1. Angina pectoris, also known as angina, is chest pain due to ischemia (a lack of blood and therefore oxygen supply) of the heart muscle, which is commonly as a result of obstruction or spasm of the coronary arteries. Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. Coronary spasm can reduce coronay blood flow by causing dynamic stenosis of coronary arteries.
Prinzmetal angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm.
Although most patients with Prinzmetal angina have underlying fixed coronary lesions, some have angiographically normal coronary arteries. Unstable angina (UA) may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel.
Thus in stable angina the angina is predictable, depending on the intensity of the exertion, while in unstable angina, it is independent of the activity.
2. Coronary artery disease (CAD) (or atherosclerotic heart disease) is accumulation of atheromatous plaques within the walls of the coronary arteries that supply the myocardium . As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium.
The risk factors are
Age, Gender ( Men are at greater risk), Family history, Smoking ( Nicotine constricts blood vessels, and carbon monoxide damages the walls, High blood pressure (Uncontrolled high blood pressure can result in hardening and thickening of arteries), High blood cholesterol levels, Diabetes (Diabetes is associated with an increased risk of coronary artery disease). Obesity and Physical inactivity
3. Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. An MI can cause severe effets on the heart, like damage t myocardium, with poor contractility, development of low ejection fraction, cardiac tampanade, cardiac rupture, pulmonay edema, Valvular insufficiency, pericarditis, ventricular aneurysm, and mural thrombus. The lifestyle of the person is severely effected. There are severe diet changes, with restrictions on lipid intake, smoking , alcohol. Physical exercise needs to be started. Other conditions like diabetes and hypertension needs aggressive management.
4. Chest pain, usually across the anterior precordium is typically described as tightness, pressure, or squeezing.
Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is more frequently affected; however, a patient may experience pain in both arms.
Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia. Dyspnea may be the patient’s anginal equivalent, and, in an elderly person or a patient with diabetes, it may be the only complaint.
Nausea, abdominal pain, or both often are present in infarcts involving the inferior or posterior wall. The patient presents with Anxiety, Lightheadedness with or without syncope, Cough, Nausea with or without vomiting, Diaphoresis, Wheezing,
4 S3 – The third heart sound is benign in youth and some trained athletes, but if it re-emerges later in life it may signal cardiac problems like a failing left ventricle as in dilated congestive heart failure
S4 – The rare fourth heart sound is sometimes audible in healthy children and again in trained athletes, but when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff/hypertrophic ventricle. It is a sign of a pathologic state, usually a failing left ventricle.
Heart murmurs are also generated by turbulent flow of blood, which may occur inside or outside the heart, but the sound has different characteristics than normal heart sounds. Murmurs may be physiological (benign) or pathological (abnormal). Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Valve insufficiency (or regurgitation) allows backflow of blood when the incompetent valve closes with only partial effectiveness
6. crackles are indicative of pulmonary edema, which is a sign of right ventricular failure ( congestive heart failure.)
7. Troponin (TnI and TnT) – TnI: Less than 0.3 micrograms per liter (mcg/L). TnT: Less than 0.1 mcg/L
Elevated troponin may be present when you have heart muscle injury. Blood levels of troponin typically rise within 4 to 6 hours after a heart attack, reach their highest levels within 10 to 24 hours, and fall to normal levels within 10 days.
Total CPK (creatine phosphokinase) – 55–170 international units per liter (IU/L)- vCPK levels generally rise within 4 to 8 hours after a heart attack, reach their highest levels within 12 to 24 hours, then return to normal within 3 to 4 days.
CPK-MB -Less than 3.0 nanograms per milliliter (ng/mL) (0% of total CPK). Blood levels of CPK-MB typically rise within 2 to 6 hours after a heart attack, reach their highest levels within 12 to 24 hours, and fall to normal levels within 3 days. An ongoing high level of CPK-MB levels after 3 days may mean that a heart attack is progressing and more heart muscle is being damaged.
The patient has remarkably raised CK, CK-MB and TpI levels, which are indicative of myocardial damage
8. The ST changes are indicative of angina with involvement of territory of the left anterior descending artery, that is the anterolateral myocardial wall. The ST segment elevation is the most important sign of ischemia, so also the q wave presence. An MI associated with ST segement elevation is amenable to thrombolysis. Q wave MI is indicative of a transmural MI
9.An echogram is done for the following reasons- to assess the ejection fraction of the heart, tho see the myocardial wall motility and if certain segments are not contracting, which are indicative o f infarction, to look for cardiac tomaponade and pericardial effusion, vlavular dysfunction, and the flow of blood across valves, and congestive heart failure, to look for cardiac tumors and clots.
10. NTG has its main use in Mi due to its role as an arterrial vasodilator rather than as a anti hypertensive. NTG allows immediate vasodilation of coronary arteries, allowing immediate symptomatic relief of the arterial vasospasm. This allows blood to reach the myocardium, limiting the extent of MI and relieving the pain. It also reduces the afterload, thus reducing the load on the heart.
11. aspirin is given in the emergency department due to its antithrombotic role. It blocks cyclooxygenase enzyme , and prevents the clotting process. Thus clot propagation is prevented, thereby reducing the extent of myocardial infarction
Abciximab- is a platelet aggregation inhibitor mainly used during and after coronary artery procedures like angioplasty to prevent platelets from sticking together and causing thrombus (blood clot) formation within the coronary artery. Its mechanism of action is inhibition of glycoprotein IIb/IIIa.
Ticlopidine- Ticlopidine (trade name Ticlid) is an antiplatelet drug in the thienopyridine family. It inihibits platelet aggregation by altering the function of platelet membranes.it is an alternative drug to aspirin, often given in more severe cases of thrombosis, an d severe myocar dial ischemia
12 Enoxaparin is a low molecular weight heparin. Enoxaparin binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and Iia. enoxaparin’s inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation.
Heparin – Heparin binds to the enzyme inhibitor antithrombin (AT) causing a conformational change. The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. Heparin acts as an anticoagulant, preventing the formation of clots and extension of existing clots within the blood. While heparin does not break down clots that have already formed (unlike tissue plasminogen activator), it allows the body’s natural clot lysis mechanisms to work normally to break down clots that have already formed.
Thus the role of the two anticoagulants in MI
13. Morphine is a highly potent opiate analgesic drug. morphine acts directly on the central nervous system (CNS) to relieve pain, and at synapses of the nucleus accumbens in particular. This is the mode of action of morphine as is relevant to ischemic cardiac conditions. Its main use here is the relief of pain.
14. Beta blockers are agents which block the beta adrenergic receptors of catecholamines and thus prevent their action. This prevents the catecholamines stimualted chronotropic and inotropic action on the heart, amongst others. Their blockade allows the heart to contract in a more relaxe fashion, allowing it to recover from ishemic insult but better perfusion match. Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction. Thus the beta blockers like metoprolol are given for antiarrythmic action as well as improved cardiac perfusion status.
15 lidocaine is an excellent antiarrythmic for ventricular tachycardias. It acts by prolonging the AV nodal conduction and reducing the hyperexcitablity of the ventricles. Thus since this patient was having many ventricular tachycardias, which can be life threaterning, lidocaine is the drug of choice here.
16 . tPA or tissue plasminogen activator is an enzyme that allows the dissolution of clots. Thus the thrombus that blocks the coronary is dissolved by the use of tPA. tPA activates the tissue plasminogen which is a fibrinolytic agent. The dissolution of clots also release fibrinogen degradation products which prevents further clotting. Thus tPA is used as a firstline agent instead of angioplasty in an attempt to stabilise the patient, and limit the damage, particularly in transmural MI’s. The effectiveness of thrombolytic therapy is highest in the first 2 hours.
17 tPA – Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI, and for the treatment of individuals with evidence of cardiogenic shock, blee ding disor ders, oesophageal varices, esophagitis,
18. percutaneous transcoronary angiography – this is an invasive proce dure where a catheter is directe d percutaneously through the femoral artery, in to the coronaries, to localise the area of the block. This is indicated in this patient, since all conservative measures given were not successful, an d it was this essential to exactly localise the block in the coronary an d assess for possible stenting. Complications of the proce dure inclu de trauma to arteries ( femoral, coronary), infection, thrombosis at local site, bleeding and hematoma at puncture site.
19. a stent is a device to maintain the patency of the artery. In an atherosclerotic coronary the lumen is normally reduced. Thus after an angiography, the stent is placed across the area of blockade and opened. This allows the lumen of the artery to be opened,and blood flow is easily established across the block, reperfusing the myocardium. This was the only option in this patient, since aal conservative measures had failed, and there was a severe block of the main artery of the heart, the left anterior descending artery.
20. the reading of the RA, PACWP and the PAS pressures is a clear indicator of cardiogenic shock. The right and the left ventricle were badly affected, leading to rise in the right atrial and the left atrial pressures. This means that the outflow of the heart was affected, thus the ventricles were not able to perform properly.
21. Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI). On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilatation, and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. The evidence for this in this patient is the raised values for Pulmaonary artery studies. The severe hypotension of the patient, ventricular tachycardias, the ECG findings of ta wave inversion, evidence of shock by presence of tachycardia, paleness, cool, and diaphoresis
22. at low doses, dopamine acts as a coronary vasodilator, with vasodilatio nof the renal circualtion also, allowing better renal perfusion as well as better coronary perfusion. In high doses, dopamine is a peripheral arterial vasoconstrictor, which allows the raising of systemic vascular resistance and raising of blood pressure, in intermediate range, dopamine acts as a coronary vasodilator as well as a systemic vasoconstrctor.
23. Dobutamine is a direct-acting agent whose primary activity results from stimulation of the β1-adrenoceptors of the heart, increasing contractility and cardiac output. Since it does not act on dopamine receptors to induce the release of norepinephrine (another α1 agonist), dobutamine is less prone to induce hypertension than is dopamine. It is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility,
24. IABP supports the blood pressure by providing a peripheral pump in the aorta to pump blood forward, reducing the afterload on the heart, while maintaing the blood pressure. The heart, finds that its load is reduced, and now has a better perfusion status, is able to recover. In thispatient IABP is specially indiicated as even after stenting, the heart was not able to take over the functions, and could not maintain the blood pressure, and went into failure.
25. inserion of IABP is difficult and requires access in to the femoral artery, via a canula. Since the patient is already under antithrombotic control, there is a great risk of hematoma and bleeding at the site of insertions, and any vascualr trauma by the IABP is going to be disastrous
26. a calcium channel blocker is required to reduce the afterload on the heart, since these are arterial blockers. CCB’s control blood pressure and prevent arrythmias developing by slowing the conduction across the AV node.
28. captopril is an angiotensic converting enzyme inhibitor. It is a peripheral vasodilator. This allows better diastolic filling of the heart, with better pumping action. In addition it has a beneficial effect on the blood pressure and diabetes. It has a role in congestive cardiac failure, as has occurred in this patient. So this is an excellent choice for this patient.
eMedicine – Myocardial Infarction : Article by Drew E Fenton. Accessed on 16 July, 2008 from www.emedicine.com/emerg/TOPIC327.HTM
Angina Pectoris Causes, Symptoms, Diagnosis, Treatment, and. Accessed on 16 July, 2008 from www.emedicinehealth.com/angina_pectoris/article_em.htm
Cite this Badly Disease “Angina Pectoris”
Badly Disease “Angina Pectoris”. (2016, Jun 26). Retrieved from https://graduateway.com/angina-pectoris/