Cardiac Flashcards
What does an ECG measure?
The collective electrical activity of the heart.
Can prolonged tachycardia cause angina?
Yes, because coronary blood flow occurs during diastole. If systole occurs to fast, there is no time for the coronary blood to flow.
What are two shockable rhythms?
Ventricular fibrillation and ventricular tachycardia.
What is a myocardial infarction?
Any acute condition whereby the myocardium is irreversible damaged and becomes necrotic (infarcted) due to the lack of oxygen (ischemia) and hypoxia.
This is a result from acute obstruction of a coronary artery.
What cardiac markers in the blood will be elevated after myocardial infarction?
Trooponin 1 or 2 and creatine kinase are elevated.
Creatine kinase is an enzyme found in your heart muscle, skeletal muscle and brain, when any of these get damaged, they leak creatine kinase into your bloodstream.
Troponin is a globular protein involved in muscle contraction. Any damage to cardiac muscle can cause troponin to spill into circulation.
What is a NSTEMI?
Non ST elevated myocardial infarction.
Is evident by myocardial necrosis shown by cardiac markers in the blood but has not acute ST segment elevation. ECG changes such as ST segment depression or T Wave inversion - or maybe both.
What is a STEMI?
ST elevation myocardial infarction.
Myocardial necrosis with ECG changes showing ST segment elevation that is not quickly reversed by nitroglycerine. Troponin 1 or creatine kinase are elevated.
ST elevation occurs within minutes of the onset of infarction and indicates the presence of ischaemic tissue.
What does a Q wave indicate?
A infarct is virtually certain if Q Waves appear during the course of the illness.
Where can MI pain radiate to?
Radiate to jaw, arm or back.
What are the signs and symptoms of MI?
Nausea, diaphoresis, dyspnoea, fear, anxiety, dysrhythmias, chest pain, impeding sense of doom.
What does each wave of an ECG represent?
P Wave - atrial depolarisation - initiated by the SA node.
QRS complex - ventricular depolarisation and atrial repolarisation occurs.
T Wave - ventricular repolarisation.
What is atherosclerosis?
Atherosclerosis is a specific type of arteriosclerosis (hardening of the arteries), where lipid plaques cause arteries to become narrowed and harden. It often affects coronary arteries, which provides oxygen and nutrients to the hearts tissues. This can often lead to angina.
What is the clinical indication for the use of nitrates?
Treat acute episodes of angina. Nitrates are very lipid soluble and can be absorbed quickly through various body surface areas. Nitrates are readily distributed and quickly metabolised.
What is the pharmacological action of nitrates?
Nitrates are changed into nitric oxide in the smooth muscle of blood vessels. This alters the calcium in the cells. With less calcium in the cells, the blood vessels will dilate. These nitrate drugs are peripheral vasodilators and wok on both the arteries and veins. The effect if decreasing the preload and afterload is to decrease the workload of the myocardium, thus reducing the myocardial oxygen demand.
What are most common nitrate drugs?
Glyceryl trinitrate and isosorbide dinitrate.
How does diuretics such as furosemide assist in ischaemic heart disease?
Frusemide blocks sodium and potassium transport. The sodium and potassium are not reabsorbed but stay in the tubular fluid. This makes the extracellular fluid hypotonic (having a lower osmotic pressure) and creates an osmotic pull, increasing the volume of tubular fluid and therefore increase urine output. This therefore create a reduction in blood volume which will reduce the preload and thus the myocardial workload.
What is diaphoresis?
excessive sweating
What is diapedesis?
The passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.
How do beta-blockers benefit ischaemic heart disease?
Betablockers are used to reduce the force of contraction of the myocardium (negative inotropic effect) and to reduce the heart rate (negative chronotropic effect). This reduces the myocardial oxygen demand and prevents myocardial ischemia
How do ACE inhibitors benefit ischaemic heart disease
ACE inhibitors inhibits the dilation of blood vessels by preventing angiotensin converting enzyme from converting angiotensin 1 to angiotensin 2. It also increases sodium and water excretion and therefore decreases blood pressure.
How do antiplatelet drugs benefit ischaemic heart disease
When blood vessels are damaged, platelets adhere to the damaged surface and secrete a platelet activating factor called thromboxane A2 the platelet aggregation is also dependent on the activation of glycoprotein llb/llla receptors. This causes platelet aggregation, thus platelets play an important role in thrombus formation. This process of platelet aggregation is not beneficial to a patient with ischaemic heart disease. To prevent intravascular thrombus formation, antiplatelet drugs are prescribed. In ischaemic heart disease, the drugs of choice are aspirin, clopidogrel and sometimes heparin.
Why is morphine the drug of choice when treating chest pain
Morphine had added benefits for use in ischaemic heart disease. It causes vasodilation which reduces preload. Angina pectoris is chest pain by definition and thus it would make sense to give the patient analgesia. The pain is due to the build-up of lactic acid and may result in inflammation of the myocardium and may or may not cause tissue injury.
The first choice of analgesia is the narcotic morphine.
What is the difference between stable and unstable angina
Stable – relationship between workload or demand and ischemia is usually relatively predictable. Goes away when exercise is stopped.
Unstable – clinically worsening angina. Angina at rest or with increasing frequency and/or intensity of episodes. Doesn’t go away when exercise has stopped.
What is the benefit of using calcium channel blockers with ischaemic heart disease?
Calcium channel blockers are used to treat angina and hypertension. The drugs stop calcium entering the cells by blocking the calcium channels. The result is muscle relaxation, which causes vasodilation. When coronary arteries dilate, more oxygenated blood can flow to the myocardium. Angina is relieved because calcium channel blockers both increase oxygen supply to the myocardium and reduce myocardial oxygen demand.
