Wk Six - STEMIs and Ventricular Rhythms

STEMI management steps sheet

Heparin Indis/Contras Etc.. Sheet

Tenectaplase Indis/Contras Etc.. Sheet

Morphine Indis/Contras Etc.. Sheet

What happens when you bleed? (Steps)

1. Injury (Bleeding, release of signalling molecules)

2. Vasoconstriction (local immeadiate control)

3. Platelet formation

4. Coagulation (Fibrinogen forms fibrin mesh)

5. Fibrinolysis (Plasminogen forms plasmin)

Clotting Cascade

The complex series of events in your body when bleeding is stopped by forming a clot. The three main pathways are Intrinisc, Extrinisic & Common

CC Intrinisc Pathway

Activated within the blood vessel often by damage to the endothelium or expose to collagen. Factor XII (Hageman) is activated > XIIa. This activates XI > XIa, which activates IX > IXa, and IXa + factor VIIa + calcium & phospholipids activates factor X which forms a blood clot.

CC Extrinisc Pathway

Triggered by external trauma that causes the blood to escape from the vessel. Damaged tissue releases Tissue Factor (III) which binds wih factor VII > VIIa, and the TF-VIIa complex activates Factor X.

CC Common Pathway

Where both pathways meet and lead to clot formation. Factor X is activated to become Xa, combined with factor V makes the prothrombin complex. This converts Prothrombin to Thrombin, which converts Fibrinogen to Fibrin, which activates Factor XIII which cross links fibrin into a stable clot.

Haemostasis

the psyiological process that stops bleeding after a vessel is injured

Haemostasis steps

• Vasoconstriction (vessel is damaged, surrounding muscle constricts to reduce blood flow)

• Platelet Plug Formation (Platelets attracted to site, adhere to exposed collagen to form a temporary plug)

• Coagulation Cascade

• Fibrin Clot Formation (fibrin clot, dissolves as the tissue heals & vessel is repaired

How is a blood clot broken down

Fibrinolysis - Plasmin inside the clot is triggered, which degrades the fibrin until the clot disintergrates

How does tenecteplase work?

A clot has a fibrin mesh, Plasmin breaks up that clot, Plasminogen is activated by tissue plasminogen activator (tPA) to make that plasmin.

What AMPLE factors increase suspcision of NSTEACS

DM, HTN, Hypercholesterolemia, Previous cardiac Hx, hormone replacement for menopause

Inferior Stemi Signs

ST elevation in 2 or more inferioir leads, may see hyperacute T waves, reciprocal depression in aVL, progressive development of Q waves in II III and AVF.

Complications of inferior stemis

Bradycardia, 2nd/3rd degree heart block

Anterior/Anteroseptal Stemi Signs

ST elevation in 2 or more leads. V1&2 = septal, V3&4 = anterior, V1-4 = anteroseptal
May also see hyperacute t waves, reciprocal ST depression in I leads, progressive development of Q waves in V1-4

Complications of anterior/anteroseptal stemis

Poorest prognosis (most amount of myocardium under attack), irritable myocardium (PCS & risk of VFib)

Lateral Stemi Signs

St elevation in 2 or more lateral leads, may see hyperacute T waves & reciprocal depression in inferior leads

Complications of lateral stemis

Rarely isolated infacrtions, usually part of a larger occlusion.

Kinds of Lateral Stemis

• anterolateral - STEMI due to LAD occlusion

• Inferior-positerior-lateral - STEMI due to LCx

• Isolated lateral - due to occlusion of smaller branch arteries like the ramus intermedius

Posterior Stemi Signs

ECG shows 0.5mm ST elevation in 2 or more leads V7-9

May see horizontal ST depression, tall broad R waves ?30ms and upright T waves in V1-3.

Complications of posterior stemis

Rarely isolated, usually occurs with inferior or lateral infarction. Much larger area damages, and theyre often missed!

Right Ventricle Stemi Signs

Confirmed by ST elevation in 2 or more of V3R-V6R. May see ST elevation in V1 & St dep in V2. Isoelectric ST segment in V1 with marked ST depression in V2, ST elevation in III > II

Complications of RV stemis

40% of inferior stemis. PRELOAD sensitive due to poor contractility, can develop severe hypotension in response to nitrates. Treated with fluid loading

Automati

property of cardiac cells that allows them to reach threshold potential by themselves, and depolarize spontaneously

What does rate of firing depend on?

The steepness of Phase 4

Hierarchy of pacemakers

SA Node > AV Node > Bundle Branches/Purkinje Network

Pacemakers & Their rates

SA - 60-100, sinus rhythm

AV - 40-60 junctional escape rhythm

BB/PN - <40 idioventricular rhythm

Enhanced Automaticity

cells firing at a rate beyond its inherent rate because cell membrane has become more permeable to sodium during phase four

Causes of enhanced automaticity

• increased catechloamine levels

• myocardial ischemia/infarction

• digoxin toxicity

• atropine

• hypoxia, hypercapnia, hypocalcemia, temp changes

Premature Ventricular Contraction

an unexpected beat, that can be fe;t. wide and bizzare looking - originates from ectopic source ventricles, bundle branches, PF & myocardium. there is a compensatory beat due to SA node not being depolarised. only concerning if there is multiple.

Single PVC

Multifocal PVC

Ventricular Bigeminy

a heart rhythm disorder where every other heartbeat is a premature ventricular contraction (PVC)

Ventricular Trigeminy

a heart rhythm disorder where after every two normal heartbeats is a premature ventricular contraction (PVC)

Couplet

Two consecutive premature beats

Triplet

Three consecutive premature beats

Idioventricular rhythms sheet

Idioventricular rhythm ECG

Accelerated Idioventricular rhythm ECG

Pathophys & Causes of Idioventricular rhythm

PATH:

• rate of impulses from the SA and AV node is less than the rate of the escape rhythm of the ventricle pacemaker

• electrical impulses from the atria fail to reach the ventricles due to blockage

• enhances automaticity of ventricular pacemaker

CAUSES:

• Reperfusion phase of an AMI

• Beta-sympathomimetics (adrenaline)

• Drug toxicity

• Electrolyte imbalances

• cardiomyopathy, congenital heart disease, athletic heart myocarditis

• ROSC after CA

How to treat idioventricular R

Treat the underlying cause - electrolytes, perfusion…

VT

ventricular tachycardia. 120-300bpm, not coordinated

VF

ventricular fibrilation, irregular heart rhythm, chaotic and uncoordinated