Cardiovascular Disease I (CVD I) Flashcards
1
Q
What are the definitions of arteriosclerosis, atherosclerosis and atheroma (fibro-fatty plaques)?
A
Arteriosclerosis - ‘Hardening of the arteries’ – a generic term for the thickening and loss of elasticity of arterial walls
Multiple causes (including atheroma, age-related sclerosis and calcification).
Atherosclerosis - a specific form of arteriosclerosis (athere = porridge-like; sclerosis = hardness) due to atheroma
Worldwide, may contribute to up to 50% of all deaths
Atheroma (fibro-fatty plaques) - Athere – ‘porridge-like’; oma – ‘tumour’ - refers to plaques found particularly in elastic and medium-to-large muscular arteries.
These can protrude into and variably-obstruct the lumen and also weaken the underlying media
2
Q
What are the risk factors for atheroma?
A
- Increasing age
- Sex hormone influences (M>F but this equalises by 8th decade)
- Genetics (‘Family History’ – probably polygenic)
- Hyperlipidaemia (esp. LDL-cholesterol)
- Hypertension (both systolic and diastolic levels are important)
- Cigarette smoking
- Diabetes mellitus
3
Q
Outline the pathogenesis of atheroma formation.
A
- Chronic or repetitive endothelial injury / dysfunction - leads to increase permeability, leukocyte adhesion and thrombotic potential
- Accumulation of intimal lipid - phagocytosed by macrophages to form foam cells
- Smooth muscle cell migration to, and proliferation, in the intima - accompanied by changes in the ECM (accumulation of collagen and proteoglycan)
- Fibrosis forming a fibro-lipid plaque - inflammatory reaction including macrophages, lymphocytes, endothelial cells and smooth muslce cells
- Plaque injury – thrombosis and haemorrhage - stable plaque can become unstable - resulting in MI
4
Q
Outline how a plaque can develop/evolve?
A
- Early plaque – confined to the intima – bulges out a little
- Advanced plaque – thin fibrous cap, dips out into the media - associated with weakening of the endothelial wall
- Complicated plaque – plaque that is likely to rupture driving thrombus formation
5
Q
Which arteries are normally effected by atheroma formation?
A
Elastic and medium-to-large muscular arteries:
1. Abdominal aorta
2. Coronary arteries
3. Popliteal arteries
4. Descending thoracic aorta
5. Internal carotid arteries
6. Vessels of the circle of Willis
6
Q
What are these images showing?
A
7
Q
What are the complications associated with atheromas?
A
- Calcification of the plaque - hardening of the arteries
- Ulceration and plaque rupture - expose highly thrombogenic material and discharge micro-embolic debris (cholesterol emboli)
- Haemorrhage - rupture leading to a bleed into the plaque - expand the plaque/lead to further rupture
- Super-imposed thrombosis - fully/partially occlude the lumen
- Aneurysmal dilatation - dilation of the vessel - typical in abdominal aortic aneurysms
All of these can contribute to the vessel obstruction and downstream ischaemia
Note - exact effects will depend on the artery effected
- Intermittent claudication – cramping in the lower leg due to insufficient blood supply
- Gangrene - tissue death due to a lack of blood supply
8
Q
What are the complications associated with atheromatous abdominal aortic aneurysms?
A
Sequelae:
1. Formation of an abdominal mass (pulsatile)
2. Impingement on adjacent structures eg ureter
3. Embolisation (atheroma or mural thrombus)
4. Vessel ostia obstruction - vessel openings
5. Rupture into the peritoneal cavity or retro- peritoneum with potentially massive (fatal) haemorrhage
9
Q
What are the definitions of thrombus, thrombosis and haematoma?
A
- A thrombus is a solidification of blood constituents that forms within the vascular system during life
- Thrombosis is a pathological process - denotes the formation of thrombus within the uninterrupted vascular system
- Haematoma (blood clot) - Solidification of blood constituents outside the vascular system or after death
Key difference - intra vs. extra-vascular
10
Q
What are the three drivers of thrombosis?
A
Virchow’s Triad – all work together (at different levels) to lead to thrombosis
Usually one of the three dominates – usually all three contribute though – some instances this is not the case
11
Q
How does endothelial injury contribute to thrombus formation? What are some common causes?
A
Endothelial integrity is the single most important factor especially in high-flow arterial scenarios - driver clot formation
Note - but the endothelium need not necessarily be physically disrupted to contribute to thrombosis; any perturbation in the dynamic balance of pro- and anti- thrombotic effects of endothelium can influence local clotting
12
Q
How does abnormal blood flow contribute to thrombus formation?
A
Abnormal blood flow
1. Disrupts laminar flow (may be more likely for platelets to contact endothelium)
2. Prevents the dilution of clotting factors
3. Retards the inflow of inhibitors of clotting factors
4. Causes endothelial injury - promoting endothelial cell activation
You can have…
1. Turbulence - contributes to the development of arterial and cardiac thrombi
2. Stasis - Important in the formation of venous thrombi
13
Q
How does hypercoagulability contribute to thrombus formation?
A
Refers to an alteration of the blood coagulation mechanism (particularly platelets and the clotting cascade) that in some way predisposes to thrombosis
May be….
1. Genetic - e.g. Mutations in factor V or prothrombin, Leiden mutaiton - resistant to protein C cleavage, etc.
2. Acquired - immobility, post-trauma or surgery, stasis and vascular injury
14
Q
How do arterial and venous thrombi appear morphologically?
A
Arterial thrombi
- Usually occlusive
- May be mural - attached to the wall of blood vessel or cardiac chamber
- Occur anywhere but more frequent in:
a) Coronary
b) Carotid
c) Cerebral
d) Femoral
Venous thrombosis
- Also termed phlebothrombosis
- Not to be confused with thrombophlebitis
- Occurs typically in pelvic and leg veins in association with stasis
15
Q
How do thrombi appear under the microscope?
A
16
Q
What are the complications of arterial thrombosis?
A
Arterial occlusion
1. Loss of pulses distal to the thrombus
2. Area becomes cold, pale, painful
3. Eventually tissue dies and gangrene results
17
Q
How do superficial and deep venous thrombosis differ?
A
Superficial (saphenous system)
- Congestion, swelling, pain, tenderness (rarely embolise - move)
Deep
- Foot and ankle oedema
- May be asymptomatic and recognised only when they have embolised (eg via IVC and right side of heart to the lung)
18
Q
Can thrombosis occur both in th venous and arterial systems?
A
Yes both possible - can lead to occlusion of artery or veins
Embolism
Arterial – away from the heart (distal)
Venous – towards the heart (proximal)
19
Q
What is the definition of an embolism?
A
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
99% of all emboli arise from thrombi (thromboembolism)
Unless otherwise qualified, the term embolus implies thromboembolism
20
Q
What are examples of rare/less common forms of emboli?
A
Less common / rare forms of emboli include fragments of:
1. Bone or bone marrow
2. Atheromatous debris
3. Droplets of fat
4. Tumour cells
5. Foreign bodies (such as bullets)
6. Bubbles of air or nitrogen
21
Q
What are five different types of embolism?
A
- Pulmonary embolism
- Systemic embolism
- Amniotic fluid embolism
- Air embolism
- Fat embolism
22
Q
What is a pulmonary embolism? Where do the emboli normally come from?
A
Refers to an embolism, usually thrombo-embolism, that travels to the pulmonary arteries
Occlusion of a large or medium-sized pulmonary artery is almost always embolic in origin until proved otherwise
Most (95%) of pulmonary emboli arise in thrombi within the large deep veins of the lower leg - next most common pelvic veins
23
Q
What effect does an emboli in the main pulmonary artery or a saddle embolus have?
A
Emboli lodged in the main pulmonary artery or at the birfurcation point - associated with instance collapse and sudden death
Their effect is to cause circulatory obstruction
Saddle embolus shown in the picture
24
Q
What effect can medium and smaller emboli have?
A
Smaller emboli can travel out into the more peripheral pulmonary arteries
- If these are of intermediate size they may cause pulmonary infarction - deprive downstream tissues (particularly the case in patients with cardiac failure - normally bronchial artery supply can often sustain the lung parenchyma)
- If very small and recurrent, they may lead to pulmonary hypertension
In the presence of an inter-atrial or inter-ventricular defect (cross over) they may gain access to the systemic circulation - paradoxical embolism
25
List the complications associated with large, medium and small-sized pulmonary emboli.
26
What are systemic emboli? What are the common causes?
Systemic emboli - refers to emboli that travel through the systemic arterial circulation
- 80-85% arise from thrombi within the heart
- Less common sources include thrombi developing in relation to:
1. Ulcerated atherosclerotic plaques
2. Aortic aneurysms
3. Infective endocarditis
4. Artificial heart valves and aortic grafts
27
What is the main consequence of arterial emboli? What are the major sites where they lodge?
Arterial emboli almost **always cause infarction**
Major sites for systemic emboli to lodge are:
1 Lower extremities (commonest)
2. The brain
3. Viscera (mesenteric, renal, splenic arteries)
4. Upper limbs (much less common)
28
What is the definition of an infarct?
Infarct (Latin: infarcire = to stuff) - area of ischaemic necrosis (lack of oxygen driving tissue/cell death) caused by occlusion of arterial supply or venous drainage in a particular tissue
29
What is the definition of an necrosis?
Necrosis - Refers to a spectrum of morphological changes that follow cell death in living tissue, largely resulting from the progressive action of enzymes on the lethally injured cells
30
What are the causes of infarction?
Thrombosis and thromboembolism account for the vast majority
Other causes include:
1. Vasospasm
2. Expansion of atheroma
3. Compression of a vessel
4. Twisting of the vessels through torsion (eg testis or bowel)
5. Traumatic rupture
31
What factors influence the development of an infarct?
1. Nature of the vascular supply - Single (e.g. spleen) or dual (e.g. lung, small bowel)
2. Rate of development of occlusion - Rapid occlusion more likely to cause infarction
3. Vulnerability of affected tissue to hypoxia - More metabolically active tissues more vulnerable e.g. heart
4. Oxygen content of blood - Hypoxia increases risk
32
What does the histopathology of an infarction look like?
1. Ischaemic coagulative necrosis (minutes - days) - Liquefactive necrosis in the central nervous system
2. Inflammatory response (hours - 7 days)
3. Reparative response (1 - 2 weeks)
4. Scarring (2 weeks - 2 months)
33
Can a lack of venous drainage cause an infarction?
Yes, lack of venous drainage – pressure rises – eventually arterial supply can’t get in as the pressure is too high
34
What are three requirements that are required for the coagulation cascade?
Require phospholipid surface, calcium present and optimal temperature
Note - coagulation cascade is driven by large enzyme macro-molecular complexes
1. Extrinsic tenase
2. Intrinsic Tenase
3. Prothrombinase
35
What is the haemostatic balance?
Physiological balance between bleeding and clotting – repair small little damages (occurs constantly) and bleeding
Can't have too little or too much clotting - finely tuned system
36
What is the epidemiology of Venous Thromboembolism (VTE)?
Common – incidence 1 per 1000
May present as as sudden death - pulmonary embolism
30% of patients develop recurrent venous thrombosis after a primary incidence of VTE
28% develop post thrombotic syndrome – longer term consequences not only acute (death)
Mortality of promptly diagnosed and adequately
treated pulmonary embolism (PE) is 2%
**A major international health problem** - 5x the number of deaths compared to the number of ALL hospital acquired infections
37
What are the risk factors of venous thromboembolism?
1. Age – increased risk with age
2. Obesity – 2-3 fold increase in obese patients
3. Varicose veins
4. Previous VTE
5. Family history of VTE
6. Thrombophilia – heritable factors for thrombosis
7. Cancer – ovarian and lung cancers
8. Other thrombotic states - Heart failure, infarction, stroke, etc.
9. Hormone therapy
10. Pregnancy
11. Immobility – travel, hospitalization, etc.
38
Is venous thromboembolism frequently unrecognised?
Yes - 80% of DVT are clinically silent - mainly times they are only found when people present with a PE
39
What are the different types of venous thrombosis?
1. Deep venous thrombosis (DVT)
2. Pulmonary embolus (PE)
3. Cerebral, mesenteric, axillary, splanchnic, splenic
Any vein can get a thrombosis – however, the distribution/incidence varies – e.g. rare in renal veins or upper limb
40
What are the clinical features of lower limb DVT?
41
How do clinicians predict the liklihood that a patient has a DVT?
Well’s pre-test probability (clinical likelihood) of DVT
Well's Scores - Stratifies patients into low-, intermediate- or high-probability categories
Online survey
42
What types of clinical investigations are used to investigate potential DVT?
1. Use of D-dimer (breakdown product of fibrinogen/fibrin) as a negative predictor of venous thromboembolism - indicates that there are elevated levels of clot formation
If D-dimer is negative it strongly indicates that there is no DVT but a positive D-dimer is indicative but not absolute - **used to rule out DVT**
2. Venous ultrasonography – gold standard
- Higher sensitivity and specificity for proximal DVTs - less sensitive for leg/calf DVTS
3. Contrast venography - Very rarely performed
43
What are the clinical features of a pulmonary embolism?
44
What investigations are performed to diagnose a pulmonary embolism?
1. X-ray is used to exclude other diagnoses – doesn’t diagnose PE directly
2. Main types of imaging
a) V/Q scan
b) CT-pulmonary angiogram (gold standard)
3. Heart strain suspected – Echocardiogram
45
What is the principle behind the venous thromboembolism (VTE) treatment?
1. **Rapid initial anticoagulation**
a) parenteral anticoagulant: heparin, low molecular weight heparin, fondaparinux,
OR
b) direct oral anticoagulant (DOAC)
Aim: to reduce the risk of thrombus extension and fatal pulmonary embolism - stop thrombus expanding and spread (does not dissolve clot)
2. **Extended therapy**
a) Orally active anticoagulant : vitamin K antagonist
OR
b) Direct oral anticoagulant
Aim: to prevent recurrent thrombosis and chronic complications such as post-phlebitic syndrome - treat with an active anticoagulant – prevent recurrent thrombosis and chronic complications
Normally use Low MW heparin or direct oral anticoagulant
46
What is the main drug used to treat VTEs?
Direct Oral Anticoagulants (DOACs)
- Dabigatran, Rivaroxaban, Edoxaban & Apixaban licensed in UK for treatment of acute DVT
- Different drugs with different actions - inhibit Xa or thrombin - all inhibit coagulation cascade
- Enables rapid initial anticoagulation orally
- Then continue a maintenance dose for 6 months, or longer for secondary prevention of VTE
Note - When using apixaban and rivaroxaban you do not need any overlap with heparin – big advantage in outpatient setting
47
What was the traditional management of VTE like?
Give LMWH or UFH (heparin) for aminimum of 5 days if uncomplicated thrombosis; or for 7 days or longer if extensive disease
**and**
Start warfarin therapy on day 1
Note - Warfarin is still used in specific circumstances – very obese patients or patients with allergies to other blood thinners - just harder to control/not a very solid safety profile
48
Apart from drug treatments, what else do you need to do if someone has a VTE?
Investigation of a procoagulant tendency
1. Full Blood Count
2. Antithrombin
3. Protein C
4. Free protein S
5. Antiphospholipid antibodies and lupus anticoagulant
6. Thrombin time/reptilase time to investigate fibrinogen function
7. Genetic tests - Factor V leiden, Prothrombin 20210A genetic tests, JAK-2 mutation
Note - Don’t need to look at all these things – but for example in young patients with DVT it may be useful to understand the underlying cause
49
Who should be tested for thrombophilia?
1. Venous thrombosis < 45yrs
2. Recurrent venous thrombosis
3. Family history of unprovoked thrombosis
4. Combined arterial and venous thrombosis
5. Venous thrombosis at an unusual site
50
What clotting factors are typically targetted by drugs?
Many different targets but factor Xa is the main target more many drugs
51
What are the two types of heparins used to treat VTE? How do they work?
Heparins
1. Unfractionated
2. Low-molecular weight heparin
Binds to unique pentasaccharide on antithrombin and potentiates its inhibitory action towards factor Xa and thrombin
52
What is the problem associated with unfractionated heparin?
Unpredictable anticoagulant response due to binding to plasma proteins
Monitoring required by activated partial thromboplastin time (APTT)
53
Compare and constrast the use of UFH and LMWH in VTE treatment.
UFH - used when there is a high risk of bleeding - can be reversed
Note - LMWH due to the reduction in chain length there is reduced capacity to inhibit thrombin compared with UFH.
UFH - short half life + can be reversed using protamine
54
What anticoagulant treatment can be used in preganant women?
Low Molecular Weight Heparin (LMWH) - Only anticoagulant that can be used in pregnant women – does not cross the placental barrier
55
How do courmarins (e.g. warfarin) function? What should be consider when administering?
Inhibit vit K dependent carboxylation of factors II, VII, IX and X in the liver - Causes a relative deficiency of these coagulation factors
Makes the blood less pro-thrombotic
Reversible by administering Vit K
Needs monitoring using the prothrombin time and international normalized ratio (INR) – measuring the effect of warfarin and establish maintenance dose (specific to each individual) – aiming a ratio of 2-3 (relative to non-warfarin use at 1)
Dietary intake of vit K also affects warfarin dose
56
Considerations and side-effects when using warfarin?
- Many drug interactions
- Requires monitoring at least monthly or more
- Most common serious side-effect: bleeding
a) Major bleeding occurs in 1% of patients each year
b) Risk of fatal intracranial haemorrhage 0.25% per annum
57
How is warfarin activity reversed?
1. Vitamin K – oral or intravenous routes
or
2. Can also reverse warfarin by administering the deficient clotting factors - Tendency to use factor concentrate (factor II, VII, IX and X)
58
What are the benefits of using DOACs over warfarin?
Benefits over warfarin:
1. MORE PREDICTABLE ANTICOAGULANT PROFILE
2. FEWER DRUG AND FOOD INTERACTIONS
3. WIDER THERAPEUTIC WINDOW COMPARED TO WARFARIN
4. ORAL ADMINISTRATION
5. NO NEED FOR MONITORING
6. SIMPLE DOSING
59
Are reversal agents available for DOACs? If not, what should be done?
Some antidotes have been developed - e.g. for dabigatran and Apixaban + Rivaroxaban
For all DOACs - basic measures:
1. Determine how long since last dose
2. Start standard resuscitation measures
3. If there is moderate to severe bleeding use...
a) Local measures
b) Fluid replacement
c) Consider fresh frozen plasma or platelets
d) Antifibrinolytic inhibitors
60
What is the reversal agent/antidote for dabigatran called?
Idarucizumab - antibody
- Binding affinity ~350 times higher than dabigatran to thrombin
- Binds to free and thrombin-bound dabigatran to neutralise activity
- No intrinsic procoagulant or anticoagulant activity
a) iv dosing by bolus or rapid infusion
b) immediate onset of action
c) Proven efficacy in clinical trials
61
What is the reversal agent/antidote for Apixaban and Rivaroxaban called?
Andexanet alfa - Recombinant human factor Xa “decoy protein” so more actual factor Xa is unaffected - Reverses the inhibition of fXa
Just starting to be used in NHS Scotland to reverse the factor Xa inhibitors, Apixaban and Rivaroxaban
62
What mechanical methods are available to prevent venous thrombosis?
Mechanical:
1. Mechanical foot pumps
2. Graduated compression stockings - TED stocking – properly applied – aid the venous return to the heart
63
Summary of the treatments used to treat venous thrombosis?
64
What are the two circulations in the body? Can both suffer from hypertension?
Two circulations
Pulmonary - low pressure circulation
Systemic - high pressure circulation
Hypertension can occur in either or both circulations
65
Does cardiac output or peripheral resistance have a larger impact on blood pressure?
Blood pressure (BP) = Cardiac output (CO) x Peripheral resistance (PR)
Blood pressure is more modulated by peripheral resistance
66
What is the definition of systemic hypertension? What are the two different classifications?
Definition
- Sustained resting blood pressure above certain level
- Usually >= 140/90 mmHg (but depends!)
- Diastolic pressure determines severity
Classification
1. Primary vs secondary (based on cause)
2. Benign vs malignant (based on clinical presentation)
67
What is more common, primary or secondary hypertension?
Classification by cause:
1. ~ 90% primary (essential) - most common - cause is unknown
2. ~ 10% secondary - less common
~ 90% due to renal disease
~ 10% due to other causes especially endocrine disease
68
What are the risk factors for primary systemic hypertension?
Idiopathic (unknown)
Risk factors:
1. Genetic susceptibility
2. High salt intake
3. Chronic stress (excessive sympathetic activity)
4. Abnormalities in renin/angiotensin-aldosterone
5. Obesity
6. Diabetes mellitus
69
What are the main causes of secondary hypertension?
**Renal disease**
- Chronic renal failure
- Renal artery stenosis
- Polycystic kidneys
**Endocrine causes**
- Pituitary – increasing ACTH
- Adrenal cortex - glucocorticoid excess (Cushing syndrome) or mineralocorticoid excess (primary hyperaldosteronism)
- Adrenal medulla - catecholamines (e.g phaeochromocytoma)
**Drug treatment** - e.g. steroids
70
What organs are typically effected by hypertension?
1. Heart - risk factors for coronary artery disease, peripheral vascular disease, cerebral vascular disease, cardiac hypertrophy and cardiac failure
2. Kidney - renal failure
3. Brain
4. Blood vessels
71
Outline the impacts that hypertension has on the heart?
1. Left ventricular hypertrophy - increase mass predicts excess cardiac mortality, predisposes people to chronic heart failure and is associated with sudden death (arrythmias)
2. Fibrosis - increased scarring
3. Contribute to the patogenesis of coronary artery atheroma and ischaemic heart disease
72
Outline the impacts that hypertension has on the kidney?
1. Cause **nephrosclerosis** (loss of nephrons)
- Hypertension causes hardening of arteries (hyaline arteriosclerosis) which in turn drives loss of nephrons - downstream ischaemia
- Proteinuria - loss of proteins
- Chronic renal failure
2. Rapid rises in blood pressure can be associated with **acute renal failure** (‘malignant’ hypertension)
73
What is the defintion/critieria for pulmonary hypertension? Is it normally primary or secondary?
The pulmonary circulation is low resistance and pulmonary BP is about 1/8th of systemic BP
Pulmonary hypertension is considered to be present if the mean pulmonary pressure reaches ¼ of systemic BP
PH is usually secondary to cardio-pulmonary
conditions that increase pulmonary blood flow and/or vascular resistance or increase left-sided heart resistance to blood flow - COPD, recurrent thrombo emoli, auto-immune disorders
Primary/Idiopathic PH is rare
74
What are the longer term consequences of
pulmonary hypertension?
Pulmonary hypertension can result in right ventricular hypertrophy, right ventricular
dilatation, and right ventricular failure
Pure RVF is termed cor pulmonale
75
What is the definition of Ischaemic Heart Disease (IHD)?
IHD - When the blood supply to the myocardium is insufficient to meet its metabolic demands - i.e. there is an imbalance between supply (perfusion) and the metabolic / functional requirements; this results in ischaemia
76
What are the causes of decreased supply and increase demand in IHD?
1. **Deficient supply**
- Coronary artery disease (commonest; 90% of cases and due to atherosclerosis)
- Reduced coronary artery perfusion
- Shock – hypovolaemia
- Severe aortic valve stenosis
2. **Excessive demand**
- Pressure overload: e.g. hypertension, valve disease
- Volume overload: e.g. valve disease
77
Definition of coronary artery disease?
Reduction in blood supply to the myocardium, resulting in a mismatch between myocardial oxygen supply and demand.
Usually caused by atherosclerosis
78
How does the body respond to coronary artery disease?
1. Initial response to luminal narrowing of the artery is auto-regulatory compensatory vasodilatation
However, when occlusion reaches >75% patients present with symptomatic ischaemia (initially e.g. on exercise), while a 90% occlusion can lead to such inadequate blood flow that there may be symptoms at rest.
2. Ischaemia can stimulate the development of collateral circulation - natural by-pass blood vessels that grow around the occluded blood vessel
79
What are three drivers/causes of cornary artery disease?
1. Atheroma-related coronary artery disease (by far the most common) - atherosclerosis - results in...
- Progressive stenosis
- Haemorrhage into a plaque
- Thrombosis
- These may cause ‘acute coronary syndromes’ (angina, acute MI and sudden death)
2. Emboli e.g. from inflamed aortic valve (endocarditis) - emboli can also arise (i.e. from aortic valve) and lodge into coronary artery
3. Vasculitis - auto-immune disorders
80
What is the defintion of myocardial infarction?
Myocardial Infarction - An area of **necrosis** of heart muscle resulting from reduction (usually sudden) in the coronary artery blood supply (primarily an ‘end-artery’)
Due to...
1. Coronary artery thrombosis
2. Haemorrhage into a coronary plaque
3. Increase in demand in the presence of ischaemia
81
What is the characteristic MI symptom? How is it diagnosed?
Clinical features - Central, ‘crushing’ chest pain
Diagnosis
1. Clinical history
2. ECG changes
3. Blood markers
- enzymes e.g. creatine kinase
- other proteins e.g. troponin
82
What are some complications associated with acute MI?
1. Sudden death
2. Dysrhythmias
3. Persistent pain - necrosis
4. Angina
5. Cardiac failure - ventricular dysfunction/dysrhythmias
6. Mitral incompetence - papillary muscles dysfunction/necrosis
7. Pericarditis
8. Cardiac rupture - weakend wall by necrosis
9. Mural thrombosis - abnormal endothelial surface
10. Ventricular aneurysm - stretching of newly formed scar tissue
83
What happens when there is chronic Ischaemic Heart Disease?
1. Chronic angina - Exercise-induced chest pain
2. Heart failure - Related to reduced myocardial function
3. Usually widespread coronary artery atheroma
4. Areas of fibrosis often present in the myocardium
84
What is cardiac failure?
Failure of the heart to pump sufficient blood to satisfy metabolic demands (hypoperfusion) and /or accommodate systemic venous return - body's demands
Leads to under-perfusion, fluid retention and increased blood volume
Two different, but linked, circulations
1. Systemic
2. Pulmonary
85
What are acute, chronic acute-on-chronic heart failure?
**Acute heart failure** - Rapid onset of symptoms, often with definable cause e.g. myocardial infarction
**Chronic heart failure** - Slow onset of symptoms, associated with, for example, ischaemic heart disease or valvular heart disease
**Acute-on-chronic heart failure** - Chronic failure becomes decompensated by an acute event
86
What classifications of hearts failure by location?
1. Left ventricular failure
2. Right ventricular failure
3. Congestive cardiac failure - Failure of both ventricles
87
What are systolic and diastolic failure (heart failure)?
**Systolic failure**
Impaired ventricular contraction and ejection – this is seen in 70% but most patients systolic failure will also have some diastolic dysfunction
**Diastolic failure**
Impaired relaxation and ventricular filling
88
What are the three general causes of heart failure?
**Pressure overload**
Hypertension (pulmonary or systemic) - leads to hypertophy - impairs normal heart function
Valve disease e.g. aortic stenosis
**Volume overload**
Valve disease e.g. aortic incompetence
**Intrinsic cardiac disease**
Ischaemic heart disease
Primary heart muscle disease
Myocarditis
Pericardial disease
Conducting system disorders
Note - actual heart failure may be a combination
89
What are the causes of left ventricular heart failure? What this typically result in?
Usually this is caused by...
1. Ischaemic heart disease
2. Hypertension
3. Aortic valve disease
4. Mitral valve disease
Results in...
1. Reduced peripheral blood flow - hypoperfusion
2. Pulmonary congestion, oedema and righ ventricular failure - back congestion from left side of the heart (traffic), resulting increased pressure in lung capillaries resulting in oedema. Back pressure will eventually lead to right sided heart failure.
90
What compensatory mechanisms are there in response to left ventricular failure?
1. Increasing the cardiac output via the Frank-Starling mechanism - increased end diastolic volume resulting in increased myocardial stretch - resulting in increased stroke volume and cardiac output
2. Ventricular remodelling to increase ventricular volume and wall thickness - initially beneficial - eventually, if untreated, leads to functional delcine.
91
What are the most common causes of right ventricular failure?
Common causes
1. Secondary to left ventricular failure (most common)
2. Related to intrinsic lung disease – ‘cor’ pulmonale
e.g. chronic obstructive pulmonary disease (COPD)
92
What are the clinical features of heart failure?
**Forward failure**
1. Reduced perfusion of tissues
2. Tends to be more associated with advanced failure
**Backward failure**
1. Due to increased venous pressures
2. Dominated by fluid retention and tissue congestion
a) Pulmonary oedema (left ventricular failure)
b) Hepatic congestion and ankle oedema (right ventricular failure)
93
How does left and right ventricular failure normally present?
94
If the cardiac SA node cells naturally fire at 80-90bpm, why are normal heart normally slower?
Cardiac SA cells – spontaneously fire – around 80-90bpm
Node – effected by para- (vagus nerve – slow heart down) and sympathetic (adrenaline/noradrenaline –speed up) neurons
Hence, the NS brings down the activity of the heart
95
In healthy people, what is the only electrical connection between the ventricles and atria?
Only connection in health between atria and ventricles – AV node – introduces time delay – ensures that ventricles have time to fill
Bundle of his, bundle branches and purkinje – conduct quickly – allow for a synchronous/rapid contraction
96
What do the Q, R and S wave in the QRS complex represent? What does the PR interval represent?
Q wave – activation of the intra-ventricular septum – from left to right
R wave – Depolarization from the base to the apex of the heart
S – wave – activation going up the walls of the left and right ventricles
PR interval – length of time between sinus node firing and AV node firing – something wrong with AV node – results in increase PR interval
97
What is a respiratory sinus arrythmia?
Sinus arrythmia - Sinus node fires at a variable rate
Normal physiological change – during inspiration there is an increase in volume of thorax as well as the heart – resulting in decrease pressure – resulting in more blood being drawn in - autonomic nervous system responds by increasing heart rate
Hence, this results in fluctuations between inspiration and expirations
a) Speeds up during inspiration
b) Slow down during expiration
This effect is mediated by changes in parasympathetic activity (vagus nerve)
98
What is sinus tachycardia? What are the physiological and pathological causes?
Sinus node fires > 100 per minute
Physiological causes:
anxiety, exercise
Pathological causes:
fever, anemia, hyperthyroidism, heart failure
shock (sepsis, bleeding, anaphylaxis)
almost any acute medical emergency
99
What is sinus bradycardia? What are the physiological and pathological causes?
Sinus node fires < 60 per minute
Physiological causes:
1. Sleep
2. Athletic training
Pathological causes:
1. Hypothyroidism
2. Hypothermia
3. Sinus node disease
4. Raised intracranial pressure - presses on brain stem - drives parasympathetic activity
many others
100
What is sino-atrial disease? What is is physiologically characterised by? What types of ECGs can it produces?
A degenerative condition affecting the atria, including the sinoatrial (SA) and atrioventricular (AV) nodes
Characterised by patchy atrial fibrosis, atrial dilatation and altered conduction
Common in individuals age > 70 years
101
What is the treatment for SA-node disease?
1. Permanent pacemaker to prevent slow rhythms
2. Antiarrhythmic drugs to prevent or moderate rapid rhythms – decreased excitability
a) beta blocker
b) digoxin
c) amiodarone
102
What is 1st degree AV nodal block?
Consistent delay in PR interval (more than 1 large square) – 1st degree AV nodal block – usually symptomless
103
What are the two types of second degree AV nodal block?
Grade 2 AV nodal block
Mobitz type 1 – increasing PR interval leading to a skipped beat – due to disease of AV node
Mobitz type 2 – normal rhythm followed by sudden QRS drop (can be multiple) – indicates bundle of his bundle block – more serious – long pauses and blackouts
104
What is grade three AV nodal block?
Grade 3 AV nodal block/Complete heart block
Complete dissociation between atrial and ventricular rhythm (different rhythms)
P wave appears randomly (can be superimposed)
QRS complexes – broad and abnormal – indicating that the ventricles are activating spontaneously
105
What are the causes of AV-nodal block?
Anything that damages and inteferes with the AV node.
106
What are the treatments for AV nodal block?
1. Remove any triggering cause (e.g. drugs)
2. IV atropine or isoprenaline (acute treatment) – stimulates and blocks parasympathetic
3. Permanent pacemaker
107
What does the following ECG show?
Atrial fibrillation
Irregular and rapid atrial activity with normal/narrow QRS complexes
108
What does the following ECG show?
Atrial flutter
Saw-tooth pattern – regular and rapid activity
Normal/narrow QRS complexes
109
What can a narrow and broad QRS complex tell us?
Normal/narrows QRS – less than 3 small squares
1. Rhythms driving from the atria – narrow QRS complexes
2. Rhythms originating from the ventricles – broader QRS complexes
110
What are the causes of atrial fibrillation and flutter?
Both atrial flutter and fibrillation cause similar symptoms
111
What are the treatments for atrial fibrillation/flutter?
112
What does the following ECG show?
Ventricular tachycardia – broad QRS, absence of P waves, abnormal axis for QRS, fast heart rate – common in patients with a previous MI/scarring in the heart
Note ST segment is elevated but in a broad QRS we can’t interpret the ST segment
113
What does the following ECG show?
Ventricular fibrillation
No organized P waves and no organized QRS complexes – cardiac arrest
114
What are the treatments for ventricular fibrillation?
