NSG-430 Exam 2 Latest Update 2024-2025 Actual
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12-lead ECG - CORRECT ANSWER: -Typically, an ECG consists of 12 leads (or views)
of the heart's activity.
-A lead consists of a positive and a negative electrode, with the positive electrode being
the "seeing eye."
-Activity coming toward the positive electrode produces an upward deflection on the
EKG paper, and one going away from the seeing eye produces a downward deflection
(this is the reason for lead tracings looking different).
-Six of the leads measure electrical forces in the frontal plane. These are bipolar
(positive and negative) leads I, II, and III (left column of tracings); and unipolar (positive)
leads aVr, aVl, and aVf.
-The remaining six unipolar leads (V1 through V6) measure the electrical forces in the
horizontal plane (precordial leads).
-The 12-lead ECG may show changes suggesting structural changes, conduction
disturbances, damage (e.g., ischemia, infarction), electrolyte imbalance, or drug toxicity.
-Obtaining 12 ECG views of the heart is also helpful in the assessment of dysrhythmias.
Nursing Considerations:
-Clip excessive hair on chest wall
-Rub skin with dry gauze
-May need to use alcohol for oily skin
-Apply electrode pad
-Artifact-movement or poor lead contact
acute coronary syndrome - CORRECT ANSWER: -When ischemia is prolonged and not
immediately reversible, acute coronary syndrome (ACS) develops.
,-ACS includes the spectrum of UA, non-ST-segment-elevation myocardial infarction
(NSTEMI), and ST-segment-elevation myocardial infarction (STEMI).
-When patients first present with chest pain, ST-elevations on the 12-lead ECG are
most likely indicative of a STEMI.
-The ECG should always be compared to a previous ECG whenever possible.
-For patients with chest pain who do not show ST-elevation or ST-T wave changes on
the ECG, it is difficult to distinguish between UA and NSTEMI until serum cardiac
biomarkers are measured.
-On the cellular level, the heart muscle becomes hypoxic within the first 10 seconds of a
total coronary occlusion. Heart cells are deprived of oxygen and glucose needed for
aerobic metabolism and contractility.
-Anaerobic metabolism begins and lactic acid accumulates.
-In ischemic conditions, heart cells are viable for approximately 20 minutes.
-Irreversible heart damage starts after 20 minutes if there is no collateral circulation
Etiology and Pathophysiology:
-ACS is caused by the decline of a once stable atherosclerotic plaque.
-The previously stable plaque ruptures, releasing substances into the vessel.
-This stimulates platelet aggregation and thrombus formation.
-This area may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or
totally occluded by a thrombus (manifesting as STEMI).
-What causes a coronary plaque to suddenly become unstable is not well understood,
but systemic inflammation (described earlier) is thought to play a role.
-Patients with suspected ACS require immediate hospitalization.
ECG Changes:
-The 12-lead ECG is a major diagnostic tool used to evaluate patients with ACS.
-The ECG changes are in response to ischemia, injury, or infarction (necrosis) of myo
acute decompensated heart failure (ADHF) - CORRECT ANSWER: -Mechanisms can
no longer maintain adequate CO and inadequate tissue perfusion results.
,-Sudden onset of signs and symptoms of HF
-Requires urgent medical care
-Life threatening condition, both of the ventricles are failing, end organ perfusion is
greatly impacted
-Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures
(universal finding)
Clinical Manifestations:
-In acute decompensated HF (ADHF), the pulmonary venous pressure increases
caused by failure of the LV. This results in engorgement of the pulmonary vascular
system.
-As a result, the lungs become less compliant, and there is increased resistance in the
small airways. To help compensate, the lymphatic system increases its flow to help
maintain a constant volume of the pulmonary extravascular fluid.
-This early stage is clinically associated with a mild increase in the respiratory rate and
a decrease in partial pressure of oxygen in arterial blood (Pao2).
-If pulmonary venous pressure continues to increase, the increase in intravascular
pressure causes more fluid to move into the interstitial space than the lymphatics can
remove. Interstitial edema occurs at this point.
•Tachypnea develops and the patient becomes symptomatic (e.g., short of breath).
-If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted
and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema).
-As the disruption becomes worse from further increases in the pulmonary venous
pressure, the alveoli and airways are flooded with fluid.
-This is accompanied by a worsening of the arterial blood gas values (i.e., lower Pao2
and possible increased partial pressure of carbon dioxide in arterial blood [Paco2] and
progressive respiratory acidemia).
-Based on hemodynamic and clinical status, patients can be c
acute kidney injury - CORRECT ANSWER: Acute kidney injury (AKI):
-Term used to encompass the entire range of the syndrome, including a very slight
deterioration in kidney function to severe impairment.
-Characterized by a rapid loss of kidney function
, -Accompanied by a rise in serum creatinine level and/or a reduction in urine output
-Severity of dysfunction can range from a small increase in serum creatinine or
reduction in urine output to the development of azotemia (an accumulation of
nitrogenous waste products [urea nitrogen, creatinine] in the blood).
-Can develop over hours or days with progressive elevations of blood urea nitrogen
(BUN), creatinine, and potassium, with or without a reduction in urine output.
-Impacts the kidney in three different ways: pre-renal, intra-renal, and post-renal
Pre-Renal Causes:
-Factors that reduce systemic circulation causing reduction in renal blood flow
-Severe dehydration, heart failure, ↓CO
-This causes ↓ to the glomerular filtration rate (GFR), leading to oliguria
-There is no damage to the kidney tissue (parenchyma)
-Caused by a decrease in circulating blood volume (e.g., severe dehydration, heart
failure, decreased cardiac output)
-Readily reversible with appropriate treatment.
-Autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine,
and antidiuretic hormone attempt to preserve blood flow to essential organs
-Prerenal azotemia results in a reduction in the excretion of sodium (less than 20
mEq/L), increased salt and water retention, and decreased urine output.
-Prerenal conditions contribute to intrarenal disease if renal ischemia is prolonged.
-If decreased perfusion persists for an extended time, the kidneys lose their ability to
compensate and damage to kidney parenchyma occurs (intrarenal damage).
Autoregulatory Mechanisms:
-GOAL: to preserve blood flow
-With a decrease in ci
aortic valve regurgitation - CORRECT ANSWER: -Aortic regurgitation (AR) may be the
result of primary disease of the aortic valve leaflets, the aortic root, or both.
