phase 1a miles benjamin daniel bradbury the peer teaching society is not liable for false or...

Phase 1a

Miles BenjaminDaniel Bradbury

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

1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)

2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias


Outline

3. Clinical Problems– Chest Pain– Leg Pain– Murmurs

Muscle

• Action potential arrives at sarcomere.

• Opening of Ca2+ channels.

• Influx of calcium ions.

• Initiates muscle contraction.


• 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 – inhibtory binds to actin, to hold

the tropomyosin – troponin complexes in place.


Troponin

• Contraction of involuntary striated muscle.– Controlled by Ca2+

– Increase in concentration causes contraction

• Sliding filament theory


Cardiac Contraction


So …


The Cardiac Cycle

• Contraction of the left and right atria.– blood pressure in

atria increases forcing blood into the ventricles.

– begins with the onset of the ‘P’ wave on ECG


Atrial Systole


Ventricular Systole• Ventricular systole is the

contraction of the left and right ventricles.

• Blood is forced out of the pulmonary and aortic valves

• “Lubb – Dub”– Lubb is the closure of AV

valves at beginning of ventricular systole.

– Dub is the closure of aortic and pulmonary at end of ventricular systole.

• QRS complex

Diastole• When do coronary arteries perfuse heart

tissue with blood?• Diastole!• In diastole the heart is in an mostly un-

contracted state• As pressure drops in ventricles, AV valves

open. Blood begins filling chambers again.



Leaving the heart• Cardiac Output

CO = SV x HR• SV = Stroke Volume• HR = Heart Rate• 5+ litres a minute• Are ventricles pumping effectively?


Electro Cardiography

• P wave– Atrial depolarization, SA node towards the AV

node, spreads from the right to left atrium.

• QRS complex– Rapid depolarization of the right and left

ventricles. Larger muscle so larger amplitude.

• T wave– Repolarisation of the ventricles.


Main waves




Outline


• Definition– The average arterial blood pressure over the

entire cardiac cycle

• Formula?


Mean Arterial Pressure

• Definition– The average arterial blood pressure over the

entire cardiac cycle

• Formula?


Physiology

MeanArterial

Pressure (MAP)

CardiacOutput

(CO)

TotalPeripheralResistance

(TPR)

= x

• Definition– Volume of blood ejected by each ventricle per

minute

• Formula?


Cardiac Output

• Definition– Volume of blood ejected by each ventricle per

minute

• Formula?


Physiology

CardiacOutput

(CO)=

Heart Rate(HR)

xStroke Volume

(SV)

• Definition– Total resistance to flow of blood by all systemic

blood vessels

• Which level of blood vessel offers the most resistance?• Arterioles offer the most resistance to vascular

flow as they can be changed by vasoconstriction or vasodilation


Physiology

• Controlling TPR– Locally

• Active hyperaemia ↑ demand by organ = vasodilation• Flow autoregulation ↓ supply to organ =

vasoconstriction

– Extrinsic• Autonomic nervous system • Hormones whole host of vasodilators/constrictors

– NO


Physiology




Outline


• Definition- Formation of plaques in the intimal

layer of medium to large sized arteries. HARDENING OF THE ARTERIES


Atherosclerosis

• PathophysiologyLDL oxidation → macrophages & lymphocytes to absorb oxidised LDL → foam cells. White cells

cannot process oxidised LDLs → inflammation & continuation of cycle. Fatty streak → fibrous plaque → atherosclerotic plaque


Atherosclerosis


Atherosclerosis• Risk Factors

– Age– FH– Obesity– Male– Smoking– Diabetes Mellitus – Hyperlipidaemia– Hypertension

• Angina• Claudication• MI• Aneurysm


Outcomes of Atherosclerosis

• Atherosclerosis of coronary arteries• Pathophysiology

– Increased demand without proportional increase in oxygen supply

• Clincal Features– SOB, Nausea, Fatigue, Chest Pain

• Stable vs. Unstable


Angina

• Diagnosis– ECG (ST depression), exercise tolerance,

coronary angiogram

• Treatment– Immediate= GTN Spray– Long Term= ????????


Angina

• Diagnosis– ECG (ST depression), exercise tolerance,

coronary angiogram

• Treatment– Immediate= GTN Spray– Long Term= Statins, Beta Blockers,

Antiplatelets:ACE inhibitors, Calcium Channel blockers


Atherosclerosis – Angina

• Complete blockage of coronary artery• Clinical Features

– Severe crushing chest pain, Dyspnoea, Nausea, Sweating, Feeling of terror

• Diagnosis– ECG, Bloods, Raised Cardiomyocyte

• Treatment– Antiplatelet, BB,Statins, PCI


Atherosclerosis – MI

• Ischaemia, usually do to atherosclerosis• Typically presents as elderly person who gets leg

pain when walking• After they rest for a few minutes the pain goes

away and they can start walking again


Intermittent Claudication

• Localised, permanent dilation of artery• Can be asymptomatic until it ruptures• Ruptured abdominal aneurysm causes sudden

severe abdominal pain – surgical emergency• Aortic dissection – blood between layers of aorta


Aneurysm




Outline



Thromboembolism

• Deep vein thrombosis• Pulmonary embolism




Outline


An acute failure of the CVS to perfuse the tissues

• Hypovolaemic – blood loss

• Anaphylactic – type I hypersensitivity

• Septic – vasodilation caused by bacterial toxins

• Cardiogenic – heart failure


Shock




Outline


• Where the heart is unable to pump enough blood to satisfy the needs of the metabolising tissues.

• Breathlessness, tiredness and fatigue are associated with a cardiac abnormality that reduces cardiac output.


Heart Failure


Left Heart Failure• Fatigue and weakness• Exertional breathlessness• Orthopnoea • paroxysmal nocturnal

dyspnoea• Cough / pulmonary

oedema – crackles in ;lung bases.


Right Heart Failure• Swollen ankles• Fatigue• Raised jugular venous

pressure• Abdominal

swelling/hepatomegaly• Pitting oedema• Ascites• Could be cor pulmonale –

query PE, COPD etc.


Congestive Heart Failure• Both!• Very often a case of

right heart failure due to severe left failure.




Outline


• Abnormal electrical activity in the heart.• Too fast?• Too slow?• Uncoordinated?


Arrhythmias


Normal ECG


Bradycardia• Slow heart rate (< 60bpm)• Sinus node disease, AV block, MI, beta blockers.• non-cardiac

– e.g.raised ICP – hypothermia – hypothyroidism


Bradycardia• AV Block• First degree – delayed conductance, prolongation of PR

interval.• Second degree – when one or more impulses fail to reach

ventricles.– Mobitz 1: progressive lengthening of PR interval each successive

complex until a P wave is not conducted.– Mobitz 2: PR interval constant, QRS complexes dropped intermittently

or in fixed ratio to P wave rate.

• Third degree – No conductance from atria to ventricles. Complete dissociation of P Waves and QRS complexes. Rate 30-40 / min


Tachycardia•Sinus tachycardia. Rate > 100/min•Causes

–Exercise–Thyrotoxicosis–Catecholamine stimulation (emotion)–Fever–Anaemia–Cardiac failure–Hypovolaemia


Supra Ventricular Tachycardia•Symptoms include palpitations - sudden onset

–sudden offset or gradually tails away–few seconds to hours/days

•Precipitating factors–Tea, coffee, tobacco, alcohol, exercise, –emotional upset

•Rate 120-260/min

•P-waves may or may not be present


Atrial Fibrilation•Irregularly irregular rhythm

•Atrium discharge at very high rates 300-500/min

•Ventricular rate slower and irregular


Atrial FibrilationCauses: Cardiac

- Idiopathic - Rheumatic heart disease - Ischaemic heart disease - Cardiomyopathy - WPW syndrome

Non-cardiac- Alcohol - Carcinoma of bronchus

- Pneumonia - PE

Treatments include aspirin/warfarin (for anticoag) and then drugs to alter rate (beta blockers). Pacemakers, implantable defibs?


Atrial Flutter• Macro re-entry circuit

within right atrium• On ECG there is a saw

tooth pattern – atrial rate 300/min

– ventricular rate

commonly 150/min• Treatment

– anticoagulants as for AF

– Drugs– rate control difficult – DC cardioversion – ablation


Ventricular Tachycardia• Broad and complex• Can well tolerated.• Risk factor for

hypotension.• Wide QRS with shift to

left.• Deep S wave.• Treat with drugs

(lidocaine) and DC cardioversion.

• Implantable defib?


Ventricular Fibrilation• Uncoordinated contraction of ventricles.• Quiver rather than contract.• Usually lead to cardiac arrest > cardiogenic

shock.• Treatement

– Immediate life support– 999– Defibrilation– PCI




Outline



Leg Pain• 74 year old man• Diabetes Mellitus and Hypertension• Heavy Smoker• Sharp pain in his calves when walking• Has to stop walking to relieve pain

• Characterised by cramp-like pain in the legs on exercise

• Muscles deprived of oxygen → lactate production → pain

• Occurs after a certain distance and settles on rest after a certain time

• Caused by atherosclerosis of one or more of the arteries supplying the lower limb

• Same risk factors as for MI


Intermittent Claudication


Chest Pain• A 61 year old man presents complaining of increasing SOB on exertion

and tiredness. Previous MI 9 weeks ago. You diagnose heart failure.

What is the pathophysiological definition of ‘heart failure’? (4)How does left heart failure lead to pulmonary oedema? (6)3 reasons why people with heart failure experience a progressive decline in cardiac function (3x2)Another symptom for left ventricular failure besides shortness of breath and fatigue? (2)


Murmur

phase 1a miles benjamin daniel bradbury the peer teaching society is not liable for false or...

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qrs complex slide

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right ventricles

left ventricles

heart rate