Presentation of Cor Pulmonale
Patients often asymptomatic Main presenting complaint is shortness of breath (Also caused by chronic lung disease) May also present with peripheral oedema, increased breathlessness of exertion, syncope or chest pain
Signs of Cor Pulmonale
-Hypoxia -cyanosis -raised JVP (due to backlog of blood in jugular veins) -peripheral oedema -third heart sound -murmurs (eg pan-systolic in tricuspid regurgitation) -hepatomegaly due back pressure in the hepatic vein
Management of cor pulmonale?
Management involves treating the symptoms and underlying cause Long term oxygen therapy often used Prognosis is poor unless reversible underlying cause
Define hypertensive heart disease?
Heart failure and conduction arrhythmias due to unmanaged high blood pressure
Define abdominal aortic aneurysm? (AAA)
Permanent aortic dilation exceeding 50% where diameter >3cm Typically infrarenal (below renal arteries), in elderly men
ECG changes and corrosponding coronary arteries
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Flow chart for treatment for NSTEMI or unstable angina
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Flowchart for STEMI treatment
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Prevalence of AAA?
1.3 to 12.7% in the uk, most commonly affecting elderly men Often inherited
A negative risk factor for AAA?
Diabetes but unknown reason
Risk factors for AAAs?
Smoking = biggest risk factor Increasing age Make Hypertension Connective tissue disorders - Ehlers Danos and Marfan syndrome (changes in balance of collagen and elastic fibres) Family history
Pathophysiology for AAA?
Smooth muscle, elastic + structural degredation in all 3 layers of vasuclar tunic (intima, media, adventitia) All 3 layers = true aneurysm Not all 3 = pseudoaneurysm (usually due to trauma ) Dilation in AAA typically 3cm+ A dilation that is 5.5cm+ has an increased rupture risk Rupture = surgical emergency
Inflammatory AAA?
Type that usually affects younger patients and is associated with smoking, atherosclerosis and vasculitis 5-10% of AAAs Same symptoms + pyrexia (fever)
Symptoms of AAA?
Mostly asymptomatic and discovered incidentally Symptoms generally when ruptured/impending rupture -sudden epigastric pain radiating to flank -pulsatile abdominal mass - tachycardia and hypertension
Surface potential signs of AAA?
Grey-Turner’s sign = flank bruising secondary to retroperitneal haemorrhage (also potentially haemorrhagic pancreatitis) Cullen’a sign = pre-umbilical bruising more associated with acute pancreatitis and ectopic pregnancy but also linked with AAA
Primary diagnosis tool for AAA?
Abdominal ultrasound -fast, cheap, reliable -highly sensitive and specific (Axial plane at level of the navel)
Treatment for an asymptomatic aneurysm <5.5cm?
Surveillance + offer advice to manage risk factors (decrease smoking, BMI, BP and satins)
Treatment for asymptomatic AAA and >= 5.5cm or >4.0cm and expanded more than 1cm per year?
Elective surgery Either: 1) EVAR (Endovascular aortic repair) - stent inserted through femoral/iliac artery -Less invasive but more post op complications 2) open surgery (favoured by nice unless sig comorbidities) -more invasive but fewer complications Survival for both=equivalent (EVAR)
Treatment for symptomatic AAA?
Urgent surgical repair (EVAR or open surgery)
Treatment for a ruptured AAA?
Stabilise ABCDE, fluids then urgent surgical repair -Nice says EVAR preferred in all women, and men over 70 otherwise open surgery preferred -Do not offer complex EVAR (eg BEVAR) if open surgery is suitable 20% of AAAs rupture anteriorly into peritoneal cavity= poor prognosis 80% rupture posteriorly = better prognosis 100% mortality for ruptured AAA if not treated immediately
Cause and treatment for rare AAA in thoracic aorta?
main cause = marfans/ehlers danos +atherogenesis - treatment = monitor with CT/MRI or if symptomatic—> surgery immediately
Pathophysiology of aortic dissection?
Surgical emergency!! Tear in intima resulting in blood dissecting through media and separating layers apart -due to mechanical wall stress Creates a false lumen (can propagate forwards and backwards) Abnormal flow can occlude flow through branches of aorta Decreased perfusion to end organs = shock/failure
Risk factors for aortic dissection(AD)
Hypertension = most key Connective tissue disorders (ED,Marafan) Family history of AAA/AD Truma Smoking
Most common location for aortic dissection
Sinotubular junction = where aortic root becomes tubular aorta, near aortic valve (Stanford A)
Stanford classification for aortic dissection
A = proximal to left subclavian artery (ascending + arch) (2/3=most common) B = distal to left subclavian artery (descending thoracic) (1/3=less common)
Debakey classification of aortic dissection
Type I = originates in ascending aorta and involves at least the aortic arch, but can extend distally Type II = originates and confined to the ascending aorta Type III = originates in the descending aorta and extends distally, but can extend proximally
Signs and symptoms of aortic dissection
Symptoms: -Sudden onset ripping/tearing chest pain that may radiate to the back -Syncope (fainting) red flag Signs: -Radio-radial and/or radio-femoral delay -Diastolic murmer due to aortic regurgitation -diff in blood pressure between two arms >10mmHg -hypertension -tachycardia and hypotension (commonly type A)
Differential diagnosis for AAA?
Acute pancreatitis Typically non pulsatile + more associated with grey-turner/Cullen signs
Investigations for diagnosing aortic dissection?
ECG Chest X-ray -may show widened mediastinum >8cm is suspicious (1= widened mediastinum and 2= enlarged aortic knuckle) Contrast-enhanced CT angiogram (gold standard) -v specific and sensitive and used if patient is hemodynamically stable -shows intima flap, false lumen, dilation of aorta and rupture (Type a aortic dissection)
Investigation in an unstable patient?
Transthoracic (TTE) or transoesphageal (TOE) echo TOE is more invasive but more specific for AD and v sensitive -shows intima flap and false lumen -Allows classification of AD as type A or B
Treatment for type A aortic dissection
- Blood transfusion - IV labetol (aim for systolic bp 100-120) - Urgent open surgical repair to replace ascending aorta
Treatment for type B aortic dissection
- conservative management: analgesia and bed rest - IV lavetol (aim for 100-120 systolic bp) - thoracic endovascular aortic repair (TEVAR) may be performed to reduce risk of further dissection yet not standard practice
Complications of aortic dissections?
cardio tampenade -aortic insufficiency (regurgitation) -pre renal AKI -stroke (ischemic)
Mortality rate for untreated aortic dissection?
Will result in a false channel rupture and fatal haemorrhage in 50-60% if patients within 24hrs Estimated 20% of patients die before reaching hospital and 30% die before reaching theatre 5 yr survival rate after surgery is 80%
Limits for diagnosing hypertension
> = 140/90 mmHg in clinic >= 135/85 mmHg at home (ambulatory blood pressure monitoring)
Primary vs secondary hypertension
1° = Essential hypertension (idiopathic/no known cause) 95% cases 2° = known underlying cause 5% cases
Causes of secondary hypertension
- Renal disease (CKD-most common cause due to diabetic nephropathy) - Endocrine disorders (phaeochromocytoma, conn’s, cushing’s) - Medication/iatrogenic : glucocorticoids, ciclosporin, atypical antipsychotics, combined oral contraceptive pill -pregnancy
Non modifiable risk factors for hypertension
Age African heritage Family history
Modifiable risk factors for hypertension
Obesity Sedentary lifestyle Alcohol excess Smoking High sodium intake (>1.5g a day) Stress
Define the limits for stages of hypertension
(H) = clinic reading (A) = ambulatory Discrepancy of >= 20/10mmHg between clinic and ambulatory suggests “white-coat hypertension
Malignant (accelerated) hypertension?
Severe increase in blood pressure >=180/120 mmHg (stage 3) with signs of retinal haemorrhage and/or pailloedema, associated with target organ damage = emergency assessment and treatment
Pathophysiology of hypertension
Ultimately all mechanisms will increase RAAS and SNS activity (CO) and TPR => increase in BP as BP=COxTPR
Signs of malignant hypertension
Hypertensive retinopathy Visual disturbances Cardiac symptoms eg chest pain Oliguira or polyuria Overall rare but scary and unrelated to cancer just very severe symptoms
Symptoms of hypertension
Mostly asymptomatic and found in screening May have pulsatile headache, classically occipital and worse in the morning
Signs of hypertension to consider
Signs of the underlying cause of secondary hypertension Eg phaeochromocytoma, hyperthyroidism or Cushing’s
How to diagnose hypertension
If bp reading in hospital is between 140/90 and 180/120 mmHg then offer ABPM to confirm diagnosis -bp is measured for 24h with at least 2 measurements per hour during waking hours -overall at least 14 measurements are required
Other investigations for hypertension?
Assess end organ damage (more damage = worse prognosis) : - Fundoscopy: assess for hypertensive retinopathy - 12- lead ECG: assess for LVH - Urinalysis and ACR: assess for renal dysfunction + diabetes risk - Bloods: HbA1c, U&Es, total cholesterol, HDL cholesterol
Treatment guidelines for hypertension
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If a patient has T2DM and is black or 55+, would they take CCB or ACEi?
T2DM takes precedence and they should take ACEi BUT ARBs are preferred for black patients so that might be preferable
Complications for hypertension?
Heart failure Increased IHD risk CKD/Renal failure PVD Dementia Increased risk of cerebrovascular incident
Pathophysiology of types of deep vain thrombosis (DVT)?
Formation of thrombus in a deep leg vein -around\below calf = minor veins (eg. Anterior and posterior tibial) => less concerning and more common -above calf (in thigh) = major veins (eg. Superficial femoral) occlusion may impede distal flow => life threatening and less common
Risk factors for DVT?
Dependant on Virchow’s triad: 1. Hypercoagulability 2. Venous stasis 3. Endothelial damage (abnormality in any component can result in thrombus)
Hypercoagulabilty and causes? (Virchow’s triad)
= increased platelet adhesion and clotting tendency Hereditary: - Factor V Leiden - protein C and S deficiency - antiphospholipid syndrome Acquired: - malignancy - chemotherapy - COCP/HRT - Pregnancy - Obesity
Venous stasis and cause? (Virchow’s triad)
blood flow is normally laminar to spread out platelets and clotting factors without activation Stasis —> aggregation of clotting factors = thrombus formation cause = immobility (long flights, after surgery)
Endothelial damage and causes? (virchow’s triad)
=endothelial cells normally prevent thrombosis by secreting anticoagulants, as well as blocking exposure to pro-thrombotic collagen - damaged endothelial cells cannot!! Causes: — endothelial dysfunction: - smoking — endothelial damage: - surgery - catheter (PICC lines) - Lower limb trauma
Symptom and signs of DVT?
Symptom: Unliateral calf pain, redness and swelling Signs: -unliateral swelling -oedema -tender and erythematous -distension of superficial veins Right leg = swollen and erythematous
What is phlegmasia cerulea dolens?
Occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). => ischemia and a blue, painful leg
What is a Wells score?
Calculates the risk of DVT and determines investigations + management >= 2 DVT likely =< 1 DVT unlikely (Don’t learn all but know a few)
Gold standard for diagnosis of DVT
Duplex ultrasound of leg (Duplex USS) -if unavailable, alternative is D-dimer
Flow chart of investigations when considering DVT
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Positive d-dimer and negative duplex USS? (In patient with suspect DVT)
-stop interim anticoagulation -offer repeat ultrasound 6 to 8 days later +ve= restart anticoagulation -ve= alternative diagnosis
Treatment for DVT?
Offer DOACs: apixaban or rivaroxaban If there’s a CI eg patient is renally impaired offer one of: -LMWH -Unfractionated heparin Treatment for at least 3 months or 3 to 6 months if they’re a cancer patient +mobilisation and compression stockings
Complications of DVT
Pulmonary embolism Post thrombotic syndrome Increased risk of bleeding (as on anticoagulants)
Risk of recurrence with DVT?
30% in the next five years
Differential diagnosis to DVT?
Cellulitis Skin infection-typically staph aureus + strep pyogenes -tender, inflamed swollen calf with pronounced demarcation will show leukocytosis on FBC while DVT will have normal levels
Pathophysiology of pulmonary embolism (PE)
Most commonly DVT embolises and lodges in oil on art after circulation (Could be any embolus) Can cause strain on right ventricle due to increased pulmonary vascular resistance
What can a PE cause?
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Risk factors for PE?
Virchow’s triad (Mentioned in detail in DVT)
Symptoms of PE
Pleuritic chest pain (present in only 10% of patients) Dyspnoea Cough or haemoptysis Fever Syncope 🚩
Signs of PE?
Tachypnoea and tachycardia Hypoxia DVT (swollen tender calf) Pyrexia Hypotension (SBP <90 mmHg suggests massive PE) Elevated JVP (suggest cod Pulmonale)
Wells two level score?
Used to determine probability of PE >4: high probability =<4: low probability (Don’t learn all just a few examples)
Process for investigating PE?
D-dimer is NOT diagnostic but CTPA is -CXR should be normal -ECG: Often find sinus tachycardia S1Q3T3 (classic finding but only in 20% px) RBBB and right axis deviation suggest right heart strain
Why is D-dimer not diagnostic?
Measure of clot burden; a small protein relaxers into blood when blood clot fibronlysed Is sensitive (rules PE in) Not specific (doesn’t rule out other conditions)
What’s massive PE?
Hypotensive patient with <90 systolic bp Less common that non massive
Treatment for massive PE?
Thrombolysis => alteplase (“clot buster”)
Treatment for non massive PE?
Anticoagulation (DOAC) 3 to 6 month treatment 1st line = apixaban\riveroxaban *If there’s a CI due to renal impairment offer LMWH or UFH
Another name for peripheral vascular disease? (PVD)
Peripheral arterial disease (PAD)
What is PVD?
Peripheral vascular disease is essentially reduced blood supply and ischaemia in the lower limbs due to atherosclerosis and thrombosis in the arteries
Risk factors for PVD?
Smoking = singke greatest risk factor T2DM Ageing Males affected at younger age Obesity Hypertension CKD
Three main patterns of presentation of PVD?
- Intermittent claudication (least severe) 2. Critical limb ischaemia 3. Acute limb-threatening ischaemia (most severe)
Intermittent claudication?
Reflects an inadequate increase in skeletal muscle perfusion during exercise - atherosclerotic partial lumen occlusion - pain on exertion
Critical limb ischaemia?
Advanced form of chronic limb ischaemia - big occlusion and blood supply barely adequate to meet metabolic demand - pain at rest - risk of gangrene/infection
Acute limb-threatening ischeamia?
Most commonly caused by emboli, usually cardiac origin, resulting in sudden decrease in limb perfusion - total vessel occlusion - emboli tend to lodge at bifurcations or sudden narrowing
Symptoms of acute limb-threatening ischeamia
6Ps Pulselessness Pallor Pain Perishingly cold Paralysis Paresthesia - present in chronic limb ischemia too but more you have=more limb threatening - all 6 = deadly!!
What happens when BV supplying region is occluded?
1) irreversible nerve damage (within 6h) 2) irreversible muscle damage (6-10h) 3) skin changes are last to appear =>likely gangrenous
Fontaine classifications of PVD
I) asymptomatic II) intermittent claudication- aching or burning of leg muscles -stage IIa = after 200m walking -stage IIb = after less than 200m walking Relieved within minutes of rest III) critical limb ischaemia - pain at rest + night IV) tissue loss: ulceration or gangrene
Why might symptoms be masked in PVD?
Inability to walk (eg severe heart failure) Pain insensitivity (eg diabetic neuropathy)
Signs to look for in PVD?
-Low ABPI (<0.9) or lack of lower leg pulse -Skin changes on leg (ulceration, thin, shiny, discolouration -Buerger’s test +ve -Bruits: pulsatile regions due to turbulent blood flow (aortic, femoral, carotid) -Some of 6Ps
Buerger’s test?
1) lie patient flat 2) elevate leg to 45° for 1 min 3) positive = pallor then reactive hyperaemia
Primary investigations for PVD?
1) ABPI (ankle-brachial blood pressure index) 0.8-1.3 normal 0.5-0.8 intermediate claudication <0.5 critical limb ischaemia Pulse absent = acute limb-threatening ischaemia 2) duplex ultrasound imaging- assess location and severity of stenosis 3) ECG, U+E, FBC, HbA1c - assess cardiovascular risk Ct angiography if surgery considered, not routine as more invasive
Treatment of intermittent claudication
RF management: -Supervised exercise programme if available (2 hrs per week for three months) -or if not then unsupervised exercise training -smoking cessation -bp control -diet and weight management -statins -HbA1c control -antilplatelets If 3 months exercise doesn’t improve quality of life then consider Revascularisation surgery
Treatment of chronic limb ischaemia
Revascularisation surgery (PCI if small, bypass if larger) Amputation if severe
Treatment for acute limb threatening ischeamia
Surgical emergency Revascularisation within 4-6hrs otherwise increased amputation risk
Complications of PVD
Amputation Ulceration + gangrene Permanent limb weakness Infection and poor tissue healing Increased risk of cerebrovascular accidents + CVD
What is pericarditis?
Typically acute (can be chronic); inflammation of pericardium +/- effusion -pericardium has two layers and innervated by phrenic hence inflammation results in pain
Epidemiology of pericarditis?
- males - 20-50yrs
Causes of pericarditis
1) Usually idiopathic 2) Or caused by a virus: - most common cause = coxsackievirus - mumps - EBV - VZV - HIV Less common causes: - bacterial - TB - systemic autoimmune disorders - malignancy - trauma
Pathophysiology of pericarditis
- inflamed pericardial layers rub against each other = more inflammation -cause exudate and adhesions within pericardial sac 1) may stay dry (no extra fluid needed to compensate for friction) 2) develop pericardial effusion (extra fluid) - if it becomes large enough to affect heart function = cardiac tamponade
Symptoms of pericarditis
Sudden onset sharp, pleuritic chest pain which can spread to left shoulder tip (phrenic) - Relieved by sitting up or leaning forward - Worse laying flat *may have signs of rhs failure due to constructive pericarditis -> SOB, peripheral oedema and tachycardia
Sign of pericarditis
Pericardial friction rub on auscultation - heard at left sternal edge as patient leans forward - squeaky leather “to and fro” sound
Differential diagnosis of pericarditis
Most key to rule out MI - central crushing chest pain not related to lying down - no pericardial rub
What is constructive pericarditis
granulation tissue formation in pericardium means impaired diastolic filling as it becomes thickened and hardened - late complication of pericarditis - sign of poor prognosis—> congestive heart failure - commonly associated with TB
Primary investigations to diagnose pericarditis
ECG: widespread saddle shaped ST-elevation (sensitive) and PR depression (specific) Eg. CXR: may show “water bottle” heart = pericardial effusion - pneumonia commonly seen in bacterial pericarditis Transthoracic ecg: to exclude pericardial effusion or tamponade ESR and CRP: might increase due to inflammation Troponin will be daisies if there’s an element of concomitant myocarditis
Treatment for idiopathic or viral pericarditis
1st line: NSAIDs + Colchine 2nd line: NSAIDs + Colchine + low-dose prednisolone
Treatment for bacterial pericarditis
IV antibiotics and pericardiocentesis with washout, culture and sensitivities
Treatment for cardiac tamponade
Urgent therapeutic pericardiocentesis - needle inserted between xiphisternum and left costal margin and directed towards left shoulder -sometimes done under ultrasound guidance -pericardial fluid aspirated to relieve intrapericardial presure
Compilcations of pericarditis
1) Pericardial effusion—> cardiac tamponade 2) Myocarditis 3) Constrictive pericarditis
What is cardiac tamponade
Accumulation of a large vol of fluid in the pericardial space (pericardial effusion) that begins to impair ventricle filling
Cause of Cardiac tamponade
Typically pericarditis Hence risk factors are all pericarditis related
Symptoms of cardiac tamponade
Related to pericarditis
Signs of cardiac tamponade
Beck’s triad: - hypotension (reduced cardiac output) - raised JVP (heart failure) - muffled heart sounds Pulses paradoxes: systolic bp reduction of >10mmHg on inspiration
Primary investigations to diagnose cardiac tamponade
ECG: may show electrical alternations - varying QRS amplitudes due to heart bouncing back and forth in pericardial fluid CXR: big globular heart ECHO: diagnostic tool
What is infective endocarditis
Infection of endocardium: - an abnormal endocardium - bacterial source —> vegetation
Two most common causes of infective endocarditis
1) S.aureus- most common overall + associated with IV drug use and prosthetic heart valves => increased virulence, Sx onset in days-weeks = ACUTE 2) S.viridans- second most common + usually affects a native valve and associated with poor dental hygiene => decreased virulence, Sx onset in weeks-months = SUBACUTE
Catergorisations of endocarditis
1) Acute 2) Subacute 3) Non- bacterial thrombotic ‘marantic’ - non-infective cause of endocarditis secondary to thrombus formation on the valvular surface - associated with malignancy or SLE (Libman-Sacks endocarditis)
Other less common causes of infective endocarditis
S. Bovis (associated with colon cancer) S. Epidermis (associated with in dwelling lines and prosthetic valves) HACEK organsisms (usually culture -ve) - Haemophilus - Aggregatibacter - Cardiobacterium - Eikenella - Kingella
Risk factors for infective endocarditis
Male 2.5x Elderly with prosthetic valve Young IV drug user Young with congenital heart defect Rheumatic heart disease
Which valves are more commonly affected by Infective endocarditis
Mitral valve most commonly affected overall Tricuspid valve is most associated with IV drug use (Mitral valve)
Pathophysiology of infective endocarditis
- any cause of abnormal endocardium —> turbulent blood flow and thrombus formation (platelets) - thrombus can get infected due to bacterial source - bacterial colonisation of the thrombus —> formation of vegetations —> valvular damage -typically happens around valves -causing regurgitation => aortic and mitral insufficiency and increase risk of heart failure
Symptoms of infection endocarditis
Rather vague -Fever or chills -headache -SOB -night sweats, fatigue, weight loss -joint pain (might be due to septic emboli)
Signs of infective endocarditis
1) Osler nodes (painful nodules on fingers\toes) 2) Janeway lesions (painless placques on palms and soles) 3) splinter haemmorrhages (red plum lines under nails) 4) Roth’s spots: white centred retinal haemorrhages heart murmer +- signs of heart failure
Primary investigations for infective endocarditis
-ECG (prolonged PR interval=aortic root abscess) -Blood cultures - 3 sets in 24 hours BEFORE ANTIBIOTICS -Inflammatory markers (CRP) - eg raised ESR\CRP + neutrophillia -FBC -ECHO: TOE more invasive than TTE but much more sensitive and specific = gold standard -Urinalysis
What is the modified Duke Criteria
Requires 2 major criteria, or 1 major and 3 minor, or 5 minor criteria for diagnosis of infective endocarditis
Major Duke Criteria for infactive endocarditis
- 2 positive blood cultures - ECHO TOE shows endocardia’s involvement Eg. Vegetations , abscess or regurgitation
Minor Duke criteria for infective endocarditis
-predisposing heart condition -IVDU -Fever >38°C -1 +ve blood culture -immunological phenomenon (Osler’a nodes, Roth’s spots or rheumatoid factor) -vascular abnormalities (eg. Septic/arterial emboli, pulmonary infarct)
First line treatment for infective endocarditis
IV antibiotics for 4 weeks following nice guidelines, extended to 6 weeks for prosthetic valves -local guidelines should be followed with nice antibiotic guidance below (Idk if you need to know all these but have a rough idea)
Second line treatment for infective endocarditis
Surgery: aim to remove infected tissue and repair it replace affected valves
Complications of infective endocarditis
Congestive heart failure Septic embolisation Valvular rupture or fistula Aortic root abscess
What does regurgitation cause?
Insufficiency + proximal chamber dilation -loss of structural chamber integrity and strength
What does stenosis cause?
Increase in upstream pressure + proximal chamber dilation+hypertrophy - heart becomes huge and rigid; poorly compliant
Main valve disorders?
Aortic regurgitation and stenosis Mitral regurgitation and stenosis
What do the main valve disorders cause?
Murmers
How are murmers best heard?
Using RILE Right side defects (tricuspid /pulmonary) heard on Inspiration Left sided defects (mitral\aortic) heard on Expiration
Normal size of mitral bicuspid lumen and after undergoing stenosis?
Mitral bicuspid lumen = 4-6cm2 Symptoms of stenosis start at <2cm
Causes of mitral stenosis
Most common = rheumatic fever (Post strep pyogenes infection) Also valve calcification in older patients + infective endocarditis
Pathophysiology of mitral stenosis
RHD causes mitral reactive inflammation, after years exacerbated with calcification => LA hypertrophy and chamber dilation
Symptoms and signs of mitral stenosis
malar cheek flush (due to CO2 retention) - association with Atrial Fibrillation (due to Stasis in LA and hypertrophy of LA) -dyspnoea - a wave on JVP
Mitral stenosis murmur?
Low pitched Mid diastolic murmer Loudest at apex Best heard on expiration with patient lying on left hand side
Investigations to diagnose mitral stenosis
CXR (LA enlarged) EVG (AFib, P mitrale= bifid “m” shale P waves when LA enlarged) ECHO -assess valve area, gradient, mobility (gold standard)
Treatment for mitral stenosis
Surgical Percutaneous balloon valvotomy (stent open mitral valve opening) Mitral valve replacement
Why is mitral stenosis more atrial fibrillation associated?
Mitral stenosis causes left atrium hypertrophy - more chances of embolisation as blood actively pumped harder
Causes of mitral regurgitation
Myxomatous mitral valve (most common valve disease) = mass of cells in valve connective tissue makes leaflets heavier + prolapse
What is mitral regurgitation
Heart valve disease in which the valve between the left heart chambers doesn’t close completely, allowing blood to leak backward across the valve
Risk factors for mitral regurgitation
Females Older Decreased BMI Prior MI Connective tissue disorder (marfan, ehlers danos)
Symptoms of mitral regurgitation
Exertion dyspnoea (due to pulmonary hypertension from back logging of blood)
Mitral regurgitation murmer?
Pan systolic blowing murmur radiating to axila (at apex) soft S1, prominent S3 in heart failure (severe cases)
Investigations for diagnosing mitral regurgitation
ECG CXR ECHO (gold standard) - check left atrium size and left ventricle function analysis Also assess valve structure to decide treatment
Treatment for mitral regurgitation
ACEi, Bb + serial ECHO monitoring If severe - (symptoms at rest) = valve repair\replacement
What is aortic stenosis
Pathological narrowing or aortic valve -decrease in flow Normal area 3-4cm Symptoms at 1/4 lumen size Most common valve disorder- results in LV dilation + hypertrophy
Symptoms of aortic stenosis
SAD Syncope (exertional) Angina Dyspnoea (relates to heart failure)
Aortic stenosis murmur
Ejection systolic crescendo decrescendo, radiating to carotids heard at right sternal border, second IC space -prominent S4 seen in LVH - narrow pulse pressure + slow rising pulse (not collapsing corrigan’s pulse)
Investigations to diagnose aortic stenosis
ECG CXR ECHO = gold standard for LV size and function + aortic valve area
Treatment for Aortic stenosis
General: Fastidious dental care to prevent IE As it is a mechanical problem-drugs are not effective Surgical if symptomatic: - in a healthy patient -> open repair\valve replaced (definitive) - more at risk (eg 75+) ->TAVI (transcutaneous aortic valve implant) less invasive and stents valve open
Differential diagnosis for aortic stenosis
Hypertrophic cardiomyopathy may also cause S4 - associated with sudden death in young men
What is aortic regurgitation
Leaky aortic valve which makes it insufficient
Causes of aortic regurgitation
Congenital bicuspid valve RHD Connective tissue disorders (Marfan/ehlers danos) Infective endocarditis
Symptoms and signs of aortic regurgitation
Collapsing carrigon’s pulse with wide pulse pressure -Quincke’s sign (nailed pulses when pressed) -De Musset sign (head bobbing in time with arterial pulsation)
Aortic regurgitation murmur
Early diastolic blowing murmer at right sternal border 2nd intercostal space - Austin fling murmer (severe) - mid diastolic low pitched rumble - heard when regurgitation is so severe blood bounces if mitral valve cusps and makes sound
Investigations to diagnose aortic regurgitation
ECG CXR ECHO gold standard, evaluates aortic valve, root, dimensions
Treatment for aortic regurgitation
Consider IE prophylaxysis (consider as differential diagnosis) Surgical valve replacement if symptoms
Epidemiology of rheumatic fever
Almost exclusively in developing countries only In young people
Cause of rheumatic fever
Systemic response to B haemolytic group A strep (Strep pyogenes) Typically pharyngitis
Rheumatic heart disease?
In 50% of cases of rheumatic fever it goes on to affect the heart
Histological appearance of rheumatic fever
Valves affected show Aschoff Bodies (Seen on the right)
Pathophysiology of rheumatic fever
M protein from S. pyogenes reacts with valve tissue of the heart Antibodies vs this “cross-link” results ins auto-antibody mediated destruction +- inflammation Molecular Mimicry!! * mostly affects the mitral valve (70% just mitral and 25% mitral and aortic) Typically thickens leaflets causing mitral stenosis
Symptoms of rheumatic fever
New murmur (esp mitral stenosis) - Syadenham’s chorea (neurological disorder that results in uncoordinated jerky movements) - arthritis - Erythema nodosum (swollen fat causing red patches\bumps) - pyrexia - evidence of strep a infection
Investigations to diagnose rheumatic fever
CXR= cardiomegaly/ heart failure (signs of mitral stenosis) ECHO= details extent of valvular damage
Jone’s criteria for diagnosis of rheumatic fever
1) recent S. pyogenes infection AND 2) 2 major signs (new murmur, arthritis, erythema nodosum, syndham chorea) OR 3) 1 major + 2 minor (pyrexia, increased ESR/CRP, arythalgia)
Treatment for rheumatic fever
Antibiotics- IV benzyloenicillin STAT, then phenoxypenicillin for 10days
Treatment for Sydenham’s chorea
Haloperidol
Most common congenital heart defect?
Bicuspid aortic valve 1-2% of the population M>F
Is the aortic valve bicuspid or tricuspid?
Typically tricuspid
Disadvantage of bicuspid aortic valve?
Bicuspid degenerates quicker than normal and will become regurgitative earlier Are also associated with coarction and dilation of ascending aorta Can be severely stenotic in infancy or childhood
Another name for atrial septal defect
Patent foramen ovale
Pathophysiology of atrial septal defect
Shunt of blood L->R and therefore not cyanotic (blue skin inducing) - increased flow to right side of heart and lungs - may overload RHS circulation causing RVH
Investigations to diagnose an atrial septal defect
Using an ECHO
Treatment for atrial septal defect
Sometimes there is spontaneous closure Otherwise treatment is surgical Percutaneous (key hole technique)
What is a ventricular septal defect
L->R non cyanotic shunt (not blue) Blood flows from high pressure to low pressure chamber Increased blood flow through the lungs (more in larger defects) Risk of Eisenmengers syndrome and RVH later
Symptoms of small ventricular septal defect
Typically asymptomatic Normal heart rate/size Loud systolic murmur
Symptoms of a large ventricular septal defect
Exercise intolerance Failure to thrive Murmur varies in instensity Tachycardia + increased respiratory rate Small skinny breathless baby :(
Investigation used to diagnose ventricular septal defect?
ECHO
Treatment for ventricular septal defect
Spontaneous or surgical closure in infancy if big No need for intervention if small and asymptomatic
What is an atrioventricular septal defect?
Essentially a hole down the middle of heart (no atrial or IV septum!) Can be complete or partial
What is atrioventricular septal defect associated with
Massively associated with Downs Syndrome
Symptoms of atrioventricular septal defect
Dyspnoea Exercise intolerance Complete defect: - breathless new pats with poor weight gain and feeding and needs repair wishing is surgically challenging Partial defect: Can present late in adulthood band can be left alone if no right heart dilation
Prognosis of atrioventricular septal defect
Progresses to eventually Eisenmenger’s and hard to treat
What is patent ductus arteriosus
When ductus arteriosus fails to close post birth = unusual
Pathophysiology of patent ductus arteriosus
Blood shunt from aorta to pulmonary trunk -risk of pulmonary overload and Eisenmengar’s
Symptoms of patent ductus arteriosus
Dyspnoea Failure to thrive Machine like murmur Risk of infective endocarditis
Investigations to diagnose patent ductus arteriosus
CXR ECG ECHO
Treatment for patent ductus arteriosus
Prostaglandin inhibitor (indomethacin) may induce closure Otherwise consider surgery by catheters
What is tetralogy of fallot
Cyanotic! Ventricular septal defect with right ventricular outflow obstruction - therefore O2 deficient blood is systemically shunted = blue blood passes from RV to LV
Most common congenital cyanotic heart disease
Tetralogy of Fallot 10% of all congenital birth defects
Four congenital abnormalities present in Tetralogy of Fallot
PROV Pulmonary stenosis: RV outflow obstruction Right ventricular hypertrophy Overriding aorta (over top of VSD) Ventricular septal defect (VSD)
Symptoms of tetralogy of fallot
Infants are often seen bringing their knees up to their chest as if squatting which partially occluded femoral arteries, this increases systemic vascular resistance and left ventricular pressure => relives cyanosis by reducing right to left shunt *cyanosis often exacerbated when cring or feeding
How to diagnose tetralogy of fallot
ECHO CXR - presents as boot shaped heart
Treatment of tetralogy of fallot
Full surgical repair within 2y of life and good prognosis if done Normally at 3-6months👩🏻🍼
Pathophysiology of coarction of aorta
Aorta narrows at or just distal to ductus arteriosus => blood diverted massively through aortic arch branches = increased perfusion in upper body vs lower body
Symptoms of coarction of aorta
Scapular bruits from collateral vessels Hypertension in collaterals (right arm) Murmur
Investigations to diagnose coarction of aorta
CXR: “notched ribs” dilated intercostal vessels CT angiogram
Treatment of coarction of aorta
Surgical repair or stenting of stenoses segment, even when mild to prevent long term problems
Three types of cardiomyopathy?
1) Hypertrophic 2) Restrictive 3) Dilated
What are cardiomyopathies?
Diseases of the myocardium (Muscular/conduction defects)
What is the most common cause of death in young people?
Hypertrophic cardiomyopathy
Causes of hypertrophic cardiomyopathy
Familial -inherited mutation of sarcomere proteins — troponin T and Myosin B
Pathophysiology of of hypertrophic cardiomyopathy
Thick non compliant heart = impaired diastolic filling => decrease in CO
Symptoms of hypertrophic cardiomyopathy
May present with sudden death Chest pain/angina Palpitations SOB Syncope/dizzy spells
Investigations to diagnose hypertrophic cardiomyopathy
Confirm with abnormal ECG ECHO (diagnostic) Genetic testing
Treatment for hypertrophic cardiomyopathy
Bb CCB Amiodarone (anti-arrhythmic)
What is the most common cardiomyopathy in general
Dilated cardiomyopathy
Cause of dilated cardiomyopathy
Autosomal dominant familial inheritance (cytoskeleton gene mutation) -IHD -Alcohol
Pathophysiology of dilated cardiomyopathy
Thin cardiac walls poorly contract leading to a decrease in CO LV/RV or 4 chamber dilation and dysfunction
Symptoms of dilated cardiomyopathy
SOB -heart failure (usually) -Atrial Fibrillation -thromboemboli
Investigations to diagnose dilated cardiomyopathy
ECG ECHO
Treatment for dilated cardiomyopathy
Treat underlying condition Eg Atrial fibrillation, heart failure
How common is restrictive cardiomyopathy
Rare
Causes of restrictive cardiomyopathy
Granulomatous disease (sarcoidosis,amyloidodis) -idiopathic -post MI-fibrotic
Pathophysiology of restrictive cardiomyopathy
Rigid fibrotic nyocardium fills poorly and contracts poorly => decreased CO
Symptoms of restrictive cardiomyopathy
Severe: -dyspnoea -S3 + S4 sounds -oedema -congestive heart failure -narrow pulse pressure ( normally 120/80 but here it’s 105/95 and consequently blood stasis due to the decreased gradient)
Investigations to diagnose restrictive cardiomyopathy
ECG ECHO cardiac catheterisation (diagnostic)
Treatment for restrictive cardiomyopathy
None Consider transplant Patients typically die within 1yr
What is shock
A medical emergency- life threatening -hypoperfusion -due to acute circulation failure -leads to tissue hypoxia and risk of organ dysfunction
What are the five different types of shock?
- Cardiogenic (heart pump failure) - Distributive (arterial supply to tissues): 1) septic 2) neurogenic 3) anaphylactic - Hypovolemic (affects venous return to heart and therefore preload)
Presentation of shock
1) decreased urine output 2) reduced GCS (Glasgow coma scale) 3) Skin - pale , cold, sweaty, vasoconstriction - increased capillary refill time = earliest, most accurate indicator - takes 3+ seconds for hand to turn pink after pressed for 5seconds 4) confusion 5) pulse- weak + rapid 6) prolonged hypotension = can lead to life threatening organ failure AFTER acute emergency recovery
Causes of hypovolemic shock
1) Blood loss - trauma, GI bleed 2) Fluid loss- dehydration
Symptoms of hypovolemeic shock
Clammy pale skin Confusion Hypotension Tachycardia
Treatment of hypovolemic shock
ABCDE Airways Breathing (give O2) Circulation (IV fluids)
Cause of anaphylactic shock
Due to IgE mediated Type 1 hypersensitivity vs allergen -Histamine release causes construction -causes excess vasodilation and bronchoconstriction Hypoxic!
Symptoms of anaphylactic
Hypotension Tachycardia Urticaria Puffy face flushing of cheeks
Treatment of anaphylactic shock
ABCDE IM adrenaline (SNS activation=stress response)
Key organs at risk of failure from shock?
Kidneys Lungs Heart Brain
Cause of neurogenic shock
Due to spinal cord trauma eg RTA Results in disrupted SNS, but intact PSNS
Symptoms of neurogenic shock
Hypotension Bradycardia Confused Hypothermic
Treatment for neurogenic shock
ABCDE IV Atropine (Blocks vagal tone: allows more psns inhibition, more chance for SNS to work)
Cause of cardiogenic shock
Due to heart pump failure; MI, cardiac tamponade, pulmonary emboli
Symptoms of cardiogenic shock
Heart failure signs (oedema) Increased JVP S4
Treatment of cardiogenic shock
ABCDE Treat underlying cause
Cause of septic shock
Due to uncontrolled bacterial infection
Symptoms of septic shock
Pyrexia warm peripheries Tachycardic
Treatment for septic shock
ABCDE Broad spectrum antibiotic
Tachycardia vs bradycardia?
Tachycardia = 100< bpm Bradycardia = 60> bpm
Types of bradycardia
1) RBBB/LBBB 2) 1°/2°/3° heart block 3) Sinus bradycardia
Two major groups of tachycardia’s
Supraventricular tachycardias AND Ventricular tachycardias
Types of supraventricular tachycardias (SVT)
1) AVRT (including WPW) 2) Atrial: -Sinus Tachycardia- Regular -Atrial fibrillation - Irregular -Atrial Flutter - Regular 3) AVNRT (functional) = most common SVT
Transmission pathway for heartbeats
SAN -> AVN -> Bundle of His -> Purkinje Fibres
What is atrial fibrillation
Irregularly irregular atrial firing rhythm
What is the most common cardiac arrhythmia?
Atrial Fibrillation
Causes of atrial fibrillation
Heart failure Hypertension 2° to mitral stenosis Sometimes idiopathic
Risk factors for atrial fibrillation
60+ T2DM Hypertension Valve defects (mitral stenosis) History of MI
Pathophysiology of atrial fibrillation
Regular,physiological impulses produced in the sinoatrial node are overwhelmed by the presence of rapid, uncoordinated electrical discharges produced in the atria. -Causes atrial spasm -Atrial blood pools instead of being pumped efficiently to ventricles
What does atrial blood pooling cause
Cause a decrease in cardiac output and increased risk of thromboembolic events (particularly stroke)
Potential underlying causes of Atrial Fibrillation
Pirates Pulmonary: PE and COPD Ischaemic heart disease: including heart failure Rheumatic heart disease: any valvular abnormality Anaemia, Alcohol, Advancing age Thyroid disease:hyperthyroidism Electrolyte disturbances eg hyper/hypokalaemia Sepsis and sleep apnoea
Pathophysiology pathway of atrial fibrillation
(In reality it’s an overlap of these two pathways)
Types of atrial fibrillation
1) First episode 2) Paroxysmel : recurrent episodes that stop on their own <7days 3) Persistant: recurrent episodes >7days 4) Permanent: continuous and refractory to treatment so management is aimed at rat control and anticoagulation
Symptoms and signs of atrial fibrillation
Symptoms: 1) Palpitations 2) Dyspnoea 3) Chest pain 🚩 4) Syncope 🚩 Signs: 1) irregularly irregular pulse 2) Hypotension 🚩 3) Evidence of heart failure 🚩(eg pulmonary oedema)
Investigations to diagnose Atrial fibrillation
ECG: - irregularly irregular pulse - narrow QRS (<120ms) - absent p waves
Treatment of atrial fibrillation
Determine if rate or rythm control is more appropriate
What is rate control
Rate control accepts the fact that the patient is not in sinus rythm, but aims at controlling the rate to reduce long-term deleterious effects of AF on cardiac function = decrease in heart rate
What is rythm control
Rythm control aims to restore normal sinus rythm, “cardioversion”, can be either electrical or pharmalogical =restore normal PQRS shape
When is rate control recommended for atrial fibrillation
Onset > 48 hours or unknown
When is rythm control recommended for atrial fibrillation?
- younger age - onset <48 hours - no underlying heart disease - reversible cause of AF - Failure of rate control - Haemodynamic instability acutely
Treatment for atrial fibrillation if patient is haemodynamically unstable
Emergency electrical synchronised DC cardioversion
Treatment of atrial fibrillation if patient is haemodynamically stable?
Onset of AF <48hrs: rate or rythm control Onset of AF >48hr/unknown: rate control and anticoagulation for at least three weeks Then offer rythm control if unsuccessful or still symptomatic
First line drugs for rate control
Beta-blocker OR rate limiting CCB Bispropolol OR diltiazen or verapamil Second line is to combine drugs
Pharmacological treatments for rythm control
Flecainide or amiodarone
Electrical treatments for rythm control
Synchronised DC shock starting at 150J under shirt acting general anaesthesia
Pathway for atrial fibrillation treatment
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What does a Has-bled score assess
Assess risk of major bleeds in AF patients on anticoagulants >= 3 (max 9) = regular reviews
What does the CHA2DS2-VASc assess?
Assess stroke risk and therefore the anticoagulation need for Atrial fibrillation
Scoring criteria for CHA2DS2-VASc score
Congestive heart failure Hypertension Age 75=< (2) DM Stoke (2) Vascular disease Age 65-74 Female Total: 2=< then oral coagulation required
Complications of atrial fibrillation
Heart failure Ischaemic stroke Mesenteric ischeamia
What is an atrial flutter
Irregular organisers atrial firing ~250-350bpm Less common and less severe than AF
Pathophysiology of atrial flutter
Fast atrial ectopic firing (250-350bpm) causes atrial spasm, but not as uncoordinated as A-Fib. Pathway typically from opening of tricuspid valve
Symptoms of atrial flutter
Dyspnoea Palpitations
Investigations to diagnose atrial flutter
ECG : (diagnostic) f wave “saw tooth” pattern Often with a 2:1 block (2 p waves for every QRS)
Treatment of acutely unstable atrial flutter
DC synchronised cardioversion
Treatment of stable atrial flutter
Rythm/rate control with oral anticoagulation (prevent thromboemboli) Also radiofreq ablation
What the most common supraventricular tachycardia?
AVNRT (functional)
Pathophysiology of AVNRT
Re-entrant pathway goes through AVN
Treatment for AVNRT
Same as AVRT (WPW)
What is an AVRT?
AVRT ( Atrioventricular reciprocating tachycardia) -> an accessory pathway exists for impulse conduction, not re entry through AVN Often Hereditary
Most common example of an AVRT
Wolff-Parkinson White syndrome (WPW)
Pathophysiology of WPW
Accessory pathway for conduction= Bundle of Kent A pre excitation syndrome (excites ventricles earlier than typical pathway so that’s why you see delta waves)
Symptoms of WPW
Palpitation Dizziness Dyspnoea
Investigations to diagnose WPW
Ecg: 1) slurred delta waves 2) short PR interval 3) wide QRS
Treatment for WPW
First line: Valsalva manoeuvre (Forceful exhalation against a closed airway.. close nose and mouth and breath hard like ur trying to pop ur ears) This triggers never to slow down electrical signals in the heart Carotid massage 2nd line: if 1st unsuccessful IV Adenosine (will temporarily cease conduction; when patient feels like dying) 6mg, then 12mg, then further 12mg (additional doses if 6mg is unsuccessful) Can also consider surgical radiofrequency ablation of bundle of Kent
What is long QT syndrome?
Ventricular tachycardia Typically congenital channelopathy disorder where mutation affects cardiac ion channels and therefore heart conduction QT interval 480ms+
Causes of long QT syndrome
-Romano ward syndrome (autosomal dominant) -Jervell - lang - Nielsen syndrome (autosomal recessive) -Hypokalemia + hypocalcemia (non-inherited) -Drugs (Amiodarone,magnesium)
What is torsades de pointes?
-Polymorphic ventricular tachycardia in patients with prolonged QT -Rapid irregular QRS complexes which “twist” around baseline - can cease spontaneously or develop to ventricular fibrillation
Initial management of MI
Get in to hospital quickly- 999 call Paramedics-if ST elevation, contact primary PCI centre for transfer Take 300g aspirin immediately Pain relief
Causes of ACS
Rupture of atherosclerotic plaque and consequent arterial thrombosis is the main cause Uncommon causes: - stress induced cardiomyopathy - coronary vasospasm without plaque rupture - drug abuse
What is troponin?
Protein complex regulates actin:myosin contraction Highly sensitive marker for cardiac muscle injury Not specific for acute coronary syndrome May not represent permanent muscle damage
Examples of PY12 inhibitors
Clopidogrel Prasugrel Ticagelor
Why are GPIIb//IIa antagonists used selectively?
Increase risk of major bleeding But still used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS
Alternative treatment to PCI for NSTE ACS
CABG used in about 10% of patients But uncommonly, patients may have severe CAD not amenable to revascularisation
Pain relief used in ACS management?
Opiates (can delay absorption of P2Y12 inhibitor so only if necessary) Nitrates for unstable angina/coronary vasospasm (GTN spray) (may be ineffective for MI)
Clopidogrel vs pasugrel
Pasugrel is much more reliable and useful because it has a direct liver breakdown pathway while clopidogrel effectiveness relies on genetics alongside other factors
Ticagrelor vs clopidogrel
Ticagrelor decreases risk of myocardial infarction and cardiovascular death in comparison to clopidogrel
What is ventricular fibrillation?
Shapeless rapid auscultations on ECG Patient becomes pulseless + goes into cardiac arrest (no effective cardiac output) 1st line treatment-> electrical defibrillation But jinn synchronised as patient is pulseless
Is rate control or rythm control preferred?
Rate control is generally preferred and first line for all patients unless they meet specific criteria
Most common congenital heart disease?
Ventricular septal defect 25-30%
Prevalence of patent ductus arteriosus
10-20%
Prevalence of tetralogy of fallot
4-10%
Exacerbating factors for IHD
Supply: -Anemia -hypoxemia Demand: -hypertension -tachycardia -valvular heart disease
Environmental exacerbating factors for IHD
Exercise Cold weather Heavy metals Emotional stress
Physiology of IHD
Myocardial ischemia occurs when there is an imbalance between heart’a oxygen demand and supply, usually from an increase in demand accompanied by limitation of supply: 1) impairment of blood flow by proximal arterial stenosis 2) increased distal resistance eg. Left ventricular hypertrophy 3) reduced oxygen-carrying capacity of blood eg. Anaemia
What is microvascular angina (syndrome X)
‘ANOCA’ Angina with apparently normal (main) coronary arteries Females mostly Cause unknown
Which risk factor drastically increases incidence of IHD
Age
Symptoms that don’t associate with angina
No fluid retention (unlike heart failure) Palpitation (not usually) Syncope or pre-syncope (very rare)
How to assess chest pain?
OPQRST Onset Position (site) Quality (nature/character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment
Differential diagnosis for myocardial ischemia
Pericarditis/myocarditis Pulmonary embolism/pleurisy Chest infection/ pleurisy Gastro-oesophageal (reflux/spasm/ulceration) Musculoskeletal Physcological
Treatment for myocardial ischemia
Reassure Lifestyle - smoking - weight - exercise - diet Advice for emergency Medication Revascularisation
Advantages and limitations of CT angiography (fuzzier than normal angiography)
Good diagnostic test and at spotting severe disease Not so good at moderate disease Anatomical, not functional
Advantages and drawbacks to exercise testing
Good functional test Relies on patients ability to walk on a treadmill (useless for elederly, obese, arthritis etc)
Side effects of beta blockers
Tiredness, nightmares Erectile dysfunction Bradycardia Cold hands and feet
Contraindication for beta blockers?
Asthma- do not give
Side effect of aspirin
Gastric ulceration
Pros and cons of PCI
Pro: - less invasive - convenient - repeatable - acceptable Cons: - risk stent thrombosis - can’t deal with complex disease - dual antiplatelet therapy
Pros and cons of CABG
Pros: - prognosis - deals with complex disease Cons: - invasive - risk of stroke - can’t do if frail - one time treatment -time for recovery
Which veins can a CABG use?
Internal mammary artery (from chest) Saphenous vein (from leg)
PCI and CABG use
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If you don’t get chest pain when you run.. how likely is IHD?
Very low probability
Prognosis of pericarditis
Majority of cases (viral and Idiopathic) are self limiting, whereas bacterial (purulent) pericarditis can be fatal if untreated.
Heart sound S1?
Mitral + Tricuspid close
Heart sound S2?
Aortic + Pulmonary close
Heart sound S3?
Shows RAPID VENTRICULAR FILLING in early diastole * normal in young/pregnant * pathological in mitral regurgitation + heart failure
Heart sound S4?
Pathological “gallop” * due to blood forced in to stiff hypertrophic ventricle (LVH + aortic stenosis)
What does P represent on a normal ECG?
Atrial depolarisation
What does PR interval represent on a normal ECG?
AVN conduction delay
Average length of PR interval?
0.12-0.2s
What does QRS interval represent?
Ventricle depolarisation + atrial repolarisation
Average length of a QRS interval?
0.08-0.1s 0.12=< is abnormal
Why does ST segment represent on a normal ECG?
Isovolemic ventricular relaxation
What does T represent on a normal ECG?
Ventricular repolarisation
What are ECGs useful in diagnosising?
-MI (STEMI, NSTEMI) -Arrhythmias -Electrolyte disturbance: K+, CA++ -Pericarditis -Chamber hypertrophy -Drug toxicity (eg. digoxin)
Scale for ECG paper?
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ECG leads for RCA
aVF + II + III (Inferior)
ECG leads for LAD
V1-V4 (Anterior + septal)
ECG leads for LCx
V5 + V6 + aVL + I (Lateral)
What is a 1° AV block?
PR interval prolongation (200ms+) Every P is followed by a QRS
Symptoms of 1° heart block?
Asymptomatic
Treatment of 1° heart block
No treatment as it is mild
Causes of 1° heart block
Drugs (Bb, CCB, digoxin —> block AVN conduction)
The difference between different degrees of heart block?
Severity 1° may not cause symptoms 2° sometimes troublesome symptoms 3° most serious = medical emergency
What is 2° heart block?
When some p waves are conducted but others aren’t
Two types of 2° heart block
Mobitz I (Weinkebach’s) Mobitz II
What is Mobitz I?
PR prolongation until a QRS is dropped (PR interval progressively elongates)
Causes of Mobitz I?
Same as 1° heart block (Bb, CCB, Digoxin) Inferior MI
Treatment of Mobitz I?
No treatment unless symptomatic eg syncope Treatment—> pacemaker
Symptoms of Mobitz I?
May have syncope
What is Mobitz II?
PR interval consistently prolonged (not progressively enlarging) with random dropped QRS
Causes of Mobitz II?
Drugs, Inferior MI, Rheumatic fever
Symptoms of Mobitz II?
Syncope SOB Chest pain
Treatment for Mobitz II?
Pacemaker
What is 3° heart block?
AV dissociation (complete heart block; atria + ventricles beat independently of each other) * ventricular ESCAPE rythm is sustaining heartbeat —> SAN (best) if dysfunctional, AVN takes over —> if dysfunctional ventricle pacemakers take over (worst, firing rate 20-40bpm)
Causes of 3° heart block
Acute MI Hypertension Structural heart disease
Treatment for 3° heart?
IV atropine + permanent pacemaker
What is a bundle branch block?
Blocks of bundles of His
Two types of bundle branch block?(BBB)
RBBB right LBBB left
Causes of RBBB
Pulmonary emboli IHD VSD
Causes of LBBB
IHD Valvular Disease
Pathophysiology of RBBB?
RV later activation than LV
Pathophysiology of LBBB?
LV activation later than RV
ECG presentation of RBBB?
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ECG presentation of LBBB?
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Epidemiology of hypertrophic cardiomyopathy
Affects 1 in 500 people
What is LVOT?
Left ventricular outflow tract obstruction is a recognised feature of hypertrophic cardiomyopathy
Cause of arrhythmogenic hypertrophy
Desmosome gene mutations
Main symptom of arrhythmogenic cardiomyopathy
Arrhythmia
What do all cardiomyopathies carry a risk of?
Arrhythmias
Likely cause of sudden cardiac death in a young person?
Often due to an inherited condition Most likely a cardiomyopathy or ion channelopothy
What is the cause of inherited arrhythmia? (Channelopothy)
Caused by ion channel protein gene mutations
Which ions do cardiac channelopothies relate to?
Potassium Sodium Calcium
Examples of cardiac channelopothies?
Long QT Short QT Brugada CPVT
Cardiac channelopothies effect on heart structure?
No effect- have a structurally normal heart
Symptom of cardiac channelopothy?
Syncope
QT prolonging drugs?
Many drugs on this list that may be used to treat other conditions eg some antidepressants But they can kill people with long QT syndrome
SADS sudden arrhythmic death syndrome?
Usually refers to normal heart/arrhythmia
Familial hypercholesterolaemia (FH)?
Inherited abnormality of cholesterol metabolism
What does familial hypercholesterolaemia lead to?
Serious premature coronary and other vascular diseases
Aortavascular syndromes
Marfan Loeys-Dietz Vascular Ehler Danos
What type of inheritance are inherited cardiac conditions usually?
Dominantly inherited Offspring have a 50% chance of inheritance
Why is screening important for inherited cardiac conditions?
Genetic testing is available Risk (arrhythmic death, vascular dissection) needs to be assessed for each individual Life saving treatments are available (ICD, beta blockers, statins, vascular surgery) Lifestyle modifications can save lives
Why is screening for inherited cardiac conditions highly contentious?
Because long QT has only a 1/5000 prevalence so it will very rarely be picked up and not a huge benefit to it in the normal population But for first degree relatives- 1/2 chance of it being passed on so highly recommended
Why treat hypertension?
Important preventable cause of premature morbidity and mortality Major risk factors for: - stroke (ischaemic and haemorrhagic) - myocardial infarction - heart failure - cognitive decline - premature death Increases risk of Atrial fibrillation as well
The main indications for ACEi?
Hypertension Heart failure Diabetic neuropathy
Examples of ACEi?
Ramipril Enalapril Perindopril Trandolapril (Largely do the same job but vary in price)
Main side effects of ACEi?
Due to reduced angiotensin II formation: - hypotension - acute renal failure - hyperkalemia - teratogenic effects in pregnancy Due to increased kinins: - cough - rash - anaphylactoid reactions
Main clinical indications for ARBs?
Hypertenison -diabetic neuropathy -heart failure (when ACEi contraindicated)
Examples of ARBs?
Cadersartan (most common) Losartan Val sat tan Irbesartan Telmisartan
Main side effects of ARBs?
Symptomatic hypotension Hyperkalemia Potential for renal function Rash Angioedema Generally very well tolerated
Contraindication of ARBs?
Pregnancy
Main clinical indications of CCBs?
Hypertension ischaemic heart disease - angina Arrrhythmia (tachycardia)
Examples of CCBs?
Amlodipine Diltiazem Verapamil Felodipine Lacidipine Nifedipine
Dihydropyridines CCBs?
Nifedipine Amlodipine Felodipine Lacidipine Preferentially affect vascular smooth muscle = peripheral arterial vasodilators
Phenylyalkylamines CCBs?
Verapamil Main effects in the heart = negatively chronotropic and inotropic
Benzothiazepines CCBs?
Diltiazem = immediate heart/peripheral vascular effects
Main side effects of peripheral vasodilation? (CCBs)
Flushing Headache Oedema Palpitations
Main side effects due to negatively chronotropic effects? (CCBs)
Bradycardia Atrioventricular block
Main side effects due to negatively ionotropic effects? (CCBs)
Worsening of cardiac failure
Side effect of verapamil?
Constipation
Main clinical indications for Bb?
Ischameic heart disease - angina Heart failure Arrhythmia Hypertension
Examples of B1 selective Bb?
Metoprolol Bisoprolol
An example of a less selective B1 Bb?
Atenolol
B1/B2 (non-selective) Bb examples?
Propranolol Nadolol Carvedilol
Are beta 1 selective blockers absolute?
Selectivity is relative rather than absolute
What percentage of beta adrenoreceptors in the heart are actually B1?
Only 60% 40% are B2 =hence you can’t use the term cardioselective to describe B1 selective beta blockers
Main side effects of Bb?
Fatigue Headache Sleep disturbance/ night mares Bradycardia Hypotension Cold peripheries Erectile dysfunction
Contraindications of Bb?
Worsening of : - asthma (can be severe) or COPD - PVD - claudication or raynauds - Heart failure - if given in standard dose or acutely
Main clinical indications of Diuretics?
Hypertension Heart failure
4 classes of diuretics?
1) thiazides and related drugs (distal tubule) 2) loop diuretics (loop of henle) 3) potassium-sparing diuretics 4) aldosterone antagonists
Examples of thuazide and related diuretics?
Bendroflumethiazide Hydroclorothiazide Chlorthalidone
Examples of loop diuretics?
Furosemide Bumetanide
Examples of potassium-sparing diuretics
Spironalactone Eplerenone Amiloride Triamterine
Main side effects of loop diuretics
Hypovolemia Hypotension
General side effects of diuretics?
Hypokalemia Hyponatremia Hypomagnesaemia Hypocalcemia Hyperuricaemia- gout
Side effects of thiazides?
Erectile dysfunction Impaired glucose tolerance
Other anti hypertensives?
A-1 adrenoceptor blockers (Doxazosin) Centrally acting anti-hypersensitive (Moxonidine + methyldopa) Direct renin inhibitor (Aliskeren)
What if patients are intolerant to ACEi and ARB? (Heart failure)
Hydralazine/nitrate combination
What do nitrates do?
Arterial and venous dilators Reduction of preload and afterload Lower BP
Main clinical indications for nitrates?
Ischeamic heart disease - angina Heart failure
Main examples of nitrates
Isorbide mononitrate GTN spray GTN infusion
Main side effects of nitrates
Headache due to GTN syncope (spray)
Drug for antiplatelet therapy in angina if aspirin intolerant?
Clopidogrel
Example of an antiarrhythmic drug?
Digoxin
