Cardiovascular Flashcards
1
Q
Define Hypertension
A
- 140/90mmHg on at least 2 readings on separate occasions
- Commonest cause of cardiac failure - major risk factor for cardiovascular disease
- Hypertension is major cause of premature vascular disease, leading to cerebrovascular events, IHD and peripheral vascular disease
- Mortality rises with increasing BP
2
Q
What are the stages of hypertension?
A
Stage 1:
- BP >140/90 in clinic
White coat syndrome - BP >135/85 with ABPM/home readings
Stage 2:
- More than or equal to 160/100mmHg clinic BP
- Daytime average ABPM or HBPM greater than or equal to 150/95mmHg
Severe:
Clinic systolic BP greater than or equal to 180mmHg and/or diastolic BP greater than or equal to 110mmHg
- If there is end organ damage, start immediate anti-hypertensive drug treatment regardless of BP level
3
Q
Describe the pathology of hypertension
A
1) VASCULAR CHANGES:
- Accelerates atherosclerosis
- Causes thickening of media of muscular arteries
HEART – major risk factor for IHD
2) NERVOUS SYSTEM
- Intracerebral haemorrhage frequent cause of death
3) KIDNEYS:
- Can cause or result from renal disease
- Kidney size often reduced and small vessels show intimal thickening and medial hypertrophy
4) Malignant:
- Characteristic features
- Markedly raised diastolic BP (usually over 120mmHg)
- Progressive renal disease
- Renal vascular changes prominent
4
Q
What are the risk factors for hypertension?
A
Modifiable:
- Alcohol intake
- Sedentary lifestyle
- DM
- Sleep apnoea
(Smoking)
Non modifiable:
- Age (>65)
- Family History
- Ethnicity (Afro-Caribbean)
5
Q
What are the causes of hypertension?
A
1) Essential (Primary origin) – 95% cases
2) Secondary causes:
ROPE:
- Renal disease e.g. CKD
- Obesity
- Pregnancy (pre-eclampsia)
- Endocrine (Conn’s syndrome)
- Drugs – oestrogen-containing oral contraceptives, NSAIDs, vasopressin
6
Q
What are the signs and symptoms of hypertension?
A
- Asymptomatic – except in malignant hypertension
- May have the occasional general headache
7
Q
What are the first-line investigations for the diagnosis of hypertension ?
A
- Take BP:
- If BP is >140/90 mmHg, then confirm using
- 24-hour ambulatory BP monitor (ABPM)
- Multiple home BP monitoring (if patient can’t tolerate ABPM)
- It is believed to be able to reduce the white coat hypertension effect in which a patient’s blood pressure is elevated during the examination process due to nervousness and anxiety caused by being in a clinical setting
8
Q
How can you asses end organ-damage in hypertension?
A
- Urinalysis to check kidneys (protein, albumin: creatine ratio and haematuria)
- ECG/Echo for LV hypertrophy
- Fundoscopy to assess hypertension retinopathy
- Bloods
+Serum creatinine
+eGFR
+Glucose – assess diabetes risk - Clinical history – previous MI/strokes
- Others - HbA1c (DM) + Lipids
9
Q
What is the first-line treatment for hypertension?
A
Lifestyle changes:
- Smoking cessation
- Low-fat diet + high consumption of fruit and vegetables
- Reduce alcohol and salt intake
- Increase exercise
- Loss weight if obese
10
Q
What is the first-line drug treatment for hypertension?
A
Less than 55:
- ACEi - e.g. Ramipril
OR
- ARB e.g. Canderstan
if ACEi is contraindicated or not tolerated (e.g. due to cough)
Over 55/Afro-Caribbean:
- CCB - e.g. Amlodipine
11
Q
What is the second-line treatment for HTN?
A
- Second line – ACE-inhibitor + CCB
- Third line – ACE-inhibitor + CCB + diuretics (e.g. Bendroflumethiazide or furosemide)
- Fourth line – ACE-inhibitor + beta blocker e.g. Bisoprolol + CCB + diuretics
A,C,D + B
12
Q
What is malignant hypertension?
A
Rapid rise in BP leading to vascular damage
13
Q
What are the symptoms of malignant hypertension?
A
- Headache
- Visual disturbance
14
Q
What are the signs of malignant hypertension?
A
- Severe hypertension
Systolic > 200 mmHg
Diastolic > 130 mmHg - Bilateral renal haemorrhage = exudates = papilloedema
- Papilledema is optic disc swelling that is caused by increased intracranial pressure due to any cause.
- The swelling is usually bilateral and can occur over a period of hours to weeks.
- Unilateral presentation is extremely rare.
15
Q
What are the complications of malignant hypertension?
A
- Hypertensive emergencies e.g. acute kidney injury, HF and encephalopathy
- Cardiac failure with LV hypertrophy and dilatation
- Blurred vision and retinal haemorrhages
- Haematuria and renal failure due to fibrinoid necrosis of glomeruli
- Severe headache and cerebral haemorrhage
16
Q
What is the treatment of malignant hypertension?
A
Sodium nitroprusside
17
Q
Define Ischaemia
A
An imbalance between the supply of oxygen to cardiac muscle and cardiac demand
18
Q
What is Atherosclerosis
A
- Atherosclerosis causes narrowing of coronary arteries 🡪 ischaemia and pain i.e. Angina
19
Q
Describe the process of Atherosclerosis
A
1) INITATION – endothelial injury 🡪 lipid accumulation 🡪 local cellular proliferation 🡪 mural thrombi on surface and subsequent healing and repeat of cycle
2) ADAPTATION – as plaque progresses to 50% of vascular lumen size, vessel can no longer compensate by re-modelling and becomes narrowed 🡪 new matrix surfaces and degradation of matrix 🡪 can progress to unstable plaque.
3) CLINICAL STAGE –
- Plaques continues to impinge on lumen, running risk of haemorrhage or exposure of tissue HLA-DR antigens 🡪 T cell accumulation
PATHOLOGICAL:
Fatty Streak:
- Show macrophages filled with foam cells
- As smooth muscle cells with fat
Intimal cell mass:
- Collections of muscle cells and connective tissue without lipid “cushions”
The atheromatous plaque:
- Characterised by distorted endothelial surface containing lymphocytes, macrophages, smooth muscles cells and variably complete endothelial surface
20
Q
What are the complications of an atherosclerotic plaque?
A
- Acute occlusion due to thrombus
- Chronic narrowing of vessel with healing of local thrombus
- Aneurysm change
- Embolism of thrombus ± plaque lipid content
21
Q
What are the causes of IHD?
A
MOST COMMON CAUSE:
- Coronary artery atheroma (atherosclerotic plaques consisting of accumulations of lipids, macrophages and smooth muscle cells in the intima)
- Results in reduced blood flow or a fixed obstruction to coronary blood flow
- LV hypertrophy – increased distal resistance
- Anaemia – reduced O2 carrying capacity
- Hypoxia – reduced availability of O2
- Coronary artery thrombosis
- Coronary artery spasm
- Arteritis
22
Q
What are the Modifiable (reversible) risk factors
for IHD?
A
- Smoking
- Obesity
- Exercise
- Diet:
- High in fats (particularly saturated fat intake)
- Low in antioxidant intake (fruit and veg)
- Alcohol intake
- Sedentary lifestyle
23
Q
What are the Clinical risk factors for IHD?
A
- Hypertension
- Diabetes
- Hyperlipidaemia
- Hypercholesterolaemia
- Depression
24
Q
What are the Non-modifiable risk factors for IHD?
A
- Age
- Family history (genetics)
- Gender – M>F
- Ethnicity
25
What are the psychosocial risk factors for IHD?
- High demand, low control jobs have high stress
- Low social interaction
- Lack of support network
26
What does the QRISK2 score predict?
- The QRISK2 score predicts risk of CVD in next 10 years
It considers:
- BP
- Age
- Smoking status
- Cholesterol
- Rheumatoid Arthritis
- Diabetes Mellitus
- Anti-hypertensives
- BMI
- Ethnicity
27
Define Angina Pectoris (Stable Angina)
Descriptive term for chest pain/discomfort arising from the heart as a result of myocardial ischaemia
28
What are the different types of Angina?
- Stable – induced by effort and relieved by rest
- Unstable (crescendo) - increases in severity, occurs at rest or is of recent onset (less than 1 month)
- Variant (Prinzmetal’s) angina – caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest
- Decubitus angina – occurs lying down
- Nocturnal angina – occurs at night and may wake patient from sleep
29
What are the symptoms of Angina?
- Central crushing retrosternal chest pain that radiates to arms, jaw and neck
- Dyspnoea
- Palpitations
- Syncope
30
What are the signs of Angina?
- Chest pain comes on with exertion and rapidly resolved by rest and/or GTN
- Exacerbated by cold weather, anger and excitement
31
How would you score Angina?
- Central tight chest pain radiating to arms, neck and jaw
- Precipitated by exertion
- Relieved by rest or GTN spray
3/3 – typical angina
2/3 – atypical angina
1/3 – non-anginal pain
32
What is the differential diagnosis for Angina?
- Pericarditis/Myocarditis
- Pulmonary embolism
- Chest infection
- GORD
- Dissection of the aorta
33
What are the first-line investigation for Angina?
- First-line = 12 Lead ECG:
- Usually normal
- May show ST depression and T wave inversion
34
What is the gold-standard investigation for Angina?
- CT angiography
- Shows narrowing of a coronary artery
- Once narrowing is shown it is then possible to go in and open with a stent or balloon
35
What other tests can you do for Angina?
- Stress ECG (ischaemia inducing exercise stress test)
Bloods:
- FBC – anaemia
- Cardiac enzymes
- Glucose
- Lipid profile
- CXR – check heart size and pulmonary vessels
36
How can you manage Angina?
- Lifestyle
- Weight loss
- More exercise
- Quit smoking
- Treat underlying conditions
- HTN and DM
37
What is the pharmacological treatment of Angina?
+Symptomatic relief:
- GTN spray
+Long term symptomatic relief:
- Beta blocker or CCB
+Secondary prevention:
- Aspirin
- Atorvastatin
- ACEi
..................................
+Percutaneous Coronary Intervention (PCI)
- Stenting or ballooning the narrow artery
- Risk of restenosis (re-narrowing) or thrombosis
- Drug-eluting stents reduces risk of restenosis
- Less invasive, shorter recovery
- Coronary artery bypass graft (CABG)
38
Describe the mechanism of action of the drugs used to treat Angina
1) Glyceryl Trinitrate (GTN) spray – 1st line anginal:
- Dilates systemic veins (venodilator) --> reduces venous return to right heart --> reduces preload --> reduces work of heart and oxygen demands
- Also dilates coronary arteries
Common side effect is headache
................................
2) Beta blockers (e.g. bisoprolol, atenolol, propranolol):
- Act on B1 receptors in heart as part of adrenergic sympathetic pathway
- Reduce HR and force of contraction (negatively chronotropic and inotropic)
- Contraindicated in asthma or in patients with heart block/heart failure/hypotension
- Use a Calcium channel blocker instead e.g. amlodipine
......................................
3) CCB (E.G. amlodipine)
Dilates systemic arteries (arterodilator) --> BP drop --> reduces afterload --> less energy required for same cardiac output
- Relax coronary arteries and reduce force of LV contraction
- Ca2+ channel blocker – Arterodilators e.g. amlodipine
.................................................
4) Anti-platelet - 75mg Aspirin (inhibits platelet aggregation by inhibiting COX)
± Clopidogrel if aspirin is contraindicated
..................................................
- Statins – reduce cholesterol e.g. atorvastatin, simvastatin
HMG-CoA reductase inhibitor
.................................................
- ACE inhibitors for BP control e.g. Ramipril, lisinopril
- If severe consider angiotensin receptor blocker e.g. Candesartan or Losartan
.................................................
- Ivabradine – inhibits pacemaker current in the SAN and therefore reduces heart rate
.................................................
- Another option if beta blockers are contraindicated
39
What is the treatment when meds fail or when high risk disease identified?
- Percutaneous Coronary Intervention (PCI):
- Stenting or ballooning the narrow artery
- Convenient and less invasive
- Shorter recovery
- Risk of stent thrombosis
- Coronary artery bypass graft (CABG):
- CABG – LIMA used to bypass narrowing in LAD – good prognosis but invasive + longer recovery, risk of stroke/bleeding
40
What is Acute coronary Syndrome?
Thrombus from an atherosclerotic plaque blocking a coronary artery, causing:
1) Unstable Angina (Ischaemia)
- Cardiac chest pain with crescendo pattern
- Deterioration in previously stable angina
- Symptoms frequently occurring at rest
2) STEMI (complete occlusion)
- Develops after occlusion of a MAJOR coronary artery previously affected by atherosclerosis
- Causes FULL thickness cardiac muscle damage
- Can usually be diagnosed on ECG at presentation
3) NSTEMI (partial occlusion → subendocardial infarction)
- Occurs by developing a COMPLETE occlusion of a MINOR coronary artery or PARTIAL occlusion of a MAJOR coronary artery previously affected by atherosclerosis
- Causes infarction distally and ischaemia proximally
- Causes partial thickness cardiac muscle damage
- Usually a retrospective diagnosis after troponin results and other investigations
41
Describe the Pathology of Acute coronary syndromes
- All have same mechanism
- Rupture or erosion of the fibrous cap of a coronary artery atheromatous plaque --> subsequent formation of a platelet-rich clot (thrombosis) --> inflammation and vasoconstriction produced by platelet release of serotonin and thromboxane A2
- Unstable angina differs from NSTEMI in that in NSTEMIs the occluding thrombus is sufficient to cause myocardial damage (necrosis) and an elevation in serum markers of myocardial injury (troponin and creatine kinase)
- Rarely due to emboli, coronary spasm or vasculitis
42
How can you differentiate between the three different types of ACS?
1) Stable Angina
- Pain develops when there is increased demand in the setting of a stable atherosclerotic plaque
- The vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand - Ischaemia BUT no infarct
- ECG = Normal
- Troponins = Normal
2) Unstable Angina
- The plaque ruptures and a thrombus forms around the ruptured plaque, causing PARTIAL occlusion of the vessel
- Angina pain occurs at rest or progresses rapidly over a short period of time
- ECG = Normal, inverted T waves, ST depression
- Troponins = Normal
3) NSTEMI
- The plaque ruptures and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium (subendocardial infarct)
- ECG = Normal, inverted T waves, ST depression
- Troponins = Elevated
4) STEMI
- Complete occlusion of the blood vessel lumen = transmural injury and infarct to the myocardium
- This is reflected by ECG changes and a rise in troponins
- ECG = Hyperacute T waves or ST elevation
- Troponins = Elevated
43
Describe the ECG changes in Acute coronary syndrome (Unstable angina, STEMI & MSTEMI).
1) Unstable Angina:
- ECG = Normal, inverted T waves, ST depression
2) NSTEMI:
- ECG = Normal, inverted T waves and / or ST depression
3) STEMI:
- ST elevation and tall T waves
- Will produce pathological Q waves some time after an MI
- There may be a new LBBB in larger MIs (WiLLiaM)
V1 – W shape
V6 – M shape
44
What ECG changes can ischaemia cause?
- ST depression
| - T wave flattening or inversion
45
What does a Q wave on an ECG show?
- Pathological Q wave
- Evidence of previous infarction
- Pathological Q waves are deeper and wider than normal (>35% QRS height and wider than one small square)
- The larger the infarction is, the more likely it will result in pathological Q waves
46
If you see ST depression in an ECG of someone who has had an STEMI, why must this have occurred?
- A posterior STEMI will show ST depression in V1 to V4 as the view of the heart on the ECG is inverted.
- V7-V9 are additional leads that can be placed on someone’s back to check for a posterior MI
47
What are the causes of ACS?
- Rupture of atherosclerotic plaque and consequent arterial thrombosis
- Uncommon causes include coronary vasospasm without plaque rupture, drug abuse (amphetamines, cocaine), dissection of the coronary artery related to defects of the vessel connective tissue, and thoracic aortic dissection
48
What are the first line investigations for ACS?
1) ECG
Acute STEMI:
- Tall T waves
- ST elevation
- New LBBB
NSTEMI:
- ST depression and/or T wave inversion
Bloods:
- FBC
- U&E
- Glucose
- Lipids
49
What other tests can be done to detect ACS?
- Cardiac enzymes – released into blood stream when cardiac muscle is damaged
- Troponin T and I – highly sensitive and specific markers of cardiac muscle injury but not diagnostic:
- Rise within 3-12 hours
- Peak at 24-48 hours
- Return to baseline by 5-14 days
- <14g/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI
- Creatine kinase – catalyses conversion of creatine and utilises ATP to create phosphocreatine (PCr) and ADP
- 3 different types found in skeletal muscle, brain and the heart
- CK-MB rise within 3-12 hours of onset of pain and can be used to determine re-infarction as levels drop back to normal after 36-72 hours
- Myoglobin
Rises within 1-4 hours of onset of pain
Highly sensitive but not specific
- CT angiography
50
What are the causes of raised troponin?
Cardiac causes:
- Congestive heart failure
- Acute or chronic stable coronary artery disease
- Myocarditis (and endocarditis and pericarditis)
- Tachy/bradyarrhythmia’s
- Heart block
Non-cardiac causes:
- PE
- Gram negative sepsis
- Severe pulmonary
- Hypertension
- Renal failure
- COPD
- Diabetes
- Drugs
- Acute neurological events
51
Define Unstable Angina
- An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage
- Classified by:
1. Cardiac chest pain at rest
2. May have crescendo pattern (it gets worse and worse more readily)
3. New onset angina
- 50% of patients with unstable angina will get an infarction within 30 days if left untreated
52
What are the diagnosis and investigations for Unstable Angina?
- History
- FBC – anaemia aggravates it
- Cardiac enzymes (troponin normal) – excludes infarction
- ECG – ST depression when patient is in pain
- CT Coronary angiography
- Risk assessment (QRISK2)
– if low risk do an elective stress test
53
What is the management of Acute Coronary Syndrome?
Risk Factor modification:
- Stop smoking
- Lose weight
- Healthy diet
- Exercise
54
What is the Pharmacological treatment for STEMI (ACS)?
1) Percutaneous coronary intervention (PCI) within 120 mins
- Clopidogrel or prasugrel and aspirin
2) Fibrinolysis (anti-coagulant treatment) (if PCI not possible in <120 mins)
e. g. Alteplase
- Ticagrelor and aspirin
55
What is the Pharmacological treatment for NSTEMI (Unstable Angina)?
- Use GRACE score to predict 6 month mortality + risk of further cardio events
- Fondaparinux
Low risk:
-Ticagrelor and aspirin
Med/high risk:
- Angiography + PCI + CABG
- Prasugrel and aspirin
56
What is the secondary pharmacological treatment for ACS?
ABAS:
- ACEi
- Beta blocker
- Aspirin + Clopidogrel
- Statin
57
Explain the pharmacology of the drugs used to treat ACS
Anti-platelet therapy:
1) Aspirin (300mg initially then 75mg daily) – irreversibly inhibits COX-1 🡪 less production of thromboxane A2 🡪 less platelet aggregation
2) Dual therapy with P2Y12 receptor inhibitors - Clopidogrel (300 mg initially then 75mg for 12 months), ticagrelor (180 mg initially then 90 mg twice daily) or prasugrel
- Inhibits ADP-dependant activation of IIb/IIIa glycoproteins preventing the amplification response of platelet aggregations
- Platelet glycoprotein IIb/IIIa receptor inhibitor for high risk patients e.g. abciximab
- Anti-coagulants – Heparin interferes with thrombus formation at site of plaque rupture by inhibiting factors II (prothrombin), VII, IX and X and reduces risk of ischaemic events and death
- LMWH e.g. enoxaparin has better efficacy than unfractionated heparin
- Fondaparinux (synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin
- Nitrates – GTN spray or IV infusion
- Beta blockers – metoprolol, bisoprolol
- Statins – Reduce cholesterol e.g. atorvastatin, simvastatin
- ACE inhibitors - Ramipril
- Calcium channel blockers (if beta blocker contraindicated) – amlodipine
58
What is the difference between NSTEMI and unstable angina?
- NSTEMI and unstable angina have similar management, only difference is that an NSTEMI is an acute infarction and will not involve the whole of the heart wall like a STEMI. Both are due to a narrowing of the coronary artery lumen rather than a total occlusion like a STEMI
59
What are common Post-MI Complications?
DREAD:
- Death
- Rupture of heart septum/papillary muscles
- Edema (heart failure)
- Arrhythmias and Aneurysm:
- Tachycardia – Sinus, VF, AF
- Brachycardia – Sinus, AV block
- Dressler’s syndrome
= pericarditis following cardiac intervention/surgery
60
Define Myocardial Infarction?
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to COMPLETE occlusion of an artery by thrombus.
- Most common cause of death in developed countries
- 1/3 cases occur at night
61
Describe the pathology of an MI?
- Almost always due to a rupture of an atherosclerotic plaque which leads to clot formation which then occludes one of the coronary arteries causing myocardial cell death and inflammation
- So basically, plaque rupture --> development of thrombosis --> total occlusion of coronary artery --> myocardial cell death
62
What are the signs of an MI on an ECG?
1) STEMI:
- ST elevation
- Tall T waves
- Might present as a new LBBB (WilliaM)
- Pathological Q waves
2) NSTEMI:
- ST depression and/or T wave inversion
63
What are the risk factors for an MI?
- Age
- Male
- History of premature coronary heart disease
- Diabetes mellitus
- Hypertension
- Hyperlipidaemia
- Family history
64
What are the symptoms of an MI?
- Crushing central chest pain similar to that occurring in angina – described as “elephant sitting on chest:
- Sweating
- SOB/Dyspnoea
- Fatigue
- Nausea
- Vomiting
65
What are the signs of a heart attack?
- Occurs at rest
- Last longer than 20 minutes
- Not relived by GTN spray
- Pain may radiate to left arm, neck and/or jaw
- Pulse and BP may vary between being up or down
- Patient appears pale, sweaty and grey
- 4th heart sound – due to forceful contraction of the atria to overcome a stiff or dysfunctional ventricle
- Pansystolic murmur – due to papillary muscle dysfunction or rupture
66
Who are silent infarctions more present in?
- Silent infarctions either go unnoticed or present with hypotension, arrhythmias or pulmonary oedema.
- This occurs most commonly in elderly patients, diabetics or those with hypertension.
67
What is the differential diagnosis for an MI?
- Stable/unstable angina
- Pericarditis
- Aortic aneurysm
- Endocarditis
- Pulmonary Embolism
- Pneumothorax
68
What are the investigations for an MI?
- Clinical history
- ECG
1) STEMI:
- ST elevation
- Tall T waves
- LBBB
- Pathological Q waves follow
2) NSTEMI:
- ST depression and/or T wave inversion
- Cardiac enzymes – troponin T, creatine kinase, myoglobin
- CT angiography
- CXR
- FBC
- U&E
- Blood glucose and lipids
69
What is the acute (initial management) of an MI?
- Get to hospital immediately
MONA:
- Morphine
- Oxygen (if sats are <94%)
- Nitrates – typically fondaparinux in Sheffield
- Aspirin 300mg – chewed in order to increase absorption
- 12 lead ECG and cardiac monitor
- Beta blocker IV – contraindicated in hypotension, HF, bradycardia and asthma
- Refer for PCI, thrombolysis (IV alteplase) or CABG ASAP as long as it’s not contraindicated
70
What is the subsequent (secondary prevention) of an MI?
Modification of risk factors:
- Diabetes
- Smoking
- Hypertension
- Hypercholesterolaemia
- Exercise
- Diet – high in oily fish, fruit and veg, low in saturated fats
71
What is the subsequent pharmacological (secondary prevention) of an MI?
- Aspirin – 75mg daily
- Clopidogrel/ticagrelor (for dual antiplatelet therapy)
- Statins
- Beta blocker if contraindicated give ACEi
- ACE inhibitors – use angiotensin receptor blocker if intolerant e.g. valsartan
72
What is the general advice you would give to patient who has just had a recent MI?
- Return to work after 2 months – not all professions e.g. airline pilots, divers, air traffic controllers
- No air travel for 2 months
- No sex for 1 month
73
What is the differential diagnosis of chest pain?
- Cardiac – ACS, Aortic dissection, pericarditis, myocarditis
- Respiratory – PE, pneumonia, pleurisy, lung cancer
- MSK – rib fracture, chest trauma, costochondritis (inflammation of the cartilage between the ribs and sternum)
- GORD
- Oesophageal spasm
- Anxiety/panic attacks
74
Define Pericarditis
Inflammation of the pericardium with/without serous/haemorrhagic effusion
75
What is the Pericardium?
- If the heart is the inside bit of an orange, the pericardium is the peel around it.
- The pericardium is a fibroserous, fluid-filled sack that surrounds the muscular body of the heart and the roots of the aorta, pulmonary vessels and the superior and inferior vena cava.
76
What does the pericardium consist of?
The pericardium is made up of two layers:
1) External fibrous layer:
- Continuous with central tendon of diaphragm
- Fibrous pericardium made up of tough connective tissue and is relatively non-distensible
- Rigid structure prevents overfilling of the heart
2) Internal serous layer:
Divided into:
- Outer parietal layer that lines the internal surface of the fibrous pericardium
- Internal visceral layer that forms the outer layer of the heart (epicardium)
- Each layer is made up of mesothelium
77
What is present between the outer and inner serous layers?
- In between the outer and inner serous layers is the pericardial cavity, which contains 50 mL of lubricating serous fluid
- This serves to minimise friction generated as the heart contracts
78
What is the function of the lubricating serous fluid?
- FIXES THE HEART in the mediastinum and limits its motion as it is attached to the diaphragm, sternum and adventitia (outer layer) of great vessels
- PREVENTS OVERFILLING OF THE HEART - Relatively inextensible fibrous layer prevents the heart from increasing in size too rapidly, therefore placing a physical limit on the potential size of the organ
- LUBRICATION from the thin film of fluid between the two layers of serous pericardium reduces friction generated by the heart as it moves within the thoracic cavity.
- PROTECTION FROM INFECTION – the fibrous pericardium serves as a physical barrier between the muscular body of the heart and adjacent organs prone to infection e.g. the lungs
79
Describe the pathology pf Pericarditis
- The pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes
- A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop
- In the UK, pericarditis is most commonly secondary to viral infection or MI
- Occurs more in men
80
What are the causes of Pericarditis?
- Idiopathic
- Infection:
- Viral– HIV, Coxsackie B, echovirus
- Bacterial – TB
- Fungal – Histoplasma spp.
- MI
- Autoimmune (immune system attacking the pericardium)
- Sjogren’s
- RA
- SLE
- Dressler syndrome (inflammation of pericardium after MI damaging it)
- Uraemia
- Trauma
- Malignancy – breast, lung, leukaemia and lymphoma
............................................
- Main causes = TB, MI, Autoimmune, SLE, Dressler syndrome
81
What are the symptoms of Pericarditis?
- Central chest pain
- Severe
- Sharp and pleuritic -stabbing- pain (without constricting crushing character of ischaemic pain)
- Often in middle/left side of the chest
- Retrosternal and may radiate to the back or neck
- Sitting up and leaning forward tends to ease the pain, while lying down and breathing deep worsens it.
- Dyspnoea
- Hiccups – phrenic involvement
- Fever
82
What are the signs of pericarditis?
- Pericardial friction rub (scratching sound) heard by
auscultation
- Chest pain worse on inspiration and lying flat
- Relieved by sitting forward
- May radiate to neck and shoulders
- Raised JVP
83
What is the first line investigation for Pericarditis?
- First-line diagnostic = ECG
- Concave (saddle-shaped)
- ST segment elevation in all leads (global ST elevation)
- PR depression
- PeRicardiTiS
84
What other investigations can be done for Pericarditis?
Bloods:
- Cardiac enzymes (troponin)
- ESR
- C-reactive protein
- FBC
- Echocardiogram
- CXR:
- Bottle-water shaped silhouette
- May show cardiomegaly in cases of effusion (enlargement of the heart)
85
What is the first-line management of pericarditis?
- NSAIDS and gastric protection (proton pump inhibitor e.g. lansoprazole)
- Systemic corticosteroids used when resistant to NSAIDs
- Colchicine (anti-gout medication) – inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence
86
What other management options are available for pericarditis?
- Pericardiocentesis – drainage of fluid if there is cardiac tamponade or symptomatic pericardial effusion
- Rest until symptoms resolve
- Treat underlying cause if there is one e.g. steroid for autoimmune causes
87
What are the complications of pericarditis?
- PERICARDIAL EFFUSION:
- Accumulation of fluid in the pericardial sac
- CARDIAC TAMPONADE – When there is enough pericardial effusion in the pericardium that it restricts diastolic ventricular filling (ability for heart to expand) and causes reduced BP and CO
- CHRONIC OBSTRUCTIVE PERICARDITIS – persistent inflammation of acute pericarditis causes the heart to be encased with a rigid fibrotic pericardial sac which prevents adequate diastolic filling of the ventricles
88
What causes Pericardial effusion and tamponade?
- May result from any of the causes of pericarditis.
| - Hypothyroidism also causes a pericardial effusion which rarely compromises ventricular function
89
What are the signs and symptoms of Pericardial effusion?
- Effusion obscures apex beat, and heart sounds are soft
- Hypotension
- Tachycardia
- Elevated JVP – rises with inspiration (Kussmaul’s sign)
- Pulsus paradoxus:
- A fall in BP of more than 10mmHg on inspiration
- Caused by increased venous return to the right side of the heart during inspiration
- The increased RV volume therefore occupies more space within the rigid pericardium and impairs LV filling
90
What are the investigations for Pericardial effusion?
- Echocardiography – diagnostic, shows echo-free space around heart
- CXR – shows globular heart
- ECG – shows low voltage complexes with sinus tachycardia
91
How would you diagnose pericardial effusion?
Pericardial effusion:
- CXR – large heart
- ECG – low voltage QRS complexes and sinus tachycardia
- Echocardiogram
Cardiac Tamponade:
- CXR – large heart
- Beck’s triad; Falling BP, Rising JVP, Muffled heart sounds
- ECG
- Echocardiogram
92
What is the management of pericardial effusions?
- Most pericardial effusions resolve spontaneously
- Tamponade requires emergency pericardiocentesis ( also called pericardial tap, is a medical procedure where fluid is aspirated from the pericardium)
- If effusion recurs, excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics
93
What is constrictive pericarditis?
- Constrictive pericarditis is a chronic, progressive disorder in which the pericardial sac becomes thick and stiffened, and restricts the filling of the heart.
- Mild cases can sometimes be treated by aggressively addressing the underlying medical disease, but usually, surgical treatment is necessary.
- This is different to cardiomyopathy- as cardiomyopathy is where the WALLS of the heart are rigid.
- Thus the heart is restricted from stretching and filling with blood properly.
- It is the least common of the three original subtypes of cardiomyopathy: hypertrophic, dilated, and restrictive.
94
Describe the aetiology of Constrictive Pericarditis?
- In UK, most cases are idiopathic in origin or result from intrapericardial haemorrhage during heart surgery.
- Must be distinguished from restrictive cardiomyopathy
95
Describe the signs and symptoms of Constrictive Pericarditis?
Similar features of right sided HF:
- Jugular venous distension
- Dependent oedema
- Hepatomegaly
- Ascites
- Kussmaul’s signs – JVP rises paradoxically with inspiration
- Pulsus paradoxus
- AF
- Pericardial knock caused by rapid ventricular filling
96
What are the investigations for Constrictive Pericarditis?
- CXR – shows normal heart and pericardial calcification
- CT or MRI – diagnostic, shows pericardial thickening and calcification
- Echocardiography
97
What is the treatment of Constrictive Pericarditis?
- Surgical excision of pericardium
98
What is infective endocarditis?
- Infection of the heart valves and/or other endocardial lines structures within the heart e.g. septal defects, pacemaker leads, surgical patches
99
Describe the epidemiology of Infective endocarditis?
- Used to be a disease of the young affected by rheumatic heart disease (Streptococcus pyogenes)
- Now it is a disease of:
- The elderly (in an ageing population)
- Young IV drug abusers
- Young congenital heart disease
- Anyone with prosthetic heart valves or pacemakers
- Poor dental hygiene
- More common in males
100
What are the causes of Infective Endocarditis?
- S. Aureus (IVDU, Diabetes and surgery) – most common cause
- Pseudomonas aeruginosa
- Streptococcus viridans (DENTAL PROBLEMS) – gram positive, alpha haemolytic and optochin resistant
101
What are the symptoms of Infective Endocarditis?
1) Fever plus:
- Prosthetic material in heart
- Risk factor for IE e.g. IVDU
- Newly developed
ventricular arrhythmias or conduction disturbances
2) General:
- Headache
- Fever
- Malaise
- Confusion
- Night sweats
102
What are the signs of Infective Endocarditis?
FROM JANE:
- Fever
- Roth’s spots – retinal haemorrhages with white or clear centres on fundoscopy
- Osler’s nodes – painful/ tender nodules in fingers
- Murmur - arrhythmia
- Janeway lesion – painless spots, haemorrhages and nodules on nail beds of fingers
- Anaemia
- Nail-bed splinter haemorrhages (splinter)
- Emboli – MI, stroke, PVD
- Clubbing
103
How would you diagnose Infective Endocarditis?
Modified Duke’s criteria:
- 2 major criteria:
1) Bugs grown from blood cultures
2) Evidence of endocarditis on echo, or new valve leak
- 5 minor criteria:
1) Predisposing factors
2) Fever
3) Vascular phenomena
4) Immune phenomena
5) Equivocal blood cultures
Definite IE:
- 2 majors
- 1 major + 3 minors
- 5 minors
Possible IE:
- 1 major
- 1 major + 3 minors
- 5 minors
104
What investigations would you do to diagnose Endocarditis?
1) Transoesophageal Echo (TOE) - DIAGNOSTIC
- Generally safe but risk of perforation or aspiration
- Easiest if ventilated (but never ventilate just for TOE)
2) Transthoracic echo (TTE)
- Safe
- Non-invasive
- No discomfort
- Often poor images so lower sensitivity
- ECG
- CXR – cardiomegaly
- Blood cultures
105
What is the treatment for Endocarditis?
- Antimicrobials – IV for around 6 weeks, choice of agent(s) based on culture sensitivities
- Not staphylococcus, use penicillin – BENZYLPENICLLIN and GENTAMYCIN
- If staphylococcus, use VANCOMYCIN and RIFAMPICIN
- Treat complications – arrhythmia, HF, heart block, embolisation, stroke rehab, abscess drainage etc.
- Surgery
106
Define Cardiomyopathy
- Cardiomyopathy is a general term for diseases of the heart muscle, where the walls of the heart chambers have become STRETCHED, THICKENED or STIFF
- This affects the heart's ability to pump blood around the body.
- They are a group of disease of myocardium that affect mechanical or electrical function of heart
- The abnormal heart muscle seen in cardiomyopathy is not caused by blocked arteries in the heart (coronary artery disease), high blood pressure (hypertension), disease of the heart valves (valvular disease) or congenital heart disease.
- Most types of cardiomyopathy are inherited and are seen in children and younger people.
107
What are the 4 different types of Cardiomypoathy?
1) Hypertrophic
2) Dilated
3) Arrhythmogenic
4) Restrictive
108
What are the risk factors for Cardiomyopathy?
- Family history
- Hypertension
- Obesity
- Diabetes
- Previous MI
109
What is Hypertrophic Cardiomyopathy?
- Characterised by unexplained primary cardiac hypertrophy
- Most common cause of sudden death in young and adults
- Diastole is main issue NOT systole – hearts are stiff and don’t relax properly
- LV becomes hypertrophied and hypertrophy is asymmetrical, blocking LV outflow tract during systole
110
What are the causes of Hypertrophic Cardiomyopathy?
- Passed on genetically via an autosomal dominant mutation
| - 50% chance of inheriting the condition
111
How does Hypertrophic Cardiomyopathy present?
- Angina
- Dyspnoea
- Palpitations
- Dizzy spells
- Syncope
- Crescendo-decrescendo murmur – similar to aortic stenosis
- S4 sound
112
How would you investigate Hypertrophic Cardiomyopathy?
1) ECG:
- Usually always abnormal
- Deep T wave inversion
2) Echocardiogram
3) Microscopically
4) Myocyte disarray
- Ultrastructural level, myofibrils are in disarray
- When stained it turns blue
- Fibrosis is an electrical insulator – electrical current has to go around the fibrosis and causes arrhythmia
- Hypertrophy can occur in coronary arteries – causes ischaemia
113
What are some complications of Hypertrophic Cardiomyopathy?
- Abnormal heart rhythms, or arrhythmias, such as atrial fibrillation or heart block can happen as a result of having HCM
- You might also be at risk of endocarditis, an infection of the hearts inner lining
114
What is the treatment for Hypertrophic Cardiomyopathy?
- Amiodarone – anti-arrhythmic medication (A for Amiodarone and A for anti-arrhythmic)
- Calcium channel blocker e.g. amlodipine, diltiazem
- Beta blocker – atenolol
- DIGOXIN IS CONTRAINDICATED
- Surgery
- DIGOXIN is used to treat Atrial Fibrillation & Heart failure ONLY, it is contraindicated in Ventricular fibrillation & Hypertrophic cardiomyopathy
115
What is Dilated Cardiomyopathy?
- The most common form of Cardiomyopathy
- Makes the muscle walls become stretched and thin (dilated) --> weak contraction --> less pumped out = BIVENTRICULAR CONGESTIVE HEART FAILURE
- Affects left ventricle more
116
What are the causes of Dilated Cardiomyopathy?
- Idiopathic – majority of time
- Infection – coxsackie B
- Ischaemia
- Alcohol
- Thyroid
- Genetic
117
How does Dilated Cardiomyopathy present?
- Heart failure symptoms:
1) Dyspnoea (breathlessness)
2) Swollen ankles and legs, (oedema)
3) Fatigue
- Arrhythmias
- Increased JVP
118
What are the investigations for Dilated Cardiomyopathy?
- CXR – large heart
- ECG
- Echo
119
What is the treatment for Dilated Cardiomyopathy?
- HF and AF treated in normal way
- Left ventricular assist device
- Heart transplant
120
What is Arrhythmogenic Cardiomyopathy?
- Also known as Right Ventricular Cardiomyopathy, is an inherited heart disease
- ACM is caused by genetic defects of the parts of heart muscle known as desmosomes - desmosome gene mutations
- Desmosomes are areas on the surface of heart muscle cells which link the cells together
- May be little structural change or may diffusely involve RV and LV
121
How does Arrhythmogenic Cardiomyopathy present?
- Arrhythmia is the main feature of arrhythmogenic cardiomyopathy
- Syncope
- RHF
122
What are the investigations for Arrhythmogenic Cardiomyopathy?
1) Histologically:
Red – normal myocardium
Blue – fibrous tissue
White – not stained
2) ECG changes:
- In leads V1, 2 and 3
- Epsilon wave
- T wave inversion
3) Echocardiogram
4) Genetic testing
123
What is the treatment for Arrhythmogenic Cardiomyopathy?
- Arrhythmias - amiodarone
| - Beta blockers e.g. bisoprolol
124
What is Restrictive Cardiomyopathy?
- Restrictive cardiomyopathy is a form of cardiomyopathy in which the walls of the heart are rigid.
- Thus the heart is restricted from stretching and filling with blood properly.
- Restrictive physiology – ventricles stiffer and less compliant 🡪 less CO 🡪 HF
- Poor dilatation of heart restricts its ability to take on blood and pass it to the rest of body
- It is the least common of the three original subtypes of cardiomyopathy: hypertrophic, dilated, and restrictive
125
How does Restrictive Cardiomyopathy present?
- Dyspnoea
- Elevated JVP
- Hepatomegaly
- Ascites
- 3rd and 4th heart sounds
126
What are the investigations for Restrictive Cardiomyopathy?
- CXR
- ECG – low amplitude signals, smaller QRS
- Echo
- Cardiac catheterisation
127
What is the treatment for Restrictive Cardiomyopathy?
- Treatment – treat underlying cause, heart transplant
128
Summarise the 4 different types of Cardiomyopathy?
1) Hypertrophic - affects diastole
2) Dilated - affects Ventricles + Ventricular contraction
3) Arrhythmogenic - Right heart failure
4) Restrictive - Ability of the heart to take on blood + pass it to the rest of the body is restricted
129
What is valvlular heart disease?
- Cardiac valves may become incompetent (regurgitant) or stenotic (narrow) or both
- Abnormal valves produce turbulent blood flow, which is heard as a murmur on auscultation, a few murmurs are also felt as a thrill on palpation
- Murmurs may be heard with normal hearts, often reflecting a hyper-dynamic circulation e.g. pregnancy, anaemia and thyrotoxicosis
130
What are the most common valvular heart problems?
1) Aortic stenosis
2) Mitral stenosis
3) Mitral regurgitation
4) Aortic regurgitation
131
What is systolic blood pressure?
Systolic Blood Pressure is the pressure of blood exerting against the artery walls when the heartbeats
Whereas,
Diastolic Blood Pressure is the pressure of blood exerting against the artery walls when the heart is resting between beats.
132
What are the different heart sounds (phases of systole)?
- In a healthy adult, the heart makes two sounds, commonly described as 'lub' and 'dub
- The third and fourth sounds may be heard in some healthy people, but can indicate impairment of the heart function.
- S1 and S2 are high-pitched and S3 and S4 are low-pitched sounds.
- A S4 heart sound is almost always pathologic.
- S1 – closing of mitral and tricuspid valve
- S2 – closing of aortic and pulmonary valve
- S3 – when blood strikes a compliant LV during passive LV filling
133
What are the different types of Aortic Stenosis?
- Supravalvular – above valve
- Subvalvular – below valve
- Valvular – most common
134
Describe the pathology of Aortic stenosis?
- Due to the narrowing of the aortic valve, there is obstructed LV emptying 🡪 a pressure gradient develops between the LV and aorta 🡪 increased afterload 🡪 LV hypertrophy
- Afterload = Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction)
- In turn this results in increased myocardial oxygen demand --> relative ischaemia of the myocardium --> consequent angina, arrhythmias and LV failure
- LV systolic function is typically preserved in aortic stenosis
- Aortic stenosis = LV hypertrophy NOT LV function deterioration
135
What are the causes of Aortic Stenosis?
1) Calcification of congenital bicuspid aortic valve (BAV) – most common and presents in middle age
2) Degeneration and calcification of a normal valve – presents in elderly
3) Rheumatic heart disease
- (Repeated strep infections (Streptococcus pyogenes causes the immune system to react against the tissues of the body --> inflaming and scarring heart valves
therefore,
- Rheumatic fever = Rheumatic heart disease
136
What are the risk factors for Aortic stenosis?
- Congenital BAV
= predisposed to aortic stenosis and regurgitation
- A bicuspid aortic valve is an aortic valve that has two leaflets instead of three --> blood flow from the heart into the aorta is therefore restricted with a BAV.
137
What are the symptoms of Aortic stenosis?
- Think Aortic stenosis in ANY elderly person with:
A classic triad of:
- Angina (Chest pain)
- Exertional syncope
- Dysponea - due to HF
+ Heart failure
138
What are the signs of Aortic Stenosis?
- Slow rising (pulsus tardus) and weak (pulsus parvus) carotid pulse
- Heart sounds
- Soft or absent 2nd heart sound – may become soft or inaudible when the valve becomes immobile
- Prominent 4th heart sound – due to LV hypertrophy
!!!!!!!!!!!
- Ejection systolic murmur – crescendo – decrescendo character
!!!!!!!!!!!
139
What is the first-line investigation for Aortic Stenosis?
1) Echocardiography (First line investigation + diagnostic)
2) CXR:
– Shows a normal heart size
- LVH
- Prominence of the ascending aorta (post-stenotic dilatation) and there may be valvular calcification
3) ECG:
- Shows evidence of LVH and a LV stress pattern when disease is severe;
- ST depression and T-wave inversion in aVL, V5 and V6
- Cardiac catheterisation used to exclude coronary artery disease
140
What is the management of Aortic Stenosis?
1) Surgical:
- Aortic valve replacement
– in symptomatic patients as onset of symptoms associated with 75% mortality at 3 years
If not medically fit for surgery, then:
- Transcatheter Aortic Valve Implantation (TAVI) with a balloon expandable stent
2) General:
- Dental hygiene/care – risk of infective endocarditis
- IE prophylaxis in dental procedures
141
What is an exemplar presentation of Aortic Stenosis?
- A 78-year-old man presented with episodes of loss of consciousness on exertion.
- On examination, the carotid pulse is rising slowly, there is a loud ejection systolic murmur at the aortic area, radiating to both carotid arteries
142
What is Mitral Stenosis?
- Obstruction of LV inflow that prevents proper filling during diastole
143
What are the causes of Mitral Stenosis?
- Rheumatic heart disease - reliable history or rheumatic fever not always obtained
- Caused by rheumatic fever from group A beta-haemolytic strep e.g. s. pyogenes
- Infective endocarditis
- Mitral annular calcification
- Congenital
............................................
- (Repeated strep infections (Streptococcus pyogenes causes the immune system to react against the tissues of the body --> inflaming and scarring heart valves
144
What are the risk factors for Mitral Stenosis?
- History of rheumatic fever
| - Untreated streptococcus infections
145
Describe the pathology of Mitral Stenosis?
- Thickening and immobility of valve leads to:
- Obstruction of blood flow from LA to LV 🡪 increased LA pressure 🡪 pulmonary hypertension and right heart dysfunction 🡪
--> AF is common due to elevation of LA pressure and dilatation
- Thrombus may form in the dilated atrium and give rise to systemic emboli e.g. the brain causing a stroke
- Chronically elevated LA pressure leads to an increase in pulmonary pressure and pulmonary oedema
..................................................
- Thrombus
- Pulmonary pressure changes
- AF
146
What are the symptoms of Mitral Stenosis?
- Progressive exertional dyspnoea
- Cough productive of blood-tinged sputum
- Haemoptysis – coughing up blood due to rupture of bronchial vessels due to elevated pulmonary pressure
............................
Right HF:
- Fatigue
- Weakness
- Abdominal/lower leg swelling
.........................................
- Palpitations – due to AF
- Chest pain
147
What does the 'lub-dub' heart sound represent?
- The" lub" is the sound of the tricuspid and mitral valves closing.
- The" DUB" is the sound of the aortic and pulmonary valves closing
148
What are the signs of Mitral Stenosis?
- Mitral facies or malar flushes on cheek – when MS is severe, there is vasoconstriction due to decreased CO which results in pinkish-purple patches on the cheeks
- Low volume pulse which may become irregular if AF develops
- Tapping, non-displaced apex beat due to combination of palpable first heart sound and LV backward displacement produced by an enlarging RV
- Heart sounds:
1) Loud first heart sound at apex:
- The presence of a loud second heart sound, parasternal heave, elevated JVP, ascites and peripheral oedema indicate that pulmonary hypertension inducing right ventricular overload has developed
2) Diastolic murmur – heard when blood flows over a valve:
- Low-pitched diastolic rumble at apex
Heard best when patient is lying on left side with help expiration
149
What are the investigations for Mitral Stenosis?
1) Echocardiogram
2) CXR:
- LA enlargement
- Pulmonary hypertension
- Calcified mitral valve
(sometimes)
3) ECG:
– AF and LA enlargement
150
What is the treatment for Mitral Stenosis?
- Rate control if patient has AF – BETA BLOCKERS, DIGOXIN
- Anticoagulation with warfarin for AF patients to prevent clot formation and embolisation
- Diuretics for heart failure e.g. furosemide
- Percutaneous mitral balloon valvotomy – access to mitral valve obtained via catheterisation through the femoral vein, RA and interatrial septum and a balloon is inflated to open the commissures
151
What is an exemplar presentation of a patient with Mitral Stenosis?
- A 45-year-old lady, who moved to the UK from India 5 years ago, presented with increasing exertional dyspnoea and orthopnoea and malar flushes
- On examination, the apex beat is tapping, with a loud first heart sound and an apical-mid diastolic rumble
152
What is Mitral regurgitation?
- Backflow of blood from LV to the LA during systole
153
What are the cause of Mitral regurgitation?
- Myxomatous degeneration
- Mitral valve prolapse
- Rheumatic heart disease – from rheumatic fever
- Infective Endocarditis
- Ischaemic mitral valve
- Dilated cardiomyopathy
154
What are the risk factors for Mitral regurgitation?
- Female
- Lower BMI
- Advanced age
- Renal dysfunction
- Previous MI
155
What is the pathology for Mitral regurgitation?
- Pure volume overload due to leakage from LV into LA 🡪LA dilatation
Compensatory mechanisms:
- LA enlargement
- LV hypertrophy – since LV must put in same effort to pump less blood
- Increased contractility
- Progressive LA dilatation and RV dysfunction due to pulmonary hypertension
- Progressive LV volume overload leads to dilatation and progressive HF
156
What are the symptoms for Mitral regurgitation?
- Exertional dyspnoea
- Fatigue and lethargy
- Palpitations
- Right sided HF and can lead to congestive heart failure
157
What are the signs for Mitral regurgitation?
- Collapsing pulse with wide pulse pressure
- Hyperdynamic and displaced apex beat
Heart sounds:
- Soft S1
- PANSYSTOLIC MURMUR at apex radiating to axilla
- Diastolic blowing murmur at left sternal border
- AUSTIN FLINT murmur (at apex) – regurgitant jet impinges on anterior mitral valve causing it to vibrate
- SYSTOLIC EJECTION MURMUR– due to increased flow across AV
158
What are the investigations for Mitral Regurgitation?
- CXR – shows enlarged LA and LV
- Echocardiogram – estimation of LA, LV size and function
- ECG
159
What is the treatment for Mitral Regurgitation?
- General: consider IE prophylaxis
...................................
Medical:
- Vasodilators - ACE inhibitors and hydralazine
- Rate control for AF – beta blockers, calcium channel blockers, digoxin
- Anticoagulant for AF and flutter
- Diuretics - furosemide
.....................................................
- Serial Echocardiograms: to monitor progression
....................................................
Surgical Treatment to replace valve if patient has:
- ANY symptoms at rest or exercise
- Asymptomatic:
- -If IE < 60%, LVESD > 45mm
- -If new onset AF/raised PAP
160
What is Aortic Regurgitation?
- Leakage of blood into LV during diastole due to ineffective coarctation of aortic cusps
161
What are the causes of Aortic regurgitation?
- Congenital bicuspid aortic valve - chronic
- Rheumatic heart disease (rheumatic fever) - chronic
- Infective endocarditis - acute
162
Describe the pathology of Aortic regurgitation?
- Combined pressure and volume overload 🡪 LV dilatation and LVH
163
What are the symptoms for Aortic regurgitation?
- Exertional dyspnoea
- Orthopnoea
- Paroxysmal nocturnal
dyspnoea
- Palpitations
- Angina
- Syncope
164
What are the signs for Aortic regurgitation?
- Collapsing (water hammer) pulse
- Wide pressure pulse
- Quincke’s sign – capillary pulsation in nail beds
- De Musset’s sign – head nodding with each heart beat
- Muller’s sign – visible pulsations of uvula
Heart sounds:
- Displaced hyperdynamic apex beat
- Early diastolic murmur heard at left sternal edge in 4th intercostal space
- Accentuated when the patient sits forward with their breath held in expiration
- Systolic ejection murmur
165
What are the investigations for Aortic regurgitation?
- Echocardiogram
- ECG – shows evidence of LVH
- CXR - shows a large heart (cardiomegaly) and occasional dilatation of the ascending aorta
166
What is the treatment for Aortic regurgitation?
- IE prophylaxis
- Vasodilators – ACE inhibitors e.g. Ramiprils only if symptomatic or hypertension
- Surgical – replace valve before LV dysfunction
167
What is pulmonary stenosis?
Narrowing of the outflow of the right ventricle
168
What does pulmonary stenosis present as?
Severe:
- Right ventricular failure as neonate
- Collapse
- Poor pulmonary blood flow
- RV hypertrophy
- Tricuspid regurgitation
Moderate/mild:
- Well tolerated for many years
- Right ventricular hypertrophy
169
What is the treatment for pulmonary stenosis?
- Balloon valvuloplasty
- Open valvotomy
- Open trans-annular patch
- Shunt (to bypass the blockage)
170
What is Heart Failure?
- It is a clinical syndrome rather than one specific disease.
Defined as:
- A symptomatic condition where breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output (HR x SV)
- A state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
- Results from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump and maintain CO to meet the demands of the body.
- Can be high output (the requirements of the body are too high e.g. pregnancy) or low output (the heart is not functioning efficiently)
171
Describe the epidemiology of Heart failure
- Annual incidence of 10% in patients over 65
| - 50% of patients die within 5 years
172
What are the causes of heart failure?
- ISCHAEMIC HEART DISEASE – most common cause in the world
- Hypertension – most common cause in Africa
- Cardiomyopathy:
Dilated is main cause
Hypertrophic and restrictive less common but still cause HF
- Valvular heart disease – aortic stenosis
- Congenital heart disease
- Alcohol and chemotherapy
- Factors that increase myocardial work – arrhythmias, anaemia, pregnancy, obesity, hyperthyroidism
173
What are the risk factors for heart failure?
- Age – 65+
- Obesity
- Gender – male
- People who have had a previous MI
174
What are the different types of Heart failure?
Systolic:
- Failure to contract
- Ejection fraction <40% (SV/EDV)
Diastolic:
- Inability to relax and fill
- There is reduced preload because there is abnormal filling of the LV
- Ejection fraction >50%
175
What is Systolic heart failure caused by?
- IHD
- MI
- Hypertension
- Cardiomyopathy
176
What is Diastolic heart failure caused by?
- Constrictive pericarditis
- Cardiac tamponade
- Hypertension
177
What is the difference between low output heart failure or high output heart failure?
- In high output, (the requirements of the body are too high e.g. pregnancy) or low output (the heart is not functioning efficiently)
178
What is low output heart failure caused by?
1) Decreased CO, fails to increase with exertion
2) Could be due to:
- Pump failure – systolic HF, may be due to decreased heart rate e.g. anti-arrhythmic drugs
- Excessive pre-load - Mitral regurgitation, fluid overload
- Chronic increased afterload – occurs in aortic stenosis, hypertension – difficult for the heart muscle to push against it
179
What is high output heart failure caused by?
- Anaemia
- Pregnancy
- Hyperthyroidism
