Cardiology Flashcards
What is acute coronary syndrome?
Umbrella term that describes ST elevation MI, unstable angina, non-ST elevation MI
All have same pathology - plaque rupture leads to thrombosis and inflammation
Rarely due to emboli, coronary spasm and necrosis
What is an ST elevation MI?
Complete occlusion of a major coronary artery previously affected by atherosclerosis Full thickness damage of heart muscle Pathological Q waves some time after MI ST segment is elevated Tall T waves May be new LBBB in larger MIs
What is unstable angina?
Angina of recent onset
Cardiac chest pain with crescendo pattern
Deterioration in previously stable angina with symptoms frequently occurring at rest
Angina of increasing frequency or severity, occurs on minimal exertion or even at rest
What is a non-ST elevation MI?
Occurs by developing a complete occlusion of a minor vessel or partial occlusion of a major artery previously affected by atherosclerosis
Retrospective diagnosis made on troponin results
Partial thickness damage of heart muscle
Non-Q wave infarction - ST depression and/or T wave inversion
Thrombus occluding vessel, rise in serum troponin or creatinine kinase
What are the 5 types of MI?
Type 1 - spontaneous MI with ischaemia due to a primary coronary event
Type 2 - MI secondary to ischaemia due to increase O2 demand or decreased supply such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
Type 3,4,5 - MI due to sudden cardiac death, relatd to PCI and related to CABG respectively
Name 5 factors that could increase your risk of having an ACS
Age Male Family history of IHD - MI in first degree relative below 55 Smoking Hypertension DM Hyperlipidaemia Obesity, sedentary lifestyle
Name 5 causes of ACS
Atheroma/stenosis of coronary arteries impairing blood flow
Valvular disease
Aortic stenosis
Arrhythmia
Anaemia - loss O2 transported to heart muscles
What occurs to the heart during an ACS attack?
Death of cardiac myocytes due to myocardial ischaemia
Rupture or erosion of fibrous cap of coronary artery plaque
Leads to platelet aggregation and adhesion, localised thrombus formation, vasoconstriction, and distal thrombus embolisation
Thrombus formation -> fibrotic plaque -> atherosclerotic plaque -> plaque rupture/fissure and thrombosis -> MI or ischaemic stroke or critical leg ischaemia or sudden CVS death
Unstable angina - partial occlusion, plaque has necrotic centre and ulcerated cap
MI - plaque has necrotic core but thrombus results in total occlusion
How does unstable angina present?
Chest pain, new onset, at rest with crescendo pattern
Breathlessness
Pleuritic chest pain
Indigestion
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily
exercise
Troponin normal, normal/undetermined ECG
How does MI present?
Acute central chest pain lasting more than 20 minutes associated with sweating, nausea, dyspnoea, fatigue, SOB, palpitations May present w/o chest pain in elderly or diabetics Distress/anxiety Pallor Increased pulse and reduced BP Reduced 4th heart sound Signs of HF - increased JVP Tachy/bradycardic Peripheral oedema
What could be a differential diagnosis of ACS?
Stable angina Pericarditis Myocarditis Aortic dissection Pulmonary embolism Pleurisy Oesophageal reflux/spasm Rib fracture, chest trauma, costochondritis GORD Anxiety/panic attack
How is ACS treated?
Pain relief - GTN spray (angina), IV opioid Anti-emetics Oxygen - if hypoxic Antiplatelets - aspirin, P2Y12 inhibitors, glycoprotein IIb/IIIa agonists Beta-blockers Statins ACE inhibitors Coronary revascularisation Risk factor modifications
How does ischaemia present on an ECG?
ST depression and T wave flattening
What investigations would you do on a patient with suspected unstable angina?
FBC - anaemia aggravates it
Cardiac enzymes - excludes infarction
ECG - when pain shows ST depression
Coronary angiography
What is a myocardial infarction?
Plaque rupture leads to clot formation that occludes one of the coronary arteries causing myocardial cell death and inflammation
What are the symptoms of an MI?
Acute central chest pain radiating to jaw or shoulder Lasting > 20 mins Nausea SOB Plapitations
What are the signs of an MI?
Clammy and pale
4th heart sounds
Pansystolic murmur
May later develop peripheral oedema
How would you manage an acute MI?
12 lead ECG
O2 if stats < 94%
IV access for bloods and enzymes
Brief history = RFs pulse, BP, JVP, murmurs, signs of congestive cardiac failure
300mg aspirin PO
Morphine 5-10mg IV and an anti-emetic
Refer for PCI or thrombolysis ASAP as long as not contraindicated
B-blocker IV and ACE-I if evidence of HF and patient normotensive
What management would you put in place for a patient who had had an acute MI?
Aspirin 75mg OD, reduces risk of repetition
B-blocker - long term, if contraindicated then verapamil
ACE-I if in HF
Statin - reduced cholesterol post-MI beneficial
Address modificable risk factors
Return to work after 2 months
Encorage exercise and no air travel for 2 months
What is an acute myocardial infarction?
Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombosis
How common are MIs?
5/1000 per annum in UK of STEMI
STEMI most common medical emergency
Worse prognosis in elderly and those with left ventricular failure
Early mortality - 30% outside hospital, 15% in
Late mortality - 5-10% first year, 2-5% annually after
What are the 2 types of MI?
STEMI - complete occlusion of major coronary artery previously affected by atherosclerosis
NSTEMI - complete occlusion on minor or partial occlusion of major coronary artery
Name 5 risk factors for development of an MI
Increasing age Male History of premature coronary heart disease Premature menopause Diabetes Smoking Hypertension Hyperlipidaemia Obesity and sedentary lifestyle Family history of IHD - MI in first degree relative below 55
What pathology occurs in a STEMI?
Sub-endocardial myocardium initially affected but continued ischaemia, infarct zone extends through sub-endocardial myocardium, producing a transmural Q wave MI
Early reperfusion may salvage regions of myocardium - reducing future mortality and morbidity
How does an NSTEMI present on an ECG?
Diagnosis made retrospectively after troponin results
ST depression and T wave inversion
Troponin I or T increased
Myoglobin released
Name 5 complications of an acute MI?
Sudden death - due to ventricular fibrillation
Arrhythmias - electrical instability following infarction
Pericarditis - transmural infarct resulting in inflammation of pericardium in STEMI
Cardiac rupture
Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue
What is angina?
Chest pain or discomfort as a result of reversible myocardial ischaemia
Usually implies narrowing of one or more of the coronary arteries
Tends to be exacerbated on exertion and relieved by rest
How common is angina?
More common in men
1.7% deaths per year
7% CV events per year
What are the different types of angina?
Stable angina - induced by effort, relieved by rest
Unstable angina - crescendo angina, angina of recent onset (less than 24h) or deterioration in previously stable angina with symptoms frequently occurring at rest, occurs on minimal exertion or even at rest
Prinzmetal’s angina - caused by coronary artery spasm (rare)
Give 5 risk factors for developing angina
Smoking Sedentary lifestyle Obesity Hypertension DM Family history Genetics Age Hypercholesterolaemia Depression/anxiety Stress - high demand/low control Hostile, competitive behaviour
Give 5 possible causes of angina
Atheroma/stenosis of coronary arteries impairing blood flow (most common)
Valvular disease
Aortic stenosis
Arrythmia
Anaemia - less O2 transported to heart muscle
What occurs during angina?
Mismatch between blood supply and metabolic demand
Ischaemic metabolites including adenosine stimulate nerve endings producing pain
Athersclerosis
Plaque continues to encroach upon lumen - increased risk of haemorrhage or exposure to tissue HLA-DR antigens which might stimulate T cell accumulation
Drives inflammation reaction against part of plaque contents
Complications develop including ulceration, fissuring, calcifcation and aneurysm change
How does Ohm’s law link to angina?
Adaptation
As plaque progresses to 50% vascular lumen size, vessel can no longer compensate by re-modelling and becomes narrowed
Drives variable cell turnover within plaque with new matrix surfaces and degradation of matrix
May progress to unstable plaque
How does stable angina present?
Central chest tightness and heaviness
Provoked by exertion, especially after meal or in the cold weather or by anger or excitement
Relieved at rest or by GTN spray
Pain may radiate to one or both arms, neck, jaw or teeth
Dyspnoea, nausea, sweatiness, faintness, palpitations, syncope
How is stable angina diagnosed?
12 lead ECG - often normal, possible ST depression, flat/inverted T waves, look for signs of past MI
Treadmill test - ECG whilst patient running uphill on treadmill, monitor time can exercise for, ST depression, sign of late ischaemia, many patients unsuitable
CT scan calcium storing - CT heart if atherosclerosis in arteries calcium will light up white, significant Ca indicates angina
SPECT/myoview - radiolabelled tracer injected into patient, taken up into coronary arteries as good blood supply, areas of little blood supply will not light up, no light after exercise indicative of myocardial ischaemia
Cardiac catheterisation
Bloods - anaemia
CXR - heart size, pulmonary vessels
Angiogram - shows luminal narrowing
Name 5 differential diagnoses of angina
Pericarditis/myocarditis PE Chest infection Dissection of aorta GORD Costochondritis
How is stable angina treated?
Reassure
Modify modifiable risk factors
Treat underlying conditons
Drugs - aspirin, statins, b-blockers, GTN spray, CCB, ivabradine
Revascularisation - stents, only when patient not stable on drugs
CABG, PCTA
What is a coronary artery bypass graft?
Bypass surgeries Internal mammary artery for left side Saphenous vein for right side Good prognosis but longer recovery Not for frail
What is PCTA?
Stenting or ballooning the narrowing, risk of restenosis or thrombosis, less invasive
What is atherosclerosis?
Deposition of fatty deposits within inner walls of arteries
Causes hardening of arteries
Formation of focal elevated lesions in intima of large and medium sized arteries such as coronary arteries
Fatty streaks present from around 10 years of age
What coronary arteries are most commonly occluded by atherosclerosis?
LAD, circumflex and right coronary
Name 5 risk factors for developing atherosclerosis?
Age - tends to be over 50s, progressive, chronic disease Tobacco smoking - free radicals damage endothelium High serum cholesterol Obesity - metabolic syndrome, increase systemic lipids Diabetes FHx Hypertension - shearing forces Sex Race Sedentary lifestyle Alcohol consumption Stress
What is that pathophysiology of atherosclerosis?
Formed of lipid, necrotic core, connective tissue, fibrous cap
Injury to epithelial cells leading to endothelial dysfunction
Activation of endothelial cells - signals sent to circulating leukocytes which accumulate and migrate into vessel wall - monocytes and T helper cells
Inflammation
LDL deposited in intima, accumulates in arterial wall, undergoes oxidation and glycation
Monocytes -> macrophages that then phagocytose LDLs and become foam cells
Foam cells promote migration of SMC from media to intima and SMC proliferation
Increase SMC proliferation leads to more collagen synthesis
Foam cells die releasing contents driving growth of plaque
Growth of plaque increases pressure causing plaque to rupture leading to coagulation cascade in blood vessel leading to thrombosis
Name 5 conditions atherosclerosis can cause
MI
Angina - stable and unstable
Stroke
Gangrene
How is atherosclerosis treated?
Percutaneous coronary artery intervention (PCI) Toxal, sirolimus Aspirin - COX-1 inhibitor Clopidogrel/ticargrelor Statins
How is an atherosclerotic plaque composed?
Central lipid core
Cap of fibrous tissue
Covered by arterial endothelium
Cap - made of collagen (produced by SMCs), inflammatory cells reside here (macrophages, T lymphocytes, mast cells)
What are foam cells?
Macrophages that have phagocytosed oxidised lipoproteins, also release chemokines to attract more macrophages, release IGF1 (growth factor) causing SMC to migrate to intima and to proliferation, proinflammatory cytokines, DNA
Why is diabetes a risk factor for atherosclerosis?
Increased free radicals which increases oxidation of LDLs
Less NO so less relaxation of blood vessels
What primary prevention methods could you use to prevent atherosclerosis?
Lifestyle changes
- Decrease alcohol intake
- Improve diet - less fats, salt and sugar
- Increase amount of physical activity
- Stop smoking
- Try to lose some weight
What secondary prevention methods could you used to prevent the progression of atherosclerosis?
Statin treatment Aspirin Anti-hypertensives Help with nicotine replacement therapies to help stop smoking Lifestyle advice Diabetic clinic and refer to dietician GTN spray Gym voucher Weight loss groups
What is heart failure?
Inability of heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues despite the normal or increased cardiac filling pressures
Impairment of heart contractility - LV systolic dysfunction most common
State where heart unable to pump enough blood to satisfy the needs of metabolising tissues
Symptomatic condition where breathlessness, fluid retention and fatiuge are associated with a cardiac abnormality that reduces CO
What is heart failure with diastolic function?
Heart requires energy to relax, problem with not relaxing (hypertension)
Preserved ejection fraction
What is ischaemic HF?
Reduced blood supply to heart
What is valvular HF?
Damage or defect in one of four valves
What is myopathic HF?
Disease of heart muscle, makes it harder to pump blood around body
What is hypertensive HF?
Due to overworking of heart
What is cor pulmonale?
High BP in pulmonary arteries leading to right sided HF
How common is HF?
Common 2-20% 2% NHS expenditure Disabiling Deadly 80% HF death within 5 years Treatable Median age 80 Majority chronic
What are the different types of HF?
Actute HF = acute decompensated CHF
- Generally under 70, male, LV ejection fraction < 40%
Acute heart failure - 71-76, equally male and female, 50% LVEF > 40%
Chronic HF
What is the NYHA classification?
New York Heart Association classificaiton
Class I - high risk of developing HF
Class II - slight limitation (mild HF)
Class III - marked limitation (moderate HF)
Class IV - inability to carry out any physical activity without discomfort (severe HF)
What are the stages of HF?
A - high risk of developing HF
B - asymptomatic HF
C - symptomatic HF
D - end-stage HF
Name 5 causes of HF
Hypertension Alcohol excess Cardiomyopathy Endocardial Pericardial MI Obesity Superimposed infection AF and arrhythmias Excess alcohol Endocrine NSAIDs
Name 5 risk factors for developing HF
Hypertension Cardiomyopathy Hypertension Coronary artery disease Heart attack Diabetes Certain medications - NSAIDs Congenital heart defects Valvular heart disease Viruses Alcohol, smoking Obesity Irregular heart beats
What are the symptoms of HF?
SOB Fatigue Ankle swelling Non-specific symptoms Cold peripheries
What are the signs of HF?
Acute - pleural oedema
Chronic - ankle oedema and abdominal ascites
Crackles and tachycardia non-specific but sensitive
Murmurs
How is HF diagnosed?
CXR/blood tests - FBC, LFTs, U&Es, BNP, TFTs, B-type natriuretic peptide (raised in HF)
Cardiac enzymes - creatinine kinase, troponin I and T
ECG
Echo (TTE) - done within 48 hours
Myocardial perfusion imaging
Raised NTproBNP - 72% chance of having HF
CXR
Name 5 differential diagnoses of HF
COPD PE Pneumothorax Anaphylaxis Asthma Pneumonia Foreign body obstruction ACS
How is HF treated?
Loop diuretics - to treat severe oedema, symptomatic treatment of congestion
ACE-I
Aldosterone antagonist
B-blockers
ARB (angiotensin II receptor blockers) - instead of ACEI if contraindicated
Calcium glycoside
Surgery - mitral/aortic valve repair/replacement
Defibrillator
Palliative care
1st line - ACEI, low dose, slow uptitration
2nd line - aldsoterone antagonist
Digoxin/ivabradine
Lifestyle - education, obesity control, diet, smoking cessation, cardiac rehab
Give 5 complications of HF
Renal dysfunction Rhythm disturbances Systemic thromboembolism DVT and PE LBBB and bradycardia Hepatic dysfunction Neurological and psychological complications
How is CO calculated?
CO = HR x SV
What is the difference between systolic HF and diastolic HF?
Sytolic - Failure to contract - EF < 40% - IHD, MI, CM Diastolic - Inability to relax and fill - EF > 50% - Constritive pericarditis, cardiac tamponade (accumulation of fluid in pericardial space), hypertension
What is the difference between low output HF and high output HF?
Low
- Decreased CO, fails to increase with exertion
- Could be due to pump failure, excessive pre-load, chronic increased afterload
High
- Anaemia
- Pregnancy
- Hyperthyroidism
What occurs during HF?
Once heart begins to fail compensatory changes occur
As HF progresses, these compensatory changes become overwhelmed (pathological)
What compensatory changes occur in HF?
Sympathetic stimulation - increases afterload by causing peripheral vasoconstriction
RAAS - salt and water retention, increases afterload and preload (increases volume and vasoconstriction)
Cardiac changes - ventricular dilatation, myocyte hypertrophy
Increased preload
What are the symptoms of left-sided heart failure?
Exertional dyspnoea
Fatigue
Paroxysmal noturnal dyspnoea
Nocturnal cough - pink, frothy sputum
What are the signs of left-sided heart failure?
Cardiomegaly (displaced apex beat) 3rd and 4th heart sounds Crepitations in lung bases Weight loss Reduced BP Tachycardia Cool peripheries Heart murmur
What are the symptoms of right sided HF?
Peripheral oedema
Ascites
Nausea
Anorexia
What are the signs of right sided HF?
Raised JVP Hepatomegaly Pitting oedema Ascites Weight gain (fluid)
What can cause right sided HF?
LV failure
Pulmonary stenosis
Lung disease (cor pulmonale)
What can be seen on a CXR in HF?
ABCDE Alveolar oedema Kerley B lines (interstital oedema) Cardiomegaly Dilated prominent upper lobe vessels Pleural Effusion
How do you treat acute HF?
100% oxygen Nitrates - GTN (dilate vessels) IV opiates IV furosemide (to reduce fluid overload) Inotropic drug - to increase contractility of dilated vessels
How do you treat chronic HF?
ACEI/ARB (valsartan)
B-blockers
CCB and other vasodilators
Diuretics and digoxin (furosemide)
What is the difference between primary and secondary hypertension?
Primary - high BP that doesn’t have a secondary cause
Secondary - high BP that does have a secondary cause eg kidney disease, adrenal disease, thyroid problems, obstructive sleep apnoea, high aldosterone
Most cases primary
What is the epidemiology of hypertension?
Often symptomless - requires screening Major risk factor in CVD Remains under diagnosed, under treated and poorly controlled Prevalence in those older than 35 More common in men
What is stage 1 hypertension?
More than or equal to 140/90mmHg clinic BP
Daytime ABPM greater than or equal to 135/85mmHg
Don’t need to treat unless increased risk of CVS events due to diabetes/end-organ damage (stroke, TIA, MI) or high QRISK
30-40% increased risk of death per 10mmHg
5 year lower life expectancy on average if untreated
What is stage 2 hypertension?
More than or equal to 160/100mmHg clinic BP
Daytime averge ABPM greater than or equal to 150/95mmHg
What is stage 3 hypertension?
Clinic systolic BP greater than or equal to 180mmHg and/or diastolic greater than or equal to 110mmHg
Start immediate anti-hypertensive drug treatment
What are the possible causes of essential/primary hypertension?
Primary cause unknown Multifactorial involving Genetic susceptibility Excessive sympathetic nervous system activity Abnormalities of Na/K membrane transport High salt intake Abnormalities in RAAS
What are the potential causes of secondary hypertension?
Renal disease
Pregnancy
Endocrine causes - Cushing’s (corticosteroids), Conn’s (aldosterone), phaemochromocytoma (catecholamines - vasoconstriction, increased cardiac contractility, increased in HR)
Coarctation of aorta
Drugs - corticosteroids, cyclosporin, erythropoietin, contraceptive pill, SSRIs, NSAIDs, immunosuppressives, cold cures
Alcohol, amphetamines, ecstasy, cocaine
Name 5 risk factors for developing hypertension
FHx Age Race - more common in Afro-Caribbean population Overweight/obese Sedentary lifestyle Smoking Too much salt Alcohol Diabetes Stress
What vascular changes occur in hypertension?
Accelerates atherosclerosis due to shearing forces exerted on vessel walls
Thickening of media of muscular arteries
Smaller arteries and arterioles typically affected
Results in endothelial cell dysfunction associated with impaired NO mediated dilatation and enhance secretion of vasoconstrictors including endothelins and prostaglandins
What is hypertension a major risk factor for?
IHD
Intracerebral haemorrhage
Renal disease (cause and result) - kidney size often redued, small vessels show intimal thickening and medial hypertrophy, numbers of sclerotic glomeruli increased
What is malignant hypertension?
Markedly raised diastolic pressure, usually over 120mmHg and progressive renal disease
Rare
Renal vascular changes prominent and usually evidence of acute haemorrhage and papilloedema
Can occur in previously fit individuals, often black males in 30s-40s
How does malignant hypertension present?
Proteinuria - if affecting kidneys
Haemorrhages/papilloedema (swelling of optic nerve) - worse prognosis than cancer
How is malignant hypertension diagnosed?
Look for end-organ damage
Urinalysis - albumin-creatinine ratio, protein, haematuria
Blood tests - serum creatinine, eGFR, fasting glucose, cholesterol
Fundoscopy/ophthalmoscopy
ECG - LV hypertrophy, past MI
Echo - LV hypertrophy
24h ABPM
How is hypertension treated?
Treatment goal 140/90mmHg Change diet - high consumption of fruit/veg and low fat Regular physical exercise Reduce alcohol intake Reduce salt intake Lose weight if obese Stop smoking - increases CVS risk ACD pathway Lifelong treatment Check BP every 6 months Withhold certain drugs in pregnancy Withhold during surgery
What is the ACD pathway?
For treating hypertension in under 55s or non-Afro-Caribbeans
ACE-I eg ramipril (or ARB if ACE-I contraindicated)
CCB
Diuretics
Beta-blockers if combination of all 3 don’t work
Also consider addition of spironolactone, high dose thiazide-like diuretic, alpha-blocker
How do you treat hypertension in over 55s and Afro-Caribbeans?
CCB 1st line
Add ACEI/ARB after CCB not working
What are the potential complications of hypertension?
Stroke MI HF Angina T2DM Vascular dementia
What are the two types of aortic aneurysm?
Abdominal aortic aneurysm - aortic diameter exceeding 3cm
Thoracic abdominal diameter
When is AAA more common?
More commonly occurs below renal arteries
Incidence increases with age
More common in men
5% of population over 60
When is TAA more common?
Ascending thoraco-abdominal aneurysms occur more commonly in patients with Marfan’s or hypertension
Descending/arch TAAs secondary to atherosclerosis
Name 5 risk factors for developing AAA?
Severe atherosclerotic damage FHx Smoking Male Increasing age Hypertension COPD Trauma Hyperlipidaemia
Name 5 risk factors for developing TAA
Strong genetic link - autosomal dominant trait Certain connective tissue disorders - Marfan's, Ehler's-danlos, Loeys-dietz Mycotic aneurysm endocarditis Aortic dissection Weight lifting, cocaine, amphetamine use - rise in BP Hypertension Increasing age Smoking Bicuspid/unicuspid aortic valves Atherosclerosis COPD Renal failure Previous aortic aneurysm repair
Why does an AAA occur?
Degradation of elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and SMC loss
Dilatation affects all 3 layers of vascular tunic
Doesn’t then pseudoaneurysm
Why does TAA occur?
Inflammation, proteolysis and reduced survival of SMCs in aortic wall
Once aorta reaches crucial diameter, loses all distensibility so rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture
How does an unruptured AAA present?
Often asymptomatic
Picked up via routine examination
Pain in abdomen, back, loin or groin
Pulsatile abdominal swelling
How does a ruputred AAA present?
More likely if hypertension, female, smoker, strong FHx Intermittent/continuous abdominal pain (radiating to back, iliac fossa/groin) Pulsatile abdominal swelling Collapse Hypotension Tachycardia Profound anaemia Sudden death
How does a TAA present?
Most asymptomatic Diagnosed incidentally Pain in chest/neck/upper back/mid-back/epigastrium Aortic regurgitation Fever if infective cause Symptoms due to compression of local strucutures Acute pain Collapse, shock, sudden death Cardiac tamponade Haemoptysis
Give 5 differential diagnoses of AAA
GI bleed Ischaemic bowel MSK pain Perforated GI ulcer Pyelonephritis Appendicitis
Give 4 differential diagnoses of TAA
Thoracic back pain
Arterial ischaemia
Collapse
MI
How is an AAA diagnosed?
Abdominal ultrasound - can assess aorta to degree of 3mm
CT an MRI angiography scans
How is TAA diagnosed?
CT/MRI
Aortography - assess position of key branches relative to aneurysm
Transoesophageal echo
Ultrasound
How is an AAA treated?
Small aneurysms below 5.5cm generally monitored
Treat underlying causes
Modify risk factors
Smoking cessation
Vigorous BP control
Lowering of lipids in blood
Surgery - if larger than 5.5cm and expanding yearly and symptomatic - open surgical repair/endovascular repair
How is a TAA treated?
Immediate urgent surgery required for ruptured Symptomatic - surgery regardless of size Regular CT/MRI monitoring every 6 months Rigorous BP control with B-blockers Smoking cessation Treat underlying cause
What is an aortic dissection?
Tear in aorta causing inner and middle layer of aortic wall to separate
How common is aortic dissection?
Medical emergency that can lead to death
Affects more men than women
Most common between 50-70, rare below 40
Very rare in children
How is aortic dissection classified?
Classified by timing of diagnosis from origin of symptoms
Acute - less than 2 wks
Subacute - 2-8 wks
Chronic - more than 8 wks
What are the potential causes of aortic dissection?
Inherited
Degenerative eg cystic medial disease (degenerative disease of aortic wall)
Atherosclerotic
Inflammatory eg giant cell arteritis
Trauma eg shearing stresses in RTA
Connective tissue disorders eg Marfan’s and Ehlers-Danlos
What occurs when an aortic dissection happens?
Begins with tear in intima
Blood under pressure then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection
Blood forms a haematoma separating the intima from the adventitia and creating a false lumen
False lumen extends for a variable distance in either direction - anterograde/retrograde
Where is an aortic dissection most likely to happen?
Within 2-3cm of aortic valve
Distal to left subclavian artery in descending aorta
How does an aortic dissection present?
Sudden onset of severe and central chest pain radiating to back and down arms - mimics an MI
Pain often described as tearing in nature - may be migratory
Hypertension
Pain maximal from time of onset - unlike MI where pain gains in intensity
Shock
Neurological symptoms secondary to loss of blood supply to spinal cord
Aortic regurgitation, coronary ischaemia and cardiac tamponade
Distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia
Peripheral pulses may be absent
Name 5 differential diagnoses for aortic dissection
ACS, MI, aortic regurgitation without dissection, MSK pain, pericarditis, cholecystitis, atherosclerotic embolism
How is aortic dissection diagnosed?
CXR - widened mediastinum
Urgent CT, transoesophageal echo or MRI will confirm diagnosis
How is aortic dissection treated?
If hypertension - urgent anti-hypertensive medication to reduce BP to less than 120mmHg - IV B-blockers or vasodilators Analgesia - morphine Surgery to replace aortic arch Endovascular intervention with stents Long term follow up with CT or MRI
What is aortic stenosis?
Narrowing of aortic valve resulting in obstruction of left ventricular stroke volume leading to symptoms of chest pain, breathlessness, syncope and fatigue
Normal aortic valve 3-4cm2
Symptoms occur when valve area 1/4 of normal
What is aortic regurgitation?
Leakage of blood into LV from aorta during diastole due to ineffective coaptation of aortic cusps
Can be associated with aortic stenosis
What is the classification of aortic stenosis?
Supravalvular
Subvalvular
Valvular - most common
What are the main causes of aortic stenosis?
Calcific aortic valvular - essentially calcification of aortic valve resulting in stenosis
Calcification of congenital bicuspid aortic valve
Rheumatic heart disease
What are the main causes of aortic regurgitation?
Rheumatic fever
Congenital bicuspid aortic valve
IE
What are the risk factors that could lead to aortic stenosis?
Congenital bicuspid aortic valve
Male
What are the risk factors that could lead to aortic regurgitation?
Marfan’s and Ehlers-Danlos syndrome
SLE
Aortic dilatation
IE or aortic dissection
What occurs during aortic stenosis?
Narrowing obstructed LV emptying and pressure gradient develops between LV and aorta resulting in increased afterload
Increased LV pressure and compensatory LV hypertrophy
Results in relative ischaemia of LV myocardium and consequent angina, arrhythmias and LV failure
Obstruction to LV emptying relatively more severe on exercise
When compensatory mechanisms exhausted LV function rapidly declines
What occurs during aortic regurgitation?
Reflux of blood from aorta through aortic valve into LV during diastole
LV dilation and hypertrophy to maintain total volume of blood ejected from LV
Progressive dilation leads to HF
Diastolic pressure falls due to regurgitation so coronary perfusion decreases
Large LV size mechanically less efficient, demand for O2 greater and cardiac ischaemia develops
Combined pressure and volume overload
How does aortic stenosis present?
Syncope Angina HF Dyspnoea on exertion due to HF Sudden death Slow rising carotid pulse and decreased pulse amplitude Heart sounds - soft/absent S2, prominent S4 due to LV hypertrophy, ejection systolic murmur (crescendo-decresendo) Pulsus tardus - late Pulsus parvus - weak
How does aortic regurgitation present?
Asymptomatic for years Exertional dyspnoea Orthopnoea - dyspnoea lying down Paroxysmal nocturnal dyspnoea Palpitations Angina Syncope Wide pulse pressure Apex beat displaced laterally Early diastolic murmur at L sternal border Systolic ejection murmur Collapsing water hammer pulse Quincke's sign - capillary pulsation in nail beds De Musset's sign - head nodding with heart beat Pistol shot femoral - sharp bang heard
What could be a differential diagnosis for aortic stenosis?
Aortic regurgitation
Subacute bacterial endocarditis
What could be a differential diagnosis for aortic regurgitation?
HF
IE
Mitral regurgitation
How is aortic stenosis diagnosed?
Echo - LV size and function, doppler derived gradient and valve area, diagnostic
ECG - LV hypertrophy, LA delay, LV strain pattern due to pressure overload - depressed ST segments and T wave inversion in leads orientated towards LV
CXR - LV hypertrophy, calcified aortic valve
How is aortic regurgitation diagnosed?
Echo - evaluation of aortic valve and aortic root, measurement of LV dimensions and function, cornerstone decision making and follow up evaluation
CXR - enlarged cardiac silhouette and aortic root enlargement
ECG - LV hypertrophy due to volume overload, tall R waves and deeply inverted T waves in left-sided chest leads, deep S waves in R side leads
How is aortic stenosis treated?
Rigorous dental hygiene, IE prophylaxis in dental procedures
Limited role for medication as mechanical problem
Vasodilators contraindicated in severe as may trigger hypotension and syncope
Surgical aortic valve replacement definitive treatment - any patients with severe, decreasing EF, undergoing CABG with moderate/severe
Transcatheter aortic valve implantation (TAVI) - if not fit for surgery
How is aortic regurgitation treated?
Vasodilators such as ACEi improve stroke volume and reduce regurgitation but only if symptomatic
Serial echos to monitor progression
Surgery for valve replacement before LV dysfunction
What is atrial fibrillation?
Choatic irregular atrial rhythm at 300-600bpm, AV node responds intermittently, hence irregular ventricular rate
Mechanically ineffective
How common is AF?
Most common sustained cardiac arrhythmia
Males more than females
5-15% patients over 75
Paroxysmal (self-terminating) or persistent
How is AF classified?
Acute - onset within previous 48h
Paroxysmal - stops spontaneously within 7 days
Recurrent - 2 or more episodes
Persistent - continuous for more than 7 days and not self-terminating
Permanent
What can cause AF?
Idiopathic Any condition resulting in raised arterial pressure, increased muscle mass, atrial fibrosis or inflammation and infiltration of atrium Hypertension HF Coronary artery disease Valvular heart disease especially mitral stenosis Cardiac surgery Cardiomyopathy Rheumatic heart disease Acute excess alcohol intoxication Thyrotoxicosis
Name 5 risk factors for developing AF
Older than 60 Diabetes Hypertension Coronary artery disease Prior MI Structural heart disease
What occurs during atrial fibrillation?
Continuous rapid activation of atria by multiple re-entry waves 300-600/min
Rapidly depolarising automatic foci, located within pulmonary veins
Atria respond electrically at this rate, no coordinated mechanical action, only proportion of impulses conducted to ventricles due to refractory period of AVN
Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone
CO drops 10-20% as ventricles not primed reliably by atria
Higher risk of thrombotic events, blood pools and remains still and clots
HR - 120-180bpm
How does AF present?
Asymptomatic Palpitations Dyspnoea or chest pains Fatigue HF No P waves Rapid and irregular QRS rhythm Apical pulse rate greater than radial rate 1st heart sound variable intensity Irregularly irregular pulse
How is AF diagnosed?
ECG - absent P waves, irregular and rapid QRS complex
What could be a differential diagnosis of AF?
Atrial flutter
Supraventricular tachyarrhythmias
How if AF treated?
Acute management - when due to acute precipitating event, cardioversion (conversion to sinus rhythm electrically or pharamcologically), ventricular rate control with drugs that block AV node eg CCB, B-blocker, digoxin, anti-arrhythmic
Long term and stable patient management
- Rate control - AV nodal slowing agents plus oral coagulation - B-blockers/CCB/digoxin
- Rhyhtm control - for younger, symptomatic and physically activate patients, cardioversion and amiodarone, anti-coagulation
Calculate stroke risk - 5x risk of stroke (embolism due to thrombus formed in atrium)
What is the target INR with treatment with warfarin?
2-3
What is atrial flutter?
Organised atrial rhythm with an atrial rate typically between 250-350bpm
How common is atrial flutter?
Often associated with atrial fibrillation and frequently require similar initial therapeutic approach
Paroxysmal or persistent
Much less common than atrial fibrillation
Name 5 things that can cause atrial flutter
Idiopathic Coronary heart disease Obesity Hypertension HF COPD Pericarditis Acute excess alcohol intoxication
What is a risk factor for developing atrial flutter?
Atrial fibrillation
What occurs during atrial flutter?
Continuous rapid activation of atria by multiple re-entry wavelets
Rapidly repolarising automatic foci, located within pulmonary veins
Atria respond electrically at this rate, no co-ordinated mechanical action, only proportion on impulses conducted to ventricles
Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone
CO drops 10-20% as ventricles not primed reliably by atria
Higher risk of thrombotic events, blood pools and remains still and clots
How does atrial flutter present?
Palpitations Breathlessness Chest pain Dizziness Syncope Fatigue Atrial rate - 300bpm Ventricular rate - 150bpm
How is atrial flutter diagnosed?
ECG - definitive
Regular saw-tooth like atrial flutter waves between QRS complexes due to continuous atrial depolarisation
F waves may be unmasked by slowing AV conduction by carotid sinus massage or IV adenosine
What could be a differential diagnosis of atrial flutter?
Atrial fibrillation
Supraventricular tachyarrhythmias
How is atrial flutter treated?
Electrical cardioversion but anti-coagulated before
Catheter ablation - create conduction block
IV amiodarone to restore sinus rhythm and use beta-blocker to suppress further arrhythmias
How is atrial flutter different to atrial fibrillation?
Atrial flutter - atria beat regularly but more often
Atrial fibrillation - atria beat irregularly and faster
What is a cardiac arrhythmia?
Abnormality of cardiac rhythm
Give 5 complications of cardiac arrhythmias
Sudden death Syncope HF Chest pain Dizziness Palpitations Asymptomatic
What is bradycardia?
Heart rate slow < 60 bpm during day and < 50 bpm at night
Usually asymptomatic unless heart very slow
Normal in athletes due to increased vagal tone and thus parasympathetic activity
What is tachycardia?
Heart rate fast > 100 bpm
More symptomatic when arrythmia fast and sustained
How can tachycardias be further classified?
Supraventricular tachycardia - arise from atrium or AV junction
Ventricular tachycardia - arise from ventricles
What can cause bradycardia?
Extrinsic (treat underlying cause) - drug therapy BB digoxin, hypothyroidism, hypothermia, raised intracranial pressure
Intrinsic (treat with atropine or temporary pacing in acute cases) - acute ischaemia, infarction of SAN, sick sinus syndrome
What is long QT syndrome?
ECG where ventricular repolarisation (QT interval) is greatly prolonged
What can cause long QT syndrome?
Congenital - Jervell-Lange-Nielsen syndrome (autosomal recessive mutation in cardiac potassium and sodium-channel genes), Romano-Ward syndrome (autosomal dominant)
Acquired - hypokalaemia, hypocalcaemia, drugs (amiodarone, tricyclic antidepressants), bradycardia, acute MI, diabetes
How does long QT syndrome present?
Syncope
Palpitations
Polymorphic ventricular tachycardia usually terminates spontaneously but may degenerate to ventricular fibrillation
How do you treat long QT syndrome?
Treat underlying cause
If acquires give IV isoprenaline (contraindicated for congenital)
What is mitral stenosis?
Obstruction of left ventricle inflow that prevents proper filling during diastole
Normal valve area = 4-6cm2
Symptoms begin at less than 2cm2
What is mitral regurgitation?
Backflow of blood from LV to LA during sytole
Mild physiological MR seen in 80% normal individuals
What can cause mitral stenosis?
Rheumatic heart disease secondary to rheumatic fever (infection with group A beta-haemolytic streptococcus), inflammation leads to commisural fusion and reduction in mitral valve orifice area causing charateristic pattern seen on echo
Progresses to valve thickening, cusp fusion, calcium deposition, severely narrowed valve orifice and progressive immobility of valve cusps
Prevalence and incidence decreasing due to a reduction of rheumatic heart disease
Also - IE, mitral annular clacification, congenital
What can cause mitral regurgitation?
Abnormalities of valve leaflets, chordae tendinae, papillary muscles/LV
Mitral valve prolapse
Ischaemic mitral valve
Rheumatic heart disease
IE
Papillary muscle dysfunction/rupture, dilated cardiomyopathy
Name 2 risk factors for developing mitral valve stenosis
History of rheumatic fever
Untreated strep infection
Name 5 risk factors for developing mitral regurgitation
Female Lower BMI Advanced age Renal dysfunction Prior MI
What happens to the heart in mitral stenosis?
Thickening and immobility of valve leads to obstruction of blood flow from LA to LV
LA pressure increases = LA hypertrophy and dilatation
Pulmonary venous, arterial and right heart pressure increases
Increase in pulmonary capillary pressure = pulmonary oedema
Partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction
Pulmonary hypertension leads to RV hypertrophy, dilatation and failure with subsequent tricuspid regurgitation
What happens to the heart in mitral regurgitation?
Regurgitation into LA = LA dilatation but little increase in LA pressure in longstanding regurgitation
Pure volume overload due to leakage of blood into LA during sytole
LA enlargement, LV hypertrophy to maintain CO and increases contractility
Progressive LA dilatation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilatation and progressive HF
How does mitral stenosis present?
No symptoms until 2cm2
Progressive dyspnoea due to LA dilatation (pulmonary congestion) worse with exercise, fever, tachycardia, pregnancy
Haemoptysis - rupture of bronchial vessels due to increases pulmonary pressure
RHF - pulmonary hypertension, weakness, fatigue, abdominal and lower limb swelling
AF - LA dilatation = palpitations
Systemic emboli (AF)
Mitral facies - bilateral, cyanotic or dusky pink discolouration over upper cheeks due to vasoconstriction in response to lowered CO
Heart sounds - diastolic murmur, lower opening S1 snap, tapping non-displaced apex beat
Chest pain
Low volume pulse
How does mitral regurgitation present?
Auscultation - soft S1 and pan systolic murmur at apex radiating to axilla, prominent S3, displaced hyperdynamic apex
Exertional dyspnoea - pulmonary venous hypertension
Fatigue and lethargy - reduced CO
Increased SV felt as palpitation
RHF symptoms and eventually congestive HF
How is mitral stenosis diagnosed?
CXR - LA enlargement, pulmonary oedema/congestion, calcified mitral valve
ECG - AF, LA enlargement
Echo - assess mobility, gradient and area
How is mitral regurgitation diagnosed?
ECG - LA englargement, AF, LV hypertrophy
CXR - LA enlargement, central pulmonary artery enlargement, LV enlargement
Echo - estimation of LA and V size and function, valve structure assessment, transoesophageal
How is mitral stenosis treated?
Mechanical problem B-blocker control HR (if in AF) and prolongue disatole for improved diastolic filling Diuretics for fluid overload Anticoagulate - warfarin Percutaneous mitral balloon valvotomy Mitral valve replacement
How is mitral regurgitation treated?
Vasodilators - ACEI HR control for AF - BBs, CCB, digoxin Anticoagulation for AF and flutter Diuretics for fluid over load Serial echo - Mild 2-3 years - Moderate 1-2 years - Severe 6-12 months Surgery for any symptomatic patient at rest or exercise for repair If asymptomatic EF less than 60%, new onset AF
What is pericarditis?
Inflammatory pericardial syndrome with/without effusion
What can cause pericarditis?
Viral (most) - enterovirus, herpesvirus, adenovirus, parvovirus B19, EBV, mumps, coxsackie B
Bacterial - mycobacterium TB, pneumonia, rheumatic fever, staph, strep
Autoimmune - Sjorgren’s, RA, scleroderma, systemic vasculitis
Neoplastic - secondary metastatic tumours, lymphoma
Metabolic - uraemia, myoxedema
Traumatic and iatrogenic - early onset (rare - direct/indirect injury), delayed onset (pericardial injury syndromes, iatrogenic trauma)
Other - amyloidosis, aortic dissecion, pulmonary arterial hypertension, chronic HF, post-MI
How does a major pericarditis present?
Fever > 38 Subacute onset Large pericardial effusion Cardiac tamponade Lack of response to aspirin/NSAIDs after at least 1 wk therapy
What can cause a minor pericarditis?
Myopericarditis
Immunosuppression
Trauma
Oral anticoagulation therapy
How does pericarditis present?
Chest pain - severe, sharp pleuritic pain, rapid onset, left anterior chest/epigastrium, radiates to arm, relieved by sitting forwards
Dyspnoea, cough, hiccups
Viral prodrome, antecedent fever
Skin rash, joint pain, eye Sx, weight loss
How is pericarditis diagnosed?
Pericardial rub Sinus tachycardia Tachypnoea Fever Signs of effusion Beck's triad - hypotension, elevated jugualr veins, distant muffled heart sounds ECG Bloods - FBC, CRP, cardiac enzyme CXR Echo
Name 5 differential diagnoses of pericarditis
Pneumonia Pleurisy PE Chostocondritis GORD Myocardial ischaemia/infarction Aortic dissection Pneumothorax Pancreatitis Peritonitis Herpes zoster - shingles ECG pericarditis Blood tests
How is pericarditis treated?
Sedentary activity until resolution of symptoms and ESR/CRP - mainly for athletes 3 months
NSAID (ibuprofen 600mg TDS 2 wks) or aspirin (750-1000mg BD 2wk) large dose for pain and inflammation
Colchicine (0.5mg BD 3 wk) limited by nausea and diarrhoea, reduces recurrence
Corticosteroids for symptomatic relief
Manage complications
What does a saddle-shaped ST and PR depression suggest?
Pericarditis
What do tall tented T waves and pathological Q waves suggest?
Hyperkalaemia
What does ST depression suggest?
Stable angina
What do absent P waves suggest?
Atrial fibrillation
What does an early diastolic heart murmur suggest?
Mitral stenosis
What does and early-systolic click suggest?
Mechanical heart valve
What does an ejection systolic crescendo-decrescendo murmur suggest?
Unstable angina
What does an end-diastolic heart murmur suggest?
Aortic stenosis
What does a pansystolic murmur suggest?
Mitral regurgitation
What is peripheral vascular disease?
Partial blockage of leg or peripheral vessels vy an atherosclerotic plaque and/or resulting thrombus in insufficient perfusion of lower limb resulting in lower limb ischaemia
Commonly caused by atherosclerosis and usually affects aorta-iliac and infra-inguinal arteries
What is acute lower limb ischaemia?
May occur because of embolic or thrombotic disease
Rapid decrease in lower limb blood flow due to acute occlusion of peripheral artery
What is thrombotic disease?
Chronic atherosclerotic stenosis in patient who has previously reported symptoms of claudication
In whom is peripheral vascular disease more common?
Men
Name 5 risk factors for developing peripheral vascular disease
Smoking Hypertension Diabetes Hypercholesterolaemia Physical inactivity Obesity
What occurs in chronic lower limb ischaemia?
Always due to atherosclerosis of arteries distal to aortic arch
Symptoms of ischaemia
What occurs in mild ischaemia?
Stress induced by physiological malfunction
Exercise induced angina
Intermitted claudication - cramping pain induced by exercise
Pain as a result of lactic acid produciton
Leg pulses often absent
Pain distal to site of atheroma
What occurs in moderate ischaemia?
Structural and functional breakdown
Ischaemic cardiac failure
Critical limb ischaemia
Vascular dementia
What occurs in severe ischaemia?
Infarction
Gangrene
How does thrombotic disease present?
6Ps Pain Pallor Perishingly cold Pulselessness Paralysis Paraesthesia The more Ps, the more sudden and complete the ischaemia
Name 3 differential diagnoses for PVD?
Osteoarthritis of hip/knee due to knee pain at rest
Peripheral neuropathy - paraesthesia
Arteritis
How do you diagnose PVD?
Exclude arteritis - ESR/CRP raised in arteritis
FBC - Hb to exclude anaemia/polycythaemia
ECG - cardiac ischaemia
Ankle/brachial pressure index 0.5-0.9 = intermittent claudication, less than 0.5 = critical leg ischaemia
Colour duplex ultrasound
MRICT
How do you treat PVD?
Risk factor modification - smoking cessation. antiplatelets ect
Revascularisation for critical ischaemia
Bypass procedure
Amputation for severe
How do you treat acute ischaemia?
Surgical emergency - revascularisation within 4-6hrs to save limb
What is intermittent claudication?
Ischaemic pain
Tissue not dying just suffering
Moderate/mild exercise, O2 debt resulting in lactic acid - pain
What is critical ischaemia?
Tissue dying and suffering at rest
Blood supply inadequate to allow basal metabolism
No reserve available for increased demand
Resting pain - typically nocturnal
Gangrene/infection risk
Give 2 signs/symptoms of critical ischaemia
Severe nocturnal pain in all toes of left foot only relieved by hanging foot over edge of bed (gravity for perfusion)
Non-healing painful ulcer on big toe with no trauma
Give 3 signs/symptoms of acute ischaemia
Acute MI
Loss of use of R side of body
Fast, irregular pulse
What is shock?
Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised hypoxia and/or an inability of cells to utilise oxygen
Low BP systolic < 90mmHg
What can cause hypovolaemic shock?
Low blood volume
What can cause cardiogenic shock?
Heart not pumping
What can cause distributive shock?
Septic shock
Anaphylactic shock
Neurogenic shock
What can cause anaemic shock?
Not enough O2 carring capacity
What can cause cytotoxic shock?
Cell poisoned
What is ‘Tennis score’?
Score for staging of hypovolaemic shock
Class 1 - 15% blood loss, pulse below 100bpm, normal BP, PP normal, resp rate 14-20, slightly anxious
Class 2 - 15-30% blood loos, pulse greater than 100bpm (tachycardic), BP normal (autonomic response), PP decreased, resp rate 20-30, mildly anxious
Class 3 - 30-40% blood loss, pulse above 120bpm, resp rate 30-40, PP decreased, confused
What occurs in hypovolaemic shock?
Secondary to haemorrhagic shock
Loss of blood due to GI bleed, trauma, peri/post operative, splenic rupture
Loss of fluid - dehydration, burns, pancreatitis
What can cause cardiogenic shock?
Cardiac tamponade - limits CO PE - flow of blood to lungs blocked Acute MI Fluid overload Myocarditis - inflammation of muscle
What occurs in septic shock?
Shock when infection becomes out of control
Disruptive shock
Systemic inflammatory response associated with infection
Sepsis complicated by persistent hypotension that is unresponsive to fluid resuscitation
Acute vasodilation from inflammatory cytokines
What occurs in anaphylactic shock?
Release of IgE due to allergic response
Intense allergic reaction
Massive release of histamine and other vasoactive mediators causing haemodynamic collapse
Accompanied by breathlessness and wheeze due to bronchospasm
What happens in the heart during shock?
Reduction in ventricular filling leading to a fall in BP and SV reducing hypotension
Reduced stimulation of baroreceptors in aortic arch and carotid sinuses resulting in increases sympathetic activity with release of noradrenaline and adrenaline
Vasoconstriction and increased myocardial contractility and HR to help restore BP and CO
Reduction of perfusion of renal cortex stimulating juxtaglomerular apparatus to release renin
Vasopressin released in response to decreased blood volume - aquaporin 2 channels increased water retention
Cortisol - fluid retention
Glucagon - raised blood sugar levels
How does shock present?
Skin pale, cold, sweaty and vasoconstricted Pulse weak and rapid PP reduced Reduced urine output Confusion, weakness, collapse, coma
How does hypovolaemic shock present?
Skin cold, pale, clammy, slate grey Drowsiness and confusion - inadequate tissue perfusion Increased sympathetic tone Tachycardia - narrow PP, weak pulse Sweating BP maintained but later hypotension
How does cardiogenic shock present?
Signs of heart failure
Raised JVP
Gallop rhythm
Basal crackles and pulmonary oedema
How does septic shock present?
Pyrexia and rigors Nausea and vomiting Vasodilation with warm peripheries Bounding pulse Temp > 38 or < 36 Tachycardia > 90bpm RR > 20 breaths/min WBC > 12 x10^9/L or < 4x10^9/L
How does anaphylactic shock present?
Signs of profound vasodilation Warm peripheries Low BP Tachycardia Bronchospasm Pulmonary oedema
How is shock diagnosed?
Capillary refill time
More than 3 seconds to refill after 5 seconds compression = bad
How is shock treated?
ABC
B - 100% O2 and correct immediately if life threatening problems such as congestive HF, bronchospasm, tension pneumothorax
C - establish IV access, fluids and blood if acute blood loss, ensure haemostasis
In septic shock - take blood cultures before antibiotics
What is a potential complication from shock? And where might be most affected?
Organ failure after recovery
Kidneys, lungs, heart, brain
What can cause neurogenic shock?
Spinal cord injury
Epidural
Spinal anaesthesia
What is the difference between sepsis, severe sepsis, septic shock and septicaemia?
Sepsis - life-threatening response to organisms that can lead to tissue damage, organ failure and death
Severe sepsis - sepsis with sepsis-induced organ-dysfunction or tissue hypoperfusion
Septic shock - when sepsis leads to a dangerously low BP and abnormalities in cellular metabolism
Septicaemia - blood poisoning
What is tachycardia?
HR > 100bpm
Physiological response to exercise and excitement
What is AVNRT?
AV-nodal re-entrant tachycardia
More common in women
Strikes without obvious provocation
Attack may stop spontaneously or continue indefinitely
What is AVRT?
Atrioventricular re-entrant tachycardia
What is supraventricular tachycardia?
Arises from atria/atrioventricular junction
AVNRT and AVRT paroxysmal SVTs
Presents between 12-30
Young patients with no/little structural heart disease
AV node essential component
What is ventricular tachycardia?
Pulse of more than 100bpm with at least 3 irregular heartbeats in a row
Found in patients with structurally normal hearts - benign condition
May lead to cardiomyopathy if untreated
Inadequate filling of ventricles due to rapid ventricular beating and less time for filling
Reduced CO and decrease in amount of oxygenated blood circulating
What is sustained ventricular tachycardia?
Ventricular tachycardia for longer than 30 seconds
Name 5 risk factors for AVNRT
Exertion Emotional stress Coffee Tea Alcohol
What is the pathophysiology of AVNRT?
Short refractory period and slow conduction or long refractory period with fast conduction (more common)
Atrial impulse occurs early slow pathway toakes over in propagating atrial impulses to ventricles
Once propagates fast pathway finished refractory period and transmits pulses again
Repeats - re-entrant loop at AV, sends signals through AV node at faster rate tan normal pacemaker so tachycardia
Atria contract slowly in first cycle then fast in next
What is the pathophysiology of AVRT?
Atrial activation after ventricle activation
Prone to AF
Wolff-Parkinson-White syndrome
Premature beat from SAN -> AVN accessory pathway in refractory period, so travels down IV septum via purkinje cells until meets accessory pathway
Out of refractory period conducts impulse back to atria - re-entry circuit leading to tachycardia
What is the pathophysiology of Wolff-Parkinson-White syndrome?
Normal AV conduction but with accessory pathway
SAN depolarises impulse travels to AVN via atria as well as accessory pathway
Accessory pathway - quick conduction, abnormal depolarisation of ventricles
Pre-excitation ECG - short PR interval, wide QRS
How does AVNRT present?
Rapid regular palpitations with abrupt onset and sudden termination
Chest pain and breathlessness
Neck pulsations - atrial conductions against closed AV valves
Polyuria
How does AVRT present?
Palpitations
Severe dizziness
Dyspnoea
Syncope
How does VT present?
Breathlessness - lack of lung perfusion
Chest pain - lack of heart perfusion
Palpitations
Light headed or dizzy - lack of brain perfusion
How does SVT present?
Dizziness Syncope Hypotension Cardiac arrest Pulse rate between 120-220 bpm
How is AVNRT diagnosed?
ECG - QRS complexes typical BBB, P waves either not visible or seen immediately before or after QRS complex due to simultaneous atrial or ventricular activation
How is AVRT diagnosed?
ECG - short PR, wide QRS
How is SVT diagnosed?
ECG - rapid ventricular rhythm, broad abnormal QRS complex greater than 0.14 seconds
How are AVNRT and AVRT treated?
Emergency cardioversion if haemodynamically unstable
Vagal manoeuvres if stable
- Breath holding
- Carotid massage
- Valsalva manoeurvre
IV adenosine
Surgery - catheter ablation of accessory pathway in AVRT and modification of slow pathway AVNRT
How is VT treated?
B-blockers to slow sinus rate
How is SVT treated?
Haemodynamically unstable - emergency cardioversion
Stable - IV beta-blocker, IV amiodarone
What can also cause tachycardia?
Anaemia Fever HF Thyrotoxicosis Acute PE Hypovolaemia Atropine
What is a supraventricular tachycardia?
Any tachycardia that arises from atrium/atroventricular junction
4 main types - AF, atrial flutter, AVNRT and AVRT
What is tetralogy of Fallot?
Most common form of congenital heart disease
Cyanotic cardiac disorder with highest survival to adulthood
What occurs in tetralogy of Fallot?
Large, maligned ventricular septal defect
Overriding aorta
RV outflow obstruction
RV hypertrophy
Stenosis of RV outflow (pulmonary stenosis) leads to RV being at higher pressure than left
Blue blood passes from RV to LV
Patients are blue
How does tetralogy of Fallot present?
Central cyanosis Low birth weight and growth Dyspnoea on exertion Delayed puberty Systolic ejection murmurs Toddler's may squat
How is tetralogy of Fallot diagnosed?
CXR - boot shaped heart
How it tetralogy of Fallot treated?
Full surgical treatment during first 2 yrs of life due to progressive cardiac debility and cerebral thrombosis risk
Often get pulmonary valve regurgitation in adulthood and require redo surgery
What is ventricular ectopic?
Premature ventricular contraction
Most common post-MI arrhythmia
Can also occur in healthy patients
What is a risk factors for developing a ventricular ectopic?
MI
What occurs during a ventricular ectopic?
Extra/missed/heavy beats
LV dysfunction if ectopics are frequent
Broad and bizzare QRS as arise from abnormal site in ventricular myocardium
Complete compensatory pause as AV node or ventricle is refractory resulting in missed beat
Can provoke ventricular fibrillation
How does a ventricular ectopic present?
Uncomfortable especially when frequent
Pulse irregular owing to premature beats
Usually asymptomatic
Can feel faint/dizzy
How is a ventricular ectopic diagnosed?
ECG - widened QRS complex
How is ventricular ectopic treated?
Reassure patient
Give beta-blockers if symptomatic - to slow down sinus rate
What is an atrial-septal defect?
Abnormal connection between two atria
Patent foramen ovale
How common is atrial-septal defects?
Often first diagnosed in adulthood
1/3 congenital heart disease
More common in women
What occurs in the heart in an atrial septal defect/
Slightly higher pressure in LA than RA
L -> R shunt
NOT blue
Increased flow from R heart to lungs
If untreated - R heart overload and dilation, R ventricle dilates to accommodate increased pulmonary flow
- RV hypertrophy
- Pulmonary hypertension - Eisenmenger’s reaction
- Increases risk of IE
As heart compliance falls with age, the shunt increases
Can lead to heart failure and shortness of breath by 40
How does an atrial-septal defect present?
Dyspnoea Exercise intolerance Atrial arrhythmias from RA dilation Pulmonary flow murmur Fixed split second heart sound
How in an atrial-septal defect diagnosed?
CXR - large pulmonary arteries, large heart
ECG - right BBB due to RV hypertrophy
ECHO - hypertrophy, dilation of right side of heart and pulmonary arteries
How is an atrial-septal defect treated?
Surgical closure
Percutaneous (keyhole)
What is the difference between primum ASD and secundum ASD?
Primum - earlier presentation, may involve AV vales
Secundum - may be asymptomatic until adulthood
What is Eisenmenger’s complex?
Shunt reversed due to development of pulmonary hypertension -> cyanosis and organ damage
What is an atrio-ventricular septal defect?
Hole in very centre of heart
Includes - ventricular septum, atrial septum, mitral and tricuspid valves
Can be complete or partial
Associated with Down’s syndrome
What occurs in the heart in atrio-ventricular septal defect?
Instead of 2 separate atrio-ventricular valves, just on big malformed one which usually leaks
How does a complete atrio-ventricular septal defect present?
Breathlessness as neonate
Poor weight gain and feeding
Torrential pulmonary flow - Eisenmenger’s resulting in cyanosis over time
How does a partial atrio-ventricular defect present?
Can present late in adulthood
Presents similar to a ventricular/atrial defect - dyspnoea, tachycardia, exercise intolerance
How is an atrio-ventricular defect treated?
Pulmonary artery banding if large defect in infancy - band reduces blood flow to lungs reducing pulmonary hypertension and Eisenmenger’s syndrome
Surgical repair challenging
Partial defect left alone if no R heart dilatation
What is a bicuspid aortic valve?
2 cusps aortic valve
Can go undetected, can be severely stenotic in infancy or childhood
How common is a bicuspid aortic valve?
Most common form of cogenital heart disease
More common in males
Degenerate quicker than normal valves
Regurgitant earlier than normal valves
Associated with coarctation and dilation of ascending aorta
May eventually develop aortic stenosis - requires replacement - IE
What should patients with a bicuspid aortic valve avoid? Why?
Intense exercise may accelerate complications
Yearly ECHO on affected patients
What does a bicuspid aortic valve lead to?
Aortic stenosis +/- aortic regurgitation
Can also pre-dispose individual to IE, aortic dilation, aortic dissection
How is a bicuspid aortic valve treated?
Treat surgically with a valve replacement
What is coarctation of the aorta?
Narrowing of aorta at or just distal to, to insertion of ductus arteriosis
In whom is coarctation of the aorta more common in?
Men
What happens in the heart with coarctation of the aorta?
Net narrowing of aorta just after arch, with excessive blood flow being diverted through carotid and subclavian vessels into systemic vascular shunts to supply to rest of the body
Stronger perfusion to upper body compared to lower
Associated with Turner’s syndrome
Resultant decreased renal perfusion, leads to systemic hypertension that persists even after surgical correction
What can coarctation of aorta lead to?
Berry aneurysms and patent ductus arteriosis
Increased risk of IE
How does coarctation of the aorta present?
Often asymptomatic for years
Right arm hypertension
Bruits over scapulae and back from collateral vessels
Murmur
Headahces and nose bleeds
Hypertension in upper limbs
Discreptant blood pressure in upper and lower body
Long term - hypertension - early coronary artery disease, early strokes, sub-arachnoid haemorrhage
Radio-femoral delay
How is coarctation of the aorta diagnosed?
CXR - dilated aorta indented at site of coarctation
ECG - LV hypertrophy
CT - accurately demonstrate coarctation and quantify flow
How is coarctation of the aorta treated?
Surgery
Balloon dilatation and stening
Risk of aneurysm and at site of repair
What is the difference between severe and mild coarctation of aorta?
Severe - block aorta, collapse with heart failure
Mild - raised BP, systolic murmur (best heart over left scapula (scapula briut)
What is infective endocarditis?
Infection of endocardium or vascular endothelium of heart
Subacute bacterial endocarditis
Who is more at risk of IE?
Valves with congenital or acquired defects
R sided IE more common with IV drug users
Normal valves with virulent organisms such as streptococcus pneumoniae or S aureus
Prosthetic valves or pacemakers
Who is more at risk of IE?
More common in developing countries Disease of - elderly, those with prosthetic valves, young IV drug user, young with congenital heart disease More common in men Those with poor dental hygiene Dental treatment IV cannula Skin and soft tissue infection Cardiac surgery Pacemaker
What pathogens cause IE?
S aureus
P aeruginosa
S viridans
What is the pathophysiology of infective endocarditis?
Consequence of 2 factors - presence of organisms in bloodstream and abnormal cardiac endothelium facilitating adherence and growth
Poor dental hygiene - bacteria from dental plaques get into blood, IVDU, soft tissue infections
Damage endocardium promotes platelets and fibrin deposition allowing organism to adhere and grow, leading to infected vegetation
Aortic and mitral valve most affected - IV drug users exception where R
Virulent organisms destory valve they are on resulting in regurgitation and worsening heart failure
How does infective endocarditis present?
New valve lesion/regurgitant murmur
Embolic events unknown origin
Sepsis of unknown origin
Haematuria, glomerulonephritis, suspected renal infarction
Fever plus risk factor
Headache, fever, malaise, confusion, night sweats
Finger clubbing
S aureus - high fever, feel ill rapidly
Valve dysfunction
Splinter haemorrhages on nail beds of fingers
Embolic skin lesions
Osler nodes - tender nodules in digits
Janeaway lesions - haemorrhages and nodules on fingers
Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy
Petechiae
How is IE diagnosed?
Dukes criteria
Blood cultures - 3 from different sites over 24 hrs, take before antibiotics started
If not staph - penicillin - benzylpenicillin and gentamycin
If staph - vancomycin and rifampicin
Treat complications
Surgery - remove valve and replace with prosthetic one - if infection can’t be cured, remove infected devices, remove large vegetations before they embolise
Good oral health for prevention
What is patent arteriosus?
Where ductus arteriosus fails to close after birth
What happens to the heart with a patent ductus arteriosus?
Ductus arteriosis persistent communication between the proximal left pulmonary artery and descending aorta
Foeatal pulmonary vascular resistance high and right heart pressure exceeded that of left - flow from right to left atrium through foramen ovale and pulmonary artery to aorta via ductus arteriosus
Some premature babies and cases of maternal rubella ductus arteriosus doesn’t close
Remains open then there is abnormal left-to-right sunt and eventually means that lung circulation overload with pulmonary hypertension and right-side cardiac failure subsequently
Increases risk of IE
How does patent ductus arteriosus present?
Continuous machinery murmurs
Bounding pulse
Large then large heart and breathlessness
Eisenmenger’s syndrome with differential cyanosis that is clubbed with blue toes but pink and not clubbed fingers
Tachycardia
How is patent ductus arteriosus diagnosed?
CXR - large shunt in aorta and pulmonary arterial system may be prominent
ECG - demonstrate left arterial abnormality and LV hypertrophy
ECHO - dilated LA and LV
How is patent ductus arteriosus treated?
Can be surgically or percutaneously
Low risk complications
Venous approach may require and AV loop
Indometacin can be given to stimulate duct closure
What is the symptoms of peripheral arterial disease?
Cramping pain in calves, thighs and buttocks relieved by rest
What are the signs of peripheral arterial disease?
Absent pulses
Punched out ulcers
Postural colour change (Bueger’s test)
6Ps - pain, pallor, pulselessness, paraesthesis, paralysis, perishingly cold
What investigations do you need to do in peripheral arterial disease?
Exclude DM, arteritis, anaemia, renal disease, lipids
ABPI - normal is 1-1.2, PAD is 0.5-0.9
Colour duples USS - quick and non-ivasive, can show vessels and blood flow within them
MRI/CT angiography - to identify stneoses and quality of vessels
Blood tests - raised CK-MM, shows muscle damage
How do you manage peripheral arterial disease?
Risk factors modification - quit smoking, treat HTN, lower cholesterol, improve DM control, lower fat diet
Medications - antiplatelets, clopidogrel is recommended as 1st line
Exercise programmes - reduce claudication by improving blood flow
PTA or surgery if severely stenosed
How common is structural/congenital heart defects?
1% of all lives births have some form of cardiac defect
Vary from all minor to incompatable with life ex-utero
Overall male predominance
Atrial septal defect and patent dutus arteriosus occur more commonly females
Name 5 risk factors for having a structural/congenital heart disease
Affected sibling Maternal prenatal rubella infection - persistent ductus arteriosus and pulmonary valvular and arterial stenosis Maternal alcohol misuse Single genes Drugs Diabetes of mother Genetic abnormalities
When do you get finger clubbing?
Prolonged cyanosis
What is a ventricular septal defect?
Abnormal connection between 2 ventricles
Many close spontaneously during childhood
20% of congenital heart defects
What occurs in the heart with a ventricular septal defect?
Higher pressure in LV then RV
L to R shunt - not blue
Increased blood through lungs
How do large ventricular septal defects present?
Pulmonary hypertension Eisenmenger's complex Cyanosis Small, breathless, skinny baby Increased resp rate Tachycardia
How do small ventricular septal defects present?
Large systolic murmur
Thrill (buzzing sensation)
Well grown
What do large ventricular septal defects look and sound like?
What do small ventricular septal defects look and sound like?
Large defects - CXR (big heart), murmurs vary in intensity (pansystolic), cause more problems in infancy
Small defects - normal HR, normal size, asymptomatic, increase IE risk, louder murmur/thrill
How are ventricular septal defects treated?
Medical initially since many will spontaneously close
Surgical closure
If small - no intervention required
Prophylactic antibiotics
Moderately size lesion - furosemide, ACEi
What is pulmonary stenosis?
Narrowing of outflow of RV
Can be valvular, subvalvular or supravalvular
How does severe pulmonary stenosis present?
RV failure as neonate Collapse Poor pulmonary blood flow RV hypertrophy Tricuspid regurgitation
How do you treat pulmonary stenosis?
Balloon valvoplasty - place catheter with balloon with balloon through femoral vein then inflate balloon at stenosis to crush it - can result in regurgitation
Open valvotomy
Shunt - to bypass blockage
What is cardiomyopathy?
Group of diseases of myocardium that affects the mechanical or electrical function of the heart
What are the different types of cardiomyopathy?
Hypertrophic
Dialted
Restricted
Arrhythmogenic right ventricular
What is hypertrophic cardiomyopathy?
Ventricular hypertrophy/thickening of muscle
Quite common, second most common cardiomyopathy
1/500
Autosomal dominant - familial
May present at any age
Most common cause of sudden cardiac death in the young
What is dilated cardiomyopathy?
Dilated left ventricle which contracts poorly/has thin muscle
Most common cardiomyopathy
Autosomal dominant
Can be caused by ischaemia, alcohol, thyroid disorder, familial/genetic
What is restricted cardiomyopathy?
Rare
Caused by amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis
What is arrhythmogenic right ventricular cardiomyopathy?
Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium
Familial form autosomal dominant but can be recessive
What can increase your risk of having a cardiomyopathy?
Family history
What occurs in hypertrophic cardiomyopathy?
Sarcomeric protein gene mutations eg troponin T and B-myosin
All in absence of hypertension and valvular disease
Hypertrophic, non-compliant ventricle impair diastolic filling resulting in reduced stroke volume and thus cardiac output
Thick powerful heart is disarray of cardiac myocytes so conduction affected
What occurs in dilated cardiomyopathy?
Caused by cytoskeletal gene mutations
Left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction
Poorly generated contractilve force leads to progressive dilatation of heart with some diffuse interstitial fibrosis
What occurs in restrictive cardiomyopathy?
Normal or decreased volume of both ventricles with bilateral enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filling
Restrictive physiology
Poor dilation of heart restricts its ability to take on blood and pass it to the rest of the body
Rigid myocardium restrict diastolic ventricular filling
What occurs in arrhythmogenic RV cardiomyopathy?
Desmosome gene mutation
RV replaced by fat and fibrous tissue
Muscle dies and replaced by fat as part of inflammatory process
How does hypertrophic cardiomyopathy present?
Hypertrophy of myocardium Sudden death Chest pain, angina, dyspnoea, dizziness, palpitations, syncope LV outflow obstruction Cardiac arrhythmia Ejection systolic murmur Jerky carotid pulse
How does dilated cardiomyopathy present?
SOB and fatigue Heart failure Arrhythmias Thromboembolism Sudden death Increased JVP
How does restricted cardiomyopathy present?
Dyspnoea Fatigue Embolic symptoms Elevated JVP with diastolic collapse and elevation of venous pressure with inspiration Hepatic enlargement Ascites Dependent oedema 3rd and 4th heart sounds
How does arrhythmogenic cardiomyopathy present?
Cardiac cells held less together
Arrhythmia most common
Syncope
R heart failure
How is hypertrophic cardiomyopathy diagnosed?
ECG - abnormal, LV hypertrophy sings, progressive T wave inversion, deep Q waves
Echo - ventricular hypertrophy, small left ventricle cavity
Genetic analysis
How is dilated cardiomyopathy diagnosed?
CXR - cardiac enlargement
ECG - tachycardia, arrythmia, non-specific T wave changes
Echo - dilated vessels
How is restrictives cardiomyopathy diagnosed?
CXR, ECHO, ECG - abnormal but non-specific
Cardiac catheterisation helps diagnose restrictive cardiomyopathy
How is arrhythmogenic cardiomyopathy diagnosed?
ECG - usually normal by may show T wave inversion
ECHO - could be normal, advanced disease show right ventricular dilation
Genetic testing
How is hypertrophic cardiomyopathy treated?
Amiodarone - anti-arrythmatic medication
CCB
B-blocker
How is dilated cardiomyopathy treated?
HF and AF treated in normal way
How is restricted cardiomyopathy treated?
No specific treatment with poor prognosis
Patients die within a year
Cardiac transplantation
How is arrhythmogenic cardiomyopathy treated?
B-blockers
Amiodarone for symptomatic arrhythmias
Occasionally cardiac transplant indicated
What is heart block?
Block in either AV node/HIS bundle results in AV block
Block in lower conduction system produces bundle branch block
What can cause heart block?
Coronary artery disease
Cardiomyopathy
Fibrosis of conducting tissues in elderly
What are the different types of AV block?
First degree
Second degree - type 1 and 2
Third degree
What is first degree AV block?
‘If the R is far from the P then you have first degree’
Prolongation in PR interval greater than 0.22 seconds
Every atrial depolarisation followed by conduction to ventricles but with delay
Asymptomatic so no treatment
What can cause first degree heart block?
Hypokalaemia, myocarditis, inferior MI, AVN blocking drugs eg b-blockers, CCB, digoxin
What is second degree heart block?
‘Longer longer longer drops, then you have a Wenkebach’ (Mobitz I
‘If some Ps don’t get through, then you have a Mobitz II’
When some P waves conduct, others don’t
What is a Mobitz I heart block?
PR interval before blocked P wave longer than after blocked P wave
Light headedness, dizziness, syncope
Doesn’t require a pacemaker unless poorly tolerated
Progressive PR interval prolongation until beat dropped, P wave fails to conduct then cycle restarts
What can cause a Mobitz I heart block?
AVN blocking drugs
Inferior MI
What is a Mobitz II heart block?
PR interval constant and QRS interval dropped
Failure of conduction through His-Purkinje system
SOB, postural hypotension, chest pain
High risk of developing sudden complete AV block and pacemaker should be inserted
What can cause a Mobitz II heart block?
Anterior MI Mitral valve surgery SLE Lyme disease Rheumatic fever
What is a third degree heart block?
‘Ps and Qs don’t agree, the you have a third degree’
Complete AV block
Spontaneous escpae rhythm originated below block keeps ventricles going
P waves completely independent of QRS
What can cause third degree heart block?
Structural heart disease, IHD, hypertension, endocarditis, Lyme disease
How is third degree heart block treated?
IV atropine or permanent pacemaker insertion
What is bundle branch block?
Usually asymptomatic
Slightly widening of QRS complex - incomplete BBB
What is RBBB?
R bundle no longer conducts, ventricles don’t get impulses at same time
QRS M wave in V1, W in V5 and V6 (MaRRoW)
What can cause RBBB>
PE, IHD, A/VSD
What is LBBB?
Late activation of LV
Deep S wave leads I and V6, tall late R in V1
WiLLiaM - QRS in V1 and 2, M in V4-6
What can cause LBBB?
IHD, aortic valve disease
What are ACEI used for?
Hypertension, heart failure, diabetic nephropathy
Name 3 examples of ACEi’s
Ramipril Enalapril Perindopril Liniopril Trandolapril
What are the main adverse effects of ACEI’s?
Related to angiotensin II formation - hypotension, acute renal failure (release more renin causing BP to drop further), hyperkalaemia, teratogenic effects in pregnancy (angiotensin II important for baby development)
Related to increased kinin production - dry chronic cough (ACE also breaks down bradykinin so inhibited = more bradykinin), rash, anaphylactiod reaction
How do ACEi’s work?
Block action of ACE enzyme in lungs preventing conversion of angiotensin I to angiotensin II
What does angiotensin II do?
Potent vasocontrictor
Stimulates aldosterone release
Increases peripheral resistance
What does aldosterone do?
Increases Na+
Therefore water retention
Increased blood volume and BP
What are ARBs used for?
Hypertension
Diabetic neuropathy
heart failure (when ACEI contraindicated)
How do ARBs work?
Block AT-1 receptor that angiotensin II works at preventing the action of angiotensin II
Name 3 examples of ARBs
Candesartan Losartan Valsartan irbesartan Telmisartan
What are the main adverse effects of ARBs?
Symptomatic hypotension Hyperkalaemia Potential renal dysfunction Rash Angio-oedema Contraindicated in pregnancy Generally well tolerated
What are CCBs used for?
Hypertension, IHD eg angina and arrhythmia
Which CCBs have an effect on electrial conductivity?
Diltiazem and verapamil
Name 3 examples of CCBs
Amlodipine Diltiazem Verapamil Nifedipine Felodipine Lacidipine
How do L-type CCBs work?
Block calcium ion channels
Dihydropyridine - nifedipine, amlodipine, felodipine, lacidipine preferentially affect vascular smooth muscle, peripheral arterial vasodilators
Phenylalkylamines - verapamil main effect on heart, reduced HR and force of heart contraction
Benzothiozepines - diltiazem, intermediate heart/peripheral vascular effects
What are the main adverse effects of CCBS?
Due to peripheral vasodilation - flushing, headache, oedema, palpitations (decreased BP so body tried to correct by increasing HR)
Due to -vely chronotropic effects - bradycardia, atrioventricular block, postural hypotension
Due to -vely inotrophic effects - worsening of cardiac failure
Verapamil causes constipation
How to beta-adrenoceptor blockers work?
Block beta-adrenoceptors causing slowing down of heart rate
What are b-blockers used for?
IHD - angina, heart failure, arrythmia, hypertension
Name 3 examples of B-blockers
Bisoprolol Carbvedilol Propranolol Metoprolol Atenolol Nadolol
Which B-blockers are more B-1 selective?
Metoprolol
Bisoprolol
Which B-blocker is in the middle in terms of selectivity?
Atenolol
Which B blocker is non-selective?
Propranolol
Nadolol
Carvedilol
Why do you need to be careful with B-blocker selectivity?
Seletive B1 in asthma since non-selective used will also block B-2 resulting in airway constriction and thus worsening of asthma
What are the main adverse effects of B-blockers?
Fatigue Headache Sleep disturbance/nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction Bronchospasm Worsening of asthma/COPD by bronchospasm PVD - claudication or raynauds HF is given standard dose acutely - give in small doses and increase slowly
What are diuretics indicated for?
Hypertension and heart failure
What are the different classes of diuretics and give an example for each?
Thiazides - cause Na+ and thus water loss in urine, act on distal tubule, less potent - bendroflumethiazide, hydrochlorothiazide, chlorothalidone
Lopp diuretics - act on loop of Henle, more potent, furosemide (blocks Na/K/2Cl transporter), bumetanide
Potassium-sparing diuretics - spironolactone, eplerenone
Aldosterone antagonists
What are the main adverse effects of diuretics?
Hypovolaemia (mainly loop) Hypotension (mainly loop) Hypokalaemia Hyponatraemia Hypomagnesaemia Hypocalcaemia Hyperuricaemia - gout Erectile dysfunction (thiazides) Impaired glucose tolerance (thiazides)
Name an alpha-1 adrenoceptor blocker
Doxazosin
Name a centrally acting anti-hypertensive
Moxonidine
Methyldopa - can be used in pregnancy
Name a direct renin inhibitor
Aliskiren
What are the cardiac natriuretic peptides?
ANP - atria
BNP - brain natriuretic peptide - ventricle
When are the natriuretic peptides released?
When stretching of atrial or ventricular muscle cells
Raised atrial or ventricular pressures
Volume overload
What are the main effects of the natriuretic peptides?
Increased renal excretion of sodium and water
Relax vascular smooth muscle
Increase vascular permeability
Inhibit action/release of aldosterone, angiotensin II, endothelin and ADH
In HF raised natriuetic peptdes in serum blood
How do nitrates work?
Arterial and venous dilators
Reduce pre-load and afterload
Lower BP
What are nitrates used for?
IHD (angina) and HF
Give 3 examples of nitrates
Isosorbide mononitrate (long acting)
GTN (glyceryl trinitrate) spray - commonly gives headache, potent vasodilator
GTN infusion
What are the main potential side effects of nitrates?
Headache
GTN spray syncope
Potential tolerance to drug
How are antiarrhythmic drugs classified?
Vaughan Williams classification
Classes 1 and 3 - rhythm control
Classes 2 and 4 - rate control
What are class I antiarrhythmic drugs?
Sodium channel blockers - flecainide
What are class II antiarrhythmic drugs?
B-blockers
What are class III antiarrhythmic drugs?
Prolong action potential
Amiodarone, sotalol
What are class IV antiarrhythmic drugs?
CCBs - verapamil, diltiazem, amlodipine
How does digoxin work?
Cardiac glycoside
Inhibits Na/K pump - found everywhere
Main effect on heart - bradycardia (increased vagal tone), increased ectopic activity, increased force of contraction by increased intracellular Ca2+
Slowing AV conduction
Narrow therapeutic range otherwise side effects
What are the potential side effects of digoxin?
Nausea, vomiting, diarrhoea, confusion
When is digoxin used?
AF to reduce ventricular rate response
Severe HF as positive inotropic
How does amiodarone work?
Blocks potassium rectifier current that are responsible for repolarisation of heart
What are the potential adverse effects of amiodarone?
QT prolongation Polymorphic ventricular tachycardia Interstitial pneumonitis Abnormal liver function Hyperthyroidism/hypothyroidism Sun sensitivity Slate grey skin discolouration Optic neuropathy Multiple drug interacton Large volume of distribution
