Ammad Mahmood GUMSA Revision Lectures

Cardiovascular Cardiovascular SystemSystem

TopicsTopicsAnatomyPhysiologyHeart sounds and ECG5 min break!AnginaHeart FailureExamination

Cardiac Anatomy

Cardiac AnatomyFour chambers – left and right atria and

ventriclesDivided by:

Interatrial septum between atriaInterventricular septum between ventriclesInterventricular valves between atria and

ventriclesThe heart lies slightly to the left of the

mediastinum with “RA to the right, RV at the front, LA to the left and LV at the back”

AtriaWhen collapsed form flaps called auricles; inner

surface contains muscular ridges called pectinate muscles

Right Receives blood from:

SVC – head, neck, upper limbs, chestIVC – rest of the trunk, viscera, lower limbsCardiac veins – drain into RA through the coronary sinus

Interatrial septum contains a shallow depression called the fossa ovalis at the site of the now closed foramen ovale

Left Receives blood from the four pulmonary veins (2 left, 2

right)

ValvesAtrioventricular valves

Mitral valve (between LA and LV)Tricuspid valve (between RA and RV)Anchored by chordae tendinae which are attached to

papillary muscles in the ventricles – prevents valve prolapseSemilunar valves

Aortic valve (between LV and aorta)Pulmonary valve (between RV and pulmonary arteries)Closed by backflow of blood, prevented from prolapsing by

the valve leaflets supporting each other like the legs of a tripod. Also less movement of the base of the valve as it is not contracting

All valves have three leaflets or cusps except the mitral (or bicuspid) valve which has two

Purpose – prevent backflow of blood

Ventricles Large muscular chambers; left considerably larger than rightDistal end is the apex, proximal end the base Inner surface is covered by muscular ridges called

trabeculae carnaePapillary muscles – anterior and posterior in both ventricles.

Septal papillary muscle only in RV for 3rd cuspThe RV has a ridge called the moderator band which

connects the conduction system of the heart to the anterior papillary muscle causing contraction of the muscle before ventricular contraction

Contraction of the LV involves shortening of the distance between apex and base and shortening of its diameter

Contraction of the RV pushes blood against the LV creating much lower pressure, it is facilitated by contraction of the LV

Aortic sinusesSac-like dilations at the base of the aorta

which fill due to blood backflow closing the aortic valve and allowing entry of blood into the coronary arteries

CoronaryCoronary CirculationCirculation

Cardiac Conduction SystemSpontaneously initiates and distributes the

stimulus to contract to the cardiac muscle without neural/hormonal input

Consists of:Sinoatrial (SA) node

Lies in posterior wall of RA, connected to AV node by internodal pathways

Atrioventricular (AV) nodeSole electrical connection between atria and ventricles,

other conduction is prevented by the fibrous skeleton of the heart

Conduction through AV node is delayed to allow atrial contraction to precede ventricular conduction

Atrioventricular bundle, bundle branches and Purkinje fibresAV bundle (Bundle of His) extends towards apex and

branches into left and right bundle branches. Purkinje fibers extend from the apex back towards the base allowing contraction to take place as a wave from apex to base

Cardiac WallThree layers:

Pericardium – outer covering, parietal and visceral (epicardium), cavity contains pericardial fluid

Myocardium – muscular layerEndocardium – innermost layer lines the

ventricles, simple squamous epithelium which is continuous with the great vessels

Cardiac Physiology

Cardiac Muscle CellsSimilar in structure to skeletal muscle except:

Cells are smaller, shorter and there is usually 1-2 nuclei

T-tubules are short and broad, and only contact the SR, do not form triads

Larger numbers of mitochondria as it depends mainly on aerobic metabolism

Adjacent cells are joined by intercalated discs which provide a stronger mechanical, electrical and chemical connection

Cardiac muscle can be considered as a functional syncytium ie a fused mass of cells

Cardiac action potentialsResting state

K+ inside the cell, Na+ and Ca2+ outside, resting potential -90mVFour stages of action potentialRapid Depolarisation – AP brings membrane to threshold

opening Na+ channels and causing large Na+ influx and depolarisation

Initial Recovery – K+ channels open in response and cause small repolarisation

Plateau Phase – Influx of Ca2+ through L-type Ca channels opened by depolarisation balances the K+ outflow maintaining membrane potential at around 0mV

Recovery – as the Ca2+ channels slowly close the K+ outflow repolarises the cell

Excitation contraction couplingIn skeletal muscle the AP travels along the T-

tubules to the junction with the sarcoplasmic reticulum to cause Ca2+ release from the terminal cisternae

In cardiac muscle the AP opens Ca2+ channels in the T-tubules themselves (the same channels responsible for the plateau phase)

This Ca2+ then opens further Ca2+ channels in the sarcoplasmic reticulum causing a massive flow of Ca2+ into the cytosol

This is called calcium-induced calcium release

Pacemaker potentialThe cell membranes of certain cells in the

conducting system cannot maintain a resting potential and gradually depolarise back to threshold after each repolarisation

The rate of spontaneous depolarisations varies across the conduction system, the fastest rate predominates:SA node – 80-100bpm (meaning heart is

usually under parasympathetic tone)AV node – 40-60bpmSome cells in Purkinje network – 20-40bpm

Pacemaker potentialThere are four ion currents to consider:

IF current – flow of Na+ into cell causing depolarisation. Open as the cell repolarises as opposed to other channels

K+ outflow causing repolarisationT-type Ca2+ channels – open briefly during

depolarisation to provide push towards thresholdL-type Ca2+ channels – open at threshold to cause

large Ca2+ influx creating AP (role of Na+ in other cells)Process is continuous – after K+ has caused

repolarisation the IF current slowly depolarises the cell to activate T-type Ca2+ channels which bring the cell to threshold activating the L-type Ca2+ channels creating the AP and again activating the K+ outflow to repolarise the cell

Cardiac cycleFour (overlapping) phases:

Atrial systole – the ventricle has largely filled passively and is topped up by contraction of the atria to the end-diastolic volume (EDV)

Atrial diastole – atria rests until next atrial systoleVentricular systole – as it begins pressure in the ventricles exceeds

that in the atria and the AV valves shut. There is a period of isovolumetric contraction rapidly increasing pressure inside the ventricle until it exceeds that in the aorta (/pulmonary arteries) and the blood is ejected. The volume ejected is the stroke volume and the percentage of the EDV it makes up is the ejection fraction (usually ~60%). Pressure in the ventricle then drops and as blood starts to backflow the semilunar valves shut – this produces a small rise in arterial pressure knows as the dicrotic notch. The blood left in the ventricle is the end systolic volume (ESV)

Ventricular diastole – isovolumetric relaxation allowing pressure in the ventricle to fall below that in the atria opening the AV valves and allowing passive filling of the ventricles until the next atrial systole

Cardiovascular PhysiologyCardiac outputStroke volumeHeart RateMean Arterial PressureTotal Peripheral ResistanceCardiovascular Response to Exercise

Cardiac outputVolume of blood the heart pumps in litres

per minuteCalculated as heart rate x stroke volume

(HRxSV)Average for adults is 5l/min (ie one blood

volume)Can increase to 20-25l/min or even higher

in athletes through changes in either heart rate

Heart rate (HR)Normal HR is ~72bpm (under parasympathetic stimulation)Mechanisms for altering heart rate:

Sympathetic stimulation (noradrenalin acting on β-adrenergic receptors) Increases the IF current to reach threshold faster Increases conduction through the conduction system Increases contractility of the heart

Parasympathetic stimulation (Acetylcholine acting on muscarinic receptors) Opposite of the above Increases permeability to K+ to hyperpolarise the membrane –

further from thresholdPlasma adrenalin acting on β-adrenergic receptorsChanges in body temperatureOther hormones eg noradrenalin, thyroxineAdenosine – a metabolite released by cardiac myocytes

Stroke volume (SV)Blood volume ejected with each beat – usually 70mlEjection fraction = stroke volume/EDV as a percentageMechanisms for altering stroke volume:

Frank Starling mechanismIncrease of EDV (ie venous return) increases SV. This is because

sarcomeres are stretched further which increases the force of contraction. Unlike skeletal muscle, cardiac muscle at rest is not at the optimal length for contraction, it is on the rising phase of the relationship

Sympathetic stimulation to increase contractilityStronger, quicker contraction and quicker relaxation at any given

EDVBrought about by faster and larger changes in cytosolic Ca2+

concentrations during contraction – more pumps opened, faster binding of calcium and troponin, increased activity of Ca2+ pumps in SR

Mean Arterial Pressure (MAP)“Average blood pressure” – reflection of the

perfusion pressure of the major organs (except lungs)

Normally between 70 and 110mmHgMAP = Cardiac output x Total peripheral resistance

(COxTPR)TPR is the total amount of resistance to blood flow in

the arterial system – mainly controlled by arteriolesMAP is maintained by various homeostatic

mechanisms by altering CO and TPR eg if TPR decreases due to vasodilation in one area then either another area can vasoconstrict to increase TPR or CO can increase to maintain MAP

Also calculated as:MAP = Diastolic pressure + 1/3(Systolic – diastolic)

Total peripheral resistanceCan be altered by local or extrinsic controls affecting the

vascular tone in arteriolesLocal:

Active hyperaemia – increased blood flow to metabolically active tissues activated by release of mediators from the tissues eg CO2, H+, adenosine, hypoxia

Flow autoregulation – the rate of flow determines arteriolar tone ie increased flow causes vasodilation through stretch receptors

Reactive hyperaemia – extreme form of flow autoregulation caused by occlusion of proximal blood vessel

Part of the inflammatory responseExtrinsic:

Sympathetic stimulationHormones such as adrenalin, angiotensin II, vasopressin

(ADH)Extrinsic controls may cause vasoconstriction (eg

adrenalin); local mediators produced due to metabolism then cause vasodilation helping to direct blood flow to the metabolically active areas

Cardiovascular response to exercise Even before exercise begins control centres in the brain activate

autonomic neurons – feed-forward system Sympathetic stimulation causes vasoconstriction especially to

abdominal organs Local mediators released due to metabolism cause vasodilation

and increased blood flow to heart, skin, muscle etc CO increases due to increased venous return (Frank Starling

mechanism) but mostly due to increased contractility due to sympathetic stimulation

Overall TPR decreases, but the larger increase in CO means there is a small increase in MAP with a wider pulse pressure

Chemo-, mechano- and baro-receptors feedback to the medullary cardiovascular centre to adjust the cardiac parameters as needed. Baroreceptors which would normally counter the rise in BP are reprogrammed upward

Two types of exercise:Dynamic eg running – cause small increase in MAP as lots of areas

vasodilateStatic eg weight-lifting – causes large increase in MAP as only specific

areas vasodilate, more dangerous form of exercise for cardiac patients and predisposes to LVH

Factors which limit exerciseVO2 – the capacity of the circulatory system to

deliver oxygen to the tissues. At VO2MAX more blood can be oxygenated by the lungs but cannot be delivered by the heart. This is because CO cannot increase any further as at the upper limits of HR the time for ventricular filling is too short

Respiration – respiration rate and depth increase greatly in exercise but pO2, pCO2 and pH only change in heavy exercise

Muscle massAge Cardiac disease

Cardiac Investigations

Cardiac Examination……

Heart soundsMajor heart sounds are caused by closure of

the valvesFour heart sounds:

S1 – closure of the AV valvesS2 – closure of the semilunar valvesS3 – blood flowing into ventriclesS4 – atrial contraction

MurmursHeart murmurs are caused by turbulent blood flow

eg due to stenosis, regurgitation or can be physiological

Murmurs to know about at this stage are the murmurs of the left heart valves:Systolic – Aortic Stenosis, Mitral RegurgitationDiastolic – Aortic Regurgitation, Mitral Stenosis

Murmurs should be described in terms of site, grade, systolic/diastolic, radiation, duration and character

If you want to hear what they are like: www.youtube.com/user/Drparth2008

Other murmurs include “innocent murmurs” of childhood and murmurs caused by congenital heart disease

ECGTracing of the electrical activity of the heart

through skin electrodesStandard “12 lead” ECG uses 10 physical

leads to produce 12 separate signals which are used for analysis

ECG componentsP wave – atrial depolarisation

Absent in atrial fibrillationQRS complex – ventricular depolarisation

widened in problems in the conduction system eg bundle branch block

T wave – ventricular repolarisationInverted in many conditions eg post MI

PR intervalprolonged in heart block

ST segmentElevated or depressed in myocardial ischaemia

QT intervalProlonged in some rare conditions

ecgpedia.org

Other investigationsImaging

CXR – mostly for heart failureEchocardiography – ultrasound used to examine

heart, can look at valves, wall motion, calculate ejection fraction

MRI with contrast (gadolinium)Angiography

Exercise testingExercise tolerance test – ECG recording during

exercise on treadmill or exercise bike. Bruce protocol (speed and incline increase every 3 minutes) is used

Cardio-pulmonary testing – calculation of VO2

5 min break……..

Clinical Cardiology

AtherosclerosisPathological process affecting arterial wall; responsible for

many common diseases Involves a number of pathological processes eg

inflammation, and hyperlipidaemiaSteps:

Shear stress damages the endothelium of the artery allowing it to take up LDL which is oxidised

Monocytes bind to the endothelium and enter it to become macrophages. These express scavenger receptors allowing them to uptake the oxidised LDL becoming foam cells

These are lead down in the tunica intima forming fatty streaks

T cells are stimulated by the oxidised LDL to release cytokines causing smooth muscle cells to proliferate and migrate from the tunica media to the tunica intima

An atherosclerotic plaque is now formed which develops a fibrous cap

Images from Robbin’s Pathological Basis of Disease

Atherosclerotic DiseasesCarotid arteries

Strokes (cerebral infarct), TIACoronary arteries

Angina, ACSRenal arteries

Renal artery stenosis, hypertensionMesenteric arteries

Ischaemic colitisAorta

Aortic aneurysmsLimb arteries

Intermittent claudication, critical limb ischaemia

Angina Pectoris Occurs when an atherosclerotic plaque causes stenosis

(but not occlusion) of coronary arteries meaning the myocardial demand for oxygen via blood cannot be met during periods of exercise eg physical exertion, following a heavy meal (increased blood supply to gut), or in cold weather (peripheral vasoconstriction increases TPR)

Coronary arteries particularly at risk, especially harmful as cardiac tissue relies mainly on aerobic respiration

An inadequate oxygen supply and inadequate removal of metabolites leads to ischaemia causing lactic acidosis and build-up of other toxic metabolites

Sensory nerves are stimulated, possibly by adenosine released by ischaemic myocardium causing chest pain

Causes Atherosclerotic risk factors:

Non-modifiableAgeMale genderFamily historyEthnicity (South Asian etc)

Modifiable HyperlipidaemiaHypertensionSmokingDiabetesObesityPoor diet, sedentary lifestyle

Investigation Diagnosis is most often clinicalTests:

ECGExercise ECGCoronary angiographyMyocardial perfusion scans eg thallium scan

TreatmentMedication

Antiplatelets eg Aspirin or Clopidogrel Prevent thrombosis

ACEI eg Ramipril Counteract RAA system, reduce blood pressure and other

effectsStatin eg Simvastatin

Reduce cholestrolNitrates eg GTN, ISMN

Metabolised to nitric oxide which causes venodilation mainly reducing preload and reducing myocardial demand

β-blockers eg Atenolol Counteract sympathetic effects discussed earlier to reduce

myocardial demandCalcium channel inhibitors eg Verapamil

Reduce contrctility of the heart and block vasoconstriction to reduce myocardial demand

Potassium channel openers eg Nicorandil Hyperpolarise membranes causing vasodilation

Treatment Risk factor reduction

Smoking cessation, adjust diet and lifestyle, lose weight, control diabetes, control blood pressure and cholestrol

InterventionAngioplasty and stentingCABG

Heart FailureDefinition – complex syndrome resulting from any structural

or functional cardiac disorder which disables the heart from acting as a pump and maintaining circulation

Causes – coronary artery disease, hypertension, valvular disease, cardiomyopathies, lung disease (cor pulmonale)

Preload – the tension the ventricular walls have developed at the end of diastole before contractionIncreased by increasing venous return and vice versaEstimated as the EDV. An increase in EDV will increase the SV

(Frank Starling Mechanism) to give the same ESV regardless of EDV

Afterload – the tension the heart must generate to overcome TPRIncreased in hypertension and ventricular dilation, decreased in

LVHIncreased afterload leads to reduced SV and increased ESV

Pathology Can be thought of in terms of:

Left heart failure - systolic and diastolic dysfunctionSystolic – impaired contractility and increased afterload

lead to reduced ejection fraction and increased pressure in the heart causing pulmonary congestion

Diastolic – abnormal ventricular relaxation eg due to fibrosis of the heart following MI; leads to systemic and pulmonary congestion

Right heart failureMost commonly due to left heart failure which increases

the afterload of the right ventricleImportant to consider the compensatory

mechanisms activated by heart failure:Frank Starling mechanismNeuro-hormonal alterationsVentricular hypertrophy and remodelling

Frank Starling MechanismAs mentioned as the EDV increases due to

incomplete emptying causing the SV to subsequently increase

This is initially beneficial however when the EDV increases to the point where SV cannot increase further to compensate the LV pressure rises.

This rise is transmitted through the LA to the lungs causing pulmonary congestion

Neurohormonal alterations3 main componentsAutonomic nervous system:

Increased sympathetic and decreased parasympathetic stimulation to help increase CO and maintain BP

Renin-Angiontensin-Aldosterone systemCauses vasoconstriction and increases circulating volume to

maintain BPAntidiuretic hormone

Promotes water retention to increase blood volume & BPOthers include ANP, BNP and endothelinsThese mechanisms initially help but eventually become

pathological:Increased blood volume and venous return cause pulmonary

congestionVasoconstriction increases afterload and impairs SV and COIncreased metabolic demand on the heartSustained sympathetic stimulation causes down-regulation of

adrenergic receptors and increases inhibitory G-proteins causing a negative inotropic response

Chronic activation of the RAA system produces cytokines and activates macrophages and fibroblasts to lead to adverse remodelling of the heart

Ventricular hypertrophy & remodellingEccentric remodelling

Occurs due to chronic volume overload (eg aortic regurgitation), myocytes elongate causing ventricular hypertrophy and dilation

Concentric remodellingOccurs due to chronic pressure overload (eg

hypertension), myocytes thicken causing ventricular hypertrophy only

Wall stress = pressure x radius / 2x wall thicknessInitially hypertrophy reduces wall stress (because

of increased wall thickness) Dilation increases wall stress due to increased

radiusEventually there is pressure overload causing

heart failure symptoms

Signs and symptomsSymptoms caused by vascular congestion and

failure to adequately perfuse tissuesDyspnoea, orthopnoea, paroxysmal nocturnal

dyspnoea, nocturnal coughFatigue and weaknessImpaired urine output during day and nocturia Dulled mental statePeripheral oedema and weight gain due to

increased venous pressureTachycardia, tachypnoea and sweating due to

sympathetic stimulation

Investigations Clinical diagnosis CXR – shows pulmonary congestion and

cardiomegalyECGEchocardiogramBloods – cardiac enzymes, BNPOther imaging or biopsies dependent on

cause of heart failure

Treatment ACEI eg ramipril

Reduce vasoconstriction (reduced ATII) and prevent increase in blood volume (reduced aldosterone) causing decreased preload and afterload

Also blocks remodelling effect of angiotensinCan substitute with angiotensin receptor blockers eg

losartanDiuretics eg frusemide, eplerenone, spironolactone

Loop diuretics eg frusemide used to clear oedema by inhibiting NaCl reabsorption at the thick ascending loop of Henle

Potassium sparing diuretics eg eplerenone, spironolactone also clear oedema without losing K+ by antagonising aldosterone to prevent Na reabsorption and K+ excretion

Treatment β-blocker eg atenolol

Must be started at a low dose and titrated up, counteracts effects of chronic sympathetic stimulation

DigoxinAntagonises the Na+/K+ pump to increase intracellular Na+; through

the Na+/Ca2+ exchanger this causes increased intracellular Ca2+

Has a positive inotropic effect on the heart to increase CO and also has indirect effect to increase vagal activity

No effect on mortality but helps with symptomsToxicity is common causing ectopic beats and heart block

Other positive inotropes such as IV dobutamine can be used short term in very sick patients but may increase mortality

TreatmentTreat underlying cause of the heart failure

eg hypertension, coronary artery diseaseDevice therapy

PacemakersCRTICD

Heart transplantation

Cardiac Examination

Wash hands, introduce, consent, positionGeneral inspection – comfortable? breathless?Hands – clubbing, nail changes, temperature,

cyanosisPulse – rate, rhythm, volume, characterFace – xanthelassma, central cyanosisNeck – JVP, carotid pulsePraecordium

Inspection – scars, chest deformitiesPalpation – apex beat, thrills, heavesAuscultation – four areas – aortic, pulmonary,

tricuspid, mitralTo finish my examination….

BPLung basesAnkle and sacral oedema

Questions?