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Cardiac Dysrhythmias

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CH29 Dysrythmias 1. Catheter ablation is when wires are entered into the body through vessels beginning in your arm, groin, or neck and guided to the heart. Energy is sent through the wires to target and destroy specific heart tissue that may cause dysrhythmia. 2. A heartbeat begins with diastole in which the atria and ventricles relax and fill with blood. The electrical conduction of the heart begins at the SA node in the Right atrium which acts as the pacemaker. It travels through the muscle of the atrium causing it to contact (systole) and pumps blood into the ventricles. Next the AV node, which has a slower pace, pauses or an instant to allow the ventricles to fill with blood. The signal is then sent through the Perkinje fibers located on the walls of the ventricles and pushes blood through the pulmonary vale (from the right ventricle to the heart) and the aortic valve (from the left ventricle to the body). The signal pauses and the heart relaxes (diastole) allowing blood to fill the heart so the process can begin again.

3. Blocking ions (K+, Na+, Ca+) act to aid in dysrhythmia by interrupting the conduction system by interrupting depolarization and repolarization. Drugs include: * procainamide (Pronestyl) which blocks Na++ channels to slow impulse conduction through the heart. It helps in treating severe cases of atrial fibrilliation, ventricular tachycardia. Side effects can be dysrhythmia, hypotension, dizziness syncope, confusion, and psychosis. * proponolol (Inderal) blocks beta 1 and 3 receptors to reduce automacity and slow conduction across the myocariduim and lower BP. Its used for atrial flutter, tachycardia, hypotension, angina, and prevention of MI. Adverse effects include bradycardia, hypotension with dizziness and fainting, and hypoglycemia. * amniodarone (Cordarone) blocka K++ channels slowing the repolarization and prolongs the refractory period of the heart. It treats resistant ventricular tachycardia, atrial dysrhythmia with heart failure. Adverse effects include creating new dysrhythmia or worsen existing one, blurred vision, pneumonia like symptoms, and hypotension. * Verapamil (Calan) blocks Ca++ channels to inhibit flow of Ca++ into vascular smooth muscle, slowing conduction, lowering BP, and dilating coronary arteries. It treats supraventricular tachycardia. Side effects can be bradycardia, hypotension, and headache
CH 22 Lipid disorders 4. Genetics play a role in lipid disorder by controlling the enzymes needed to metabolize lipids causing excessive storage of fat. Environmentally, too much LDL can be consumed so that HDL cannot carry all of the cholesterol back which causes a clog up in arteries. If there is too much VLDL, liver concentration of cholesterol can increase. 5. LDLs are low density lipids and contain the highest amount of cholesterol. It transports cholesterol from liver after digestion to tissues and organs where it’s used to build plasma proteins or synthesize other steroids. It contributes to plaque deposits. VLDL is very low density lipoprotein and is the primary carrier of triglycerides through the body. It can reduce in size to LDL. HDL is high density and manufactured in liver to assist in retrieving cholesterol from the body back to the liver to broken down and put into bile and excreted. It is considered good cholesterol. 6. Prototype drug is atorvastatin and is a HMG Co-A reductase, HMG- CoA reductase serves as a primary regulatory site for cholesterol biosynthesis and is controlled through negative feedback, and high levels of LDL in the blood will shut down the production of HMG-CoA, turning off the cholesterol pathway so that less cholesterol is produced by the liver. The liver also increases the number of LDL receptors so that more cholesterol can be removed. It is a temporary change and patients on these drugs will remain so for their lifetime or until their hyperlipidemia can be controlled through diet and lifestyle changes (pg 287).

CH30 Coagulation Disorders 7. Coagulation occurs when fibrin forms a mesh to trap blood particles and form a clot. This helps control bleeding. plasma proteins are converted to an active state. The intrinsic pathway is activated in response to an injury and consists of an injury, factor x, prothrombin activator, is formed, prothrombin activator converts the clotting factor prothrombin into the enzyme thrombin. Thrombin converts fibrinogen, a plasma protein, to fibrin and the fibrin forms the framework for a clot. The extrinsic path is when blood leaks out of a vessel and enters tissue spaces. In this case, the lover releases prothrombin and fibrinogen which follow the same path of creating a fibrin mesh frame.
Fibrinolysis is clot removal. It is initiated 24 to 48 after a clot has formed and continues until it is completely dissolved. When a clot is formed, nearby blood vessel cells secrete the enzyme tissue plasminogen activator (TPA) TPA converts the inactive plasminogen to plasmin which digests the fibrin strands to remove the clot. 8. Hemostatics refers to a classification of drugs used to promote blood clotting while thrombolytics are to dissolve life threatening clots. 9. Classification of drugs include * anticoagulants (heparin, warfarin) * antiplatelets (aspirin, ADP receptor blockers, glycoproteins IIb/iia receptor antagonsits, agents for intermittent claudication) * thrombolytics (altepase) * hemostatics.
2 examples of drugs are: * clopidogral (Plavix) which changes the binding of ADP to receptors on platelets. They are permanently unable to receive signals required to aggregate. This prevents throbi formation in arteries after a stroke or MI. Abnormal bleeding can be a result (need to wait for body to remove platelets), dyspepnia, abdominal pain, dizziness, and headache * alteplase (Activase) converts plasminogen to plasmin to digest fibrin and dissolve clots. Superficial bleeding at injection site can be a results, and allergic reations.

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