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Phase 1A

The Peer Teaching Society is not liable for false or misleading information…

•Describe the main risk factors in cardiovascular disease

•Understand the pathology of atherosclerosis

•Understand the main diseases that affect the CVS


Aims


Branches of the Aorta

DIAPHRAGM


GROIN

KNEE

ANKLEFOOT

Arterial Supply of the Lower Limb


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

• 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


Physiology

• 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 end-organ perfusion

• There is also a predisposition to rupture and thrombus formation


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 plaqueEndothelium become fragile and ulcerates

Further platelet aggregation and thrombus formation

Atherosclerosis

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.The Peer Teaching Society is not liable for false or misleading information…

MI and Angina


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

The Peer Teaching Society is not liable for false or misleading information…1

Intermittent Claudication

Ischaemic Rest Pain

Ulceration/Gangrene

Cramping pain felt in the calf, thigh or buttock after walking for a fairly fixed distance and relieved by rest

Burning pain at rest (esp. At night) relieved by hanging legs over the side of the bed


Venous Thrombosis

• Blood clot within veins – generally deep veins of legs (DVT)

• Risk factors – 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


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


Cardiac physiologyThree 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.


Cardiac physiologyVENTRICULAR 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

• 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


Cardiac physiology

• 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

• 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?


ECGR-R interval (big squares)

Heart rate

1 300

2 150

3 100

4 75

5 60

6 50

• 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)


Normal ECG


Normal ECGLeads 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

-30 aVL

0 Lead 1

90 aVF

-150 aVR

120 Lead 3

Normal axisLADRAD

180

-90

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.


ECG

• 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


Bradycardia’s

• 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.


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


Tachycardia’s

• Atrial flutter- rapid re-entry of conduction within right atrium. See saw tooth pattern

• Ventricular fibrillation


Tachycardia’s

• ST segment elevated (STEMI)/ depressed (ischaemia)



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)

Bundle Branch Blocks


CVS ReflexesAim to maintain mean arterial pressureKey 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


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

• RAS • antiduretic hormone

Heart rate + cardiac contractility

TPR x CO BP

Blood volume

Na and water excretion, thirst

Vasoconstriction

TPR = Total Peripheral ResistanceRAS = Renin Angiotensin SystemAntidiuretic hormone = ADH= Vasopressin

Inability of CVS to maintain organ perfusionSymptoms: Hypotension, tachcardia, weak pulse, delayed CRP, decreased urine outputSigns: 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


Shock

• 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

• = FRANK-STARLING RELATIONSHIP


Cardiac output and Starling’s law

contractility

normal

Failure (decreased contractility)

SV

EDP

Sympathetic tone

• 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


Cardiac output and Starling’s law

• 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)


Heart Failure

PathogensisA 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 waterHowever 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.


Heart Failure


Heart Failure- ClinicallyLV 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 failureCor pulmonale = RHF due to chronic pulmonary disease


Heart soundsSystolic 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

Pulmonary regurg•Heard in pulmonary area

Tricuspid regurg •see elevated JVP/ pulsatile liver

Tricuspid stenosis •Similar to mitral stenosis but may see elevated JVP/ pulsatile liver


JVPManonmeter 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.

Development of primitive heart• Sinus venosus: Left horncoronary sinus

Right horn wall of right atrium• Primitive atrium: Right half right auricle of right atrium Left halfleft auricle of left atrium• Bulbous courdis: Right ventricle/ Outflow of right and left

ventricle


Embryology

• Origins of chambers of the heart• 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


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


Embryology

http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html

1. This is the normal duration/range of the QRS complex in msec2. This is the normal duration/range of the PR interval in msec3. This is the angle/range assessed by limb lead II in degrees4. This is the angle/range assessed by limb lead I in degrees5. This is the duration/range in msec represented by one small square on a standard ECG recording6. 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 • Less than or equal to 120 • -30 to 90 • 40• Greater than 100 • 60 • 0 • 60 to 100 • Greater than 120 • Less than 60


Questions

1. This is the normal duration/range of the QRS complex in msec2. This is the normal duration/range of the PR interval in msec3. This is the angle/range assessed by limb lead II in degrees4. This is the angle/range assessed by limb lead I in degrees5. This is the duration/range in msec represented by one small square on a standard ECG recording6. 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


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


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


Questions


Questions1. 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


Questions1. 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


QuestionsAtherosclerosis.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 LymphocytesFatty streakAneurysm formation Plaque rupture Mast cells Macrophages Lipid pool Calcification


QuestionsAtherosclerosis.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)


Questions1. 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%


Questions1. 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)


Questions1. What is Starling’s law?2. 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?


Questions1. What is Starling’s law?2. 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.

– 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.


EMQ’s1. Pulmonary embolism2. Peripheral vascular disease3. Lymphoedema4. Heart failure

• 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

5. Varicose veins6. Pulmonary oedema7. Lymphoma8. Deep vein thrombosis


Clinical ScenarioA 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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