Cardiovascular Flashcards
What is Cardiac Failure?
The failure of the heart to maintain the cardiac output required to meet the body’s demands
LHF + RHF = Congestive Heart Failure
What does it mean by ‘Output States’ in relation to Cardiac Failure?
Low Output State = heart fails to pump in response to normal exertion
High Output State = cardiac output is normal but there are higher metabolic needs such as pregnancy, anaemia, hyperthyroidism
What are the ways in which Cardiac Failure can be classified?
- By EF
- By time
- By LHF or RHF
What are the parameters for classifying Cardiac Failure by EF?
- Patients with reduced LVEF (< 35-40%) have HF-rEF
This is due to systolic dysfunction (impaired myocardial contraction) - Patients with normal (preserved) LVEF have HF-pEF
This is due to diastolic dysfunction (impaired filling during diastole)
LVEF measured using echocardiography
Causes of Systolic and Diastolic dysfunction for Heart Failure
SD
- Ischaemic Heart Disease
- Dilated CMO
- Myocarditis
- Arrhythmias
DD
- Hypertrophic Obstructive CMO
- Restrictive CMO
- Cardiac Tamponade
- Constrictive Pericarditis
What are the parameters for classifying Cardiac Failure by time?
Acute or Chronic
- Acute typically refers to an acute exacerbation of chronic
- Most urgent symptoms are often due to LV failure resulting in pulmonary oedema
What are the parameters for classifying Cardiac Failure by LHF and RHF?
HF-rEF and HF-pEF typically develop left-sided heart failure. This may be due to increased left ventricular afterload (e.g. arterial hypertension or aortic stenosis) or increased left ventricular preload (e.g. aortic regurgitation resulting in backflow to the left ventricle).
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).
History and Examination for LHF
Respiratory symptoms
- Increased heart and respiratory rate
- Arrhythmia
- Dyspnoea
- Nocturnal cough (may have pink frothy sputum)
- Fatigue
History and Examination of RHF
Swelling symptoms
- Swelling
- Fatigue
- Raised JVP
- Reduced exercise tolerance
- Anorexia
- Nausea
- Nocturia
- Ascites
Clinical Diagnosis for Cardiac Failure by Framingham Criteria
2+ majors or 1 major and 2 minors from:
Investigations for Cardiac Failure
CHRONIC
-NT-proBNP (nice)
- 2000ng/litre, urgent referral for transthoracic echo in 2/52
- 400-2000ng/litre, same as above but in 6/52
ACUTE
- BNP > 100ng/litre
- NT-proBNP > 300ng/litre
- Perform transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities
- ECG
- Bloods - FBCs, U&Es, LFTs, TFTs, BNP
- Chest X-Ray
- Transthoracic Echocardiography
- Coupled with Doppler
- Can calculate EF (normal 50-70%)
Findings for Cardiac Failure on X-Ray
- Alveolar Oedema
- Cardiomegaly
- B-lines (Kerley)
- Dilated upper lobe vessels and upper lobe
- Effusion
Management of Cardiac Failure if Acute
ABCDE approach
- Sit patient upright
- Give oxygen (target 94-98%)
- GTN infusion if concomitant myocardial ischaemia, severe hypertension or left-sided regurgitation
- Can cause hypotension
- IV furosemide for pulmonary oedema
- CPAP if not responding to treatment and in respiratory failure.
- Inotropic agents such as dobutamine should be considered with severe left ventricular dysfunction and cardiogenic shock (hypotensive).
- Stop beta-blockers if HR < 50, second or third degree heart block, or shock
Management of Cardiac Failure if Chronic
- Treat underlying cause
- Treat exacerbating factors
- Lifestyle modifications
- Drugs
- ACE inhibitor - give to all patients with LV dysfunction (reduced EF) and beta-blocker - reduce O2 demand on heart
- Aldosterone agonist
- Spironolactone, eplerenone
- Monitor potassium to avoid hyperkalaemia
- SGLT-2 inhibitors for reduced ejection fraction
- Ivabradine if sinus rhythm > 75/min and EF < 35%
- Sacubitril-valsartan if EF < 35% and symptomatic on ACEi’s or ARBs (initiate after wash-out period)
- Digoxin if coexistent atrial fibrillation
- Consider hydralazine and nitrates in Afro-Caribbean patients
- Cardiac resynchronisation therapy if widened QRS
- Annual influenza vaccine
- One-off pneumococcal vaccine
What are complications of Cardiac Failure?
- Respiratory complications
- Renal failure
- Acute exacerbations
What is Deep Vein Thrombosis?
Deep vein thrombosis (DVT) is a significant medical condition characterised by the formation of a thrombus within the deep venous system, typically in the lower extremities.
What do patients with DVT usually present with?
- Pain + tenderness + swelling in affected leg
- Warmth + redness in affected leg
- Shortness of breath and chest pain (suggestive of PE)
What scoring system is carried out for suspected DVT?
Well’s Score
Investigations for DVT
If scores from Well’s Score:
- Is >2 : Ultrasound of affected leg, D-dimer if negative
- Is <2 OR US can’t be carried out in 4 hours : D-dimer, give DOAC in meantime
- If +ve D-dimer, stop DOAC and do US in a week
Management for DVT
The management of DVT involves the following steps:
- Apixaban or rivaroxaban
- If unsuitable, severe renal impairment or antiphospholipid syndrome then low molecular weight heparin followed by vitamin K antagonist (warfarin)
- 3 months for provoked VTE
- 6 months for unprovoked VTE
- Compression stockings: These help to prevent swelling and improve blood flow in the affected leg.
- Elevation of the affected leg: This helps to reduce swelling and improve blood flow.
- Thrombectomy: This is a surgical procedure to remove the blood clot in the affected vein
What are risk factors for DVT?
- Age
- Smoking
- Alcohol
- Recent surgery
- Medication
- Trauma
- Malignancy
- Obesity
- Being inactive
- Diabetes
What is the NICE definition of Hypertension?
- A clinic reading persistently above 140/90 mmHg
- A 24 hour BP average reading of 135/85 mmHg
What are the two types of Hypertension?
Primary - no single disease causing the rise in BP, complex series of physiological changes
Secondary - precipitates from a particular disease
Renal causes of Hypertension
- Glomerulonephritis
- Chronic pyelonephritis
- Adult polycystic kidney disease
- Renal artery stenosis
Endocrine causes of Hypertension
- Primary hyperaldosteronism
- Phaeochromocytoma
- Cushing’s
- Liddle’s
- CAH
- Acromegaly
- Thyroid problems
H&E of Hypertension
Usually asymptomatic unless very high BP
Patients may experience
- Headaches
- Visual disturbance
- Seizures
Ensure there is no end-organ damage
What is very important to assess when a patient has newly diagnosed hypertension?
End organ damage
- Fundoscopy to check for hypertensive retinopathy
- Urine dipstick to check for renal disease (cause or consequence
- ECG to check for LV hypertrophy or IHD
Investigations for hypertension
24 hour BP monitoring
ABPM or HBPM
U&E - renal disease
HbA1c - DM
Lipids - Hyperlipidaemia
ECG
Urine dipstick
Management of hypertension
STEP 1
<55 or T2DM = ACEi or ARBs
>55 / Afro-caribbean + No T2DM = CCBs
STEP 2
A+C or A+D
STEP 3
A+C+D
STEP 4
If K+ < 4.5 add low-dose spirinolactone
If K+ > 4.5 add alpha or beta blocker
If still not controlled have specialist review
What is Unstable Angina?
Chest pain, considered to be present in patients with ischaemic symptoms suggestive of ACS + no elevation in troponins, +/- ECG changes indicative of ishcaemia
Troponins may elevate some hours later, treated same as NSTEMI until Troponin result known
H&E of Unstable Angina
- Chest pain
- May radiate to jaw or left arm
- Often described as ‘heavy’ or ‘crushing’
- Not relieved by rest
- Certain patients e.g. diabetics or elderly may not experience pain
Other symptoms of ACS:
- Dyspnoea
- Sweating
- N+V
Investigations for Unstable Angina
- ECG
- Cardiac markers e.g. troponin
Simplified management of NSTEMI/Unstable Angina
- Aspirin 300mg, Fondaparinux if no immediate PCI planned
- Estimate 6 month mortality with GRACE
- Low risk - Conservative - Ticagrelor
OR
Intermediate or high risk - PCI - offer immediately if unstable otherwise in 72hrs
Give prasugrel or ticagrelor, give unfractionated heparin, drug-eluting stents used in preference
Further treatment of NSTEMI/Unstable Angina
MONA
- morphine for severe pain
- oxygen if <94%
- nitrates
- aspirin 300mg
Antithrombin treatment for patients at high risk of bleeding
GRACE Risk Assessment
Takes into account:
- age
-HR, BP
- Cardiac (Killip class) and renal function (serum Cr)
- Cardiac arrest on presentation
- ECG
- Troponin levels
What is Pulmonary Embolism?
Life-threatening condition resulting from dislodged thrombi occluding the pulmonary vasculature; RHF and cardiac arrest may ensue if not aggressively treated
RF for PE?
- Age
- DVT
- Recent surgery
- Long bed rest
- Previous thromboembolic event
- Malignancy
- Trauma
- COCP
H&E of PE
- Pleuritic chest pain
- Dyspnoea
- Haemoptysis
- Collapse if severe
- Tachycardia
- Tachypnoea
- Fever
PE rule-out criteria (PERC)
Used to exclude PE in patients known to have a low pre-test probability (<15%)
Age >= 50
HR >= 100
O2 Sats <= 94%
Previous DVT or PE
Recent surgery or trauma in last 4 weeks
Haemoptysis
Unilateral leg swelling
Oestrogen use (e.g. HRT, contraceptives)
2-Level PE Wells score
Clinical signs and symptoms of DVT - 3
Alternative diagnosis less like than PE - 3
HR > 100 - 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks - 1.5
Previous DVT/PE - 1.5
Haemoptysis - 1
Malignancy - 1
PE LIKELY - MORE THAN 4 POINTS
PE UNLIKELY - 0-4 POINTS
Investigations for PE
If PE likely:
- CTPA : if +, PE diagnosed / if -, consider proximal leg vein ultrasound
- Interim therapeutic anticoagulation - DOAC
If PE unlikely:
- D-dimer test : if + = CTPA, if - = stop anticoagulation
- V/Q scan instead of CTPA if renal impairment
- Arterial blood gas
- ECG sinus tachycardia, may also see RBBB, right axis deviation, S1Q3T3
- CXR - Westermark’s sign : wedge shaped opacification
Management of PE is haemodynamically unstable (SBP<90)
- Thrombolysis (alteplase)
- Respiratory support
- Unfractionated heparin
- Then switch to DOAC
Management of PE if haemodynamically stable
- DOAC
- if severe renal impairment or antiphospholipid syndrome, give LMWH and warfarin
Give treatment for 3 months if VTE was provoked, 6 months if unprovoked
If repeat PE despite treatment consider inferior vena cava filters
VTE prevention for PE
Everyone must be VTE risk assessed within 24 hours of hospital admission
- Compression stockings
- Low molecular weight heparin (tinzaparin)
What is Pericardial Disease?
Refers to any condition that affects the pericardium, the sac-like membrane that surrounds the heart.
Can cause inflammation, fluid accumulation or constriction of the pericardium.
Acute is lasting for less than 4-6 weeks
Aetiology of Pericardial Disease
- Viral infections (Coxsackie)
- TB
- Uraemia
- Post-MI
- early (1-3 days) : fibrinous pericarditis
- late (weeks to months) : autoimmune (Dressler’s syndrome)
- Radiotherapy
- Connective tissue disease
- SLE
- RA
- Hypothyroidism
- Malignancy (lung/breast)
- Trauma
H&E of Pericardial Disease
History :
- Pleuritic chest pain
- Relieved by sitting forwards
- SOB
- Non-productive cough
- Fever
- Fatigue
- Palpitations
Exam :
- Muffled Heart sounds
- Pericardial rub
H&E of Constrictive Pericarditis
- RHF symptoms
- Elevated JVP
- Ascites
- Oedema
- Hepatomegaly
- Pericardial knock : Loud S3
- Positive Kussmaul’s sign : paradoxical rise in JVP on inspiration
Investigations for Pericardial Disease
- First-line is ECG
- PR depression
- Saddle-shaped ST elevation
- All patients with suspected acute pericarditis should have a transthoracic echo
- Bloods : CRP and ESR
- Raised troponin indicates myopericarditis
- CXR for constrictive pericarditis
- Pericardial calcification
Management of Pericardial Disease
- Combination of NSAIDs and Colchicine for patients with acute idiopathic or viral
- Until symptom resolution and normalisation of inflammatory markers, taper doses
- High-risk features e.g. fever and raised troponin, treated as inpatient
- Treat any underlying cause
- Avoid strenuous physical activity
- If pericardial effusion is causing significant symptoms of haemodynamic compromise, pericardiocentesis may be necessary
- If cases of chronic or constrictive pericarditis, surgical interventions such as pericardiectomy or pericardial window may be required
What is Haemochromatosis?
- Autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation
- Caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*
- Often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia
H&E of Haemochromatosis
Early symptoms include fatigue, ED and arthralgia (often hands)
Reversible symptoms:
- ‘bronze’ skin pigmentation
- cardiac failure secondary to dilated CMO
Irreversible symptoms:
- DM
- Liver : stigmata of CLD, hepatomegaly, cirrhosis, hepatocellular deposition
- Hypogonadism (2nd to cirrhosis and pituitary dysfunction)
- Arthritis
Screening of Haemochromatosis
Screening:
Gen. Pop.
- Transferrin saturation is considered the most useful marker
- Ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
Family members:
- Genetic testing for HFE mutation
Investigations for Haemochromatosis
Typical iron study profile in patient with haemochromatosis
- Transferrin saturation > 55% in men or >50% in women
- Ferritin raised and iron
- Low TIBC
Also:
- LFTs
- Molecular genetic testing for C282Y and H63D mutations
- MRI to quantify liver and cardiac iron
- Liver biopsy if suspected cirrhosis
Management of Haemochromatosis
- Venesection
- Transferrin saturation should be kept below 50% and serum Ferritin concentration below 50 ug/L
- Desferrioxamine may be used second line
What are Acute Coronary Syndromes?
Umbrella term covering a number of acute presentations of IHD
- STEMI
- NSTEMI
- Unstable Angina (present in patients suggestive of ACS w/o elevation of troponins +/- ECG changes)
What is Ischaemic/Coronary Heart/Artery disease?
Gradually build up of fatty plaques leading to:
- Gradual narrowing, resulting in blood loss and therefore oxygen loss reaching the myocardium - leads to angina
- Risk of sudden plaque rupture - leads to occlusion of artery
RF of ACS
Unmodifiable: age, gender (M>F), FHx
Modifiable: smoking, DM, HT, high cholesterol, obesity
H&E of ACS
Key:
- Chest pain (central/LHS, crushing/heavy, radiates to jaw or LA)
- Dyspnoea
- Sweating
- N+V
Investigations for ACS
1st:
- ECG
- Cardiac markers e.g. Troponin
- Bloods
ECG lead changes in ACS
Anterior/Septal = V1-V4 = Left anterior descending
Inferior = II, III, aVF = Right coronary
Lateral = I, V5-V6 = Left circumflex
General Management of ACS
MONA
- Morphine (for severe pain)
- Oxygen (if <94%)
- Nitrates (caution if hypotensive)
- Aspirin 300mg
Management of STEMI is PCI possible
- Aspirin 300mg
- PCI within 120mins
- give prasugrel
- unfrac. heparin
- bailout glycoprotein IIb/IIIa inhibitor
- drug elluting stents should be used in preference
ASSUMING
- Patient presents within 12 hours of symptoms
- Patient is not a high bleeding risk
- Patient is not on DOAC
Management of STEMI if PCI not possible
- Aspirin 300mg
- Fibrinolysis
- Give antithrombin at the same time
- Following procedure give Ticagrelor
- Conduct ECG 60-90 mins after fibrinolysis - if persisting consider PCI
ASSUMING
- Patient presents within 12 hours of symptom
- Patient is not high bleeding risk
- Patient is not on DOAC
Management of NSTEMI/ Unstable Angina if LOW RISK
- Aspirin 300mg + Fondaparinux if PCI not immediate
- GRACE risk </3% = low risk
- Give Ticagrelor
Management of NSTEMI/ Unstable Angina if HIGH RISK
- Aspirin 300mg + Fondaparinux if PCI not immediate
- GRACE risk >/3% = high risk
- PCI if clinically unstable, otherwise within 72 hours
- Give prasugrel/ticagrelor
- Unfractionated heparin
- Drug eluting stents used in preference
Assumptions made in treatment of ACS + alternatives
Patient is high bleed risk:
- STEMI : switch prasugrel to ticagrelor/ ticagrelor to clopidogrel
- NSTEMI/UA : fondaparinux for alternative antithrombin/dose
Patient is on DOAC :
- STEMI : swap prasugrel for clopidogrel
- NSTEMI/UA : swap ticagrelor/prasugrel for clopidogrel or switch prasugrel to ticagrelor/ ticagrelor to clopidogrel
Patient presents after 12 hours = PCI immediately if ongoing MI
After event management of ACS
Lifelong:
- Aspirin
- Second antiplatelet (clopidogrel)
- Beta-blocker
- ACEi
- Statin
What are beta-blockers and what are they used for?
B1 antagonists
Used for IHD, CHF, AF, SVT, resistant hypertension, migraine prophylaxis and thyrotoxicosis
Contraindications and adverse effects of beta-blockers
Contraindications in asthma (can cause bronchospasm), heart block and severe hypotension
Effects :
- Fatigue, cold extremities, headaches, GI upset, sleep disturbance + nightmares, erectile dysfunction
In HF, start with low dose and gradually increase
Reduce dose in significant liver failure
Adverse effects of Statins
Common side effects:
- muscle pain, headache, digestive issues, and fatigue
More serious but rare side effects include:
- liver damage, kidney damage
- rhabdomyolysis (muscle breakdown)
- raised CK
Serious adverse effect of Gentamicin
It is nephrotoxic
What are ACEi + side effects?
Inhibit conversion of angiotensin I to angiotensin II
- Cough
- Angioedema
- Hyperkalaemia
What are CCBs + side effects?
Block VG calcium channels, relaxing vascular smooth muscle and force of myocardial contraction
- Flushing
- Headaches
- Ankle swelling
What are Thiazide diuretics + side effects?
Inhibit sodium absorption at beginning of DCT
- Hyponatraemia
- Hypokalaemia
- Dehydration
What are A2RBs + side effects?
Block effects of angiotensin II at AT1 receptor
- Hyperkalaemia
What is an Aortic Aneurysm?
Weakening of vessel wall of aorta specifically abdominal portion
- Usually result of the failure of elastic proteins within ECM
- Diameters >3cm are considered aneurysmal (M-1.7, F-1.5)
- 90% occur below renal arteries
- True aneurysms = all three layers expanding
H&E of Unruptured AAA
- Usually asymptomatic
- Pulsing sensation in abdomen
- May have abdominal/lower back pain
H&E of Ruptured AAA
- Severe, central abdominal pain radiating to back
- Dizziness
- Sweaty, pale and clammy skin
- Tachycardia
- Dyspnoea
- Syncope
RF of AAA
- Smoking
- FHx
- HT
- High cholesterol
- Syphilis
- CT disorder e.g. Ehlers Danlos T1, Marfan’s
Investigations for AAA
Abdominal US to detect presence
CT angiogram to detect is ruptured (if stable)
Bloods - crossmatch in case of surgery
Management of AAA
<3cm = no further action
3-4.4cm = small = rescan yearly
4.5-5.4cm = medium = rescan every 3 months
> / 5.5cm = large = refer within 2 weeks to vascular surgery for probable intervention (only 1 in 1000)
If large + symptomatic or rapidly enlarging - 2 week vascular surgery
If ruptured immediate vascular review and emergency endo vascular repair (open repair if unsuitable) - complication is endoleak
What is an Aortic Dissection?
Tear in aortic intima that allows blood to flow into new false lumen in between inner and outer layers of tunica media
Stanford classification of Aortic Dissection
Type A - ascending aorta, 2/3 cases
Type B - descending aorta, distal to left subclavian origin, 1/3 cases
DeBakey classification of Aortic Dissection
- Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
- Type II - originates in and is confined to the ascending aorta
- Type III - originates in descending aorta, rarely extends proximally but will extend distally
H&E of Aortic Dissection
- Acute severe chest pain (more common in type A and upper back pain is type B)
- Deficit pulse
- L/R BP difference
- Aortic regurgitation
- Features of Ehlers-Danlos/ Marfan’s
Symptoms of Aortic Dissection due to blockage of branching arteries
- Carotid = blackouts, dysphasia
- Coronary = angina
- Subclavian = loss of consciousness
- Renal = anuria, renal failure
RF of Aortic Dissection
- HT
- Trauma
- Biscuspid aortic valve
- CT disorders
- Coarctation of aorta
Investigations of Aortic Dissection
- CT angiogram - false lumen
(Trans oesophageal echo if unstable) - ECG (often normal)
- CXR - widened mediastinum
- Bloods + cardiac enzymes
Management of Aortic Dissection
- IV antihypertensives + beta-blocker
- O2 + analgesia
- Type A - surgery, control BP to 100-120 systolic
- Type B - conservative management, IV labetalol to reduce BP
Surgery associated with significant risk of paraplegia
What is Arterial Thrombosis?
Blood clot that forms in an artery
Can block flow of blood to affected area - causing damage or death to tissue
Occurs in antiphospholipid syndrome, Polycythaemia Vera, Hyperosmolar Hyperglycaemic state
H&E of Arterial Thrombosis
Depend on location of the clot
Common symptoms include:
- Sudden pain in chest, arm or leg
- Dyspnoea
- Dizziness
- Numbness or tingling in face, arm or leg
- Vision problems
- Seizures
Investigations of Arterial Thrombosis
Depends on location and severity
- Duplex US
- Angiography
- CT scan
- ECG
- Bloods
Management of Arterial Thrombosis
Depends on location and severity
May include:
- Thrombolytic therapy
- Anticoagulation therapy
- Surgical intervention
What are Venous Ulcers?
Complication of chronic venous insufficiency
- increasing leg pain
- fatigue
- heaviness with prolonged standing
Typically seen above medial malleolus
H&E of Venous Ulcers
- Large + shallow
- Sloping, sides not well-defined
- Gaiter region (between ankle and knee)
Symptoms of venous insufficiency
- swelling, itching, aching
Investigations for Venous Ulcers
- Duplex US of lower limbs
- ABPI : <0.9 = arterial disease - impairs healing
- Swab for microbiology
- Biopsy
Management of Venous Ulcers
- Four layer compression bandaging
- Debridement and cleaning
- Measure SA to monitor progression
- Oral pentoxifylline (peripheral vasodilator) to improve healing rate
- Abx if infected
What is Vasovagal Syncope?
- Type of neurally mediated reflex syncope (NMRS)
- MC cause of loss of consciousness in young people
- Syncope is sudden, temporary and self-terminating loss of consciousness associated with inability to maintain postural tone with rapid and spontaneous recovery
H&E of Vasovagal Syncope
- Hx of recurrent faints
- Absence of structural heart disease
- Provocative factor
- Nausea
- Lightheadedness
- Pallor
- Diaphoresis
- Bradycardia
RF of Vasovagal Syncope
- Prior syncope
- Prior Hx of arrhythmias, MI, HF or CMO
- Severe aortic stenosis
- Prolonged standing, emotional stress, dehydration
Investigations for Vasovagal Syncope
- 12-lead ECG
- Serum Hb
- Plasma blood glucose
- Serum beta-hCG
- Cardiac enzymes
- D-dimer levels
- Serum cortisol
- Urea or serum creatinine
Management of Vasovagal Syncope
- Patient education
- Physical techniques
- Volume expansion
What is Myocarditis?
Describes inflammation of the myocardium
Wide range of underlying causes - should particularly be considered in young people with chest pain
Causes of Myocarditis
- Viral : coxsackie B, HIV
- Bacteria : diphtheria, clostridia
- Spirochaetes : Lyme disease
- Protozoa : Chagas’, toxoplasmosis
- Autoimmune
- Drugs : doxorubicin
H&E of Myocarditis
- Usually young patient with acute Hx
- Chest pain
- Dyspnoea
- Arrhythmias
Investigations for Myocarditis
Bloods
- inc. inflammatory markers in 99%
- inc. cardiac markers
- inc. BNP
ECG
- tachycardia
- arrhythmias
- ST/T waves changes including ST-segment elevation and T wave inversion
Management of Myocarditis
- Treatment of underlying causes e.g. Abx if bacterial
- Supportive treatment e.g. of heart failure or arrhythmias
Complications of Myocarditis
- HF
- Arrhythmias
- Dilated CMO : usually late complication
Causes of Aortic Stenosis
- Degenerative calcification (MC > 65 years)
- Bicuspid aortic valve (MC < 65 years)
- William’s syndrome (supravalvular aortic stenosis)
- Post-rheumatic disease
- Subvalvular : HOCM
H&E of Aortic Stenosis
- Chest pain
- Dyspnoea
- Syncope/presyncope
- Murmur (Ejection systolic, radiates to carotids, decreased following Valsalva manoeuvre)
Features
- narrow pulse pressure
- slow rising pulse
- delayed ESM
- soft/absent S2
- S4
- thrill
- left ventricular hypertrophy or failure
Investigation for Aortic Stenosis
- Echocardiography to assess valve area, gradient, jet velocity
Management of Aortic Stenosis
Asymptomatic : observe
Asymptomatic but valvular gradient >40mmHG + LV systolic dysfunction : consider surgery
Symptomatic : valve replacement
Options for replacement:
- Surgical AVR : young or low/medium risk
- TAVR : for high operative risk
Balloon valvuloplasty : in children with no calcification or adults not fit for surgery
What is Aortic Regurgitation?
Leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole
Can be caused by disease of aortic valve or distortion or dilation of aortic root and ascending aorta
Causes of Aortic Regurgitation
Chronic due to valve : rheumatic fever (MC in developing world), calcification, CT disorder, biscuspid AV (both valve and root)
Chronic due to root : bicuspid AV, HT, syphilis, CT disorder, spondylarthropathies
Acute due to valve : infective endocarditis
Acute due to root : aortic dissection
H&E of Aortic Regurgitation
Mild can be asymptomatic but severe can cause:
- Fatigue
- Shortness of breath
- Chest pain
- Fainting
- Swelling of ankles and feet
- Heart palpitations
On exam:
- early diastolic murmur: intensity increased by handgrip manoeuvre
- collapsing pulse
- wide pulse pressure
- Quincke’s sign (nailbed pulsation)
- De Musset’s sign (head bobbing)
- Mid-diastolic Austin-Flint murmur in severe AR
Investigation of Aortic Regurgitation
Echocardiogram
Management of Aortic Regurgitation
Medical management of any associated HF
Surgery : AV indications include
- symptomatic patients with severe AR
- asymptomatic patient with severe AR who have LV systolic dysfunction
Types of Atrial Fibrillation
First detected episode : first time irrespective of symptomatic or self-terminating
Recurrent : 2 or more episodes of AF
- If AF terminates spontaneously (usually last <7days) = PAROXYSMAL
- If AF not self-terminating (usually >7days) = PERSISTENT
Permanent : continuous AF, which cannot be cardioverted or if unable to do so, treatment goals are rate control and anticoagulation
H&E of Atrial Fibrillation
- Palpitations
- Dyspnoea
- Chest pain
- Irregularly irregular pulse
Investigations for Arrhythmias
ECG
Management of Atrial Fibrillation
If haemodynamically unstable, cardioversion, otherwise, rate or rhythm control
Rate control if >48 hours or uncertain
- Beta blocker
- If they don’t work, combination of any 2 of:
- Beta blocker
- Digoxin
- Diltiazem
Rhythm control
- Beta blocker
- Amiodarone
- Flecainide if no structural heart disease
After an episode of paroxysmal atrial fibrillation, CHA2DS2-VASc score should be calculated, and a DOAC considered if the score is 1 or more.
- Apizaban, dabigatran, edoxaban or rivaroxaban
- Warfarin if DOAC is contraindicated or not tolerated
Management of Supraventricular Tachycardia
Acute management:
- vagal manoeuvres:
- Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
- carotid sinus massage
- IV adenosine
- rapid IV bolusof6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
- contraindicated in asthmatics - give verapamil
- rapid IV bolusof6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
- electrical cardioversion if unstable
Prevention of episodes:
- beta-blockers
- radio-frequency ablation
Management of Ventricular Tachycardia
DC cardioversion if unstable
Drug therapy:
- amiodarone: ideally administered through a central line
- lidocaine: use with caution in severe left ventricular impairment
- procainamide
Verapamil should NOT be used in VT
If drug therapy fails:
- electrophysiological study (EPS)
- implantable cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
Manage torsades de pointes with IV magnesium sulphate
What are the types of rhythms in cardiac arrest?
Shockable - VF / pulseless VT
Non-shockable - asystole / pulseless-electrical activity (PEA)
Reversible causes of Cardiac Arrest
Hs - hypoxia, hypovolaemia, hyperkalaemia, hypokalemia, hypoglycaemia, hypocalcaemia, hypothermia
Ts - thrombosis, tension pneumothorax, tamponade, toxins
H&E of Cardiac Arrest
- Unresponsive
- Absence of normal breathing, circulation
- Cardiac rhythm disturbance
Investigations of Cardiac Arrest
- Continuous Cardiac monitoring
- FBC
- U&Es
- ABG
- Cardiac biomarkers
Management of Cardiac Arrest
- Chest compressions : 30:2, continued while defib charges
- Defib : single shock for VF/Pulseless followed by 2 minutes of CPR, if cardiac arrest in monitored patient do 3 shocks
- Drugs should be delivered by IV, if not possible use interosseous route
- Adrenaline : 1mg ASAP for non-shockable rhythms, during VF/VT, 1mg given once CPR have restarted after 3rd shock and then repeat 1mg every 3-5mins whilst ALS continues
- Amiodarone : 300mg given to VF/pulseless VT after 3 shocks, further 150mg after 5 shocks, lidocaine if not available
- Thrombolytic drugs : considered if PE is suspected, if given, CPR continued for extended period of 60-90 mins
Signs of Tricuspid Regurgitation
- pan-systolic murmur
- prominent/giant V waves in JVP
- pulsatile hepatomegaly
- left parasternal heave
Causes of Tricuspid Regurgitation
- right ventricular infarction
- pulmonary hypertensione.g. COPD
- rheumatic heart disease
- infective endocarditis (especially intravenous drug users)
- Ebstein’s anomaly
- carcinoid syndrome
What is Mitral Valve Stenosis?
Describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle
Leads to increase pressure within the left atrium, pulmonary vasculature and RHS of the heart
Causes of Mitral Stenosis
- Rheumatic fever
RARE
- Mucopolysaccharidoses
- Carcinoid and endocardial fibroelastosis
H&E of Mitral Stenosis
- Dyspnoea - inc. left atrial pressure leads to pulmonary venous hypertension
- Haemoptysis - due to pulmonary pressures and vascular congestion
- Mid-late diastolic murmur (best on expiration)
- Loud S1
- Opening snap
- Low volume pulse
- Malar flush
- AF
SEVERE
- Length of murmur increases
- Opening snap becomes closer to S2
Investigations for Mitral Stenosis
- CXR - Left atrial enlargement
- Echocardiography - tighter cross-sectional area of valve
Management of Mitral Stenosis
- patients with associated AF require anticoagulation - currently warfarin - DOACs for mild MS who develop AF
- Asymptomatic patients - monitored with echo
-Symptomatic patients - percutaneous mitral balloon valvotomy or MV surgery
RF for Mitral Regurgitation
- Female
- Low BMI
- Age
- Renal dysfunction
- Prior MI
- Prior MS or valve prolapse
- Collagen disorders
H&E of Mitral Regurgitation
- Mild to moderate are asymptomatic
Symptoms due to failure f LV, arrhythmias or pulmonary HT:
- Fatigue
- Dyspnoea
- Oedema
Signs:
- Blowing pansystolic murmur - best at apex and radiating into axilla
- S1 may be quiet
- Severe MR may cause widely split S2
Investigations for Mitral Regurgitation
- ECG - broad P wave
- CXR - cardiomegaly
- Echo is crucial to diagnosis and assess severity
Management of Mitral Regurgitation
- Acute cases: nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
- If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone
- In acute, severe regurgitation, surgery is indicated
- Repair over replacement
- When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
Associations of Mitral valve prolapse
- congenital heart disease: PDA, ASD
- cardiomyopathy
- Turner’s syndrome
- Marfan’s syndrome, Fragile X
- osteogenesis imperfecta
- pseudoxanthoma elasticum
- Wolff-Parkinson White syndrome
- long-QT syndrome
- Ehlers-Danlos Syndrome
- polycystic kidney disease
Features of Mitral Valve Prolapse
- atypical chest pains or palpitations
- mid-systolic click (occurs later if patient squatting)
- late systolic murmur (longer if patient standing)
- complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death
What is a TIA?
Brief period of neurological deficit due to vascular cause, typically lasting less than an hour
H&E of TIA
Similar to stroke symptoms
- Unilateral weakness
- Aphasia or dysarthria
- Ataxia, vertigo or loss of balance
- Visual problems - diplopia, homonymous hemianopia, loss of vision in one eye
Immediate treatment of TIA
Give Aspirin 300mg unless:
1) Patient has bleeding disorder or is on anticoagulants (immediate admission for imaging to exclude haemorrhagic stroke)
2) Patient already taking low-dose aspirin (continue dose until reviewed by specialist)
3) Aspirin contraindicated (discuss management with specialist)
Specialist review for TIA
If patient has had >1 TIA/ suspected cardioembolic source/ severe carotid stenosis - discuss admission or observation with specialist
If patient has had suspected TIA in last 7 days - arrange urgent (<24hrs) by specialist
If patient has had suspected TIA over 7 days - refer specialist ASAP <7days
ADVISE PATIENT NOT TO DRIVE UNTIL SEEN
Investigations for TIA
CT - should not be done unless other diagnosis suspected that can be picked up by CT
MRI - preferred, same day as specialist assessment
Carotid imaging - urgent carotid doppler unless not candidate
Management of TIA
Secondary prevention - antiplatelet therapy following initial aspirin therapy
CLOPIDOGREL first-line
Aspirin + Dipyridamole if Clopidogrel not tolerated
High intensity statin - reduce non-HDL by >40%
What is Pulmonary Hypertension?
Defined as a mean pulmonary arterial pressure >/ 20mmHg at rest
Classification of Pulmonary Hypertension based on underlying etiology
Group 1 - pulmonary arterial HT
Group 2 - left heart disease
Group 3 - lung disease +/ hypoxia
Group 4 - chronic thromboembolic pulmonary HT
Group 5 - miscellaneous
What is Pulmonary Arterial Hypertension?
Subtype of Pulmonary Hypertension
- elevated pulmonary artery pressure
- normal capillary wedge pressure
- inc. pulmonary vascular resistance
Can be idiopathic or associated with CT diseases, HIV, congenial heart disease
H&E of Pulmonary Hypertension
- Dyspnoea, fatigue, chest pain, syncope
- On exam : RV hypertrophy +/ failure, elevated JVP, peripheral oedema and prominent pulmonary component S2
Investigations for Pulmonary Hypertension
Echo is first-line - estimate of pulmonary artery pressure, RV function or any underlying structural abnormalities
Right heart catheterisation confirms diagnosis
Further - pulmonary function test, ABG, CXR, CTPA
Classification of Pulmonary Hypertension based on activity
- Ordinary physical activity = no symtpoms
- Ordinary physical activity = symptoms, not when resting
- Slight physical activity = symptoms, not when resting
- Symptoms when resting + worse on activity
Management of Pulmonary Hypertension
- Treatment of pulmonary hypertension is dependent on the underlying cause and severity of the condition.
- Patients with PAH are typically treated with targeted pulmonary vasodilator therapy, such as
- prostacyclin analogues,
- endothelin receptor antagonists (bosentan, ambrisentan)
- and phosphodiesterase type 5 inhibitors (sildenafil and tadalafil)
- Other treatment options may include oxygen therapy, diuretics, and anticoagulation.
- In severe cases, lung transplantation may be considered.
Typical patient presentation for Infective Endocarditis
- Previous normal valve (50%), MV most affected
- Rheumatic valve disease (30%)
- Prosthetic valves
- Congenital heart defects
- IVDU, TV most affected
- Recent piercings
Causes of Infective Endocarditis
- Staph. aureus - MC cause
- Strep. viridans - poor dental hygiene or following dental procedure
- Staph. epidermidis - indwelling lines + valve replacement
- Strep. bovis - colorectal cancer
- Non-infective - SLE + malignancy (marantic)
H&E of Infective Endocarditis
- Fever
- Malaise
- Myalgia, arthralgia
- Confusion
- New regurgitant murmur
- Vasucilitic lesions - Roth’s spots, Osler’s nodes, Janeway lesions, splinter haemorrhages
Investigations for Infective Endocarditis
- Bloods - high neutrophils, normocytic anaemia, RF positive
- Blood culture
- Duke’s classification - 2 major, 1 major + 3 minor, 5 minor
- Transthoracic Echo - first line imaging
Indications for surgery for Infective Endocarditis
- Severe valvular incompetence
- Aortic abscess (indicated by prolonged PR)
- Infections resistant to Abx/ Fungal infections
- Cardiac failure refractory to standard treatment
- Recurrent emboli after Abx therapy
Blind management of Infective Endocarditis
- Amoxicillin for native valve
- Vancomycin + gentamicin if penicillin allergic, MRSA or sepsis
- Vancomycin + rifampicin + gentamicin for prosthetic valve
Management of Infective Endocarditis if Staph.
Native valve
- Flucloxacillin
- Vancomycin + rifampicin if penicillin allergic or MRSA
Prosthetic valve
- Flucloxacillin + rifampicin + gentamicin
- Vancomycin + rifampicin + gentamicin if penicillin allergic or MRSA
Management of Infective Endocarditis if Strep.
Fully-sensitive
- Benzylpenicillin
- Vancomycin + gentamicin if penicillin allergic
Less-sensitive
- Benzylpenicllin + gentamicin
- Vancomycin + gentamicin if penicillin allergic
Three main patterns of presentation + RF for PVD
- Intermittent claudication
- Critical limb ischaemia
- Acute limb-threatening ischaemia
RF : elderly, male, Hx of HT, smoking, previous stroke/TIA
H&E of Intermittent Claudication
- Aching or burning in leg following walking
- Patients can typically walk a predictable distance before symptoms
- Usually relieved within minutes of stopping
- Not present at rest
H&E of Critical limb ischaemia
1 or more of:
- Rest pain in foot for >2 weeks
- Ulceration
- Gangrene
Patients report hanging their legs out of bed at night to ease pain
H&E of Acute limb-threatening ischaemia
1or more of the 6 P’s:
- Pale
- Pulseless
- Painful
- Paralysed
- Paraesthetic
- Perishingly cold
Factors suggesting Thrombus for PVD
- Pre-existing claudication with sudden deterioration
- No obvious source of emboli
- Reduced or absent pulse in contralateral limb
- Evidence of vascular disease
Factors suggestive of Embolus in PVD
- Sudden onset of painful leg (<24hrs)
- No Hx of claudication
- Clinically obvious source of embolus
- No evidence of PVD
- Evidence of proximal aneurysm
Investigations for PVD
Duplex US for intermittent claudication
ABPI
Handheld arterial Doppler for Acute limb ischaemia
- If signals present, ABPI
- <0.5 indicates Critical limb ischaemia
Magnetic Resonance Angiography before any intervention
Management of PVD
- Clopidogrel
- Smoking cessation + exercise training
- Treat comorbidities
- Atorvastatin 80mg if established CVD
Management of severe PVD or Critical limb ischaemia
Endovascular revascularization
- percutaenous transluminal angioplasty +/- stent placement
- endovascular techniques are typically used forshort segment stenosis (e.g. < 10 cm), aortic iliac disease and high-risk patients
Surgical revascularization
- surgical bypass with an autologous vein or prosthetic material
- endarterectomy
- open surgical techniques are typically used forlong segment lesions (> 10 cm), multifocal lesions, lesions of the common femoral artery and purely infrapopliteal disease
Amputation if not suitable for other interventions
Management of Acute limb-threatening ischaemia
- ABC approach
- IV opioids
- IV unfractionated heparin if surgery not immediate
- Vascular review
Definitive management:
- Intra-arterial thrombolysis
- Surgical embolectomy
- Angioplasty
- Bypass surgery
- Amputation if irreversible
Symptoms of Lacunar Stroke
Small infarcts around basal ganglia, internal capsule, thalamus and pons
May result in pure motor, pure sensory, mixed signs or ataxia
Effects of Stroke in Anterior Cerebral Artery
Contralateral hemiparesis and sensory loss, lower>upper
Effects of Stroke in Middle Cerebral Artery
Contralateral hemiparesis and sensory loss, upper>lower
Contralateral homonymous hemianopia
Aphasia
Effects of Stroke in Posterior Cerebral Artery
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Effects of Stroke in PICA
AKA lateral medullary syndrome / Wallenberg syndrome
Ipsilateral facial pain and temperature loss
Contralateral limb/torso pain and temperature loss
Ataxia
Nystagmus
Effects of Stroke in AICA
AKA lateral pontine syndrome
Similar to PICA but
Ipsilateral facial paralysis and deafness
Effects of Stroke in Retinal/Opthalmic Artery
Amaurosis Fugax
Effects of Stroke in Basilar Artery
Locked in Syndrome
Effects of Weber’s Syndrome Stroke
Branches of PICA that supply midbrain
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Investigations for Stroke
Non-contrast CT head scan
Acute ischaemic strokes
- May show areas of low-density in grey and white matter of territory (may take time to show)
- Other signs are hyper dense artery sign (visible immediately)
Acute haemorrhagic strokes
- Show areas of hyper dense material (blood) surrounded by low density (oedema)
Management of Ischaemic Stroke
The patient should be offeredthrombolysis (alteplase) if:
- patients present with 4.5 hours of onset of stroke symptoms
- the patient has not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant etc.
Once haemorrhagic stroke has been excluded patients should be given aspirin 300mg as soon as possible and antiplatelet therapy should be continued.
Mechanical thrombectomy if confirmed occlusion of proximal anterior circulation.
Management of Haemorrhagic Stroke
- Specialist consultation
- Supportive measures
- Stop anticoagulants and antithrombotics, reverse any coagulation
