What is Pathology - Ventricular Tachycardia
Pathophysiology • In ventricular tachycardia (VT), the ventricles take over as the heart's pacer from the sinoatrial (SA) node. PVCs frequently follow VT. • MI, cardiac irritability, and cardiomyopathy are possible causes of VT. Digoxin toxicity, RA, SLE, and respiratory acidosis; abnormally low amounts of K+, Ca++, and Mg+. • Pacing cables and catheterization of the heart. Evaluation and Diagnostic Results • Rapid ventricular beat, absence of P waves, absence of a PR interval, and a QRS complex longer than 0.11 seconds are all visible on the ECG. • The client may experience sudden diaphoresis as well as palpitations, lightheadedness, nausea, and chest discomfort. The client's blood chemistry, heart enzymes, ABGs, and serum digoxin levels are evaluated. The client may pass out and become pulseless. Complications • Ventricular fibrillation and mortality can result from prolonged VT. • CHF after numerous incidents. Medical Attention and Surgical Procedure • Defibrillation; ACLS protocol-compliant antiarrhythmic, vasopressor, and oxygen delivery. • Replacing electrolytes and giving magnesium to calm the ventricular myocardium. • Inform clients that any time they experience chest discomfort, lightheadedness, or syncope, they should call 911 because prehospital stabilisation can boost survival rates. • Clients who have serious cardiac problems should be on telemetry because they may have VT. • examine the customer as well as the ECG. • Track blood drug levels, cardiac enzymes, and electrolyte levels.
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What is Pathology - Atrial Fibrillation
Pathophysiology Atrial fibrillation (AF), also known as quivering of the atria, is brought on by impulses entering the atrioventricular (AV) node repeatedly. • A decrease in atrial pulse. • The tension of surgery, aging, illness (such as hyperthyroidism), and stimulation of the sympathetic nervous system can all cause AF. Paroxysmal, chronic, permanent, and lone AF are a few of the different types. Evaluation and Diagnostic Results • There are no P waves visible on the ECG, and the rhythm is erratic with a shortened QRS complex. The PR gap is not measurable. • The client might express palpitations, irregular heartbeats, and nervousness. • Blood studies such as the complete blood count (CBC), cardiac enzymes, thyroid function tests, serum drug levels, serum toxicology, and blood chemistry to check for infections, MI, thyrotoxicosis, the toxicity of prescribed cardiac medications or their side effects, renal failure, or abnormal electrolyte levels. • CXR or TEE to check for inflammatory or structural illness. Complications • Blood stasis results in the development of thrombi, which can induce CVA, MI, or pulmonary embolism. (PE). • Left ventricle dysfunction. Medical Attention and Surgical Procedure • Beta-adrenergic blockers, heart glycosides, antiarrhythmic medications, intravenous anticoagulants, and calcium channel blockers. • Ablation or maze treatment (cardiac catheterization approach), pacemaker, implantable cardioverter defibrillator (ICD), electrical cardioversion, or open-heart maze procedure. • Teach clients to report palpitations, particularly those who already have cardiac conditions. • Emphasize to clients the worth of keeping track of laboratory results. • Pay close attention to ECG, INR, and PT readings. Any SOB that may be a PE should be reported. What is Pathology - Cardiogenic Shock
Pathophysiology • Because the right or left ventricles become less contractile as a result of AMI, the cardiac flow to all organ systems in the body is reduced. • Pericarditis and the ensuing heart tamponade may be the cause of CS. Heart valve stenosis or persistent tachycardia can result in CS. • Drugs prescribed for angina, arrhythmias, or preexisting hypertension may accumulate to toxic amounts and result in CS. Evaluation and Diagnostic Results • Cyanosis, muffled heart noises, crackles and wheezes in the base of the lungs, and jugular venous distention. • BP less than 90 mm Hg for more than 30 minutes; an elevated ST-segment on the ECG, which is indicative of an AMI. • Extreme cold; alteration in mental state. • A urine production of 20 to 30 mL or less per hour. • A rise in heart enzyme levels. • Electrolyte levels, CBC showing inflammation, ABG for acidosis, BNP, and coagulation studies. Cardiopulmonary collapse, fatal arrhythmias, renal failure, thromboembolism, and stroke are complications. Medical Attention and Surgical Procedure • Vasodilators, natriuretic peptides, vasopressors, inotropic drugs, phosphodiesterase enzyme inhibitors, platelet aggregation inhibitors, and opioid analgesics. • Monitoring of hemodynamics. • intra-aorta balloon device; LVAD. • Inform customers about the early symptoms and signs of AMI and urge them to get help right away. • Keep an eye on your blood pressure, heart rate, pulse oximetry, and ECG. • Maintain a calm atmosphere and reassure the customer to reduce sympathetic outflow. What is Pathology - Congestive Heart Failure
Pathophysiology The heart has two pumps. The pump's structural flaws will result in cardiac failure. • A buildup of fluid in the lungs is a result of left-sided cardiac failure. • The inferior and superior venae cavae become clogged with liquids when the heart fails on the right side. • As PVR rises, preload expands and afterload becomes challenging to surmount. Evaluation and Diagnostic Results • SOB, crackling or diminished breath noises at the base of the lungs, the existence of the third and fourth heart sounds, orthopnea, cough, pale, clammy skin, anxiety, and restlessness. • Elevated pulmonary wedge pressures, CXR showing pleural effusion and/or atelectasis, transesophageal echocardiogram (TEE) displaying reduced ejection fraction and low cardiac output, exercise or drug-induced stress test showing poor myocardial perfusion pattern, abnormal ECG. • Elevated endothelin 1 (ET-1), a vasoconstrictor, reduced PaO2 in the ABG, as well as elevated ANP and BNP. PND-related pleural fluid, hepatomegaly, splenomegaly, left ventricular thrombus/embolism, and cardiogenic shock are all complications. Medical Attention and Surgical Procedure • Hemodynamic monitoring, daily weights, oxygen, high Fowler's posture, bed rest, IV opioids, IV inotropic agents, IV vasodilators, IV human B-type natriuretic peptide. Heart failure can be avoided with yearly physicals, a healthy diet, exercise, and medicine. • Keep an eye out for changes in your everyday weights, urine output, breath sounds, and BNP. What is Pathology - Myocardial Infarction
Pathophysiology • The sympathetic nervous system is triggered when blood flow to the heart muscle declines, increasing blood pressure and heart rate. The heart cells' requirements for oxygen and glucose rise as a result. Necrotic cardiac tissue will never regain its previous capacity to contract instead forming scar tissue. Cardiac necrosis from lack of perfusion occurs centrally, surrounded by various degrees of ischemic tissue radiating outward from the site. • Damage to the heart's pacing mechanism can result in deadly arrhythmias. Evaluation and Diagnostic Results · ECG variations (ST segment elevation). • Disturbing 12-lead ECG results. • An increase in heart enzymes. • Increased blood pressure and pulse; reduced oxygen saturation. • Elevated white blood cells on the complete blood count (CBC); irregular electrolytes. Complications • Sudden demise, fatal dysrhythmias, cardiogenic shock, valvular dysfunction, and heart failure. Medical Attention and Surgical Procedure • Antiplatelet medications, oxygen, morphine sulfate, nitrates, vasodilators, beta blockers, and regulators of the angiotensin-converting enzyme. • CABG, or cardiac angioplasty with stent implantation. • A healthy lifestyle is the best way to prevent atherosclerosis; however, some individuals are genetically predisposed to it. • Inform customers of the symptoms and signs of MI to encourage prompt medical attention. • Women experience unusual signs and symptoms (nausea, indigestion, and possibly no pain), but diagnostic tests should be carried out if they also experience loss of breath or other symptoms. • Although thrombolytic therapy has a 6-hour window, it is best to observe the "60 minutes to treatment" guideline. Time is like a muscle. • Arrhythmia patients who have access to defibrillators in public spaces often survive. What is Pathology - Angina Pectoris
Pathophysiology • Atherosclerotic plaque obstructs the coronary arteries, which supply the heart tissue. Because of narrowing and resistance to dilation, increased oxygen demands cannot be satisfied. Ischemic pain develops as a consequence and is referred to the sternum, between the scapulae, inner upper arms, and jaw. • The 4 Es—eating a big meal, excitement, environment (very cold or very hot), and exercise—as well as smoking, are considered causative events. Stable angina, variant angina (Prinzmetal's), unstable angina, which can quickly result in MI, and silent ischemia, which is typically experienced by older people and damages the heart without causing any symptoms, are among the types. Evaluation and Diagnostic Results • Chemical stress testing with radioisotope imaging (showing "cold spots" or regions of decreased cellular metabolism); ECG; exercise; graded testing; and ECG during exercise. • ECHO stress. heart enzymes; Crp. Heart failure can result from complications like MI and permanent heart muscle injury. Medical Attention and Surgical Procedure • Cardiac catheterization, which includes stent and balloon angioplasty insertion. • CABG. • Vasodilators, calcium channel blockers, beta-adrenergic blockers, ACE inhibitors, ANRBs, lipid-lowering medications, and anticoagulant medications. • Inform the customer about a healthy diet, regular exercise, and avoiding angina triggers. • Inform the customer how to use nitroglycerin. • Attacks from the devil and MI need to be distinguished. ECG and cardiac enzymes help with identification. Angina should be handled as a MI up until a MI has been ruled out. What is Pathology - Coronary Artery Disease
Pathophysiology • As a consequence of atherosclerosis, CAD results in blood flow interruption that may result in ischemia or infarction. Low-density lipoproteins (LDL) are drawn to the inflammatory location and bound there by the LDL. The intima's sublayer receives a spillover of the LDLs' triglyceride centre. These lipids are encapsulated by macrophages, also known as "foam cells." • The "fatty streak" that can be seen in the early phases of atherosclerosis is this. More LDL, macrophages, platelets, and smooth muscle fibres are attracted to the spot as the area grows and accumulate under the intima, narrowing the vessel and increasing blood pressure in the tiny coronary vessels. Evaluation and Diagnostic Results • Crp to identify bodily inflammation; blood lipid profile to measure LDL and cholesterol. • A stress test using thallium nuclear imaging, which reveals "cold spots" in regions that aren't well-perfused. • Stress echocardiography; irregular ECG. • A quick CT scan to look for calcium buildup in the vessels. The ultimate standard for diagnosis is cardiac catheterization. Complications include a myocardial infarction that can cause lasting cardiac muscle damage and heart failure, as well as activity intolerance with angina pectoris. • Arrhythmias brought on by a reduction in blood flow to the conduction system. Medical Attention and Surgical Procedure • Drugs that reduce cholesterol; dietary changes. • Depending on the degree, cardiac catheterization combined with balloon angiography and stent placement. • CABG. • Explain to customers that while some risk factors for CAD (such as quitting smoking, maintaining a healthy diet, and exercising) may be genetic, others can be changed. • Changes in lifestyle can rectify CAD. Measure your breathing difficulty while exercising. What is Pathology - Malignant Hyperthermia
Pathophysiology • Autosomal dominant disorder wherein exposure to a specific anaesthetic agent results in a rise in body temperature and muscular rigidity. • Mainly impacts skeletal muscular tissue. Multiple skeletal muscle contractions can result from free ionised calcium concentrations rising to harmful amounts. The hypermetabolic condition results in lactate formation, which leads to acidosis. The temperature may increase to over 105°F from repeated contractions. Evaluation and Diagnostic Results ● Family ties. • An rise in body temperature after anaesthesia. • Muscle stiffness and soreness. • Rhabdomyolysis-related renal insufficiency; dark brown pee (myoglobin in urine). • The blood's composition. Complications • Death; arrhythmia. • Renal problems. • Brain tissue destruction; seizures. Medical Attention and Surgical Procedure • Stop using the anaesthetic right away. • Cooled intravenous dantrolene and intravenous water to flush kidneys of myoglobin. • Antipyretics and a cooling comforter. • Inform clients that they should disclose any personal or kin experience of adverse reactions to anaesthesia. • Rapid contractions caused by an overabundance of calcium cause muscle tissue to be destroyed. Myoglobin is produced as muscle is destroyed and travels through the bloodstream to the kidneys, where it can cause acute tubular necrosis; sufficient hydration is required to flush the kidneys. Antipyretics and cooled intravenous fluid must be administered to bring the temperature down to normal. Blood chemistry should be monitored for elevated amounts of enzymes, creatinine, and BUN. What is Pathology – Encephalitis
Pathophysiology Causative agents include viruses, ticks, mosquitoes, parasites, toxins, bacteria, vaccines, or fungus. Damaged and inflamed neurons cause brain edoema and elevated ICP. The very young, the very old, and people with weakened immune systems are at particular danger. The disease's most prevalent non-insect-borne source may be the herpes simplex virus. Evaluation and Diagnostic Results • A high body temperature, headache, dizziness, nausea, and overall malaise. • Tremors, ataxia, irregular sleep patterns, and hemiparesis. • LP, MRI, and CT imaging to evaluate CSF. Cerebral edoema is identified by MRI and CT imaging. The WBC and protein amounts in the CSF are elevated, and the glucose levels are normal. Seizures, motor impairments, personality changes, blindness, and cognitive deficits are complications. • Death and swelling of the brain. Medical Attention and Surgical Procedure • Corticosteroids, antipyretics, painkillers, sedatives, and AEDs. • ICP tracking using invasive or noninvasive MRI techniques. • Intravenous antiviral drugs. • Inform the client's relatives and friends about the disorder. • Keep a peaceful atmosphere with few distractions to reduce cerebral edoema. • Explain that the purpose of medication and ventilator treatment is to lower ICP. • Noisy stimuli make ICP worse; keep the customer calm and the surroundings quiet. • Keep track of CBC, ABG, and ICP measurements. • Check for epidermis deterioration. • Keep an eye on ventilation; only open the airways when absolutely necessary to prevent ICP rises. What is Pathology - Guillain-Barré Syndrome
Pathophysiology • The GB syndrome (inflammatory polyneuritis) is an inflammatory condition marked by a clear paralysis development. GB frequently occurs after a viral illness. occurs more frequently in Caucasians than in African Americans and in people over the age of 45. • Immune cells invade peripheral nerves, causing inflammation and axonal demyelination. Starting in the knees, paralysis progresses upward. Respiratory support is necessary if the illness affects the lungs. Although the plateau stage is the worst, it marks the conclusion of the progression because remyelination takes place and the symptoms go away. • The illness has a progressive form. Ataxia and additional ocular paralysis but no respiratory or sensory loss are brought on by Miller-Fisher syndrome. Evaluation and Diagnostic Results • CSF for LP. indicates a rise in protein. • Tests for the EMG and nerve conduction rate. • Tests of pulmonary function. Complications include immobility, skin breakdown, PE, muscular atrophy, and DVT. They also include infections, depression, anxiety, and respiratory failure. Medical Attention and Surgical Procedure A plasmapheresis. • Supplemental air and ventilation. • steroid use. • Inform patients and carers of the steps being taken to reduce symptoms; an interim ventilator support system may be required. • Explain the disease's typical course of development. • Offer mental comfort and distraction. • Controlling pain; evaluating the health of the epidermis and nutrition. |
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