For Phase 1a Maria Digby & Rowena Speak

For Phase 1a

Maria Digby & Rowena Speak

Cardiology

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

1st Half* Physiology* Pharmacology* Anatomy* ECG

2nd Half* Pathophysiology + Clinical Scenarios* More Pharmacology!* Question time

What we’re going to cover…


Ventricles


* Phase 0: depolarisation – Na+ in

* Phase 1: partial repolarisation – Na+ channels shut, K+ out

* Phase 2: plateau – Ca2+ in through L-type channels

* Phase 3: repolarisation – K+ out

* Phase 4: resting potential – (-90mV) – Na+/K+ ATPase

SAN


* Phase 4 = pacemaker potential – less K+ out, Na+ in through F-type channels, Ca2+ in through T-type channels

* Phase 0 = slower depolarisation – Ca2+ in through L-channels NOT Na+ in like depolarisation ventricles!)

* Phase 3 = repolarisation – K+ out

Antiarrhythmic drugs: Vaughan Williams classification


* Class I: Na+ channel blockers1a) Quinidine – moderate blocker 1b) Lignocaine – weak blocker1c) Flecainide – strong blocker

* Class II: Beta blockers: block sympathetic stimulation - atenolol

* Class III: K+ channel blockers: prolong repolarisation - amiodarone

* Class IV: Ca2+ channel blockers: verapramil

I

IV

Phase 4

Phase 0

Phase 1

Phase 2

Phase 3

0 mV

-80mV

II

III

Cardiac cycle


- AP = aortic pressure- LVP = left ventricular

pressure- LAP = left atrial pressure- LVEDV = left ventricular

end diastolic volume- LVESV = left ventricular

end systolic volume

Cardiac cycle: Systole


• Systole

- After ventricular filling, pressure in ventricles > in atria = AV valves close (SOUND 1 = “lub”)

1. Isovolumetric contraction: ventricles contracts when all valves are shut (this increases pressure in ventricles)

2. Ventricular ejection: pressure in ventricles > in pulmonary artery/aorta = semilunar valves open and blood flows out of ventricle

Cardiac cycle: Diastole


• Diasystole

- After ventricular ejection, pressure in pulmonary artery/aorta > than in ventricles = semilunar valves shut (SOUND 2 = “dub”)

1. Isovolumetric relaxation: ventricles relax when all valves are shut (this decreases the pressure in the ventricles)

2. Ventricular filling: pressure in ventricles < in atria = AV valves open

Cardiac cycle: “atrial kick”


• Ventricular filling is mostly a passive process

• But towards the end of diastole, the atria contract causing a small increase in pressure in the ventricles = “atrial kick”

Cardiac cycle: dicrotic notch


• When the aortic valve closes, blood rebounds against the valve causing a decrease then a rebound of aortic pressure = dicrotic notch

Equations: learn these!!


* SV = EDV - ESV* CO = HR x SV* MAP = DP + 1/3(SP-DP)* BP = CO x TPR

Monitoring MAP: Baroreceptors


Where are the arterial baroreceptors?

a) Carotid sinus + b) Aortic arch

Baroreceptors detect changes in arterial pressure Afferent nerve (Glossopharyngeal) CNS (Medullary Cardiovascular Centre) Efferent nerve i. Sympathetic outflow to heart and arterioles ii. Parasympathetic (Vagus) outflow to heart

Maintaining MAP (BP = CO x TPR)


BP

CO TPR

Maintaining MAP: 1. Changing CO


CO = HR x SV

Change Heart Rate* Sympathetic nervous

stimulation of the heart* Parasympathetic nervous

stimulation of the heart (Vagus)

* Plasma adrenaline

Change Stroke Volume* Sympathetic nervous

stimulation of the heart* Plasma adrenaline* End-diastolic ventricular

volume (preload) – FRANK-STARLING MECHANISM

FRANK-STARLING MECHANISM – learn this!


At any given heart rate….

Any ↑ Venous Return….

Causes ↑ End-Diastolic Volume…

Causes ↑ stretch in the cardiac muscle (Preload)…

Causes ↑ forceful contraction…

Which ↑ Stroke Volume and thereby the Cardiac Output

Maintaining MAP: 2. Changing TPR


The arterioles are the principle site of resistance to blood flow

Vasoconstriction* Local: Endothelin-1, internal

blood pressure (myogenic response)

* Neural: Sympathetic nerves* Hormonal: Adrenaline (on

alpha receptors), Angiotensin II, Vasopressin (aka Antidiuretic hormone)

Vasodilation* Local: decrease in Oxygen,

increase in CO2/H+, Nitric Oxide, Eicosanoids, Prostacyclin

* Neural: Neurons that release Nitric oxide

* Hormonal: Adrenaline (on beta 2 receptors), Atrial Natriuretic Peptide

Important point…


* There is sympathetic stimulation to both the heart and arterioles

* But there is no parasympathetic stimulation to the arterioles, only to the heart

Terms to understand…


Active hyperaemia – vasodilation in response to an increase in metabolic activity

Flow autoregulation – vasodilation in response to decreased pressure

Reactive hyperaemia – when a tissue’s blood supply has been completely occluded, on removal of the occlusion there is a profound, transient increase in blood flow

GO LOOK AT…


VANDERS - especially page 399 (12th edition)

Long term regulation of MAP


The Baroreceptor reflex is a short term regulator. They end up adapting to a maintained change in pressure.

The most important long-term regulator of arterial pressure is blood volume – this is regulated by the Renin-Angiotensin-Aldosterone System (RAAS)

ACE inhibitors inhibit RAAS to reduce blood volume

(have a quick look at RAAS – try to understand it but don’t worry about memorising it until Phase 1b!)

RAAS


Haemostasis


1. Platelet plug2. Clotting cascade

* Clotting factors dependent upon Vitamin K: II, VII, IX, X

* Haven’t got time to talk about this now – make sure you understand the principles of it

* Important for understanding pharmacology of Aspirin, Clopidogrel, Warfarin, Heparin and Fibrinolytics

Anatomy - valves


Valve Surface marking Auscultation area

Tricuspid 4th intercostal space-midline

5th intercostal space-right and left sternal edge

Pulmonary 3rd costal cartilage-sternal junction-left

2nd intercostal space-left sternal edge

Mitral 4th intercostal cartilage-midline

5th intercostal space-left, midclavicular line

Aortic 3rd intercostal space-left half of sternum

2nd intercostal space-right sternal edge

Anatomy - valves


Valve pathology


Pathology Cause MurmurMitral stenosis Rheumatic fever Mid-diastolic

Mitral regurgitation Ischaemic heart disease, MI, Rheumatic fever

Pan-systolic

Aortic stenosis Calcific valve disease, Rheumatic fever

Ejection-systolic

Aortic regurgitation Rheumatic fever, bicuspid aortic valve

Diastolic

Rheumatic fever


• Endocarditis • Post-Streptococcus pyogenes infection• (Scarlet fever, Strep throat)• Damages heart valves

Anatomy – heart borders


Right: formed by right atrium, runs between 3rd and 6th right costal cartilages approximately 2-3cm from the midline in the adult

Left: formed by left atrial appendage + left ventricle, apex 2nd left intercostal space 2-3cm from midline

Inferior: formed by right atrium and right ventricle + tiny bit of left ventricle

Anatomy – aorta


Thoracic* Right + left coronary arteries* Brachiocephalic (aka innominate)

artery* Left common carotid artery* Left subclavian artery

Passes through diaphragm at T12

Abdominal* Abdominal aortic aneurysm –

expansile, pulsatile mass, midline, above umbilicus

Bifurcates at L4

Electrocardiography (ECG) – heart rate


Heart Rate– Quick estimation = 10 x no. of QRS complexes on

one rhythm strip (check speed of ECG is 25mm/s)

• Sinus bradycardia < 60bpm• Sinus tachycardia >100bpm• Normal PR interval = 0.12-0.20s• Normal QRS complex = 0.08-0.12s

ECG – AV block


1st degree – PR interval prolonged, >0.20sec

2nd degree:-1. Mobitz type I - progressive lengthening of PR interval with

each successive complex until a P wave is not conducted2. Mobitz type II – PR interval constant, QRS complexes

dropped intermittently or in fixed ratio to P wave rate

3rd degree - Complete dissociation of P Waves and QRS complexes

ECG


Atrial flutter = saw tooth pattern

Atrial fibrillation = irregularly irregular rhythm

ECG – Ventricular fibrillation: fine and coarse


Ventricular fibrillation

Useful websites


• http://www.cvphysiology.com• http://www.cvpharmacology.com/

http://www.cvphysiology.com/



http://www.cvpharmacology.com/

http://www.cvpharmacology.com/

Pathology/Pathophysiology

• Normal arterial structure


Getting old ain’t pleasant

• Progressive fibrous thickening of intima

• Fibrosis + scarring of muscular or elastic media

• Accumulation of mucopolysaccharide-rich ground substance

• Fragmentation of elastic laminae

• ATHEROSCLEROSIS


Atherosclerosis

Some predisposing factors?

Prevented?


Atherosclerosis

• Effects medium and large arteries

Risk factors:• Aging• Male • Hypertension • Smoking • Diabetes mellitus

• Hyperlipidemia • Increase LDL• Decreased HDL• Having a factor 7

genetics• Lifestyle- Exercise - Obesity- Diet- Stress and personality


Drugs – ‘all’s well that ends well’ ;)

• Drugs• Calcium channel blockers “ipine”s eg:

amlodipine• ACE Inhibitors “il”s eg: ramipril• Angiotensin Receptor Blockers “sartans” eg:

candesartan• Diuretics “ide”s eg: loop – furosemide,

thiazide – bendoflumethiazide and K sparing - Amiloride

• Beta blockers “olol”s eg: atenolol• Statins “statin”eg: simvastatin


• Clopidogrel - is an oral, thienopyridine class antiplatelet agent

• Anticoagulants “rin” eg: warfarin and heparin

• NSAIDS “profen” eg: ibuprofen, aspirin *so doesn’t work for everything



Angina Pectoralis

• Caused by chronic heart disease

• Atherosclerosis in the coronary artery

• Means less O2 to heart muscle

• Crushing chest pain • No troponin • No new changes on

ECG

• Stable or unstable? • Stable - Caused by activity / stress (watching Barnsley)- relieved by GTN/rest• Unstable - NOT relieved by GTN /rest - Can occur at rest


MI

What is an MI? How does it occur?How does it present? How is it prevented?

• ST elevation myocardial infarction

• Non-ST elevation myocardial infarction


MI - STEMI

• Crushing chest pain • Feeling of

“impending doom” in Barnsley – “gonna miss Barnsley play at weekend” ;)

• Nausea • Sweating• SOB• Clammy skin

• Raised Troponin level

• ST elevation on ECG


MI - STEMI

• STEMI • Ambulance • MONA

• A and E • β blocker (atenolol)• Thrombolytics (tPA

or streptokinase)• ACE inhibitor

(lisinopril)• Clopidogrel

• Back at home• Warfarin• Aspirin• β Blocker

(metoprolol)• ACE inhibitor• Statin (simvastatin)


MI - NSTEMI

• Infarct • Feeling again same

“impending doom” - Barnsley be relegated?

• Nausea • Sweating• SOB • Clammy skin

• Raised Troponin• No new ECG

changes


MI - NSTEMI

NSTEMI Ambulance • MONA• M= Morphine • O = Oxygen• N = Nitrates• A = Aspirin

A and E • β blocker (atenolol)• LMW heparin• GPIIb/IIIa antagonist

(tirofiban)• Nitrates• Clopidogrel Back at home • Warfarin• Aspirin• β Blocker (metoprolol)• ACE inhibitor • Statin


Heart Failure

• Heart failure = pathophysiological state in which the heart is unable to pump sufficient blood to meet the needs of the metabolising tissues or can only do so with elevated filling pressures

• R, L or Congestive • Systolic / diastolic /Both• Excessive salt and water retention• Low cardiac output and raised peripheral

resistance


Causes:- 1. Ischaemic heart disease – 34%2. Dilated cardiomyopathy – 32% 3. Primary valvular disease and

congenital heart disease – 12% 4. Hypertensive heart disease – 11% 5. Other -5%


• Physiological– A state where the heart is unable to

pump enough blood to satisfy the needs of the metabolising tissues

• Clinical– A symptomatic condition where

breathlessness, tiredness and fatigue are associated with a cardiac abnormality that reduces cardiac output


Key concepts - Pathophysiology

1. Initial insult2. Fall in cardiac output 3. ↑Preload to maintain ventricular

performance4. ↑Afterload limits ventricular performance5. Maladaptive hormonal responses6. Progressive left ventricular remodelling 7. Progressive decline in cardiac

performance


Left heart failure

• Symptoms:

• fatigue,

• exertional breathlessness,

• orthopnoea

• paroxysmal nocturnal dyspnoea

• Signs: (occur late)

• cardiomegaly,

• added heart sounds,

• tachycardia,

• crackles in lung bases


Right heart failure

• Symptoms:

• -swollen ankles, fatigue, anorexia

• Signs: (occur early)

• -raised jugular venous pressure

• -hepatomegaly

• -pitting oedema

• -ascitesThe Peer Teaching Society is not liable for false or misleading information…

Congestive

• A mixture of both left and right heart failure!

• Almost always right heart failure secondary to severe left heart failure…


Tetralogy of Fallot

• Congenital defect – most common form of cyanotic congenital heart disease

Causes:-Low O2 levels in the blood leading to cyanosis



Classic form includes 4 defects of the heart and its major blood vessels

1. Ventricular septal defect 2. Narrowing of the pulmonary outflow

tract3. Overriding aorta - shifted over to

the RV and ventricular septal defect (usually just from LV)

4. Right ventricular hypertrophy


Factors that increase risk

• Alcoholism in mother • Diabetes • Mother who is over 40 years old• Poor nutrition during pregnancy• Rubella or other viral illnesses during

pregnancy • Children more likely to have Downs

syndrome


Symptoms

• Cyanosed (blue skin)• Clubbing of fingers • Difficulty feeding • Failure to gain wt• Passing out • Poor development • Squatting during episodes of

cyanosis


Signs and tests• Chest Xray• Complete blood count • ECHO • MRI (usually after surgery)TreatmentSurgery to repair tetralogy of Fallot is done when the infant is very youngOutcome – 90% survive to adulthood and live an active, healthy and productive life• Do have to have regular cardiology

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

Problem solving time

• 50 year old man presents with “crushing chest pain”, he was rushed in to AandE from the local Barnsley vs Owls, smoker for 35 years, the chest pain radiates to his jaw. He feels sweaty, nauseous and vomited.


a) MIb) Angina c) Tetralogy of Fallotd) Right heart failuree) Football fever


• 80 year old retired postman complains of severe onset central chest pain which comes on when he is walking his cat Jess. He sometimes gets it when sitting reading the sports section of the Barnsley Chronicle.

• Any ideas?


a) MI b) Unstable Angina pectoralisc) Palpitationsd) Intermittent claudication e) Stable angina pectoralis


• A 50 year old lady diabetic (type 2) complains of pain when walking in her calves and is relieved by rest.

• She used to smoke until 2 years ago and is a telesales rep


a) Crampb) Intermittent Claudication c) DVT (deep vein thrombosis)d) Pulled a muscle e) Been stabbed in the leg in the past


Thank you for your attention

Documents

For Phase 1a Maria Digby & Rowena Speak