CCRN-Adult VCE Exam Download

A high mixed venous O2 saturation (SO2) indicates that the tissue cells are not extracting enough oxygen from the blood, which can be due to impaired cellular metabolism or increased oxygen delivery. In septic shock, there is often a mismatch between oxygen delivery and consumption, resulting in a high SO2 despite tissue hypoxia. Therefore, SO2 alone is not a reliable indicator of tissue perfusion in septic shock.

References:

• Mixed venous oxygen saturation (SvO2) monitoring • LITFL • CCC
• SvO2 to monitor resuscitation of septic patients: let’s just understand the basic physiology | Critical Care | Full Text
• Reference Guide for CCRN (Adult), page 14.

The actions taken by the nurse are best described as evidence-based practice. By reviewing the literature and developing a proposal referencing peer-reviewed articles, the nurse used current research findings to inform and change clinical practice. This approach ensures that patient care is based on the best available evidence, leading to improved patient outcomes.References: = CCRN Exam Handbook, page 59

The first priority in the management of an acute gastrointestinal (GI) hemorrhage is fluid resuscitation. This is critical to maintaining hemodynamic stability and ensuring adequate perfusion of vital organs. Monitoring of serial hemoglobin and hematocrit (Hgb and Hct) levels, while important for ongoing assessment, is secondary to the immediate need to stabilize the patient's circulatory status. Pain relief and insertion of a Sengstaken-Blakemore tube may be part of the overall management plan but are not the first priority. References: CCRN Exam Handbook, AACN, page 27, section on GI emergencies.

The patient’s present clinical status is most likely a result of a ventricular septal defect (VSD), which is a hole in the wall between the left and right ventricles. A VSD can occur as a mechanical complication of MI, usually within the first week, due to necrosis and rupture of the ventricular septum. A VSD causes a left-to-right shunt of blood, which leads to increased pulmonary pressure, pulmonary edema, and reduced cardiac output. The patient’s symptoms and signs are consistent with a VSD, such as severe chest pain, hypotension, tachycardia, respiratory distress, high PAOP with large V waves, low CI, cool and clammy skin, inspiratory crackles, and a loud blowing holosystolic murmur at the apex. A papillary muscle rupture, a cardiac tamponade, and an acute aortic insufficiency are other possible mechanical complications of MI, but they have different clinical manifestations. A papillary muscle rupture causes acute mitral regurgitation, which presents with a soft systolic murmur at the apex and pulmonary congestion1. A cardiac tamponade causes compression of the heart by pericardial fluid, which presents with hypotension, muffled heart sounds, and jugular venous distension2. An acute aortic insufficiency causes backflow of blood from the aorta to the left ventricle, which presents with a diastolic decrescendo murmur at the left sternal border and a wide pulse pressure3.

References:

• 1: Mechanical complications of acute myocardial infarction - UpToDate4, p. 2-3.
• 2: Cardiac tamponade - Symptoms, diagnosis and treatment | BMJ Best Practice US, p. 1-2.
• 3: Acute aortic regurgitation - Symptoms, diagnosis and treatment | BMJ Best Practice US, p. 1-2.