Part 7

Which troponin have specific cardiac types 

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 

Most common type of MI 

Lower cholesterol 

Lower BP 

ACE inhibitor 

Aspirin 

Statins 

Beta blockers 

Life style (smoking and diabetes) 

Progressive disease affecting the intima of elastic and muscular arteries.

Characterised by focal atheroma's 

Lipid core covered by fibrous cap 

Calcification in the media of muscular arteries 

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

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) 

Commonest 

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 

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 

Further arrhythmias and subsequent heart failure 

Pericarditis 

Papillary muscle dysfunction (mitral valve complication) 

Mural thrombosis in ventricle 

Ventricular rupture 

Papillary muscle rupture 

Ventricular aneurysm 

Post MI sundrome 

Ischaemia 

Reinfarction 

1-5% of cases 

Commenest 4-7 days post infarct 

Ventricular free wall 

Haemopericardium 

Cardiac tamponade 

Rupture of intraventricular septm 

Left to right shunt 

Rupture of papillary muscles -> severe acute mitral incompetence 

2nd or 3rd day 

Fibrinous or fibrinohaemorrhagic 

Usually localised to region overlying necrotic area 

Transfer of abnormal material via bloodstream and impaction in vessel 

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 

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

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

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 

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 

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

Pressure overload (HTN, aortic stenosis) 

Volume overload (Valve regurgitation) 

Contractile dysfunction (ischaemic heart disease, congenital cardiomyopathies) 

Peripheral vasoconstriction 

Increased HR 

Contractility 

All returning BP to normal 

Vasconstriction at tissues

Stimulates aldosterone release 

Stable 

Mixed

Unpredictable 

Vasospastic 

Microvascular - syndrome X 

Unstable 

B-blockers 

Ivabradine 

Ranolazine 

CCB 

K+ channel activators 

Nitrates 

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

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  

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) 

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 

Class 1 anti-arrhythmic drug 

Class 2 anti-arrhythmic drug 

Class 3 anti-arrhythmic drugs

Class 4 anti-arrhythmatic drugs 

Rate control drugs 

Rhythm control drugs 

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 

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. 

Chaotic disorganised electrical activity 

Caused by MI, ischaemia, cardiomyopathy but sometimes idiopathic 

No organised ventricular beat therefore no CO 

The two non-shockable rhythms (defib)