Chapter 35 care of the patients with cardiac problems 1. What are the dlinical m
ID: 240327 • Letter: C
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Chapter 35 care of the patients with cardiac problems 1. What are the dlinical manifestations of digoxin toxicity? 2 What are beta-adrenergic blockers how do they work how do they improve the patient's cardiac function and what do you instruct the patient about the medication? 3. How does continuous positive airway pressure improves heart failure? 4. How does cardiac resynchronization therapy improve heart failure? 5. How does gene therapy play a role in heart failure? What does ventricular assistive devices do for heart failure? 6. Explain heart reduction surgery and what role it plays with heart failure? B. What are the nursing interventions and teaching for this patient? 7. What are your heart failure self-management teaching with medications activity weight diet and symptoms? What is the most effective education method to provide heart failure education to heart failure patents? Make sure you review the indications of worsening or recurrent heart failure as well as drug therapy for patient and family education you also want to review the Nutrition Therapy and understand and know your advance directive information. 10. What is the outcomes are the expected outcomes for the heart failure person? VALVULAR HEART DISEASE Know the following Mitral stenosis Mitral regurgitation Mitral valve prolapse Aortic stenosis Aortic regurgitation What is your assessment for these patients? What testing would do you expect to be ordered? What is your management when it comes to drugs therapy?Explanation / Answer
1) Manifestation of Digoxin toxicity
The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or yellow vision). It is also associated with cardiac disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.Digoxin toxicity produces CNS, visual, GI, and cardiac manifestations.
2) Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta-blockers are used for treating hypertension, angina, myocardial infarction, arrhythmias and heart failure.
Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drugs.
Effect on cardiac
Beta-blockers bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both 1 and 2 adrenoceptors, although the predominant receptor type in number and function is 1. These receptors primarily bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood. Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.
Beta-adrenoceptors are coupled to a Gs-proteins, which activate adenylyl cyclase to form cAMP from ATP. Increased cAMP activates a cAMP-dependent protein kinase (PK-A) that phosphorylates L-type calcium channels, which causes increased calcium entry into the cell. Increased calcium entry during action potentials leads to enhanced release of calcium by the sarcoplasmic reticulum in the heart; these actions increase inotropy (contractility). Gs-protein activation also increases heart rate (chronotropy). PK-A also phosphorylates sites on the sarcoplasmic reticulum, which lead to enhanced release of calcium through the ryanodine receptors (ryanodine-sensitive, calcium-release channels) associated with the sarcoplasmic reticulum. This provides more calcium for binding the troponin-C, which enhances inotropy. Finally, PK-A can phosphorylate myosin light chains, which may contribute to the positive inotropic effect of beta-adrenoceptor stimulation.
Because there is generally some level of sympathetic tone on the heart, beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy (heart rate), inotropy (contractility), dromotropy (electrical conduction) and lusitropy (relaxation). Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate. These drugs have an even greater effect when there is elevated sympathetic activity.
Blood vessels
Vascular smooth muscle has 2-adrenoceptors that are normally activated by norepinephrine released by sympathetic adrenergic nerves or by circulating epinephrine. These receptors, like those in the heart, are coupled to a Gs-protein, which stimulates the formation of cAMP.In vascular smooth muscle an increase in cAMP leads to smooth muscle relaxation. The reason for this is that cAMP inhibits myosin light chain kinase that is responsible for phosphorylating smooth muscle myosin. Therefore, increases in intracellular cAMP caused by 2-agonists inhibits myosin light chain kinase thereby producing less contractile force (i.e., promoting relaxation).
Compared to their effects in the heart, beta-blockers have relatively little vascular effect because 2-adrenoceptors have only a small modulatory role on basal vascular tone. Nevertheless, blockade of 2-adrenoceptors is associated with a small degree of vasoconstriction in many vascular beds. This occurs because beta-blockers remove a small 2-adrenoceptor vasodilator influence that is normally opposing the more dominant alpha-adrenoceptor mediated vasoconstrictor influence.
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