Transcript CV - March 22 - Alex Bradwell and Sam Gaffing

Phase 1A
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Aims
• Describe the main risk factors in cardiovascular disease
• Understand the pathology of atherosclerosis
• Understand the main diseases that affect the CVS
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Branches of the
Aorta
DIAPHRAGM
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Arterial Supply of the
Lower Limb
GROIN
KNEE
ANKLE
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Venous Drainage of the Lower Limb
• DEEP vs. SUPERFICIAL VEINS
• Blood drains from superficial to deep veins via the perforating
veins
• Superficial Veins
– Great Saphenous – runs up medial side of leg and thigh to join the
femoral vein at the saphenous opening
– Short Saphenous – drains postero-lateral aspect of the leg and joins the
popliteal vein behind the knee
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Physiology
• Mean Arterial Pressure (MAP) determines the
pressure of blood entering the tissue
• Systolic Pressure (SP) = max. arterial pressure
occurring just before contraction
• Diastolic Pressure (DP) = min. arterial pressure
occurring just before ventricular contraction
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Atherosclerosis
• Harderning and thickening of arteries which reduces their
elastic properties
• Involves the formation of an atheroma within the walls of the
vessel
• Results in a ↓ in the arterial lumen diameter and a ↓ in endorgan perfusion
• There is also a predisposition to rupture and thrombus
formation
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Atherosclerosis
Endothelium damage, LDL moves into intima
Monocytes migrate into intima and become
macrophages, take up LDL and become foam
cells.
Platelets adhere to endothelial cells, release
PDGF, causes smooth muscle migration into
intima
Lesion develops, pressure causes the media to
atrophy and the muscle to be replaced by
collagen. Fibrous cap of collagen forms.
There is ↑ free lipid in the plaque
Endothelium become fragile and ulcerates
Further platelet aggregation and thrombus formation
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MI and Angina
Underlying pathology and risk factors is the same eg
atheroslcerosis
• Angina: Reduction in blood flow
– Can be made better via GTN
– Central chest pain and radiation, SOB, variable triggers
• Myocardial infarction: Plaque rupture
– STEMI/NSTEMI
– As above not relived by GTN, may have no precipitations
Consequences: Heart failure, infarction, arrthymia’s, depression,
decreased ADL’s.
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Peripheral Vascular Disease
• = obstruction of large arteries (not within the coronary, aortic
arch or brain vasculature)
• Main cause is atherosclerosis
• Risk Factors
– Smoking(!), diabetes, HTN, sedentary lifestyle, ↑cholesterol, obesity
• Investigations
– Bloods, ABPI, arterial duplex, MR angiography
• Management
– Conservative measures – lose weight, ↑exercise, anti-hypertensives,
statins, STOP SMOKING
– Surgery – angioplasty, surgical bypass, amputation
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Intermittent
Claudication
Cramping pain felt in the calf, thigh or buttock
after walking for a fairly fixed distance and
relieved by rest
Ischaemic Rest
Pain
Burning pain at rest (esp. At night) relieved by
hanging legs over the side of the bed
Ulceration/
Gangrene
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Venous Thrombosis
• Blood clot within veins – generally deep veins of legs (DVT)
• Risk factors
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Lower limb trauma, surgery or immobilisation in a plaster cast
Bedridden for >3 days or surgery within the last 4 weeks
PMH of DVT/PE
Malignancy
IVDU
Pregnancy
OCP/HRT
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Venous Thrombosis
• Investigations
– D-dimer
– Compression USS
• Management
– Prevention – stop OCP 4 wks pre-op, mobilise pts early, prophylatic
anticoagulation
– Treatment – Anticoagulation (LMWH then warfarin)
• Complications
– Pulmonary Embolism - SOB, haemoptysis, pleuritic CP, syncope
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Cardiac physiology
Three types of troponin:
Troponin C – calcium binds to cause a conformational change in Troponin I.
Troponin T – binds to tropomyosin, forming a tropomyosin – troponin complex.
Troponin I – binds to actin, to hold the tropomyosin – troponin complexes in place.
When calcium binds to troponin C it causes tropomyosin to move out of the way in
order to exposure the actin binding sites on the myosin molecules.
Therefore enabling the muscle to contract, in the absence of calcium tropomyosin
interferes with myosin so the muscle remains relaxed.
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Cardiac physiology
VENTRICULAR FILLING (DIASTOLE)
• Passive filling of the ventricles – Ventricular volume and pressure increases
• AV valves are open
• Semi lunar valves are closed
ISOVULUMETRIC CONTRACTION (SYSTOLE)
• Ventricular pressure> Atrial pressure
• Causing the AV valves to close
EJECTION (SYSTOLE)
• Ventricular pressure> Atrial pressure
• Causing the semi lunar valves to open.
ISOVOLUMETRIC RELAXATION (DIASTOLE)
• Both semi lunar and AV valves are closed
• When ventricular pressure < atrial pressure, AV valves open
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Cardiac physiology
•
Electrical changes in the myocardium
– Depolarisation initiated in the SAN which has an
inherent rhythm (see later) but also controlled
via vagus nerve. It has the fastest rate of
discharge in the heart therefore it is the
pacemaker, but sometimes other tissue can
conduct to the AV node (=ectopics)
– Spreads from RA  LA causing systole
– At AVN the depolarization is delayed by 0.1s so
the atria can contract
– Conduction continues through bundle of His to
its L and R branches
– Spreads to purkinje fibres and the rest of the
ventricle
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ECG
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•
Detects electrical impulses through the heart
1 small square = 0.04s
1 large square = 0.2 s
Use these to work out the heart rate
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Check the patient details - is the ECG correctly labelled?
What is the rate?
Is this sinus rhythm? If not, what is going on?
QRS axis
Are the P waves normal (Good places to look are II and V1)
What is the PR interval?
Are the QRS complexes normal? Specifically, are there:
– significant Q waves? (seen before R wave- previous MI)
– widened QRS complexes?
Are the ST segments normal, depressed or elevated?
•
R-R interval
(big squares)
Heart rate
1
300
2
150
3
100
4
75
5
60
6
50
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Normal ECG
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Regular sinus rhythm 60-100 beats per mintue
P wave (atrial depolarisation)
PR interval 0.12-0.2 s
QRS (ventricular depolarisation) < 0.12s (3 small squares)In
general as proceed from V1-6 the R waves get taller and the S
waves get smaller
• T wave (ventricular repolarisation)
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Normal ECG
Leads
What they look at
V1, V2
Right ventricle and anterior LV
V2, V4
I.V. Septum and anterior LV
V5, V6
Anterior and lateral wall of LV
Lead 1, aVL, aVR, aVF.
Left side of heart
Lead 2 +3, aVF
Inferior surface of the heart
aVR
Right atrium
-150 aVR
-90
-30 aVL
0 Lead 1
180
120 Lead 3
90 aVF
Normal axis
LAD
RAD
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ECG
Axis
•One quick, non-specific method can be used to determine
the QRS axis. When depolaristion moves towards a lead
Rwave> S wave i.t QRS is more +ve
•If the QRS complex is upright (positive) in both lead I and
lead aVF, then the axis is normal
•If the QRS is upright in lead I and downward (negative) in
lead aVF, then the axis is leftward.
•If the QRS is predominately downward in both leads I and
aVF, then the axis is rightward.
•If the QRS is downward (negative) in lead I and upward
(positive) in lead aVF, then the axis is indeterminate.
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Bradycardia’s
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•
Sick sinus syndrome, B-blockers, raised intracranial pressure
AV Block
– 1st degree heart block. All atrial pulses reach the ventricle but the conduction
is delayed through AV node
– ECG: P-R interval > 200ms
– 2nd degree heart block. Some atrial pulses reach the ventrical eg not all p
waves are followed by a QRS complex
• Mobitz type 1: P-R increases over a number of beats followed by an
unconducted p wave
• Mobitx type 2: P-R interval is constant but QRS complexes are dropped
intermittently eg 2:1, 3:1
– 3rd degree heart block. Complete dissociation of p and QRS complexes
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Tachycardia’s
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•
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Exercise, fever, anemia, hypovolaemia, emotion, caffiene
Wolf Parkinson white- abnormal conducting pathway between atria and
ventricle via an accessory pathway e.g it does not pass through the AV
node and so there is no delayed conduction therefore see shortened PR
and slurred upstroke in QRS as normal bundle of His pathway catches up
Re-entry tachy
– Orthodromic – A.V conduction sets off accessory pathway bypassing
AV node- see rapid upstroke and narrow QRS and supressed p wave
– Antidromic- Accessory pathway goes back up through AV node. QRS
is wide and p wave comes after and is inverted.
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Tachycardia’s
• Atrial fibrillation- caused by high firing in the atrium but slower and
irregular ventricle response as not all impulses are conducted by the AV
node
– No p waves
– Flutter in V1
– Irregularly irregular rhythm
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Tachycardia’s
• Atrial flutter- rapid re-entry of conduction within right atrium. See saw
tooth pattern
• Ventricular fibrillation
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• ST segment elevated (STEMI)/ depressed
(ischaemia)
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Bundle Branch Blocks
RBBB and LBBB- Delay in conduciton at I.V. Spetum
leads to widening of QRS (>120)
WiLLiaM (W in V1, M in V6 for LBBB)
MaRRow (M in V1, W in V6 for RBBB)
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CVS Reflexes
Aim to maintain mean arterial pressure
Key components: blood vessels, heart and kidney
Pathways controlling MAP
• Local eg temperature
• Neural control
• Vascular reflexes eg stretch leads to contraction
• Hormonal factors and local metabolic factors eg
angiotensinogen II, NO, K, adenosine
CO= HR x SV
CO = MAP/TPR
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CVS Reflexes
A volume / arterial BP  activation of cardiopulmonary receptors (in atria/
ventricles) / baroreceptors (in aortic arch + carotid sinuses)
Which leads to activation of CNS
• Sympathetic tone
• Vagal tone
Vasoconstriction
 Heart rate +  cardiac contractility
 TPR x  CO   BP
 Blood volume
• RAS
 Na and water excretion,  thirst
•  antiduretic hormone
TPR = Total Peripheral Resistance
RAS = Renin Angiotensin System
Antidiuretic hormone = ADH= Vasopressin
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Shock
Inability of CVS to maintain organ perfusion
Symptoms: Hypotension, tachcardia, weak pulse, delayed CRP, decreased
urine output
Signs: Cool skin, low BP, tachyoponea, confusion, thirsty, loss of conciousness
• Hypovolaemic: Causes: Trauma, haemorrhage, burns eg rapid fluid loss
causing mechanisms to be activated (see above)
• Septic: Infection results in release of toxins causing increased
permeability
– Fever, chills, sweating
• Anaphylatic- Severe allergic reaction
– angiodema and narrowing of airways
• Cardiogenic: Damage to myocytes causing ineffective pumping eg MI
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Cardiac output and Starling’s law
• CO = Stroke volume x heart rate
• SV is influenced by the filling pressure (preload), the force of the cardiac
muscle and the pressure against which the heart has to pump (afterload).
• The volume of blood in the ventricle before systole (contraction) is the end
diastolic volume. This is dependant on the end-diastolic pressure and the
compliance of the ventricle i.e. how easy it relaxes.
• If EDP and therefore EDV rises then the force of the next contraction and
the stroke volume will increase
 Sympathetic tone
• = FRANK-STARLING RELATIONSHIP
 contractility
normal
SV
Failure
(decreased
contractility)
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EDP
Cardiac output and Starling’s law
• Starlings Law = The energy released during contraction depends on the
initial fiber length
• The consequence of this is to match left and right ventricular output
otherwise if RV>LV it would lead to an increase in pulmonary blood
pressure and may result in pulmonary oedema.
• Due to starlings law any increase in blood flow would increase the filling
pressure and hence EDV within the LV . This would result in an increase in
LV output and would prevent any rise in pulmonary pressure.
• Therefore an increase in central venous pressure e.g. in exercise will also
result in an increased cardiac output, conversely a decrease in central
venous pressure eg sitting to standing will lead to a fall in CO
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Heart Failure
• Occurs when the heart is no longer able to maintain sufficient tissue
perfusion for normal cellular metabolism.
Due to,
• Damaged cardiac muscle eg IHD
• HBP (increased afterload means the heart has to work harder)
• valular heart disease (increase afterload and so increase the work of the
heart)
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Heart Failure
Pathogensis
A decrease in LV systolic dysfuction results in a decrease in contractility and
shifts the starling curve to the right. This results in a decreased force of
contraction. The body then tries to compensate by increasing the filling
pressure (EDP).
Its does this by
• Increased sympathetic activity  HR and force
• Peripheral vasconstriction   EDP (but also afterload!!)
• RAS activation  Retention of Na and water
However these responses eventually overwhelm the heart and prolonged
excessive filling leads to dilatation which leads to ineffectual contraction and
possible valvular incompetence. Dilation also increase the work of the
myocytes (Laplace’s law) thus predisposing the myocardium to ischeamia and
damage. This leads to further cardiac remodelling, which leads to a further
reduction in CO.
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Heart Failure- Clinically
LV Failure
RV Failure
Dysponea
Peripheral oedema (pitting)
Poor excersize tolerance
Ascites + hepatomegaly
Orthopnea
Nausea
Paroxysmal nocturnal
dysponea
Anorexia
Wheeze
Raised JVP
Cold peripheries
Facial swelling
Can get both = Congestive cardiac failure
Cor pulmonale = RHF due to chronic pulmonary disease
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Heart sounds
Systolic
Diastolic
Aortic stenosis
•Aortic area
•Ejection click
•Radiates to carotids
Aortic regurg
•Aortic area
•Loudest in early diastole
Mitral regurg
•Pansystolic
•Blowing
•Best heard at apex
•Radiates to left axilla
Mitral stenosis
•Heard at apex with patient
in left lateral position
•Opening snap, rumbling
sound
Rare!
Pulmonary stenosis
•Heard in pulmonary area
Tricuspid regurg
•see elevated JVP/ pulsatile
liver
Pulmonary regurg
•Heard in pulmonary area
Tricuspid stenosis
•Similar to mitral stenosis
but may see elevated JVP/
pulsatile liver
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JVP
Manonmeter of right atrial pressure. Observed
with the patient at 45o
Distinguish from carotid artery as it
•Multiphasic
•Non- palpable
•Occludable
•Varies with head tilit
•Varies with respiration
Elevated due to
•Fluid overload
•SVC obstruction
•RVF
•Constrictive pericarditis
•Tricuspid stenosis/ regurg
a wave represents atrial systole
c wave represents closure of the tricuspid
valve
x descent represens the fall in atrial
pressure during ventricular contraction.
v wave represents the atrial filling against
the closed tricuspid.
y descent represents opening of the
tricuspid valve.
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Embryology
Development of primitive heart
• Sinus venosus: Left horncoronary sinus
Right horn wall of right atrium
• Primitive atrium: Right half right auricle of right atrium
Left halfleft auricle of left atrium
• Bulbous courdis: Right ventricle/ Outflow of right and left
ventricle
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Embryology
• Origins of chambers of the heart
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•
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Left atrium: is formed from 4 primitive pulmonary veins
Right atrium: primitive atrium and sinus venosus (right horn)
Ventricles: (L)- primitive ventricle, (R)- Bulbous cordis
Pulmonary trunk/ aorta: bulbous courdis/ Truncus ateriosus
SA Node/ AV Node and bundle- sinus venosus/ AV canal
Pericardium- Septum transversum
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Embryology
Aortic arch development week 4-7 (nb no 5th arch!)
Left
Right
1st arch
Regress into part of maxiallry
artery
2nd arch
Regress into stapedial artery
3rd arch
Left/ right common/internal/
external carotid arteries
4th arch
Part of aortic arch
Part of right subclavian artery
6th arch
Left pulmonary artery and Ductus
arteriosus
Right pulmonary artery
7th segmental artery
Left subclavian artery
Part of right subclav artery
Dorsal aorta
Descending thoracic aorta
Regress into part of righ subclav
artery
http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html
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Questions
1.
2.
3.
4.
5.
6.
This is the normal duration/range of the QRS complex in msec
This is the normal duration/range of the PR interval in msec
This is the angle/range assessed by limb lead II in degrees
This is the angle/range assessed by limb lead I in degrees
This is the duration/range in msec represented by one small square on a standard ECG recording
This is the duration/range of the QRS complex in msec in lead V6 in an ECG showing complete left bundle
branch block
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•
•
120 to 200
Less than or equal to 120
-30 to 90
40
Greater than 100
60
0
60 to 100
Greater than 120
Less than 60
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Questions
1.
2.
3.
4.
5.
6.
This is the normal duration/range of the QRS complex in msec
This is the normal duration/range of the PR interval in msec
This is the angle/range assessed by limb lead II in degrees
This is the angle/range assessed by limb lead I in degrees
This is the duration/range in msec represented by one small square on a standard ECG recording
This is the duration/range of the QRS complex in msec in lead V6 in an ECG showing complete left bundle
branch block
•
•
•
•
•
•
•
•
•
•
120 to 200 (2)
Less than or equal to 120 (1)
-30 to 90
40 (5)
Greater than 100
60 (3)
0 (4)
60 to 100
Greater than 120 (6)
Less than 60
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Questions
Aortic Arch Embryology .For each of the following post-natal structures, indicate their
embryological origin.
1. Ductus Arteriosus.
2. Aortic Arch.
3. Left Common Carotid Artery.
Left 1st arch
Right 2nd arch
Left 3rd arch
Right 3rd arch
Left 4th arch
Right 4th arch
Left 5th arch
Right 5th arch
Left 6th arch
Right dorsal aorta
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Questions
Aortic Arch Embryology .For each of the following post-natal structures, indicate their
embryological origin.
1. Ductus Arteriosus.
2. Aortic Arch.
3. Left Common Carotid Artery.
Left 1st arch
Right 2nd arch
Left 3rd arch (3)
Right 3rd arch
Left 4th arch (2)
Right 4th arch
Left 5th arch
Right 5th arch
Left 6th arch (1)
Right dorsal aorta
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Questions
1. A circulating count of less than 80 x 109/L of this blood constituent is associated with
increased risk of bleeding whilst an excess is associated with increased risk of thrombosis.
2. This blood constituent plays the major role in maintaining oncotic pressure and retaining fluid
in the intravascular space.
3. These differentiated B lymphocytes produce antibodies in response to non-self protein
antigens.
4. The number of these in the blood is regulated by erythropoietin
• Platelets
• Eosinophils
• Plasma cells
• Monocytes
• Erythrocytes
• Leukocytes
• Albumin
• Immunoglobulins
• Haemoglobin
• Coagulation factors
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Questions
1. A circulating count of less than 80 x 109/L of this blood constituent is associated with
increased risk of bleeding whilst an excess is associated with increased risk of thrombosis.
2. This blood constituent plays the major role in maintaining oncotic pressure and retaining fluid
in the intravascular space.
3. These differentiated B lymphocytes produce antibodies in response to non-self protein
antigens.
4. The number of these in the blood is regulated by erythropoietin
• Platelets (1)
• Eosinophils
• Plasma cells (3)
• Monocytes
• Erythrocytes (4)
• Leukocytes
• Albumin (2)
• Immunoglobulins
• Haemoglobin
• Coagulation factors
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Questions
Atherosclerosis.
1. These cells enter the artery wall in response to chemokines and facilitated by adhesion molecules such as
VCAM-1 where they may interact with antigens such as oxidised LDL.
2. This is the first lesion in the progression from normal vessel wall to obstructive or ulcerating atheroma.
3. This event underlies the majority of myocardial infarctions and strokes.
4. This can be quantified in coronary arteries using modern CT scanning methods
Platelet aggregation
Eosinophils
T Lymphocytes
Fatty streak
Aneurysm formation
Plaque rupture
Mast cells
Macrophages
Lipid pool
Calcification
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Questions
Atherosclerosis.
1. These cells enter the artery wall in response to chemokines and facilitated by adhesion molecules such as
VCAM-1 where they may interact with antigens such as oxidised LDL.
2. This is the first lesion in the progression from normal vessel wall to obstructive or ulcerating atheroma.
3. This event underlies the majority of myocardial infarctions and strokes.
4. This can be quantified in coronary arteries using modern CT scanning methods
Platelet aggregation
Eosinophils
T Lymphocytes (1)
Fatty streak (2)
Aneurysm formation
Plaque rupture (3)
Mast cells
Macrophages
Lipid pool
Calcification (4)
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Questions
1. The SAN is supplied by the RCA in what percentage of people?
2. The AVN is supplied by the RCA in what percentage of people?
3. Left dominance of the coronary arteries occurs in what percentage of the population?
10%
20%
40%
60%
70%
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Questions
1. The SAN is supplied by the RCA in what percentage of people?
2. The AVN is supplied by the RCA in what percentage of people?
3. Left dominance of the coronary arteries occurs in what percentage of the population?
10% (3)
20%
30%
60% (1)
90% (2)
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Questions
1.
2.
What is Starling’s law?
A 68 year old presents to his GP with HBP. He is given some medication. Later he
goes home but presents to A+E complaining of muscle weakness and aches,
muscle cramps and palpitations, he then collapses.
–
–
–
–
–
Normal BP range and if diabetic?
Risk factors for high blood pressure?
What class of medication was given?
Where does this act?
How does this account for the gentlemens symptoms?
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Questions
1.
2.
What is Starling’s law?
A 68 year old goes to his GP he is known to suffer from HBP, he is given
additional medication to control his HBP. Later he goes home but presents to A+E
complaining of muscle weakness and aches, muscle cramps and palpitations, he
then collapses.
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–
–
–
–
Normal BP range and if diabetic? 140/90 , 130/80
Risk factors for high blood pressure? Age, ethnicity, gender, family history, smoking activity level/
excersize, diet
What class of medication was given? Thiazide diuretics
Where does this act? Distal convoluted renal tubule
How does this account for the gentleman’s symptoms? Side effect of thiazides is it blocks Na/Cl
channel in the tubule. To compensate more K+ is excreted leading to hypokalamiea.
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EMQ’s
1.
2.
3.
4.
Pulmonary embolism
Peripheral vascular disease
Lymphoedema
Heart failure
5. Varicose veins
6. Pulmonary oedema
7. Lymphoma
8. Deep vein thrombosis
•
A 49 yr old diabetic man complains of pain in his calves which comes on
when walking and is relieved by rest
•
A 64 yr old retired teacher who suffers from breast cancer complains of
some unsightly swellings on her calves which bleed when knocked
•
A 47 yr old gentleman has recently returned from abroad and within
hours is complaining of an aching, swelling and redness in his left calf. He
was previously fit and well
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Clinical Scenario
A 69 year old gentleman presents to vascular clinic with severe cramping pain
in his right calf. He can only walk about 900 yards before the pain starts,
which is relieved by rest. He smokes 30 cigarettes a day and suffers from
angina. On examination his right dorsalis pedis, posterior tibial and
popliteal pulses are absent but otherwise the rest of the examination is
unremarkable.
What is the most likely diagnosis?
Which artery is likely to be affected?
Question from themastersurgeon.com
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