Part 7


I and T

Which troponin have specific cardiac types 

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Site - diffuse ant chest, left arm and neck 

Character - Tight, pressure, weight, constriction, dull 

Triggers - exercise, cold, meals, psychological stress 

Relief - rest, GTN (if anginga) 

Duration - >30mins 

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Most common type of MI 

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Prevention of an MI

Lower cholesterol 

Lower BP 

ACE inhibitor 



Beta blockers 

Life style (smoking and diabetes) 

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Progressive disease affecting the intima of elastic and muscular arteries.

Characterised by focal atheroma's 

Lipid core covered by fibrous cap 

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Monckeberg's medial sclerosis

Calcification in the media of muscular arteries 

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Proliferation or thickening of hyaline in the wall of small arteries and arterioles 

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Stages of plaque development

Type 1 = lipid present in macrophages in intima, take up LDL 

Type 2 = Lipid present in both macrophages and SM cells - start producing collagen that goes on to form the fibrous cap 

Type 3 = Fibrous plaque 

Type 4 = Complex plaque (fibrous cap over a lipid core) 

8 of 40

Transmural (STEMI)


Regional infarct 

Ischaemic necrosis that involves the full or nearly full thickness of the ventricle wall in distribution of a single coronary artery. 

Associated with coronary artherosclerosis -> plaque rupture -> superimposed thrombus 

9 of 40

Subendocardial (NSTEMI)

Inner one third or at most half of the ventricle wall 

Diffuse stenosing coronary atherosclerosis and global reduction of coronary flow (shock) 

But no plaque rupture or thrombus 

10 of 40

Early Post MI complications

Further arrhythmias and subsequent heart failure 


Papillary muscle dysfunction (mitral valve complication) 

Mural thrombosis in ventricle 

Ventricular rupture 

Papillary muscle rupture 

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Late post MI complications

Ventricular aneurysm 

Post MI sundrome 



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Cardiac rupture

1-5% of cases 

Commenest 4-7 days post infarct 

Ventricular free wall 


Cardiac tamponade 

Rupture of intraventricular septm 

Left to right shunt 

Rupture of papillary muscles -> severe acute mitral incompetence 

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2nd or 3rd day 

Fibrinous or fibrinohaemorrhagic 

Usually localised to region overlying necrotic area 

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Transfer of abnormal material via bloodstream and impaction in vessel 

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Different types of emboli

Fragment of thrombus 

Material from ulcerating atheromatous plaques (commonest in distal leg A) 

Septic emboli 

Fragment of tumour growing into a vein 

Fat globules (following fractures) 

Air emboli (300ml enough to make heart stop) 

Parenchymal cells 

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Day post an operation, most common to suffer from a PE 

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Acute heart failure

Inability to provide adequate CO to support the needs of tissues - or to do so at the expense of raised filling pressure 

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Right sided heart failure

Impaired pumping causing reduced CO in both ventricles 

Systemic venous pressure rises as RV EDP rises 

Circulatory reflexes keep PAP, PVP, LV EDP and aortic pressure constant 

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Left sided heart failure

Both Ventricle CO falls 

Pulmonary venous pressure rises as LV EDP rises 

Increased PVP transmitted leading to raised PAP 

Aortic pressure and systemic remain constant 

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Congestive heart failure

Most patients 

Heart failure due to LV failure in turn affecting the RV 

Fall in CO 

Significant rise in PVP as LV EDP rises 

Modest elevation in PAP 

Rise in SVP 

Reflexes keep aortic constant

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Causes of heart failure

Pressure overload (HTN, aortic stenosis) 

Volume overload (Valve regurgitation) 

Contractile dysfunction (ischaemic heart disease, congenital cardiomyopathies) 

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Peripheral vasoconstriction 

Increased HR 


All returning BP to normal 

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Ang II

Vasconstriction at tissues

Stimulates aldosterone release 

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Types of angina





Microvascular - syndrome X 


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Anti-anginal drugs





K+ channel activators 


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Disturbance of the normal rhythmic beating of the heart - ectopic pacemaker 

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3rd degree heart block (complete heart block)

Causes - idiopathic bundle branch fibrosis, atherosclerotic CHD, dilated cardiomyopathy

Effect on cardiac rhythm - slow HR (degree depends on location of block) 

Heart rhythm is driven by escape beats, originating from the distal pacemaker just below the block

Symptoms - temporary syncope followed by recovery with breathlessness, fatigue and possible chest pain 

Prognosis - 2 mo without treatment 

Treatment - implantation of a permanent pacemaker.

QRS dissociation from P wave as atria and ventricle beat independently  

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Rapid heart rate caused by re-entry 

Occurs when adjacent areas of myocardium have different conduction rates and refractoriness (ischaemia, myocardial scarring and certain congenital conditions) 

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Atrial fibrillation

Chaotic atrial rhythm with rapid irregular ventricular rhythm 

Causes - ectopic focus or reentrant pathway in heart muscle surrounding PV or in the atrium 

Risk factors - dilation, HF, HTN, overactive thyroid, XS alcohol, old age 

Ventricular excitation occurs with atrial depolarisation sufficient to be conducted through AVN 

Symptoms - palpitations, breathlessness, dizziness, syncope 

Paroxysmal -> persistent -> permanent 

Major risk factor for stroke due to stasis of blood 

Treat with class 1-4 anti-arrhythmatic drugs, radio catheter ablation, anticoagulants or LA appendage closure 

ECG - lack of p wave, irregularly irregular QRS, time smaller f waves 

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Na+CB, suppressing conduction (flecainide)

Class 1 anti-arrhythmic drug 

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Beta blockers, inhibit AVN conduction

Class 2 anti-arrhythmic drug 

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Drugs which prolong AP and refractory period (amio

Class 3 anti-arrhythmic drugs

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CCB - inhibit AVN conduction (verapamil)

Class 4 anti-arrhythmatic drugs 

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Class 2, 4, adenosine and digoxin

Rate control drugs 

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Class 1 and 3

Rhythm control drugs 

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Rapid (120-200bpm) successive ventricular beats 

Most often due to cardiac scarring post MI or dilated cardiomyopathy, Can be congenital (LQT syndrome, brugada syndrome). Almost always due to re-entry 

Regular (monomorphic) or irregular (polymorphic) 

Symptoms - chest pain, SOB, syncope 

Implant cardioverter Defib

Class 1,2,3 drugs and radio-catheter ablation 

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Implantable defib

A connect electrode to RV and SVC 

Senses arrhytmias by rate and location 

Delivers an appropriate shock causing cardioversion (return to sinus rhythm) 

Sometimes combined with drugs to reduced freq. 

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Chaotic disorganised electrical activity 

Caused by MI, ischaemia, cardiomyopathy but sometimes idiopathic 

No organised ventricular beat therefore no CO 

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Asystole, PEA

The two non-shockable rhythms (defib) 

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