Cardiovascular Flashcards
(164 cards)
1
Q
What is haemostasis
A
A physiological process which is initiated when there is damage to a blood vessel. It involves the rapid formation of a solid plug at the site of injury.
It is protective and stops loss of blood from the circulation.
2
Q
What are the constituents of a haemostatic plug
A
Platelets, fibrin and RBCs
3
Q
Explain the process of haemostasis
A
(1) Endothelial injury leads to adhesion and aggregation of platelets.
(2) Platelets adhere to collagen by vWF and RBCs become enmeshed with the platelets, resulting in the formation of a lose platelet plug
(3) At the same time, exposure of tissue factor initiates the coagulation cascade = formation of fibrin
Fibrin stablises the loose platelet plug
4
Q
What is the role of the fibrinolytic system
A
It ensures that the haemostatic plug does not become too big- limits it to the site of injury.
Endothelial injury also initiates fibrinolysis (as well as haemostasis) and it results in plasmin formation - which breaks down fibrin to soluble products.
5
Q
What is thrombosis
A
This occurs when there is an inappropriate (ie. pathological) activation of haemostasis which overwhelms the capacity of the fibrinolytic system, resulting in the formation of a solid plug = thrombus.
6
Q
What are the constituents of a thrombus
A
The same as a haemostatic plug - platelets, fibrin and RBCs
7
Q
What is a clot composed of
A
RBCs and fibrin (no platelets)
8
Q
Explain the difference between clots and thrombi
A
(1) Composition Thrombus = RBC, fibrin, platelets Clot = RBC, fibrin (2) Location T = forms within the CVS C = forms outside the CVS (3) Blood T = forms in flowing blood (life) C = forms in stationary blood (during/after life)
9
Q
What are the 3 components of Virchow’s triad
A
3 predisposing factors to thrombus formation
(1) Endothelial injury
(2) Abnormal blood flow
(3) Hyper-coagulability
10
Q
What can cause endothelial injury
A
- Atherosclerosis
- Vasculitis
- Direct Trauma = heat / chemical injury
11
Q
What can cause abnormal blood flow
A
Turbulence:
- Atherosclerosis
- Artificial valves, stents
Stasis:
- Post-op / trauma
- Congestive cardiac failure
- Immobility
- Pelvic obstruction (mass)
- Aneurysms
12
Q
What can cause hypercoagulability
A
Too many blood cells: - Erythrocytosis - Thrombocytosis Coagulation factor defects: - Hereditary = factor V Leiden, protein C/S deficiency - Acquired = OCP, malignancy, pregnancy
13
Q
What is the most important risk factor for thrombosis in an artery
A
Atherosclerosis (results in endothelial injury and turbulence)
14
Q
What is the most important risk factor for thrombosis in a vein
A
Stasis and hyper-coagulability
15
Q
List 3 main ways in which thrombi can cause disease
A
- Partial occlusion of the vessel at the site of thombosis
- Complete occlusion at the site of thrombosis
- Embolism to distant site
16
Q
What are the complications of thrombosis
A
Partial or complete occlusion results in ischaemia - can progress to infarction.
17
Q
What is embolism
A
The occlusion of a vessel by undissolved material that is transported in the blood stream.
(In clinical practice most emboli are thromboemboli)
18
Q
List the types of emboli
A
- Thrombi
- Fat/bone marrow
- Air
- Amniotic fluid
- Tumour
- Septic emboli (eg. infective endocarditis)
- Atheromatous debris
19
Q
Where will emboli originating in the venous system occlude
A
A pulmonary artery
Symptoms and signs include swollen calf; PE - results in a pulmonary infarct
20
Q
Where will emboli originating in the arterial system occlude
A
A systemic artery e.g. mesenteric artery, cerebral artery, renal artery
21
Q
What is atherosclerotic plaque stability determined by
A
The balance between:
(A) inflammatory cells = destabilise by making MMPs that digest the fibrous cap
Can also cause the SMC in the intima to under go apoptosis
(B) smooth muscle cells = protective as they produce the fibrous cap stabilising the plaque
Also make TIMPs which inhibit MMPs
22
Q
What are the features of a stable atherosclerotic plaque
A
- contains few inflammatory cells and large numbers of SMCs
- thick fibrous cap which is resistant to rupture
- grow slowly = gradual stenosis
23
Q
What are the features of an unstable ‘vulnerable’ plaque?
A
- inflammatory cells (foam cells) > smooth muscle cells
- Thinner fibrous cap, which is more prone to rupture = may result in thrombosis/embolism
24
Q
List 3 main mechanisms by which atherosclerosis causes disease
A
(1) Gradual enlargement of a stable plaque leading to luminal stenosis and reduced blood flow through the artery
(2) Sudden rupture of a vulnerable plaque
(3) Aneurysm formation
25
What is Poiseuille's law
Flow is proportional to the radius to the power of 4
26
How does rupture of an atherosclerotic plaque result in formation of a thrombus
The rupture results in the exposure of tissue factor and other pro-thrombotic substances. As a consequence a thrombus forms over the site of the rupture - can cause occlusion at the site / embolism to a distant site
27
What is ischaemic heart disease
The term used to describe the spectrum of heart disease which results from coronary artery atherosclerosis. It includes stable angina, ACS and sudden cardiac death.
28
Why is ischaemic heart disease dangerous
The atherosclerosis causes gradual or complete occlusion of one or more coronary arteries = reduction in blood flow to the myocardium = mismatch between supply and demand of oxygen to the myocardium - resulting in ischaemia.
29
What is angina
NB: It is a syndrome not a disease.
It occurs when there is imbalance between supply and demand of oxygen to the myocardium - resulting in myocardial ischaemia, which presents as cardiac-type pain
30
How does stable angina present clinically
Predictable cardiac-type pain.
| Precipitated by exertion, lasts for 1-2 minutes and is relived by GTN.
31
What is the most common cause of stable angina
A stable but gradually enlarging atherosclerotic plaque in a coronary artery causing gradually progressive stenosis - which itself gradually reduces blood flow through the artery
32
What are acute coronary syndromes
A spectrum of diseases which occur when there is a sudden and severe reduction in myocardial perfusion - essentially a sudden change in a coronary artery atherosclerotic plaque.
Leads to ischaemia and/or infarction.
33
List the most common progression of events leading to ACS
(1) Sudden rupture of a vulnerable atherosclerotic plaque with superimposed thrombosis
(2) Sudden partial or complete occlusion of the coronary artery
(3) ACS
34
What does troponin detect
Myocardial necrosis.
Levels rise following myocardial injury - peaking at 24 hours
35
List the different forms of ACS
- Unstable angina (partial occlusion by a thrombus)
- NSTEMI (partial occlusion by a thrombus leading to a zone of necrosis)
- STEMI (complete occlusion by a thrombus leading to a zone of necrosis)
36
How would you differentiate between the forms of ACS
Unstable angina = No ST elevation, troponin -ve
NSTEMI = No ST elevation, troponin +ve
STEMI = ST elevation, troponin +ve
37
How do you determine the management of STEMI and what does the management consist of
- PCI if pt presents <12h of onset AND primary PCI can be delivered within 120 minutes
- Fibrinolytic treatment/thrombolysis (alteplase) - pts presenting within 12 hours when primary PCI cannot be delivered in 120 minutes
38
Management of NSTEMI and unstable angina
| note these are managed the same as the troponin will not rise until later; often a retrospective diagnosis
- Coronary angiography with follow-on PCI within 96h if GRACE score shows risk of cardiovascular events as imtermediate to high
- patients who are clinically unstable are offered angiography as soon as possible
39
Describe the body's response to MI
0-12h = Not visible; Myocyte necrosis
12 - 72h = Pale (<24h) --> Soft and pale (<72); Necrosis induces an acute inflammatory response - the neutrophils infiltrate between dead cardiac muscle
3-10 days = hyperaemic border; repair of the infarct - organisation
weeks - months = White scar; secondly progressive scar tissue deposition
40
How would an inferior MI be detected on ECG
ECG: leads II, III, aVF
41
How would a lateral MI be detected on ECG
ECG: leads I, aVL, V5-6
42
How would an anterior MI be detected on ECG
ECG: leads V1-4
43
Which artery is affected in an inferior MI
Right coronary artery
44
Which artery is affected in a lateral MI
Left circumflex artery
45
Which artery is affected in an anterior MI
Left anterior descending artery
46
Why do we worry about inferior MIs
Affects the RCA. Supplies the RA, RV, inferior LV and the pacemaker!
Worrying because it can affect the SAN
47
List short term complications of MIs
- Ventricular fibrillation (causes sudden death)
- Other arrythmias
- Acute Cardiac Failure / cardiogenic shock
- Myocardium Rupture
- Pericarditis
- Mural Thrombus (may embolise)
48
List long term complications of MIs
- Recurrent MI
- Chronic congestic cardiac failure (loss of contractile myocardium)
- Dressler's Syndrome
- Ventricular aneurysm formation, which predisposes to: congestive cardiac failure, arrythmia, thrombus formation within the aneurysm (due to stasis) which may embolise
49
How does an MI result in acute cardiac failure
The infarcted myocardium no longer contracts and this may cause heart failure - or if a significant proportion of the myocardium is affected may lead to cardiogenic shock
Relates to the size of the infarct - usually >45% of the LV mass
50
Myocardium rupture is a consequence of MI, but what are the consequences of myocardium rupture
(1) Cardiac tamponade - rupture of the free wall
(2) acute LVF - rupture of the papillary muscle, causing acute mitral regurg (heart can't compensate)
(3) Acute heart failure - rupture of the interventricular septum causing an acute ventricular-septal defect
51
Why does an MI predispose to the formation of a thrombus
A mural thrombus can form because there is:
- endothelial injury (transmural infarct extends to involve the endothelium causing damage to the endothelium)
- stasis (the infarcted myocardium does not contract and so there is an akinetic zone)
52
What is Dressler's syndrome
A self-limiting autoimmune pericarditis 2-10 months after full-thickness MI.
In the era of PCI it is uncommon.
53
What is a reperfusion injury
Following PCI/thrombolysis.
The process of reperfusion may damage some myocytes that were not already dead when reflow occurred.
It is due to toxic oxygen species which are overproduced on restoration of the blood supply
54
What is chronic ischaemic heart disease
There is decreased perfusion to the myocardium as a result of a stable plaque = ischaemia = over a long time the contractile myocardial tissue is replaced by non-contractile scar tissue (progressive fine diffuse myocardial fibrosis)
55
How does chronic ischaemic heart disease present
Often asymptomatic as the remaining myocardium can compensate (LVH)
However they will eventually decompensate and there will be onset of progressive chronic heart failure
56
Define an ischaemic stroke
A sudden occlusion of a cerebral artery leading to a sudden reduction in blood flow to part of the brain = infarction of brain tissue
57
What is the most common cause of ischaemic stroke
Rupture of an atherosclerotic plaque in an internal carotid artery - a thrombus then forms on the surface of the ruptured plaque and part of the thrombus embolises and occludes a cerebral artery
58
Why are patients with AF at increased risk of ischaemic stroke
Stasis within the (left) atrium as a result to fibrillation (virchow's triad) and this can result in a thrombus which may embolise to occlude a cerebal artery
Pts are anticoagulated to prevent this
59
Why are patients with infective endocarditis at increased risk of ischaemic stroke
Vegetations are present on the mitral or aortic valve - these can embolise and occlude a cerebral artery
60
Define an aneurysm
A localised, permanent, abnormal dilatation of a blood vessel by greater than at least 50% of its normal diameter
61
How can you classify aneurysms
- Saccular = spherical shape, bulges out of side of vessel
- Fusiform = Spindle shape, involvinf all the circumference of the vessel
- False = an expanding pulsatile haematoma in continuity with a vessel lumen; it is not lined by endothelium
62
What is the clinical definition of an aortic aneurysm
Aortic diameter of >3cm
63
What are the main risk factors for atherosclerosis
- Smoking
- Dyslipidaemia
- Hypertension
- DM
- FHx
- Male
64
How does atherosclerosis result in development of an aneurysm
The aorta gets its strength from the media (smooth muscle layer)
enlarging atherosclerotic plaque = pressure/ischaemic atrophy of the media and loss of elastic tissue. As a consequence the aortic wall is weakened and it may dilate, forming an aneurysm, which over time will grow in size.
65
Causes of AAA
- Atherosclerosis
- Marfan
- Ehler Danlos
66
What are complications of AAA
- Rupture (as the radius increases so does the tension in the wall - Laplace's law)
- Thrombus + embolism
67
Who gets AAA
Men (6:1)
| >65
68
What is the NHS AAA screening programme
Men aged 65
- Small (3 - 4.4) / Medium (4.5-5.4) followed up to see if it grows
- Large (>5.5) referred to a vascular surgeon
69
What is the clinical significance of AAA >5.5cm
Classified as large
| Risk of repair < risk of rupture
70
What is the management of AAA >5.5cm
Open surgery, EVAR or conservative management
71
In the case of pulmonary embolism where do the emboli originate
70-80% - vein in the leg
| 10 - 15% - vein in the pelvis
72
What would be the result of a medium sized PE
Occlusion of a segmental pulmonary artery - V/Q perfusion defect
Results in respiratory compromise - usually manifests as pulmonary infarction.
73
List clinical features of PE
- Pleuritic chest pain
- SOB
- Haemoptysis (due to infarction of the non-perfused lung tissue)
- Pleural rub
- Crackles
- Effusion
74
Explain logistics of VTE prevention
Patients admitted to hospital have a documented VTE assessment.
They should be reassessed within 24hr of admission and whenever the clinical situation changes
75
List examples of VTE prevention offered
- Encourage to mobilise as soon as possible
- Give information about VTE risk on admission and discharge
- Mechanical interventions eg. antiembolism stockings
- Dalteparin
76
What tool assesses clinical likelihood of PE
The Wells criteria
| Likely if >4 but unlikely if <4
77
What is D-dimer
Made from the degradation of fibrin via the action of plasmin.
78
What does a raised D-dimer indicate
```
PE
MI
Post-operatively
Stroke
Trauma
Pregnancy
```
79
What is more useful- a normal or a positive D dimer
Raised D-dimer can be caused by many things - not specific!
Normal is useful as >90% of these patients will not have a PE
80
When should you test for D-dimer
PE is suspected clinically but the Wells score is <4
81
What is the gold standard investigation for suspected PE
CTPA (or V:Q scan if allergy to contrast media or renal impairment)
Involves injecting radio-contrast into the circulation and a CT scan is performed. Blood vessels are filled with blood mixed with contrast so appear white, but a thrombus will appear as a darkened area because it formed before the contrast was administered
82
Pt has a suspected PE and a Wells score of 6 - how do you investigate?
CTPA
83
Pt has a suspected PE and a Wells score of 2- how do you investigate
D-dimer
84
What is hypertension
Raised blood pressure in the systemic vascular bed
>140/90mmHg
85
List causes of hypertension
95% Essential
| 5% Secondary
86
List causes of essential hypertension
Genes - those encoding angiotensinogen, renin and atrial natriuretic peptide receptor genes
Environmental - stress, diet, intrauterine environment (eg. low birth weight)
87
List causes of secondary hypertension
(1) Chronic renal disease- CKD, renal artery stenosis, PKD, acute glomerulonephritis, autoimmune disease
(2) Coarctation of the aorta
(3) Endocrine diseases- Cushing's syndrome, Conn's syndrome, phaeochromocytoma, acromegaly
(4) Drugs- steroids, COCP, NSAIDs
(5) Pregnancy
88
What are the clinical features of hypertension
Clinically silent until a complication occurs
89
What are the effects of hypertension of blood vessels
- Accelerates atherosclerosis
| - Accelerates arteriosclerosis
90
What is arteriosclerosis
Hardening of an artery / arteriole
Two types:
- Hyaline - SMC replaced by collagen
- Hyperplastic - characteristic of malignant hypertension. The very high BP causes fibrinoid necrosis in the vessel wall - tries to heal = proliferation of intimal cells
91
What effect does hypertension have on the heart
- Accelerates coronary artery atherosclerosis (worsens IHD)
| - Left ventricular hypertrophy
92
Why does hypertension lead to LVH
(1) The LV has to push harder against the increased pressure in the systemic circulation in order to eject blood into the aorta.
(2) Therefore the LV undergoes compensatory LVH
(3) As this progresses there is increasing metabolic demands of the myocardium - but the heart is less able to meet these as
(A) hypertrophy renders the myocardium stiff
(B) increasing distance across which O2 has to cross
(C) Accelerated atherosclerosis due to HTN
93
List ways in which hypertensive heart disease may manifest
- Myocardial ischaemia
- Myocardial infarction
- Arrhythmias (eg. AF)
- Progressive left heart failure
94
What is the commonest cause of AF
Hypertension
95
Why is AF dangerous
(1) Thrombi may form in the atria as a consequence of stasis. These thrombi may embolise.
(2) CO may fall due to loss of normal atrial contraction
96
How does hypertension lead to hypertensive renal disease
Progressive hyaline arteriosclerosis in the renal arterioles = chronic, progressive renal ischaemia.
Ischaemia results in development of CKD.
This is a viscous cycle as CKD can in turn worsen the HTN
97
What is the difference between atherosclerosis and arteriosclerosis
```
Arteriosclerosis = a general term describing a hardening of a medium or large artery.
Atherosclerosis = a hardening of an artery specifically due to an atheromatous plaque.
```
98
How would you investigate suspected CKD
USS - shows small kidneys (due to atrophy and fibrosis)
99
What is the most common cause of an intracerebral haemorrhage (note: presents as a haemorrhage stroke)
Hypertension
100
Describe pathophysiology behind a haemorrhagic stroke
Haemorrhage is due to the rupture of Charcot-Bouchard aneurysms - weakened by long-standing HTN
101
Describe pathophysiology of a subarachnoid haemorrhage
Due to rupture of a Berry aneurysm
102
How do berry aneurysms develop
Under the influence of HTN and atherosclerosis in people with a congenital weakness in the media of cerebral vessels.
103
What is malignant hypertension
A markedly raised diastolic blood pressure (>130 - 140) and end organ damage
104
Who does malignant hypertension usually affect
- Usually in cases of secondary HTN
| - Younger people = new cases 30-40y/o
105
What are clinical consequences of malignant hypertension
1) Acute left ventricular failure
2) Stroke (cerebral haemorrhage)
3) Acute renal failure
4) Blurred vision - due to retinal haemorrhage/exudates/papilloedema
5) Hypertensive encephalopathy (headache, irritability, alteration in consciousness)
6) Microangiopathic haemolytic anaemia and DIC
106
What is an aortic dissection
There is a tear in the intima. A split forms in the media and blood tracks in the newly formed "false lumen"
107
How does an aortic dissection present
Classically a tearing pain between the shoulder blades with HTN and asymmetrical pulses
108
What are major risk factors for aortic dissection
- HTN
- Abnormal media (eg. marfans / ehler-danlos)
- Pregnancy
109
How are aortic dissections classified
Type A: Ascending aorta
| Type B: Does not involve the ascending aorta
110
What type of aortic dissection is most dangerous
Type A are more serious
111
How are aortic dissections managed
Type A: immediate surgical repair
| Type B: Medical - rigorous BP control with surgery reserved for if there are complications
112
How do aortic dissections cause disease
False lumen reduces blood flow through the true lumen - this may extend into other arteries and cause ischaemia/infarction of the organ supplied by that artery
Dissection may rupture internally into the pleural cavity, pericardial space or abdominal space
113
What are complications of type A aortic dissections
Can compromise blood flow along branches of the aorta as it spreads along its length.
It may even track back to the root of the aorta and rupture into the pericardium causing cardiac tamponade.
Involves the root fo aorta = aortic regurg
Rupture into thoracic / abdominal cavity = exsanguination
114
What is cardiac tamponade
When fluid in the pericardium builds up and results in compression of the heart.
115
What is the role of the heart valves
Ensure one way flow through the heart
116
What are the 2 main types of mechanical defects in the heart valves
Stenosis - the failure of a valve to open completely (impairs forward flow). Usually as a result of a chronic process.
Regurgitation - failure of a valve to close completely (reverse flow). May be as a result of an acute or chronic process.
117
What is the most common valve disease
Aortic stenosis
Mitral regurg is the 2nd most common
118
List common causes of aortic stenosis
1) Cusp calcification of a bicuspid valve (note that the normal aortic valve is tricuspid, but 1-2% of the population have a bicuspid aortic valve)
2) Age related calcification of a tricuspid valve
3) Post rheumatic fever disease
119
Explain pathophysiology behind aortic stenosis
Blood flow across the aortic valve is impeded during systole. As a consequence a significantly elevated left ventricular pressure is necessary to drive blood into the aorta. As this is a chronic process, the LV hypertrophies to compensate. The hypertrophy reduces compliance = elevation of diastolic LV pressure.
120
Describe clinical presentation of aortic stenosis
A chronic procress with compensatory changes meaning there is a long asymptomatic period.
Eventually, the heart decompensates and presents with the classic triad of:
- Angina
- Syncope on exertion
- Development of congestive cardiac failure
It also is associated with an ejection systolic murmur
121
What is the most likely cause of an ejection systolic murmur
Aortic stenosis
122
List common causes of mitral regurgitation
MITRAL ANNULUS: LV dilatation (secondary stretching of the valve ring such that it cannot close properly)
CUSPS: Mitral valve prolapse; infective endocarditis; post-rheumatic fever
PAPILLARY MUSCLES: Rupture post-MI; ischaemia due to coronary artery atheroma
123
What is the most common cause of acute mitral regurgitation
Sudden onset = infective endocarditis / rupture of papilliary muscle after an MI
124
Explain the pathophysiology of acute mitral regurgitation
Sudden onset - the heart does not have time to undergo compensatory changes.
Blood flows back into the left atrium.
Increased pressure in the LA - and therefore also in the pulmonary system.
Transudation of fluid from the circulation into the lung interstitium and alveoli (pulmonary oedema).
125
What is the most common cause of chronic mitral regurgitation
Dilatation of mitral valve ring, mitral valve prolapse, post-rheumatic fever or papilliary muscle ischaemia.
126
Explain the pathophysiology of chronic mitral regurgitation
Gradual onset = heart has time to undergo compensatory changes.
LA dilates such that it can accomodate the back flow of blood without a substansial increase in LA pressure.
The LV undergoes hypertrophy - mitigates the effects of regurgitation
Asymptomatic for years - eventually LV decompensates and pts progress to left ventricular failure
127
What is the most common cause of mitral valve regurgitation
Mitral valve prolapse
128
Who gets mitral valve prolapse
Women > men
Usually an isolated finding
May be a complication of marfans/ehlers-danlos (genetic disorders of tissue synthesis)
129
What is the pathophysiology behind mitral valve prolapse
The normal dense collagen and elastic matrix of the valve is replaced with loose myxomatous connective tissue containing abundant glycosaminoglycans ('myxomatous degeneration'). The leaflets become enlarged and one of the leaflets 'prolapses' back into the La during systole
130
What is the mortality of infective endocarditis
High
Untreated = 100%
Treated = 10-30%
131
List causes of infective endocarditis
Bacterial (usually)
- streptococcus = S. viridans (weakly pathogenic)
- Staph = staph A (highly pathogenic), most common in IVDUs - usually affects the tricuspid valve.
Other bacteria eg. g-ve = E. Coli
Less commonly, fungi = candida / asperillis. This is more likely in immunocompromised, IVDU, pts with indwelling venous line
132
Describe pathogenesis of infective endocarditis
Episode of bacteriaemia = bacteria delivered to the heart.
(could be due to tooth brushing / surgery)
Organisms adhere to and invade the valve
133
What conditions must be fulfilled in order for an infection of the endocardium to occur
1) Highly pathogenic organism (staph) colonising a normal valve
OR
2) Weakly pathogenic (strep) colonising an abnormal valve - eg. prosthetic / mitral or aortic regurg / mitral valve prolapse
134
What is a vegetation and how do they form in infective endocarditis
A thrombus containing microorganisms.
As the organisms on the valves replicate, they become enmeshed within layers of platelets and fibrin on the valve surface forming vegetations.
135
What components of Virchows triad occur in infective endocarditis
Endothelial injury. if the valve is abnormal, there may be turbulent blood flow across the valve.
136
What are 3 complications of infective endocarditis
1) Disturbance of valve function (valve is destroyed by infection = regurg)
2) Embolism (vegetations can break off and embolise - mostly present as a stroke)
3) Formation of antigen-antibody immune complexes (antibodies made againts the antigen of the infection causing microorganism - can be deposited in the glomeruli = activates complement)
137
How would you confirm a diagnosis of infective endocarditis
- Blood cultures = at least 3 sets of blood cultures from different sites taken a minimum of 1h apart and before starting antibiotics (confirms diagnosis and guides appropriate ABx therapy)
- Transoesophageal echo to identify vegetations and complications
138
What criteria are used to help diagnose infective endocarditis
Duke's (this criteria places heavy emphasis on blood culturs and echo)
139
What is heart failure
A syndrome which occurs when the pumping action of the heart is inadequate for the needs of the body. Ie. the cardiac output is unable to meet the metabolic needs of the tissue
140
What is the mortality of heart failure
30% in first year
| 10% after
141
How can you classify heart failure
Acute / Chronic (depends on speed of onset)
| Left / Right (depends on dominant site of injury)
142
Describe pathophysiology of acute left heart failure
Sudden major insult to the left side of the heart
no time for compensation, CO falls catastrophically
Sudden failure of LV leads to severe congestion in the pulmonary venous system and rapid accumulation of fluid in the alveolar spaces and interstitium. This causes pulmonary oedema and presents as severe SOB. In bad cases there is underperfusion of organs = cardiogenic shock
143
What is acute left heart failure most often caused by
A complication of an MI affecting the LV
- extensive MI renders a large volume of the LV non-functional
- rupture of a mitral valve papilliary muscle
- development of an arrythmia
144
What is the most common form of heart failure
Chronic left heart (ventricular) failure
145
What are the common causes of chronic left heart failure
Damage to the LV slowly:
- chronic ischaemic heart disease (due to coronary artery atherosclerosis)
- systemic HTN
- valvular (mitral/aortic) heart disease
146
What is the relevance of heart disease occurring acute vs chronic
Can help you to determine cause.
Chronic disease means that compensation (hypertrophy) can occur and therefore there will be a period where the patient is asymptomatic, before they decompensate
147
Explain pathophysiology of chronic left ventricular failure
It is a progressive disorder in which a viscious cycle becomes established which escalates cardiac workload and worsens the degree of LVF.
Because poor cardiac output reduces tissue perfusion, the body responds by increasing the SNS - activates RAAS
Sodium and water retention - which leads to more myocardial stress and declining cardiac function
148
Explain what decompensation means in the context of chronic heart failure
Patients may decompensate if the heart is stressed.
Patients with chronic heart failure frequently experience episodes of acute worsening in their symptoms = relapsing-remiting course (acute decompensation) - commonly seen when a concurrent illness (usually trivial) places additional burden on a critically failing heart
149
Chronic left ventricular failure can be split into systolic and diastolic. What is the difference
Systolic: the underlying problem is a failure of the pumping action of the ventricle during systole. The ventricle is usually dilated and fails to contract normally such that the ejection fraction is reduced.
Diastolic: failure of the ventricle to fill due to increased stiffness of the wall
150
How do you investigate chronic left ventricular failure
1) History and Examination
2) ECG (usually abnormal)
3) CXR (cardiomegaly)
4) Echo (to confirm systolic or diastolic dysfunction and see if underlying cause eg. valvular disease)
5) BNP level
151
What is BNP
A hormone secreted by ventricular myocytes in response to volume and pressure overload of the LV. Its normal function is to promote a salt and water diuresis by the kidney.
152
What is the most common cause of right sided heart failure
Left sided heart failure. As the definition for right heart failure is when it develops in the absence of left heart failure, this is not actually right heart failure and is called congestive (biventricular) heart failure
153
What is the most common cause of acute right sided heart failure
A massive pulmonary embolism causing sudden blockage of a major pulmonary bifurcation (saddle embolus)
An MI involving the right ventricle, but sparing the left is another important cause
154
How can a massive PE result in acute right heart failure
Blocks a major pulmonary bifurcation. This causes the pressure in the pulmonary artery system to rise dramatically = development of pulmonary HTN. The heart does not have time to undergo compensation and can't generate enough force to maintain an output
155
How does acute right heart failure present clinically
Circulatory collapse, shock and/or instantaneous death
156
What is pulmonary hypertension
An increase in blood pressure in the pulmonary vasculature. It is defined as a resting mean pulmonary artery pressure at or above 25mmHg
157
What are the clinical features of chronic right heart failure
Raised JVP, hepatomegaly, ascites, peripheral oedema
158
What are the most common causes of chronic right heart failure
```
Lung diseases:
- COPD
- Pulmonary fibrosis
- Recurrent small PEs
The damage to the lungs results in pulmonary HTN, but there is time for compensation to occur.
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What is cor pulmonale
Right heart failure due to lung disease:
- massive PE = acute cor pulmonale
- COPD, pulmonary fibrosis, recurrent small PEs = chronic cor pulmonale
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What is the most common cause of cor pulmonale
COPD
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What is a non-massive PE and how does it present
A medium-sized embolus occludes a segmental pulmonary artery. This results in a segment of lung being ventilated but not perfused ie. V/Q defect = Respiratory compromise, manifests as pulmonary infarction (haemopytsis) +/- pleuritis/effusions
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What is a massive PE and how does it present
A massive embolus occludes a proximal pulmonary artery. Result = blood unable to enter lungs = sudden pulmonary HTN - acute right heart failure. Blood is also unable to pass through the lungs = decreased filling of left side of the heart and therefore decreased left ventricular output. This presents as haemodynamic compromise in the form of shock, collapse and sudden death.
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A patient presents to A+E. They have recently collapsed.
O/E:
- Tachycardia
- Hypotension
- Raised JVP
- RV heave
- Normal chest examination
- Low O2 sats
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What is wrong with them
Haemodynamic compromise due to massive PE
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What are recurrent small PEs and how do they present
Usually subclinical. But will gradually result in pulmonary HTN and can result in chronic right heart failure
