Chapter 8
Preparing for Nursing Questions
You don’t know what you don’t know until you are interviewed by a nurse manager or sit for a pre-employment online nursing test – and by then it’s too late. No one knows what you’ll be asked on a job interview or pre-employment test except the nurse manager and the people who created the pre-employment test. However, it is likely that you’ll be asked questions that involve nursing judgment and patient safety.
Like many nurses, you have good skills within your area of nursing. You can whiz through any nursing quiz in your specialty but how would you fare with questions outside your current nursing job? Can you provide the textbook approach to procedures that you perform daily? These can be challenging and trip you up during the pre-employment process. It’s not that you don’t know the answer, but you don’t remember it. Somewhere in your brain it sits. How far back depends on how long ago you graduated from nursing school.
Don’t fret. This chapter provides a review of nursing basics — a good foundation for answering critical thinking and patient safety questions. Consider this review as a tune-up – maybe a long overdue tune-up depending on how long ago you interviewed for a nursing job.
Physiological Compensation
When the patient encounters a stressful situation – a disorder — the patient’s body automatically changes from normal operations to modified operations in order to compensate for the stressful situation. Respiration increases to raise the oxygen level in the blood. Some blood vessels contract while others dilate to increase blood volume to vital organs and away from less vital organs. The heart rate escalates pumping the increased oxygenated blood throughout the body. Normal function returns once the stressful situation subsides.
This is referred to as physiological compensation. The capability of the patient’s body to compensate for abnormal situations (such as infection) is called the body’s physiological reserves. The patient requires medical intervention when the physiological reserves are low or unable to compensate for the changes. For example, the patient’s immune system destroys and removes bacteria that enter the body by increasing the white blood cell (WBC) count. The WBC count returns to normal once the bacterial infection is resolved. However, the severity of the bacterial infection may eventually deplete the patient’s physiological reserves – the immune system can’t keep up fighting the bacteria – and the patient requires antibiotic medication to help fight the bacterial infection. Without the additional help (antibiotics), the bacteria will “win” because the patient’s physiological reserves are exhausted — the patient becomes septic and dies.
The lower the physiological reserves, the more medical intervention is required to help the patient compensate for the abnormal situation. The combination of medical intervention and the patient’s physiological reserves enables the patient’s body to compensate for the disorder. The objective is to intervene before the physiological reserves are depleted and the patient develops multiple organ dysfunction syndrome (MODS) where failure of one organ to compensate has a cascading effect of taxing the physiological reserves of other organs. For example, depletion of respiratory reserves increase CO2 in arterial blood leading to an increased heart rate as the heart pumps more blood to compensate for low oxygen levels in the blood. At some point, cardiac reserves are depleted and no blood is supplied to organs. The kidneys fail. The liver fails. The heart fails. And the brain fails.
Physiological reserves decrease with:
–Aging. Parts of the body are old and don’t work like they use to work. For example, an aging liver may be unable to properly metabolize some medications leading to ineffective therapeutic effect of the medication and the risk of an overdose of medication.
–Disorders. Parts of the body are not functioning properly. For example, bone marrow and other blood forming organs produce an increasing number of immature WBC (leukemia) leading to an impaired immune system.
Estimating the Physiological Reserves
The patient’s physiological reserve can be estimated by measuring some systems of the body – but not all systems. Sometimes attempting to measure the physiological reserve of a system may produce misleading results.
–Cardiac reserve. Cardiac reserve is measured as the difference between the resting heart rate and the heart rate when ischemia and angina occurs during a stress test. A narrow range indicates a low reserve. Cardiac reserve is also measured by the mean arterial pressure (MAP), which is the average arterial pressure during a cardiac cycle. A value less than 50 mmHg indicates a low reserve.
–Pulmonary reserve. Pulmonary reserve is measured as partial pressure of the end-tidal CO2 (PaCO2) in arterial blood gas. Increased CO2 indicates a low reserve. Lower arterial oxygen levels indicate low reserve. An arterial oxygen level lower than 200 mmHg may require that the patient be placed on mechanical ventilation.
–Renal reserve. Renal reserve is measured by serum creatinine. A value greater than 5 mg/dl indicates a low renal reserve. Creatinine is a byproduct of muscle metabolism and is filtered by the kidneys and excreted in urine.
–Blood production reserve. Blood production (hematopoietic) reserve is measured by serum hemoglobin and the platelet count. Hemoglobin 7g/L indicates a low reserve. A platelet count below 50,000 indicates a low reserve.
–Liver reserve. Liver reserve is measured by total bilirubin in serum. Total bilirubin greater than 12 mg/dl indicate a low reserve.
–Coagulation reserve. Coagulation reserve is measured by the serum platelet count. A serum platelet count of less than150,000 platelets indicates a low reserve.
–Neurological system reserve. The neurological system reserve is measured by the Glasgow Coma Scale. A Glasgow Coma Scale value of less than 9 indicates a low reserve.
–Immune system reserves. The immune system reserves are measured by testing the amount of immunoglobulins (antibodies) in the patient’s blood. The white blood cell (WBC) count (B-cells and T-cells) is also an indicator of the immune system reserves. A low WBC indicates a low reserve indicating that the patient is at risk for infection.
The Call for Help
The average patient visits a practitioner when all else has failed to address the problem. The body compensates for many disorders without the patient noticing a change. For example, the immune system attacks microorganisms routinely. It is only when the immune system reserves are being overtaxed that the patient notices symptoms (for example, fever). At this point, the average patient tries to “tough it out” and let the body’s compensation take over. The patient may rest more than normal but as the symptoms become more uncomfortable the patient may use home remedies and over-the-counter (OTC) medications most of which treat the symptoms and not the underlying cause. For example, an OTC pain medication may help a headache but does nothing for the bacterial infection that triggered the inflammation response that lead to the headache. Sometimes home remedies and OTC medications are sufficient to give the body time to resolve the problem. However, when home remedies and OTC medications fail, the patient goes to the practitioner for help.
The practitioner is faced with a puzzle — diagnose the problem and develop a treatment plan that either fixes the problem (acute condition) or minimizes the symptoms (chronic condition). However, in the real world there may be more that the practitioner considers other than identifying and treating the problem.
The patient is thinking, “I hope the practitioner can fix my problem.”
The practitioner is thinking, “I hope you have a problem that I can fix.”
The practitioner creates a database of information about the patient especially focusing on the current episode. Questions are asked; a physical assessment is performed; and medical tests are likely ordered, if necessary. The direction taken by the practitioner depends on the symptoms (subjective) reported by the patients and the signs (objective) identified by the physical assessment.
The practitioner then decides if she can fix the problem. If so, a medication is likely ordered to supplement the patient’s physiological reserves. Sometimes treatment can only be performed in a hospital if the patient’s physiological reserves are low and more involved treatment is needed to supplement the physiological reserves. The practitioner may also decide to refer the patient to another practitioner if the practitioner is unable to reach a diagnosis or is unable to treat the patient.
There are times when the practitioner is capable of treating the patient but doesn’t want to treat the patient. In the real world, practitioners have the following concerns when deciding to treat a patient:
–Avoid being sued.
–Keep the professional license.
–Make money.
–Treat the patient.
Practitioners tend to build a practice (outpatient/inpatient) focused on a specific group of disorders that the practitioner finds relatively safe to treat and that is profitable. Some focus on family practice while others become experts in a specialty. This expertise is not only for diagnosing and treating patients but also navigating third party payer rules to ensure maximum profit.
The goal of the practitioner — regardless of motivation — is to fix the problem. But if this is not feasible, the goal is to return the patient to activities of daily living (ADL), to reduce the symptoms so that the patient is more comfortable than when the patient presented to the practitioner.
The Cascading Effect
A symptom may be caused by a complex array of events take place in a patient’s body. Think of each symptom as a dot. The task is to identify and connect all the dots to “see” what is really happening with the patient. This is similar to the “connect-the-dots” books that children use to “draw” pictures.
Let’s look at a patient who is a heavy smoker.
–Tobacco causes increased growth in cells in the lung that produce mucus. This leads to an overproduction of mucus (thick mucus).
–Cilia (hair-like cells) “clean the lungs.” Tobacco consumption decreases the number of functioning cilia. Mucus cannot be removed.
–The buildup of mucus clogs the airway and the patient develops a chronic cough as the body attempts to remove the mucus.
–Airway narrows reducing air flow resulting in increased CO2 levels and decreased oxygen levels in the blood.
–Wheezing is heard as air moves through mucus.
–Mucus retained in the lungs make a perfect medium for the growth of microorganism leading to chronic lung infection (chronic bronchitis and COPD).
–Over time the alveoli (the site of gas exchange in the lungs) collapse, trapping air in the alveolar sac (emphysema) thus reducing the area of the lung that can be used for gas exchange.
–Decreased gas exchange leads to decreased oxygen in the blood resulting in bluish tint seen in nail bed, nose, and earlobe (cyanosis).
–Increased levels of CO2 in blood signals the brain to compensate by increasing the heart rate (tachycardia) to pump more blood through the body to perfuse organs and increase respiration (tachypnea, shortness of breath) to increase gas exchange.
–Increased respiratory workload leads to the patient using accessory muscles to breath (raised shoulders). Accessory muscles are used to compensate for low respiratory reserve.
–The increased cardiac workload to compensate for increase CO2 levels in blood leads to right-side heart failure as cardiac reserves are depleted. The heart is unable to effectively pump blood through the cardiovascular system leading to accumulation of fluid in the legs, ankles, and eventually the lungs (edema).
–Eventually low oxygen levels affect the brain and the patient dies.
Resolving the underlying problem (that is, smoking tobacco), may reverse the cascading effect or begin to reduce dependency on the physiological reserves. Effective treatment may also reduce dependency on physiological reserves, if the underlying problem is not resolved. For example, respiratory treatment reduces some of the accumulated mucus resulting in a decreased risk of infection and possibly an increase in effective gas exchange in the lungs.
Assessments
The patient assessment is where you learn why the patient is seeking help. There are times when the patient reports classic symptoms that lead to a diagnosis. You’ll find classic symptoms for various body systems disorders later in this chapter. Classic symptoms help to define the patient’s current problem (episode); however, always consider the whole patient when making the assessment. Some symptoms may not be related to the current problem but may indicate other problems that haven’t fully materialized.
Also consider than signs that seem abnormal may be perfectly normal for the patient under the circumstances. For example, an 80-year-old male complained about random pain and drove himself to the emergency department. Blood tests were taken and his blood glucose level was near 300 mg/dL. This is considered an abnormal sign unless it was learned that the patient ate a large breakfast a little over an hour ago. This was normal.
The initial assessment is to identify systems that are being stressed by the underlying problem as indicated by signs and symptoms — and systems that are normal. The results direct the focus of the assessment to the current problem and then possible treatment options.
Quick Assessment
Remember your first bedside clinical assessment in nursing school that took nearly an hour to complete — and the five-minute assessment that you probably perform daily at bedside today?
“Mr. Jones, I’m Jim. I’ll be your nurse today. How are you feeling?”
“I’m feeling much better.”
This brief conversation tells you that the patient is breathing (no signs of any respiratory distress); heart is working (no signs of cardiac distress); alert and oriented (no signs of cognitive impairment); skin color is normal (no signs of cyanosis); he moved his head and followed you (no signs of hearing or loss of sight); he was reading, and holding a magazine when you walked in (arms and hands are functional, no tremors).
“Mr. Jones, were you able to go to the bathroom this morning?”
“No problem in that category. I went a few minutes ago.”
There is no bowel obstruction; no reported problems urinating; no incontinence; and the patient is ambulatory.
Although a quick assessment is no replacement for a thorough head-to-toe assessment, quick assessments are commonly used to identify likely causes of the patient’s complaints based on probabilities rather than possibilities. Here are three commonly used approaches to a quick patient assessment.
SAMPLE
–Signs and Symptoms (What bothers you?)
–Allergies (Is the patient having an allergic reaction to something?)
–Medication (Has the patient taken any new medications that may be causing an adverse side effect?)
–Pertinent past medical history (Has a previous problem reoccurred or lead to the present problem?)
–Last oral intake (What did you ingest recently?)
–Events leading up to the problem (Have you been doing anything different recently?)
OPQRST
–Onset: When did the problem start?
–Provocation: What makes the problem worse?
–Quality: How do you feel?
–Radiation: Does the pain or discomfort move?
–Severity: How bad is the problem?
–Time: How long have you had this problem?
PQRST
A relatively efficient way of assessing pain is to use the PQRST method.
–P = Provocation
○Where did the pain start?
○What caused the pain?
○What aggravates the pain?
○What relieves the pain?
○Was the pain sudden or gradual?
○Describe the pain as sharp, dull, stabbing, burning, crushing, throbbing, shooting, and/ or nauseating
–R = Region and Radiation
○Where is the pain located?
○Is the pain located in one place?
○Is it radiating pain? If so, where does the pain travel?
–S = Severity
○On a scale of 0 to 10 with zero being no pain and 10 being the worst pain, what is your pain?
–T = Timing
○What time did the pain begin?
○How long did the pain last?
○What time of day did you experience the pain?
○Did you ever have this pain before now?
Five P’s of musculoskeletal injury (head to toe)
–Pain
–Paralysis
–Paresthesia
–Pulse
–Pallor
Risk of Mortality
In critical situations, it is important to assess the risk of mortality resulting from multi-organ failure to determine if treatment is beneficial or futile. Remember that treatment is designed to supplement the patient’s body’s capability to compensate for the physiological imbalance. There are times when the patient’s body is no longer capable of compensating and, therefore, treatment is futile. There are four assessment models that are commonly used to assess the probability of mortality. These are:
Multiple Organ Failure (MOF)
–Multiple Organ Failure (MOF) predicts the patient’s mortality based on the number of the patient’s organs that have depleted their physiological reserves.
Mortality Probability Model (MPM)
–The Mortality Probability Model is used in the intensive care unit to predict the probability of the patient’s mortality in 24 hours, 48 hours, and 72 hours of admission. Here are the factors that are evaluated in this assessment:
○Age
○Type of admission
○Hours admitted
○Metastatic Cancer
○Cirrhosis
○Diuresis < 150 mL/8h
○Creatinine > 2 mg/dL
○Coma (Glasgow Coma Scale 3-5)
○Intracranial Mass Effect
○Vasoactive drug (increases/decreases blood pressure) >= 1h
○Mechanical Ventilation
○PaO2 < 60 mmHg
○Proven Infection
○Pt > standard + 3 sec
Simplified Acute Physiology Score (SAPS)
–The Simplified Acute Physiology Score is used after the first 24 hours of admission to a critical care unit using 12 physiological measurements. These are:
○Age
○Heart Rate
○Systolic Blood Pressure
○Temperature
○Glasgow coma score
○Mechanical ventilation in use
○PaO2
○FiO2 (A fraction of the amount of oxygen inhaled using an oxygen device)
○Urine output per hour
○BUN
○Sodium
○Potassium
○Bicarbonate
○Bilirubin
○WBC
○Hematologic malignancy
○AIDS
○Type of admission
Sequential Organ Failure Assessment (SOFA) Score
–The Sequential Organ Failure Assessment Score uses six factors to evaluate the risk of sequential organ failure. The higher the score the lower the physiological reserves. These are:
○Respiratory
○Cardiovascular
○Hepatic
○Coagulation
○Renal
○Neurological
Acute Physiology and Chronic Health Evaluation (APACHE)
–The Acute Physiology and Chronic Health Evaluation measures physiological factors during the first 24 hours of admission to measure the severity of disease for adults. The higher the APACHE score, the higher risk that the patient will die. Factors measured are:
○Age
○PaO2 or AaDO2 (which to select to assess is based on FiO2 value)
○Rectal Temperature
○Mean arterial pressure (MAP)
○Arterial pH
○Heart rate
○Respiratory rate
○Serum sodium
○Serum potassium
○Creatinine
○Hematocrit
○White blood cell count
○Glasgow Coma Scale
Baseline Assessment
The baseline assessment provides a database of information about the patient that helps you identify what is normal and potentially abnormal physiologically with the patient. Trust what the patient reports; however, be sure to verify the information with the patient’s other healthcare providers and the patient’s family. Some patients are poor historians. Develop a potential problem list reported by the patient. The practitioner will also develop a problem list containing targets for treatment.
–Age, occupation, psychosocial information
–Presenting problem that caused the patient to seek treatment
–Current/past medical problems and chronic medical conditions
–Timeline of events leading the patient to seek treatment
–Head:
○Eyes open. Pupils equal and reacting to light.
○Mouth free from trauma
○Patent airway
○All tubes are patent
–Chest:
○Heart
▪Heart sounds
▪Heart rate
▪Blood pressure
▪Mean arterial pressure to measure end-organ perfusion
▪Urinary output to measure end-organ perfusion
○Respiration
▪Respiratory rate
▪Partial pressure of arterial O2 (PaO2)
▪Partial pressure of end-tidal CO2 (PaCO2)
○Chest expansion
○Lungs
○Drainage tubes are patent
–Arms and hands:
○Skin
○Range of motion (ROM)
○Patent I.V. lines
–Abdomen:
○Bowel sounds present
○Bowel movement
○Urinary output
○Drainage tubes are patent
○Femoral line patent
–Legs and feet:
○Skin
○Range of motion (ROM)
–Blood Labs (abnormal)
○HCT low
○Hgb low
○TICB low
○Iron low
○Ferritin low
○RBC low
–Risk for bleeding
○Platelet < 37,000
○PTT high
○PT high
○INR high
–Nutrition (abnormal)
○Malnutrition
▪Prealbumin decreased
▪Albumin decreased
–Fluid balance (abnormal)
○Dehydration
▪HCT high.
▪Hgb high
▪RBC high
▪Albumin high
▪Urine specific gravity high
○Overhydration
▪HCT low
▪Hgb low
▪RBC low
▪Albumin low
▪Urine specific gravity low
○CD4 low
○WBC < 2,000
○ESR high
○Neutrophils high
○Eosinophils high
○Lymphocytes high
–Pancreas (abnormal)
○Amylase high
○Lipase high
–Liver function (abnormal)
○Albumin low
○ALT high
○AST high
○Total bilirubin high
○Direct bilirubin high
–Renal function (abnormal)
○Urine output less than 1 ml/kg/hr
○Creatinine high
○BUN high
Remember the methods used to physically examine the patient:
–All parts of the body except the abdomen
○Inspection: Look for abnormal signs.
○Palpation: Assess for location, size, texture, and consistency.
○Auscultation: Listen with a stethoscope.
○Percussion: Tap areas and listen for repercussion sounds.
–Examine the abdomen
○Inspection: Look for abnormal signs.
○Auscultation: Listen with a stethoscope.
○Palpation: Assess for location, size, texture, and consistency.
○Percussion: Tap areas and listen for repercussion sounds.
Level of Consciousness
The Glasgow Coma Scale (Table 8.1) is used to objectively measure the patient’s level of consciousness based on the patient’s eye response, verbal response, and motor response. A score of less than 13 is associated with decreased level of consciousness. The National Institutes of Health Stroke Scale (Table 8.2) is an objective way the measure impairment caused by a stroke by assessing consciousness, vision, sensory, motor responses, and speech and language function. An initial score greater than 4 indicates that the patient may benefit from thrombolytic medication to dissolve the blood clot.
Table 8.2: The National Institutes of Health Stroke Scale
Ramsay Sedation Scale (RSS)
RSS is used to assess the rousability of a patient based on six levels.
- anxious/agitated or restless, or both
- cooperative, oriented, and tranquil
- respond to commands only
- exhibits brisk response to light tap or loud auditory stimulus
- sluggish response to light tap or loud auditory stimulus
- no response
Riker Sedation-Agitation Scale (SAS)
SAS provides a clear definition of sedation and agitation that can be used to measure the patient’s sedation-agitation level throughout the course of treatment.
- Unarousable. No response.
- Very Sedated. Awakens to physical stimuli but doesn’t follow commands.
- Sedated. Difficult to arouse but awakens to gentle shaking and verbal stimuli and can follow simple commands before drifting back to the sedated state.
- Calm and Cooperative.
- Agitated. Mildly agitated or anxious but can be calm down with verbal intervention.
- Very Agitated. Unable to calm down with verbal intervention and must by physically restrained.
- Dangerous Agitation. Thrashing and is assaultive to staff.
Triage Revised Trauma Score (TRTS)
TRTS is an assessment tool (Table 8.3) that uses systolic blood pressure, respiration, and the Glasgow Coma Scale to prioritize treatment of patients in an emergency. The TRTS score ranges from 0 to 12 that corresponds to the status of the patient. Table 8.3 contains the TRTS assessment tool.
–Delayed: Walking Wounded. TRST Score 12
–Urgent: The patient can wait for a short time before being further assessed. TRST Score 11
–Immediate: The patient requires immediate attention. TRST Score 4 to 10
–Morgue: The patient is unlikely to survive TRST Score: < 4
Reverse Triage
Reverse triage is a technique used to manage scarce medical resources when assessing and treating patients. The goal is to stabilize the patient and return the medical staff to work. The initial step is to acquire information from the patient, those who accompanied the patient, and first responders (if involved in the care of the patient). Determine:
–What occurred
–When it occurred
–How it occurred
–Why it occurred
–What led up to the situation
Identify medical information gather from assessment and any treatment that was provided to the patient by first responders:
–Blood Pressure
–Pulse
–Oxygen saturation
–Respiration
–Temperature
Next, look for medical alert information on the patient (bracelets or medical alert cards in the patient’s pocket or wallet). Use your critical thinking skills to verify all information you’ve gathered from the patient and other sources. Question each source of information then compare responses. Ask yourself, “does this make sense?” How did the person arrive at this information?
The final step is to use medical resources to treat more stable patients before less stable patients except in life threatening situations. There will likely be more stable patients that require minimum time to assess and treat compared with less stable patients, therefore, more patients can be treated by limited medical resources in the shortest amount of time by using reverse triage.
Dealing with Common Stressors
Always keep in mind that the presence of the medical team and the environment may create stress that also leads to symptoms. This is commonly referred to as “white coat syndrome.” For example, a patient who presents with relatively high blood pressure each time she visits her practitioner may not have hypertension. Instead, the patient’s body is compensating for anxiety by increasing blood pressure which becomes apparent when the patient is asked to measure her own blood pressure at home twice a day for two weeks.
Patients undergo stressful experiences when seeking medical treatment that exacerbates the patient’s medical condition. An effort should be made to ease stressors by reducing the patient’s anxiety at each stage of the episode. Here are common stressors that patients experience. Some have no basis in reality but appear real to the patient.
–Fear of death
–Fear of permanent disability
–Discomfort
–Loss of autonomy
–Lack of privacy
–Separation from loved ones and friends
–Frustration by the lack of immediate resolution of the patient’s problem
Here are steps that you can take to reduce the stress level for your patients:
–Acknowledging the patient’s concerns validates the patient’s feelings.
–Educating the patient helps the patient learn about the unknowns of the patient’s care and sets realistic expectations based on facts rather than speculation.
–Establishing milestones in the patient’s experience. Explain what will happen and when it will happen.
–Making the patient comfortable at every stage of the encounter.
–Keeping the patient informed, continuing through every stage of the encounter. Don’t let the patient sit for more than 15 minutes without a brief update of the patient’s status.
–Minimizing disruptions by having fewer and longer interventions rather than frequent and short interventions.
Prepping for the “Quiz”
You may luck out and not be asked any technical questions during your interview with the nurse manager or have to take a pre-employment test that challenges your nursing knowledge. Realistically, however, expect that you’ll be asked questions about nursing, some of which focuses on specific types of assessments, disorders, and nursing interventions. The nurse manager probably wants to know if you can recognize classic signs and symptoms and respond appropriately.
The rest of this chapter helps to prepare for your pre-employment nurse manager interview and pre-employment tests. Each section focuses on assessments, disorders, and nursing interventions for systems of the body. No doubt you learned about this information in nursing school. Some information you use daily in your practice and the rest is a good review before you go for your interview.
Pre- and Post-Operative Care
Special care must be given to patients who are to undergo an operative procedure and who return from an operative procedure. These are areas that should be your focus:
Pre-Operative Care
–Assess patients for contraindication for the procedures (for example, a bleeding disorder).
–Educate the patient and family on the procedures and what to expect pre- and post-procedure.
–Identify the patient’s allergies.
–Determine if the patient signed informed consent for the procedure.
–Ensure that the patient has fasted before the procedure per practitioner’s orders (usually, eight hours for heavy meal, two hours for clear liquid).
–Make sure the patient’s vital signs are within acceptable range before the patient is transported to the procedure area.
–Address the patient’s anxiety and fear, if necessary.
–Administer pre-procedure medication per practitioner’s orders.
–Encourage the patient to void bladder and defecate before surgery.
–Ensure that baseline vital signs and laboratory tests have been completed.
–Remove all jewelry.
–Remove contact lenses.
–Remove dentures.
–Remove hair pieces.
–Remove hearing aids. Note on chart that the patient has a hearing deficiency.
–Remove makeup and dark nail polish
–Ensure that the patient has an ID band for allergies.
–Ensure that the patient’s chart goes with the patient to the procedure area.
–Ensure that the pre-op checklist is completed.
Post-Operative Care
–Vital Signs. Identify changes in the patient’s status.
–Pain Control. Ensure that the patient is free from pain.
–Monitor input and output. Ensure there is no buildup of fluids and the GI tract is working.
–Assess the wound site. Identify complications and proper drainage, if necessary.
–Apply compression stockings. Decreases the risk for deep vein thrombosis.
–Apply intermittent pneumatic compression (IPC) devices. Decreases the risk for deep vein thrombosis.
–Encourage early mobilization. Decreases the risk for deep vein thrombosis.
–Provide walking aids. Removes obstacles from early mobilization.
–Encourage deep breathing and coughing exercises. Increases lung capacity.
–Perform range of motion exercises. Regain mobility and muscle strength.
–Ensure adequate nutrition. Nutrition is required for healing.
–Turn patient every two hours. Prevents pressure sores and skin breakdown.
–Keep skin clean from urine and feces. Prevents skin breakdown.
Cardiovascular Assessment, Disorders, Interventions
Assessment
–Focus on the problem area.
–Stop the assessment if you need to intervene to stabilize the patient.
Interview
–Ask questions, short and to the point. Questions should be structured so they can be answered with a yes or no if the patient is in distress.
–Initial Questions:
○What makes you feeling that something is wrong?
○What happened prior to your noticing this problem?
○Have you recently undergone any medical procedure?
–Follow up questions:
○When did this problem start?
○How long have you had this problem?
○Can you describe the problem?
○On a scale of 0 to 10 where 0 is no pain and 10 is the worst pain, what number is your pain?
○Where is the pain?
○When did the pain begin?
○What makes the pain worse?
○What makes the pain better?
○Is the pain squeezing, burning, or tightening?
○Does the pain move or remain in one place?
○Do you feel anything unusual with your heart, such as palpitation or your heart skipping a beat?
○Do you feel short of breath?
○You do have difficulty breathing when you wake up?
○Do you feel dizzy?
○Do you awaken to urinate?
Common Classic Signs
–Difficulty awakening: Related to decreased oxygenated blood (hypoxia) and possibly decreased circulation
–Bilateral swelling in ankles or feet related to right-side heart failure.
–Skipping heart beats related to irregular heart rhythm
–Heart pounding related to hypoxia
–Heart fluttering related to irregular heart rhythm
–Shortness of breath related to decreased oxygenation or decreased circulation
–Frequent night urination is a possible sign of right-side heart failure
–Dizziness is a sign of decreased oxygenation related to decreased circulation
–Pain might be a sign of decreased circulation to the heart muscle
–Cyanosis in nail beds, tip of the nose and ear lobes related to deoxygenating blood or poor circulation
–Clubbing of fingers related to chronic deoxygenating of blood
–Pale mucus membranes in dark skinned patients related to inadequate circulation
–Loss of hair on arms and legs related to decrease arterial circulation to the area
–Bilateral swelling is a possible sign of right-side heart failure, venous insufficiency, varicosities, or thrombophlebitis.
–Flushed skin related to increased circulation due to fever
–Capillary refill more than three seconds related to decrease circulation
–Cool skin temperature related to decreased circulation
–Warm skin temperature related to increased circulation
–Sound of turbulent blood flow related to aneurysm or heart valve malfunction
–Strong long pulse indicates increased cardiac output
–Diffuse pulse related to left ventricular hypertrophy
–Weak pulse indicates decreased cardiac output or increased peripheral vascular resistance
–Bounding pulse indicates hypertension or high cardiac output
–Dull sound from percussion over lung indicates pleural effusion related to biventricular failure allowing fluid to build up between the lung and the chest wall
–Bruits over the abdominal aorta indicates abdominal aortic aneurysm
–Pulmonary congestion (lungs) indicates left-side heart failure
–Sudden, sharp, continuous pain located below the sternum and radiating to the neck or left arm that gets worse lying on back or breathing deeply might be related to pericarditis
–Sudden, stabbing pain over the back that worsens on inspiration may be related to pulmonary emboli
–Sudden, severe, pain located at the side of the chest with difficulty breathing, and deviated trachea that worsens with normal breathing is related to pneumothorax
–Sudden, severe, tearing pain located in the upper abdomen or behind the sternum is related to a dissecting aortic aneurysm
–Squeezing, aching, burning pain below the sternum radiating to the arms, neck, back, and jaw that worsens on exertion, stress, eating, and lying down is related to angina pectoris (stable angina pectoris if resting resolves pain; unstable angina pectoris if pain continues upon resting).
–Pressure, aching, burning pain across the chest and radiating to the arms, neck, back, and jaw that worsens on exertion and increased anxiety is related to acute myocardial infarction.
Angina Pectoris
Narrowing of the coronary artery (arteriosclerosis) reduces blood flow to the heart.
–Stable Angina. Chest pain follows exercise or stress and is relieved by rest.
–Unstable Angina. Chest pain can occur at rest.
–Prinzmetal’s angina (vasospastic angina). Chest pain occurs at night and at rest.
Classic Signs
–Chest pain, pressure, heaviness, squeezing, tightness for up to five minutes radiates to the jaw, back, or arms. Related to stress that increases oxygen demands on the heart
–Shortness of breath (dyspnea). Related to decrease oxygen in the blood.
–Tachycardia. The body attempting to increase oxygen flow to the heart.
–Increased anxiety. Related to decreased oxygen to cardiac muscles.
–Sweating (diaphoresis). Related to anxiety and increased cardiac workload.
Interventions
–Tell the patient to rest. Decreases cardiac workload.
–Place patient in a semi-Fowler’s position. Decreases stress.
–Monitor vital signs.
–Measure fluid intake and output. Assess for renal output and renal perfusion. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour
–Perform 12-lead ECG during episodes of chest pain per orders.
–Place patient on a low cholesterol, low sodium, and low fat diet.
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient
○Analgesic (Morphine). Decreases cardiac workload and pain.
○Nitrates (Nitroglycerin). Dilates blood vessels leading to increased blood flow to cardiac muscles.
▪Hold nitrate if systolic blood pressure < 90 mm Hg. Risk of reducing blood to the brain.
○Beta-adrenergic blocker. Decreases cardiac workload.
▪Hold Beta-adrenergic blocker if heart rate is less than 60 beats per minute. Risk of low cardiac output.
○Aspirin. Decreases formation of platelets.
Myocardial Infarction (MI)
Coronary artery blockage by atherosclerosis starves cardiac muscle of oxygen causing necrosis of cardiac muscle (infarction).
Classic Signs
–Feeling of impending doom. Related to decreased oxygen to the brain.
–Chest pain radiating to arms, jaw, back, and/ or neck that is unrelieved by rest or nitroglycerin. Related to necrosis of cardiac muscle.
–Cool, clammy, pale skin. Related to decreased circulation.
–Diaphoresis (sweating). Related to increased anxiety from decreased oxygen to cardiac muscle.
–Tachycardia. The body attempting to increase oxygen flow to the heart.
–Nausea/vomiting. Related to decreased cardiac output.
–Variable blood pressure. Related to decreased cardiac output.
–Shortness of breath (dyspnea). Related to decreased oxygen in the blood.
–Asymptomatic. Symptoms varies in degree and a patient may have no symptoms of a MI.
–Urine output decreases (< 25 ml/ hr). Related to lack of renal blood flow. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour
–Decreased pulse pressure (difference in systolic and diastolic). Related to decreased cardiac output.
Interventions
–Bed rest without bathroom privileges. Decreases cardiac workload.
–Place patient in a semi-Fowler's position. Decreases stress.
–Monitor vital signs.
–12-lead ECG during episodes of chest pain per orders.
–Place patient on a low cholesterol, low sodium, and low fat diet
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient.
○Analgesic. Decreases cardiac workload and pain.
○Nitrates. Dilates blood vessels leading to increased blood flow to cardiac muscle.
▪Hold nitrate if systolic blood pressure < 90 mm Hg. Risk of reduced blood to the brain.
○Beta-adrenergic blocker. Decreases cardiac workload.
▪Hold Beta-adrenergic blocker if heart rate is less than 60 beats per minute. Risk of low cardiac output.
○Aspirin. Decreases formation of platelets.
○Antiarrhythmics. Controls cardiac arrhythmias.
○Antihypertensive. Decreases blood pressure.
○Thrombolytic therapy (within 3 to 12 hours of an attack). Dissolves blockage.
○Heparin. Prevents formation of blood clots following thrombolytic therapy.
○Calcium channel blockers. Prevents re-infarction in a non-Q-wave infarction.
Cardiac Tamponade
The pericardium fills with fluid, blood, or pus increasing pressure in the pericardium and resulting in decreased filling of ventricles leading to decreased cardiac output.
Classic Signs
–Muffled cardiac sounds. Related to fluid, blood, or pus in the pericardium.
–Sweating (diaphoresis). Related to increased anxiety from decreased oxygen to cardiac muscle.
–Tachycardia. The body’s attempts to increase oxygen flow to the heart.
–Shortness of breath (dyspnea). Related to decreased oxygen in the blood.
–Restlessness. Related to decreased oxygen to the brain.
–Paradoxical pulse (decrease of 15 mmHg or more in systolic blood pressure on inspiration). Related to pressure change within the chest on inspiration.
–Fatigue. Related to increase cardiac workload.
–Jugular vein distention. Related to fluid overload.
Interventions
–Monitor vital signs.
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient
○Beta-adrenergic blocker. Decreases cardiac workload.
▪Hold Beta-adrenergic blocker if heart rate is less than 60 beats per minute. Risk of low cardiac output.
–Pericardiocentesis: Aspirate fluid from the pericardium.
Cardiogenic Shock
Decreased blood pressure as a result of decreased cardiac output related to cardiomyopathies.
Classic Signs
–Distended jugular veins. Related to fluid overload.
–Hypotension. Related decreased cardiac output.
–Clammy, pale skin. Related to decreased circulation.
–Confusion. Related to decreased oxygen to the brain.
–Crackles. Related to build-up of fluids in the lungs.
–Decreased skin temperature. Related to decreased circulation.
–Cyanosis. Related to poor perfusion.
–Arrhythmias. Related to irritability of cardiac muscle from decreased oxygenation.
–Oliguria (urine output < 30 ml per hour) due to decreased kidney perfusion.
–Tachycardia. The body’s attempts to increase oxygen flow to the heart.
Interventions
–Place patient on bed rest. Decreases cardiac workload.
–Monitor vital signs.
–Measure fluid intake and output. Assess for renal output and renal perfusion. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour.
–Measure weight daily. Weight increase indicates fluid retention.
–Place patient on a low sodium and low fat diet.
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient.
○Vasodilator. Dilates blood vessels and decreases cardiac workload.
○Adrenergic medication. Increases blood pressure and heart rate to perfuse organs.
○Inotropes. Strengthens cardiac contractions.
○Vasopressor. Increases blood flow.
Endocarditis
An infection of the inner lining of the heart (endocardium) and heart valves as a result of invasive medical procedures or secondary to rheumatic heart disease or degenerative heart disease.
Classic Signs
–Janeway lesions. Non-tender, small red areas on the soles and palms, or solid, elevated areas of tissue or fluid inside or under the skin of the soles or palms.
–Petechiae. Small, purple spots on fingernails and palate.
–Osler nodes. Painful, red, raised lesions found on the hands and feet.
–Fatigue. Related to increased cardiac workload.
–Murmurs. Related to turbulent blood flow caused by infected heart valves.
–Fever. Related to infection.
Interventions
–Bed rest. Decreases cardiac workload.
–Monitor for renal failure:
○Decreased urine output. Related to decreased perfusion of the kidneys.
○Increased BUN. Related to decreased perfusion of the kidneys.
○Increased creatinine clearance. Related to decreased perfusion of the kidneys.
–Monitor for embolism:
○Hematuria (blood in urine)
○Decreased mentation
○Cough or painful breathing
–Monitor for heart failure:
○Weight gain. Related to fluid retention.
○Dependent edema. Related to fluid retention.
○Jugular vein distention. Related to fluid overload.
○Crackles. Related to build-up of fluids in the lungs.
○Shortness of breath (dyspnea). Related to decreased oxygen in the blood.
○Tachycardia. The body’s attempts to increase oxygen flow to the heart.
–Blood culture and sensitivity test 3 times, one hour apart. Identifies the microorganism and treatment.
–Administer antibiotics as ordered.
Congestive Heart Failure (CHF)
Ventricles cannot contract to full capacity resulting in decreased circulation. Right-side heart failure occurs when the right ventricles are unable to fully contract resulting in blood backing up in the circulatory system leading to edema, especially in peripheral areas. Left-side congestive heart failure occurs when the left ventricles are unable to fully contract resulting in blood backing up in the lungs.
Classic Signs
Early Signs:
–Fatigue. Related to increased cardiac workload.
–Nocturia (waking up from sleep to urinate). Related to increased fluid volume.
–Shortness of breath (dyspnea) on exertion. Related to decreased oxygen in the blood.
–Bilateral crackles. Related to build-up of fluids in the lungs
Advanced Signs:
–Shortness of breath lying down (orthopnea). Related to fluids in the lungs.
–Enlarged heart (cardiomegaly). Related to overworking of the heart or underlying cardiac disease.
–Enlarged liver (hepatomegaly). Related to the backup of blood in the circulatory system.
–Frothy or pink sputum. Related to fluids in the lungs.
–Decreased hemoglobin.
–Decreased hematocrit (three times less than hemoglobin).
–High BUN. Related to decreased perfusion of the kidneys.
–High Creatinine clearance. Related to decreased perfusion of the kidneys.
–Decreased urine output. Related to decreased perfusion of the kidneys. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour.
Interventions
–Place patient in high Fowler’s position. Decreases cardiac workload.
–Measure weight daily. Weight increase indicates fluid retention.
–Monitor vital signs.
–Measure fluid intake and output. Assess for renal output and renal perfusion. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour.
–Raise legs. Decreases dependent edema.
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient.
○Diuretics. Decreases fluid volume.
○ACE inhibitors. Decreases pressure in the left ventricle.
○Beta-adrenergic blockers. Decreases cardiac contractions.
○Inotropic medication. Strengthens cardiac contractions.
○Vasodilator. Dilates blood vessels and decreases cardiac workload.
○Anticoagulant. Decreases blood coagulation.
Hypertensive Crisis
A sudden spike in blood pressure to 180/120 or higher.
Classic Signs
–Dizziness. Related to decreased oxygen to the brain.
–Confusion. Related to decreased oxygen to the brain.
–Irritability. Related to decreased oxygen to the brain.
–Nausea/vomiting. Related to decreased oxygen in the blood.
–Short of breath on exertion. Related to decreased oxygen in the blood.
–Blurred vision. Related to decreased oxygen in the blood.
–Seizure. Related to decreased oxygen in the blood.
–Decreased level of consciousness. Related to decreased oxygen to the brain.
Interventions
–Provide quiet, low-lit environment.
–Monitor blood pressure every fifteen minutes. Blood pressure should decrease no more than 25% of Mean arterial pressure (MAP) within the first two hours of treatment.
–Monitor ECG continuously.
–Monitor urine output. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour.
–Monitor pulse oximetry (arterial oxygen saturation). 95 to 100% is normal on room air without chronic pulmonary disease. A lower value is normal for a patient with chronic pulmonary disease.
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient.
○Vasodilator. Dilates blood vessels and decreases cardiac workload.
Hypovolemic Shock
Decreased intravascular volume related to decreased circulation of blood, plasma, and other body fluids leading to inadequate organ perfusion.
Classic Signs
–Tachycardia. Related to decreased blood volume.
–Agitation. Related to decreased oxygen to the brain.
–Hypotension. Related to decreased blood volume.
–Decreased skin temperature. Related to decreased circulation.
–Decreased blood pressure. Related decreased blood volume.
–Urine output less than 25 ml/hour. Related to decreased kidney perfusion. Normal is 1 ml per kg per hour. Critical is < 0.5 ml per kg per hour.
–Decreased hemoglobin. Related to decreased blood volume.
–Decreased hematocrit. Related to decreased blood volume.
–High BUN. Related to decreased perfusion of the kidneys.
–High Creatinine clearance. Related to decreased perfusion of the kidneys.
–Arterial Blood Gas.
○Decrease pH
○Increase pCO2
○Decrease pO2
Interventions
–Monitor vital signs every 15 minutes.
–Monitor for bilateral crackles. Related to build up of fluids in the lungs as a result of treatment.
–Measure urine output hourly using indwelling urinary catheter.
–Increase fluid intake if urine output is less than 30 ml/ hour.
–Insert large IV catheter (18G).
–Administer as ordered:
○2 to 4 liters 100% oxygen. Use a non-rebreather face mask to increase oxygen supply to the patient. Increase oxygen if less than 80 mmHg systolic
○Catecholamines. Increases blood pressure.
○Inotropic medication. Increases blood pressure.
○Crystalloid solutions. Expands intravascular and extravascular fluid volume.
○Fresh frozen plasma. Increases clotting.
○Blood replacement (Type O negative, universal donor).
Myocarditis
Inflamed cardiac muscle due to infection.
Classic Signs
–Shortness of breath (dyspnea) on exertion. Related to decreased oxygen in the blood.
–Chest pain. Related to necrosis of cardiac muscle as a result of infection and inflammation.
–Fever. Related to increased circulation related to the inflammation process.
–Tachycardia. Related to increased cardiac workload.
–Increased CK-MB. Related to necrosis of cardiac muscle.
–Increased troponins. Related to necrosis of cardiac muscle.
Interventions
–Bed rest without bathroom privileges. Decreases cardiac workload.
–Place patient in high Fowler’s position. Decreases cardiac workload.
–Monitor vital signs.
–Gradually return to normal activities.
–Administer as ordered:
○Antiarrhythmics. Controls cardiac arrhythmias.
Pericarditis
Inflammation of the pericardium from infection. Acute pericarditis is typically caused by a viral infection. Chronic pericarditis is typically caused by disease or medication reaction.
Classic Signs
–Anxiety. Related to pain and changes in respiratory function.
–Sharp pain over the precordium radiating to the neck, shoulders, back, and arm relieved by leaning forward or sitting up. Related to inflammation affecting a common nerve.
–Pain in the teeth or muscles. Related to inflammation affecting a common nerve.
–Arrhythmias. Related to irritability of cardiac muscle from inflammation.
–Difficulty breathing (dyspnea). Related to decreased oxygen from decreased cardiac output caused by inflammation.
–Tachypnea. Related to increased cardiac workload.
–Fever. Related to inflammation.
–Increased AST. Related to necrosis of liver cells.
–Increased LST. Related to necrosis of liver cells.
–Increased CK-MB. Related to necrosis of cardiac muscle.
–Increased WBC. Related to inflammation.
–Increased SED rate. Related to inflammation.