Disorders Cardiac Function PDF

**Hypertensive Crisis** - Hypertensive crisis - severe increase in blood pressure which may lead to a stroke. Two categories: hypertensive urgency and hypertensive emergency. - Hypertensive Urgency: Severe elevation in blood pressure, typically systolic blood pressure over...

**Hypertensive Crisis** - Hypertensive crisis - severe increase in blood pressure which may lead to a stroke. Two categories: hypertensive urgency and hypertensive emergency. - Hypertensive Urgency: Severe elevation in blood pressure, typically systolic blood pressure over 180 mmHg or diastolic blood pressure over 120 mmHg, without evidence of target organ damage. It is crucial to reduce blood pressure over a period of 24-48 hours, using oral antihypertensive medications. Captopril and clonidine - Hypertensive Emergency: This is a severe elevation in blood pressure similar to hypertensive urgency, but with evidence of impending or progressive target organ damage. This condition needs immediate reduction of blood pressure (usually within hours) using intravenous (IV) antihypertensive medications. Nitroprusside - Both conditions require immediate attention. However, the key difference lies in the presence or absence of end-organ damage - Especially in the CNS - Kidney damage or loss of consciousness - End-organ damage is not always visible and requires test to determine - Rate of increase in BP is more important than the absolute value. - Often occurs in clients with a history of hypertension who have failed to comply with medications or who have been undermedicated. - In this setting, rising BP is thought to trigger endothelial damage and the release of vasoconstrictor substances. A vicious cycle of BP elevation ensues, leading to life-threatening damage to target organs. - Hypertensive crisis related to cocaine or crack use is becoming a more frequent problem Clinical Manifestations/Complications - Hypertensive crisis can lead to significant pathophysiological changes and potential damage to target organs.: - Heart: Workload of the heart increases due to high blood pressure, which can result in left ventricular hypertrophy, coronary artery disease, congestive heart failure or myocardial infarction. - Brain: Chronic high blood pressure can lead to hypertensive encephalopathy, characterized by headache, nausea, vomiting, seizures, confusion, and coma. Stroke may occur due to hemorrhage or thrombosis. - Kidneys: Hypertensive nephropathy, resulting in proteinuria and kidney injury. - Eyes: Hypertensive retinopathy may occur, characterized by retinal hemorrhage and loss of vision. - The Blood Vessels: Damage to the endothelium of the arteries, leading to arteriosclerosis. - In a hypertensive emergency, these damages are imminent or progressive, requiring immediate medical intervention to prevent irreversible damage. **Cardiac Dysrhythmias (Arrhythmias)** - Damage to the heart\'s conduction system - Systemic causes such as electrolyte abnormalities, fever, hypoxia, stress, infection, or drug toxicity. - Interference with the conduction system may result from inflammation or scar tissue associated with rheumatic fever or myocardial infarction. - ECGs provide a method of monitoring the conduction system and detecting abnormalities - Dysrhythmias reduce the efficiency of the heart\'s pumping cycle. - Cardiac output effects perfusion in the body - A rapid heart rate prevents adequate filling during diastole, reducing cardiac output, and a very slow rate also reduces output to the tissues (perfusion), including the brain, heart, eyes, kidneys, and the heart itself. - Prompt assessment of dysrhythmias and the client's response to the rhythm is critical. **Classification of Dysrhythmias** - Atrial Dysrhythmias: - Originate in the atria. Examples include atrial fibrillation and atrial flutter. - SA node dysrhythmias, too high or too low (sinus brady or tachycardia) - AV node dysrhythmia, too high or too low - Cardio myocytes conducted electricity and are in communication with each other. If someone has a lot of scar tissue (most common reason), the signal will come but because of the scar tissue it will go around instead of through, causing the current to continue to go around, making the contractions out of unison - Big concern with this is blood pooling and then clotting - Risk factors include heart disease, cardiac surgery, increased age, and diabetes. - **Atrial flutter** refers to an atrial heart rate of 250 to 350 beats per minute - AV node delays conduction - **Atrial fibrillation** is a rate of more than 350 beats per minute. - Causes blood pooling and clots - With flutter, the AV node delays conduction, and therefore the ventricular rate is slower. A pulse deficit may occur because a reduced stroke volume is not felt at the radial pulse. - Atrial fibrillation causes pooling of blood in the atria and is treated with anticoagulant medications to prevent clotting and potential cerebrovascular accident (stroke). Ventricular filling is not totally dependent on atrial contraction, and therefore these atrial arrhythmias are not always symptomatic unless they spread to the ventricular conduction pathways. - Atrial kick - Ventricular Dysrhythmias: - Originate in the ventricles. - Examples include ventricular tachycardia and ventricular fibrillation. - Heart Block Dysrhythmias: - Electrical signal is delayed or blocked. Can occur at the atrioventricular (AV) node or along the electrical pathways in the ventricles. Understanding the type of dysrhythmia is crucial as it influences the treatment approach and potential outcomes. **Life Threatening Dysrhythmias** - Recognizing life-threatening dysrhythmias is a crucial skill. Some key dysrhythmias are: - Atrial Fibrillation (A-Fib) with Rapid Ventricular Response (RVR): - While A-Fib itself is not usually life-threatening, if it leads to a rapid ventricular rate, it can result in serious complications like stroke or heart failure. - Don't have enough time to fill and reduce cardiac output - Ventricular Fibrillation (V-Fib) - This is a chaotic rhythm where the ventricles quiver instead of pumping blood. It is the most serious cardiac rhythm disturbance and can lead to cardiac arrest and death if not treated immediately with defibrillation. - Ventricular Tachycardia (V-Tach): - This is a fast, abnormal heart rate that starts in the ventricles. It can be life-threatening, especially if it leads to V-Fib. - Torsades de Pointes: - This is a specific form of V-Tach that can lead to V-Fib if not treated quickly. - your provider can see a specific pattern of ventricular tachycardia that looks like twisting points or peaks (which is what the name means in French) on an electrocardiogram (EKG). - **Total, or third-degree**, blocks occur when there is no transmission of impulses from the atria to the ventricles. The ventricles contract spontaneously at a slow rate of 30 to 45 beats per minute, totally independent of the atrial contraction, which continues normally. In this case, cardiac output is greatly reduced, sometimes to the point of fainting (syncope), causing a Stokes-Adams attack\* or cardiac arrest. \*A sudden, brief loss of consciousness from a large drop in cardiac output. ECG shows no association between P wave and QRS complex - Each of these dysrhythmias requires immediate attention and specific treatment. Understanding their characteristics can help in prompt recognition and intervention **Sudden Cardiac Death** - Unexpected death resulting from various causes, including cardiac arrest. In many cases, SCD is not actually sudden. Etiology and Pathophysiology - Cardiac function is disrupted abruptly, causing immediate loss of CO and cerebral blood flow. - May not have a known history of CAD. - Death usually occurs within 1 hour of the onset of acute symptoms (e.g., angina, palpitations). - Some symptoms shown but may not be recognized - Acute ventricular dysrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) cause the majority of cases of SCD. - Sudden death with athletes in previous class - Aortic valve not opening - Muscle getting too big - Less commonly, SCD occurs because of a primary left ventricular outflow obstruction (e.g., aortic stenosis, hypertrophic cardiomyopathy), or long QT syndrome - It is difficult to predict who is at risk for SCD. Risk factors for SCD include (a) male sex, (b) family history of premature atherosclerosis, (c) tobacco use, (d) diabetes mellitus, (e) hypercholesterolemia, (f) hypertension, and (g) cardiomyopathy.