phase 1a jono wells rizwan malatagar the peer teaching society is not liable for false or misleading...

Phase 1A

Jono WellsRizwan Malatagar

CARDIOVASCULAR SYSTEM: Anatomy, physiology, pathology and clinical problems

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

• First half – 25mins on anatomy and physiology• Second half – 25mins on pathology and clinical

applications• Last 5mins – questions and quiz sheets.


introduction

• Know what it is, how it works, how it goes wrong and how to recognise when it does.

• Not comprehensive!• Emphasis on understanding principles then applying

these to work out signs and symptoms of disease• Know your definitions• Generally doesn’t cover management• Quiz sheet based on the kind of questions in Phase

1A exams.


Learning aims: CV system

Basics:• What is the function of the heart?

– Distributing O2 and nutrients to all body tissues– Transportation of CO2 and metabolic waste

products (eg. urea) away from the tissues– Distribution of water, electrolytes and hormones– Immune support– Thermoregulation


Cardiovascular Anatomy


Cardiovascular Anatomy

• Posterior to the sternum• Medial to the lungs• Anterior to vertebral column• Base lies beneath 2nd rib• Apex at 5th intercostal space• Lies upon diaphragm


Location of the Heart


Clinical Relevance

• Pericardium– Loose fitting double layered sac– Fibrous + Serous

• Visceral Pericardium– membrane on the surface of the heart

• Parietal Pericardium– secretes pericardial fluid


Heart coverings

SerousPericardium

• 2 main arteries R and L• Both arteries originate directly above the

aortic valve


Coronary Circulation

• Sympathetic:– Cervical and upper thoracic portions of

sympathetic trunks– +ve chronotropic, +ve inotropic, dilatatory– Norepinephrine/Epinephrine

• Parasympathetic:– Branches of the vagus– -ve inotropic, -ve chronotropic, constrictory– Acetylcholine


Nervous supply

• Not going to cover embryology in this lecture; but worth looking over no matter how boring it may seem!!


Embryology

• Three main types– Arteries– Veins– Capillaries


Blood Vessels


Blood Vessels

• Function relates to form


Histology of Blood Vessels

• Controlled by the SA node• Depolarisation spreads through adjacent atria

causing atrial systole• AV node limits the depolarisation• Continues through bundle of His• Purkinje fibres distribute impulse to cells in

endocardium• Impulse spread through the epicardium


Cardiac conduction


Cardiac conduction

• Involuntary, striated muscle• Cardiac contraction controlled by calcium

concentration• When Ca rises, the cardiac muscle contracts

and when it falls the cardiac muscle relaxes


Cardiovascular physiology

Energized cross-bridge binds to actin

Cross-bridge moves

ATP binds to myosin → cross bridge detaches

Hydrolysis of ATP → cross-bridge becomes energized


Cardiovascular physiology

• Three types of Troponin:-• C: Ca binds to C make a

conformational change to Troponin I

• T: binds to tropomyosin to form troponin-tropomyosin complex

• I: binds to actin to hold the tropomyosin-troponin complexes in place


Cardiac muscle contraction

• Approximately 0.9 seconds


Cardiac Cycle

Diastole:• Passive filling of the

ventricles• AV valves open• Semi lunar valves closed

Isovolumic Contraction:• Ventricular pressure>atrial

pressure• Causing AV valves close

Systole:Ventricular pressure>atrial pressureSemilunar valves open

Isovolumic Relaxation:• Both valves closed• When ventricular

pressure<atrial pressure; AV valves open


Cardiac Cycle


ECG representation

P wave = atrial contraction

QRS complex = ventricular contraction

T wave = ventricular relaxation

MAP = CO X TPRThe Peer Teaching Society is not liable for false or misleading information…

Regulation of MAP

CO = HR X SV


Cardiac output

mL/min Beats/min mL/beat

• What are Baroreceptors?• Located in the carotid sinus and aortic arch• Respond to the stretch of the vessel wall• Impulse carried to medulla• Increases parasympathetic drive: decreases

sympathetic drive• Decreases HR and decreases BP


Baroreceptors

• Located in carotid and aortic bodies• Hypercapnia/hypoxia/acidosis increases

excitation• Increased excitation = vasoconstriction +

bradycardia


Chemoreceptors

• “stroke volume of the heart increases in response to the volume of blood filling the heart (end diastolic volume)” – Starling’s law

• Preload: force associated with the degree of initial stretch in the ventricle from initial volume load

• Contractility: Ability of the heart to contract independently of the afterload and preload


Stroke volume

• Increased TPR = decreased venous return + decreased stroke volume

• Control:– Sympathetic nervous system (vasoconstriction)– Hormonal control:


Total peripheral resistance

• Atherosclerosis• Thromboembolism

• Shock

• Heart failure• Arrhythmia


Cardiovascular pathology

• Arteriosclerosis - thickening and hardening of arteries.

• Atherosclerosis – the process leading to arteriosclerosis where atheroma forms.

• Arteriolosclerosis – arteriosclerosis of the small vessels. Mainly caused by HTN.


Atherosclerosis - definitions

Obesity Hyperlipidemia Hypercholesterolaemia

Smoking Diabetes

Family History Old age Male gender SE Asian Alcohol

Poor diet Insufficient exercise

Low SES Type A coronary-prone

Stress


Atherosclerosis – risk factors

• Constitutional• Environmental• Lifestyle


Atherosclerosis - process


1. Endothelial injury


2. Fatty streak


3. Bulge


4. Fibrous cap

• Narrowed lumen• Occlusion• Emboli – fragmentation of plaque• Aneurysm – due to loss of elasticity

• Learn examples of each.


Atherosclerosis - outcomes

• Virchow’s triad – stasis, hypercoagulability and endothelial injury


Thromboembolism

• Thrombosis = inappropriate coagulation of blood inside a vessel

• In veins it’s fibrin rich due to low pressure, in arteries they’re platelet rich e.g. atheroma.

• Main clinical problems are DVT and PE.


Thromboembolism• Virchow’s triad – stasis, hypercoagulability and

endothelial injury

• Where? – Affects deep veins e.g. femoral, popliteal

• Presentation?– Pain, swelling, redness and possibly distended

superficial veins and distal proximal oedema• Treat with anticoagulation

• May also present as pulmonary embolism


DVT

• Definition – an acute failure of the cardiovascular system to perfuse the tissues of the body.

• 4 main types:– Hypovolaemic– Distributive– Cardiogenic– Obstructive


SHOCK!


Shock – symptoms and signsFaintness, light headedness, dizzinessReduced level of consciousness

Skin:Sweating + pallor.Cold

Rapid, weak pulse

Rapid, shallow breathing

OliguriaMuscle weakness

Intravascular compartment potential

volumeLow end organ perfusion

• External fluid loss• Internal fluid loss

• What causes these?


Hypovolaemic shock

• Total fluid volume is the same, it’s just maldistributed.

• Origin: septic or anaphylactic.• Septic – exotoxins released from bacteria or

endotoxins released when they die• Anaphylactic

– Inflammatory mediators– Peripheral vasodilatation, increased vascular

permeability and bronchoconstriction


Distributive shock

• Pump failure – the heart isn’t pumping adequately to maintain the circulation e.g. arrhythmia, MI or myocarditis.

• Usually an acute presentation but can occur due to worsening heart failure.


Cardiogenic shock

• Direct outflow obstruction -> pressure on the heart or vessels leading to inadequate end organ perfusion.– Extrinsic compression – cardiac tamponade or

tension pneumothorax– Intrinsic obstruction– Pulmonary embolism


Obstructive shock

• ‘A Syndrome of heart insufficiency’. It is failure of the heart to deliver oxygenated blood at the rate needed by metabolising tissues.

• Commonest cause is myocardial ischaemia.• Other causes include

– Pressure overload– Volume overload– Primary myocardial disease


Heart failure

• The myocardial failure leads to decreased CO and Starling’s law is impaired.

• Laplace’s law means that as heart muscle dilates, the myocytes require more energy to increase tension.

• Compensation due to sympathetic and renal system.

• Both relate to angiotensin II.


Changes in circulation

• Commonest symptoms – SOB, fatigue, ankle oedema

• Specific signs – raised JVP, displaced apex beat• Heart failure can be right sided, left sided or

mixed.• Clinical features of either right or left relate to

what’s behind that side in the vascular system.• Also get a functional regurgitation murmur.


Heart failure

• Rate• Rhythm• Cardiac axis


ECGs!


ECGs!

• Rate– 60-100 normal.

• Rhythm– look at all the waves and intervals.

• Cardiac axis– down in II and up in III.


ECGs

• Main types:– Supraventricular– Ventricular

• Or:– Bradycardias– Tachycardias


Arrhythmias

• Atrial fibrillation – irregularly, irregular.– Absent P waves, random contractions– Aetiology– Types – PPP!– Consequences – clots and death

• Atrial flutter– REALLY FAST. Sinus rhythm.– Sawtooth trace


Atrial arrhythmias

• 1st degree – prolonged PR interval• 2nd degree:

– Mobitz type 1 (Wenkebach) – PR lengthens then miss QRS

– Mobitz type 2 – PR constant lengths then loss of QRS complex

– 2:1 block – every second P wave followed by QRS• 3rd degree - discoordination


Heart Block

• Bundle branch block– william marrow V1-6

• ST elevation– Shows broken bits. Learn where leads represent

• After MI -> ST elevation within hours, T wave inversion within 24hrs and pathological Q waves after days.

• Potassium changes– Hyperkalaemia – absent P, wide QRS, tall T and VF– Hypokalaemia – small P, few T-waves, long QT


Other points

• Chest pain• Leg pain

• Murmurs


Clinical problems!

Differential diagnosis? CVS, RS, GI and MSK conditions

Key questions? Worse on breathing? Related to food intake, positional? Presence of CVS risk factors, radiation?


Chest pain

Necrosis of an area of heart muscle due to compromised blood supply.

Atherosclerotic plaque ruptures -> occlusion

Necrosis -> scar tissue


Myocardial infarction

Cardiac arrest Unstable angina Pericarditis Cardiac tamponade Mitral regurgitation – due to pap

muscles Arrhythmia Thromboembolisms


Consequences of MI

ABC 12-lead ECG MONA Consider thrombolytics, clopidogrel

and PCI.


Management

Lifestyle modification Secondary prevention drugs (AC

ABS) Surgical treatments – PCI or CABG


Treatment post-MI

• Differential diagnosis?• Vascular, musculoskeletal or neurological

• Key questions?– SOCRATES– Trauma– Risk factors for DVT or atherosclerosis


Leg pain

• Ischaemia -> low oxygen• Lactic acid in muscles• Can’t be got rid of until at rest• Remember Pouiselle’s law!

• Also acute limb ischaemia:– 6 P’s: Pallor, paraesthesia, perishing cold, pain,

pulselessness, paralysis


Science of IC

• DVT– Pain and clinical effects due partially to oedema

and inflammation of tissues.

• Rheumatological conditions

• Cellulitis


Differentials

Due to turbulent flow through valves Timed with phases of heart contraction. Usually 1 of:

Systolic (ejection, mid or pan) Diastolic (mid or early) Continuous (machinery, venous hum or pericardial rub)

Also comment on site, character and radiation.


Murmurs

S1 due to mitral/tricuspid closure, S2 due to aortic/pulmonary closure.

Added sounds: Stenosis = whistle before Insufficiency = swish after

Systolic -> aortic should be open, mitral should be closed. Diastolic -> mitral should be open, aortic should be closed.


Sounds

Damage due to: Age – mechanical stresses and impact damage Rheumatic fever Infective endocarditis Aortic root dissection Papillary muscle damage Congenital e.g. bicuspid aortic valve


Valves – acellular flaps

Aortic stenosis Mitral regurgitation Aortic regurgitation Mitral stenosis


The big 4:

Outflow obstruction Back-pressure effect on myocardium Reduced CO

Ejection systolic, aortic area, radiates to neck


Aortic stenosis

Leaks -> volume overload in LV Back pressure on LA

Pansystolic, ‘blowing’, heard at apex, radiates to axilla.


Mitral regurgitation

Leaks blood causing back pressure on LV

Early diastolic, ‘blowing, high-pitched’ at left sternal edge. Get patient to lean forward and breathe out.


Aortic regurgitation

Back-pressure causes dilatation of LA and pulmonary vasculature causing…

Mid-diastolic, ‘low rumbling’ at apex which is louder with exercise. Listen with the bell and roll onto left side.


Mitral stenosis

Heart failure CVS Respiratory Fluid congestion


Other signs and symptoms?

Surgery Starr-Edwards valve – turbulent, ‘clicks’ Tissue valve – no rejection


Treatments

Incidence 6-7/100,000 in UK Affects endothelium and heart valves. Febrile illness + murmur Consider method of infection and prosthetic valves 50% death rate for acute infection!


Infective endocarditis

Any questions?


Thanks for listening!

phase 1a jono wells rizwan malatagar the peer teaching society is not liable for false or misleading...

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