Chest pain and ACS Flashcards
what are the common causes of chest pain (order of most common to least)?
- atypical chest pain
- angina/CAD
- other cardiac causes (congestive cardiac failure, AF, dysrhythmia)
- non PE-pulmonary causes (pneumonia, pneumothorax)
- acute MI
what are the signs and symptoms of acute coronary syndrome?
Central chest pain, squeezing, heaviness, radiation to jaw etc, nausea, vomiting, dyspnoea, dizziness, weakness, rest, normal examination?, jugular venous distension, S4 gallop, holosystolic murmur, bibasilar rales, hypotensive, tachycardic, bradycardic, hypoxic
what conditions make up acute coronary syndrome?
unstable angina
NSTEMI
STEMI
what investigations are performed in a patient with suspected acute coronary syndrome?
ECG-STEMI, NSTEMI, unstable angina
CXR-normal or signs of HF such as alveolar markings
Cardiac enzymes (troponins)-elevated in STEMI and NSTEMI but not unstable angina
BNP
Coronary angioplasty
describe the coronary arteries?
The left coronary artery will divide into the circumflex and the left anterior descending artery. Subsequently, this will divide into much smaller branches. The right coronary will divide into smaller branches as well.
what is unstable angina?
blood flow obstruction causing a lack of perfusion to the myocardium. Initial perfusion starts directly from the heart into the aorta and subsequently into the coronary arteries which supply their respective portions of the heart. Unstable angina results when the blood flow is impeded to the myocardium. Most commonly, this block can be from intraluminal plaque formation, intraluminal thrombosis, vasospasm, and elevated blood pressure. Often a combination of these is the provoking factor.
what physiological factors can increase myocardial oxygen demand?
Arrhythmias Fever Hypertension Cocaine use Aortic stenosis AV shunts Anemia Thyrotoxicosis Pheochromocytoma CHF
describe the pathophysiology of an NSTEMI?
NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. Type 1 myocardial infarction (MI) is most commonly caused by a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque, and leads to non-occlusive or near-complete thrombosis of a vessel supplying the myocardium. Plaque rupture with superimposed non-occlusive thrombus or embolic events leading to coronary vascular obstruction. Dynamic obstruction, such as in vasospasm. Progressive luminal narrowing (i.e., chronic arterial narrowing from restenosis). Inflammatory mechanisms (i.e., vasculitis).
what extrinsic factors leads to poor coronary perfusion?
hypotension, hypovolaemia, or hypoxia
what is the most common cause of NSTEMI and how does this relate to cardiac biomarkers?
plaque rupture or obstructive atherosclerotic disease. In this setting, the release of myocardial biomarkers in type 1 MI is thought to be due to atherosclerotic plaque fissuring or rupture with resulting intra-coronary thrombus or platelet emboli leading to diminished myocardial blood flow
where does plaque rupture usually occur?
weakest and thinnest part of the atherosclerotic cap (often at shoulder region)
what is contained within a ruptured plaque?
large numbers of inflammatory cells including monocytes, macrophages, and T lymphocytes.
what proportion of occlusions occur at the sight with greatest stenosis?
one third of occlusions occur at a site with the greatest stenosis, most (66% to 78%) arise from lesions with <50% stenosis, and <5% arise from lesions exhibiting >70% stenosis. Approximately 25% of patients with a diagnosis of NSTEMI have a 100% occlusion of the affected artery on coronary angiography
what is the severity of myocardial damage in NSTEMI dependent on?
Duration of ischaemia and time to reperfusion
Extent of underlying atherosclerosis
Presence of collateral blood flow to the affected region (reserve blood flow)
Diameter of affected coronary vessel
Degree of occlusion
Presence of other comorbidities (i.e., diabetes, renal failure, or hypertension).
describe the pathophysiology of plaque formation?
Atherosclerotic plaques form gradually over years. They begin with the accumulation of low-density lipoprotein cholesterol and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the adhesion of leukocytes to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to this point is referred to as a fatty streak, and may be reversible to a certain extent. Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.Some of the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification as they evolve. The plaque initially evolves with the artery remodelling outwards, followed by encroachment on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing angina.
when does a STEMI usually occur?
STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque
how does a STEMI occur after abrupt disruption of cholesterol laden plaque?
exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial cell necrosis follows. On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the non-infarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank-Starling mechanism
what causes infarction expansion following STEMI?
As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction
what happens if a sufficient quanity of myocardium undergoes ischaemic injury?
left ventricular (LV) pump function becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end diastolic pressure give rise to diastolic dysfunction.
what are the signs and symptoms of stable angina?
Chest discomfort on exertion, relieved by GTN or rest, no change in intensity, frequency or duration, no associated diaphoresis, nausea/vomiting or SOB
what investigations would be considered if a patient has suspected stable angina?
ECG-no acute changes-evidence of previous infarction (Q waves) CXR-Norma or cardiomegaly Cardiac biomarkers-not elevated Stress testing Coronary angiography CT coronary angiography
what causes angina symptoms?
imbalance between myocardial oxygen supply and demand
what determines myocardial oxygen supply?
determined by coronary blood flow and arterial oxygen content.
how much stenosis is required to result in stable angina?
In the absence of collateral coronary circulation, stenoses of >70% of the cross-sectional area (equivalent to 50% of the lumen diameter by angiography) can result in stable effort angina due to inability to adequately increase coronary blood flow with exercise
what other conditions can precipitate angina?
mental and emotional stress, sexual activity, tachycardia from any cause, or the metabolic demands of fever, thyrotoxicosis, and hypoglycaemia
what is prinzmental variant angina syndrome X?
Rarely, patients may have severe coronary vasospasm in the absence of atherosclerotic plaque, resulting in angina (Prinzmetal variant angina), or angina in the presence of normal coronary arteries (syndrome X).
what are the signs and symptoms of pneumonia?
Productive or dry cough, fever, pleuritic pain associated with SOB, may have rigors, myalgias, arthralgias, recent history of travel
Decreased breath sounds, rales, wheezing, bronchial breath sounds, dullness to percussion, increased tactile fremitus
what investigations are needed in a patient with suspected pneumonia?
CXR-pulmonary infiltration, air bronchograms, pleural effusion
WBC count-elevated with left shift (increased neutrophil count)
Sputum culture
Blood culture
what is the pathophysiology of pneumonia?
Infection to the lung causing an inflammatory response to be initiated and alveolar oedema and exudate formation, alveoli and respiratory bronchioles fill with serous exudate, blood cells, fibrin, bacteria leading to consolidation of lung tissues
what are the signs and symptoms of viral pleuritis?
Pleural friction rub with or without low grade fever, sometimes reproducible tenderness to palpation of chest when perichondritis or pleurodynia accompanies pleuritis
what is the pathophysiology of viral pleuritis?
Infection/inflammation or trauma causes inflammation of pleura, irritate the sensory fibres of parietal pleura. During respiration (intensified on inspiration), the pleural membrane rub together the result is severe, sharp, knifelike pain
what investigations would be needed if a patient had suspected viral pleuritis?
CXR-usually normal
FBC-normal or leucocytosis with lymphocytic predominance
what are the signs and symptoms of GORD?
Chest pain, retrosternal burning with eating fatty meals that can be reproduced when lying supine and relieved on sitting up, relieved by antacids
No specific physical findings
what investigations would be needed if a patient had suspected GORD?
Try PPI to see if pain relieved
Oesophagogastrodeodenoscopy
what are the signs and symptoms of costochondritis?
Focal chest wall pain, precipitating injury, aggravated by sneezing, coughing, deep inspiration or twisting of the chest. Reproducible pain on chest wall palpation
what is the pathophysiology of costochondritis?
The pathophysiology is not clear, but results in inflammation of the costal cartilage.
Cartilage has a relatively poor blood supply, and use of antibiotics is usually ineffective in treating infective costochondritis.
what would CXR show in a patient with suspected costochondritis?
no specific findings
what are the signs and symptoms of anxiety/panic disorder?
Sharp chest pain with anxiety, dizziness, faintness, palpitations, sweating, trembling, fear of dying, chills, hot flushes, hyperventilation, examination normal
what investigations should be considered in a patient with suspected anxiety/panic disorder?
ECG-normal
CXR-normal
HADS (hospital anxiety and depression scale) score->11
what is an aneurysm?
True arterial aneurysms are defined as a 50% increase in the normal diameter of a blood vessel. Any artery may be affected. Commonest are the abdominal aorta and iliac arteries, with popliteal, femoral and carotid arteries less commonly affected
what are the symptoms of aneurysm?
Often few initially, so present late. First presentation is often rupture, thrombosis or distal embolization. Many picked up incidentally on ultrasound/CT performed for some other indication
what are the causes of abdominal aortic aneurysm?
Traditionally believed to be solely atherosclerotic. Although they tend to develop in older men, with a smoking history, and concomitant atherosclerosis, their aetiology is unknown. Current theories include; genetic predisposition (there is an increased familial risk of aneurysms), proteolytic (matrix metalloproteinase enzymes degrading elastin in the arterial wall), infective, auto-immune.
what are the treatment options for AAA?
Choice between conventional open surgery or endovascular aneurysm repair
describe open surgical repair?
Clamps are placed above and below the AAA, the aneurysm is opened, and a synthetic graft is sutured to the normal cuff of arterial wall. The aneurysm wall is then sutured over the graft
describe endovascular aneurysm repair?
A stentgraft (combined metal and fabric device) is placed inside the arteries (endovascularly) via the common femoral arteries at the groin. Most have at least 2 components that fit together (described as modular). It is manipulated using x-ray control, endovascularly to lie in the infrarenal aorta, and deployed to exclude the AAA from the circulation. Patient prepared, and under spinal anaesthesia both common femoral arteries (CFA’s) are exposed at the groin. A measuring angiogram is performed via the left CFA, and measurements checked. The main body of the device is introduced via the left CFA and deployed infrarenally. The position of the stentgraft, as close to the renal artery origins, without occluding them is vital. The limb extension is prepared and deployed, to extend the stengraft into the common iliac arteries. The completion angiogram shows a satisfactory position of the stent graft device, with perfusion of the renal arteries. The aneurysm is excluded from the circulation, with no leakage of blood between the aortic wall and the stentgraft (called an endoleak). Both CFA’s are repaired by clamping the arteries temporarily and suturing the defects caused by passage of the stentgraft. The groin wounds are then closed, and dressings applied
describe AAA screening?
Level 1 evidence for AAA screening. Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. 42% risk reduction in screened population. Improved technology may increase proportion of AAA suitable for EVAR. Mechanism of expansion and rupture of AAA currently unknown, but intensive research into this. Possibly drug therapy in future may stop expansion/prevent rupture, allowing conservative management of small screen-detected AAA’s
what are the consequences of MI?
- loss of viable myocardium impairs cardiac output and cardiogenic shock
- systolic and diastolic dysfunction-ischaemic myocardium
- abnormal cardiac rhythms
- baroreceptor reflexes leading to activation of neurohormonal compensatory mechanisms
- sympathetic nervous system activation-systemic vasoconstriction and cardiac stimulation, increase myocardial oxygen demand, sweating, renal hypoperfusion, renin release
what are the symptoms of MI?
include intense chest pain that may radiate into the neck, jaw or arms (i.e., referred pain), a sense of substernal heaviness, squeezing or pressure, shortness of breath (dyspnea), fatigue, fainting (syncope), nausea, sweating (diaphoresis), anxiety, sleeplessness, hypertension or hypotension (depending in part on the extent of cardiac damage), tachycardia and arrhythmias.
