- Acute coronary syndrome (ACS) represents in a range of clinical presentations sharing common pathology, causing a reduced blood flow to the heart, ranging from worsening/unstable angina, prolonged chest pain, irregular pulse and ECG changes such as
ST-elevation MI (STEMI).
- Most patients present with prolonged (>10mins) or recurrent central chest discomfort described as tightness, heaviness, squeezing or crushing sensation. The absence of these symptoms does not rule out ACS.
- Angina (pectoris): Chest pain caused by myocardiac ischemia
- Stable angina: Angina pain develops when there is increased demand in the setting of a stable atherosclerotic plaque. The vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand.
- Unstable angina: The plaque ruptures and a thrombus forms around the ruptured plaque, causing partial occlusion of the vessel. Angina pain occurs at rest or progresses rapidly over a short period of time.
- The most common form of arteriosclerosis, characterised by soft deposits of intra-arterial fat and fibrin in the vessels walls that harden over time. Fatty lesions develop between the tunica intima and media of the vessel walls, narrowing
the lumen of the vessel. These lesions can grow large enough to occlude blood flow, or they can rupture and cause the sudden development of a clot that occludes the blood vessel.
- The thickening, hardening, and loss of elasticity of the walls of arteries. This process gradually restricts the blood flow to one's organs and tissues and can lead to severe health risks brought on by atherosclerosis.
- An atheroma, or atheromatous plaque ("plaque"), is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults. The material consists of mostly macrophage cells,
or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
- Myocardial Infarction
- A heart attack or acute myocardial infarction (AMI) occurs when one of the arteries that supplies the heart muscle becomes blocked. Blockage may be caused by spasm of the artery or by atherosclerosis with acute clot formation. The blockage
results in damaged tissue and a permanent loss of contractility of this portion of the heart muscle (this is called tissue necrosis). The infarcted area continues to grow until circulation to that area is restored. Infarcted myocardium becomes non-functional and is gradually replaced by fibrous tissue. The presence of collateral circulation can reduce the amount of infarction; these pathways can develop over time with short episodes of ischaemia creating new pathways to perfuse tissue.
Injury to the endothelial cells that line the inner layer of the coronary artery occurs.The injured endothelium becomes dysfunctional, initiating an inflammatory response.
Low-density lipoproteins (LDL) infiltrate the damaged endothelium and accumulate in the intima of the coronary artery.The LDLs become oxidised as a result of exposure to free radicals including nitric oxide. Oxidation of the LDLs causes monocytes and
T-lymphocytes to migrate into the intima.
Monocytes differentiate into macrophages, and engulf the large amounts of LDLs by phagocytosis. After macrophages become laden with lipid from ingesting LDLs, they are referred to as foam cells. Eventually, foam cells undergo apoptosis and die, but the
contained lipids accumulate in the tunica intima forming a lesion called a fatty streak.
T-lymphocytes are activated and secrete cytokines, mediators and growth factors that promote smooth muscle cell migration from the media to the intima.
The smooth muscle cells proliferate, and deposit elastin and collagen on the surface of the fatty streak. This causes the formation of a fibrous capsule that covers the original fatty streak. As a result, a fibrous plaque (atheroma) is formed.
Initially, the vessel wall will expand to accommodate the growing fibrous plaque,but eventually the plaque will protrude into the lumen of the artery. The extrusion of fibrous plaque disrupts the smooth arterial lining and results in an uneven surface;
this creates turbulent blood flow.
Two types of fibrous plaques can be defined, stable and unstable.
plaques have a thick, intact fibrous capsule. These plaques are not prone to rupture, and the atheroma gradually expands to occlude the vessel.
- Unstable plaques have a thin fibrous capsule. These plaques are prone to rupture.
When rupture occurs, platelets aggravate at the injured tissue and initiate the coagulation cascade. This results in the formation of a thrombus.
The acute thrombus may suddenly occlude the affected vessel, causing an acute coronary syndrome. This can result in ischaemia and/or infarction.
- Stable angina:
- Blood flow adequate at rest
- Upon exertion, there is an iIncreased oxygen demand
- Arteriosclerosis/atherosclerosis limits blood flow
- Pain usually lasts 5 – 15 minutes
- Relieved by rest
- Nil ECG changes
- No permanent damage to myocardium
- Unstable angina:
- Blood flow interrupted by rupture of unstable plaque and resultant clot
- Pain at rest
- May also present with nausea, SOB and diaphoresis
- May have ECG changes
- T – wave inversion
- ST depression
- No permanent damage to myocardium
- Myocardial infarction:
- Biomarkers released (troponin, creatine kinase)
- May be complete or near-complete vessel occlusion
- If complete occlusion usually a smaller vessel
- Tissue Death to partial thickness of the myocardium
- ECG changes include T wave inversion and ST depression. Typically ST Elevation is not present or not meeting criteria.
- Complete occlusion of larger artery
- Results in death of full thickness of myocardium
- ECG changes include ST Elevation in 2 or more contiguous leads (minimum voltage limits). ST depression may be present in other leads.
- Sedentary lifestyle
- Cigarette smoking
- Diabetes mellitus
- Advance age (50+)
- Male gender or females after menopause.
- Family history.
- Right Coronary Artery; supplies blood to:
- Right atrium
- Right ventricle
- Sinoatrial (SA) node (55%)
- Atrioventricular (AV) node (90%)
- Inferior Left Ventricle
- Posterior Left Ventricle
- Left Coronary Artery; supplies blood to:
- Left atrium (circumflex)
- Sinoatrial (SA) node (45%, via circumflex)
- Atrioventricular (AV) node (10%, via circumflex)
- Lateral left ventricle
- Anterior left ventricle (via Left Anterior Descending artery)
- Intraventricular septum (via Left Anterior Descending artery)
- Bundle Branches (via Left Anterior Descending artery)
- Left Anterior Descending Artery: The LAD artery is the most commonly occluded of the coronary arteries. It provides the major blood supply to the interventricular septum, and thus bundle branches of the conducting system (complications
seen include a right bundle branch block (or RBBB) and left bundle branch block (or LBBB)).
- In general, the LAD artery and its branches supply most of the interventricular septum; the anterior, lateral, and apical wall of the left ventricle, most of the right and left bundle branches, and the anterior papillary muscle of the bicuspid
valve (left ventricle).
Signs and Symptoms:
- Chest pain/discomfort (ache, pressure, tightness, heaviness, burning)
- Pain radiating to jaw, arms, back, shoulders, neck, upper abdomen
- Nausea and/or vomiting
- Indigestion-like feeling
- SOB (dyspnoea)
- Lightheaded, dizzy, syncope
- Feeling of restlessness or apprehension
- The principles of management of ACS are based on reducing the imbalance between oxygen demand and supply.
- Coronary blood flow is improved by reversing vasoconstriction, preventing clotting, and reducing plaque growth and rupture.
- Myocardial oxygen consumption is reduced by manipulation of blood pressure, heart rate, contractility, and left ventricular volume.
- Nature - what does the pain feel like? (Mild, crushing, vice like).
- Severity - use PAINLOGTM to assess.
- Onset - when did it start? At rest and/or on physical exertion?
- Duration - intermittent, constant?
- Location - may be left side or retrosternal (behind the sternum/breastbone).
- Radiation - one/both arms, jaw, back?
- Aggravating or alleviating factors - effects of position, movement?
- Change on inhalation / exhalation - Does taking a deep breath make the pain worse or does it stay the same?
- A Normal ECG does not rule out Acute Coronary Syndrome (ACS).
- Monitor Vital Signs and cardiac rhythm (if possible) via ‘dot’ electrodes en route. Watch for sudden cardiac arrest. Reassure continually. Only apply Multi Function Pads to a patient that is unconscious and
- If a patient goes into cardiac arrest while you are monitoring them on the dot electrodes, it will be necessary to remove them before applying the multi function pads.
- Suspicion of acute myocardial ischaemia (
) is based entirely on field history. Do not be reassured by a "normal" rhythm strip. Treat the patient not the rhythm!
- Constant monitoring of the patient is essential. As many as 50% of patients who develop ventricular fibrillation in this setting may have NO warning arrhythmia!
- All suspected
patients are a life-threatening emergency, until a defibrillator is attached to the patient to revert sudden VF.
Critical points for Patient Care Record Form:
- Observe and record any complications, which may be present:
- Pulmonary Oedema.
- Cardiogenic shock.
- Nausea and vomiting.
- Degree of pain (occasionally patients do not have pain though they have the other signs / symptoms of a heart attack).
- Note: If an IV is in place, state the flow rate and who inserted the IV (doctor or paramedic’s name).