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When there is ANY abnormality to the conduction or heart's ability to eject and circulate blood means the CARDIAC OUTPUT is IMPAIRED. This can cause damage to organs causing entire systems to SHUT DOWN aka SHOCK

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Stage 1: AV VALVE OPEN / SL CLOSED

STAGE 2: All valves CLOSED

STAGE 3: AV VALVES CLOSED/SL VALVES OPEN

STAGE 4:ALL VALVES CLOSED

The volume of blood stretching the ventricles at the end of diastole is called preload. ​

Increased by aortic valve disease, hypervolemia, and heart failure​

Decreased by rapid heart rate and hypovolemia​

Afterload is the peripheral resistance which the left ventricle must pump against. ​

Affected by the size of the ventricle, wall tension, and elevated arterial blood pressure​

Over time, increased resistance to eject blood results in ventricular hypertrophy.​

Increased by hypertension (vasoconstriction)​

Contractility is increased by epinephrine and norepinephrine released by the sympathetic nervous system.​

Increased contractility increases the stroke volume by increasing ventricular emptying​

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Blood Pressure - BP

SYSTOLIC/DIASTOLIC mmHg

Pulse Pressure- P P

Systolic Pressure - Diastolic Pressure in mmHg

Mean Arterial Pressure - MAP

Diastolic Pressure + Pulse Pressure / 3 in mmHg

Stroke Volume SV- Blood pumped from the left ventricle IN EACH BEAT

Cardiac output / Heart Rate OR

End Diastolic Volume-End Systolic Volume in mL/beat

Cardiac Output - CO-The amount of blood ejected PER MINUTE

Heart rate X Stroke Volume in mL/min

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CARDIAC DIAGNOSTIC /THERAPUTIC PROCEDURE 

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CARDIAC DIAGNOSTIC /THERAPUTIC PROCEDURE 

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Stable angina: Starts with activity or exertion. It is relieved with rest and relaxation. It sometimes requires additional medication but should not last more than 20-30 minutes continuously. If it does not stop, immediate treatment is needed.​

Unstable angina (also called acute coronary syndrome (ACS)): Starts suddenly with minimal or no provocation. Rest or relaxation does not reduce symptoms. Medication or basic treatment is of limited help.  This requires immediate treatment.​

Symptoms in women can be different. They may include shortness of breath with no chest discomfort, pain in the middle of the back, nausea, vomiting, abdominal pain, or throat pain.​

Diabetics, especially those with uncontrolled or chronic disease can have blunted or no chest discomfort.

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Cardiodenic Shock/ End stages of all shock 

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Cardiodenic Shock/ End stages of all shock 

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CARDIA DEVICES AND APPRORIATE INTERVENTION 

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CARDIA DEVICES AND APPRORIATE INTERVENTION 

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monitor the site for signs of bleeding

hematoma development

hemothorax can also develop- so the assess the client’s lung sounds and compare them side to side to ensure this has not occurred.

Dislodgement of the pacemaker is another common complication after pacemaker placement. If the client shows signs of:

***** impaired cardiac output

*Pallor

*Diaphoresis

*Dizziness

The client should be positioned for safety and to promote easier blood flow to the vital organs. The nurse should assess the client’s heart rate

blood pressure

ECG rhythm

The heart rhythm should be normal without any evidence of ventricular ectopy.

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EKG and ECG is the same! Don't be confused!

Echo allows us to see pictures of heart while EKG/ECG allows us to see waveforms and conduction times

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ECG/EKG

PRE PROCEDURE

Position patient supine for 12 lead placement

expose chest and cleanse to remove oils, CLIP-DO NOT SHAVE- to remove hair

Attach leads

tell the patient to remain still and breathe normally

INTRAPROCEDURAL

Mointor for dysrythmias, chest pain, decreased LOC,S.O.B, and hypoxia

POSTPROCEDURE

Hit print

detach leads

Notify provider

Remove leads

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On the grided paper vertical is amplitude ans horizontal is time

Each tiny box is 0.2 seconds

p wave- 0.06-0.12

PR Interval - 3-5 small squares ( 0.12- 0.20)

QRS Complex- less than 0.12

ST- 0.12

T wave - 0.16

QT-0.34-0.43

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P wave is associated with the Atria. So any dysfunction in the atria will appear in the P wave.

Q-R-S Complex is associated with the ventricles. Any dysfunction in the ventricles will appear in the Q-R-S.

ST Elevation is a life-threatening emergency. This indicates a Myocardial Infraction (MI).

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RARELY benign but mostly life threatening are electrical dysfunctions in conduction centers( AV NODE, SA NODE OR VENTRICLES) causing negative effects on the rate and rhythm

-BRADYCARDIA + A- fib are the benign dysrhythmia ONLY if the patient is NONSYMPTOMATIC.

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 TIMING BOUNCES FROM SA NODE TO AV NODE 

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FIRST DEGREE BLOCK- SA node to AV Node trade off

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FIRST DEGREE BLOCK- SA node to AV Node trade off

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SECOND DEGREE TYPE 1 HEART BLOCK - WENKE 

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SECOND DEGREE TYPE 1 HEART BLOCK - WENKE 

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THRID DEGREE HEART BLOCK- ATRIAL VENTRICULAR INDEPENENT PACING 

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THRID DEGREE HEART BLOCK- ATRIAL VENTRICULAR INDEPENENT PACING 

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All complexes are Normal but RATE IS SLOW

occurs when SA node is firing at less than 60 bpm= inadequate perfusion unless asymptomatic

TX: Stop any drugs causing bradycardia

IV ATROPINE to increase RATE ( Dopamine and Epi can me used as well)

IF SYMPTOMATIC PATIENT WILL NEED A PACEMAKER TO KEEP HR IN NORMAL RATE AND RYTHM

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Occurs when ATRIA contraction is NOT strong enough to squeeze out all of the blood. Its a quiver not a complete squeeze.

P waves are disorganized and rplaced with fibrillatory wave

QRS is PRESENT and NORMAL

TX: Diltiazem ( Calcium Channel Blocker) , Metoprolol(Beta Blocker) , Amiodarone and Digoxin

Syncronized Cardioversion may convert this rythm bact to NSR

Cardiac Cath ABLATION

Cold cryoblation

ANTICOAGULANT THERAPY - Warfarin(Eliquis+ Riveroxaban

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Occurs when the SA node short circuits and the ATRIA contracts RAPIDLY. Due to this, the blood never completely empties which means the ventricles are NOT getting adequate blood volume to produce sustainable cardiac output.

Flutters/ saw tooth pattern replaces p waves , P-R interval is unmeasurable and QRS complexes are present and intact.

S+S: TACHYCARDIA , DYSPNEA, CHEST PAIN

TX: Amiodarone and Metoprolol

Cardioversion can convert this rhythm back to normal sinus.

Radiofrequency ablation catheter - ablation of ectopic stimuli casing dysrhythmia

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Occurs when Atria is contracting rapidly - a run of PREMATURE ATRIAL CONTACTIONS - Then a period of systole may occur

P wave will be hidden and QRS will be intact

S+S TACHYCARDIA(150-250 bpm) , Palpations, Hypotension, Dyspnea and Angina

TX: Vaga; Stimulation ( Bear Down, Cough, Cartoid Massage, valsalver manuerver

MEDS- ADENOSINE ( decrease H.R ), Diltiazem and Verapamil

Cardioversion may be used to restore normal sinus rythm - Use medication first then use cardioversion if ineffective.

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Ventricular fibrillation (VF) will be pulseless and requires immediate intervention.

-V. FIB= D FIB DEFRIBILLATION THERE IS NO PULSE ! Quality CPR in between is EXTREMELY IMPORTANT

Assessing the client is the highest priority as a disconnected lead or electrical interference can mimic VF. If the client is pulseless, assess using the ABCs of CPR and initiate a code blue.

MEDS include: Amiodarone . lidocaine( SLOWS RATE- onset 45-90 sec) and Epinephrine

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occurs when Ventricles take over Pacer. Vtach leads to vfib! can be deadly  Identify: P waves are undetectable Q-R-S is distorted + wide. 

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Ventricular tachycardia (VT) presents a threat to the client’s life because the rapid rate and loss of atrial kick decreases cardiac output. The client may or may not have a pulse with VT, so it is critical that the client be assessed using the ABCs of cardiopulmonary resuscitation (CPR) and a rapid response or code blue be initiated.

WITH PULSE : CARDIOVERSION

Elective treatment of for symptomatic patients that has a PULSE you can COUNT.

MEDS may include: Amiodarone, verapamil and adenosine

WITHOUT PULSE: DEFIBRILLATION

Defibrillation stops all electrical activity of the heart, allowing the SA node to take over and reestablish a perfusing rhythm.

Quality CPR in between is EXTREMELY IMPORTANT

MEDS may include: Amiodarone(block potassium whis is reponsible for depolarization),procainomide, lidocaine(can be use when amiodarone is NOT available- blocks sodium channels which helps decrease heart conduction) and epinephrine (Causes vsoconstriction to improve diastolic pressure )

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Treatment includes CPR, followed by drug therapy (e.g., epinephrine) and intubation. Correcting the underlying cause is critical to prognosis.

Common causes of PEA include:

hypovolemia

hypoxia

metabolic acidosis

hyperkalemia and hypokalemi​a

hypoglycemia

hypothermia

toxins (e.g., drug overdose)

cardiac tamponade

thrombosis (e.g., myocardial infarction [MI], pulmonary embolus)

tension pneumothorax

trauma

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Asystole represents no ventricular electrical activity, though P waves or atrial fibrillation may occasionally be present.

Without depolarization, the ventricles do not contract and the client will have no cardiac output.

Immediate intervention is needed with CPR, drugs (e.g., epinephrine), and intubation.

Asystole is also seen when clients on a cardiac monitor die.

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Packed red blood cells (PRCBs) are prepared from whole blood by centrifugation. One unit contains 250 to 350 mL and can be stored for up to 42 days depending on how it is processed. ​

What do I need to know?​

Administering PRBCs instead of whole blood reduces the risk of fluid volume overload, non-hemolytic febrile reactions, and mild allergic reactions, as well as the transmission of cytomegalovirus. Packed red blood cells must be transfused within 4 hours. ​

Why is this prescribed?​

Clients with severe or symptomatic anemia or acute blood loss are often prescribed PRBCs. One unit of red blood cells can increase the hemoglobin by 1 gram per deciliter and hematocrit by 3%. ​

Fresh frozen plasma (FFP) is the liquid portion of whole blood that has been separated from red blood cells and frozen. One unit contains about 250 mL. FFP contains clotting factors but no platelets. It can be stored up to 1 year but must be used within 24 hours of thawing. ​

What do I need to know? ​

FFP used to be used when treating hemorrhagic shock but is being replaced by other products, such as albumin and plasma expanders. Once thawed, one unit is administered over 15–30 minutes. ​

Why is this prescribed?​

When bleeding is caused by a clotting factor deficiency, such as disseminated intravascular coagulation (DIC), warfarin overdose, vitamin K deficiency, or liver disease, FFP is often prescribed. ​

Platelets are prepared from fresh whole blood. A single donation results in 200 to 400 mL of platelets. ​

What do I need to know?​

Platelets can be stored at room temperature in a blood bank under gentle agitation for 1 to 5 days, depending on the type of collection and storage bag used. Platelets are usually transfused over 30–60 minutes, but this varies based on facility policy.​

Why is this prescribed?​

Clients with thrombocytopenia are prescribed platelet infusions.

Albumin and cryoprecipitates can be prepared from plasma. Albumin is available in two concentrations: 5% or 25% and expands the blood volume when administered. The expansion occurs as water moves from the extravascular to intravascular space. Clients with hypovolemic shock may need albumin to recover. ​

Cryoprecipitates are rich in clotting factors and fibrinogen. Clients with a fibrinogen deficiency, including disseminated intravascular coagulation (DIC) and severe liver disease, as well as clotting factor deficiencies may need cryoprecipitate administration.

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Red Blood Cells

White Blood Cells

Cardiac enzymes: ELEVATED LEVELS DETECTABLE FOLLOWING MYOCARDINAL INJURY- Troponin , Myoglobin and Creatine Kinase

Ehection Fraction :

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Donors with O negative blood type are called the “universal donor” because their red blood cells can be transfused into any client, regardless of the client’s blood type. Even though O negative blood has the highest demand, only a small percentage of the population has this very important blood type. Clients with O negative blood type cannot receive O positive red blood cells. ​

​Almost half of the population has O positive blood type. These clients can receive O positive and O negative blood, but they can donate red blood cells to O positive, A positive, B positive, and AB positive clients. ​

(A+) A positive blood type is the second most common blood type and is transfused often. The clients of this blood type can:

Receive A positive, A negative, O positive, and O negative blood.

Donate red blood cells to A positive and AB positive recipients.

Donate platelets to A positive and O positive recipients.

Donate plasma to A positive, A negative, O positive, and O negative clients.

(A-) A negative blood type are quite rare, but red blood cells and whole blood are often needed. These clients can:

Receive A negative or O negative blood only.

Donate red blood cells to A negative, A positive, AB positive, and AB negative recipients.

A negative plasma and platelets can be used by A negative, A positive, O negative, and O positive recipients.

(B+) B positive blood type can:

Receive B negative, B positive, O negative, and O positive blood.

Donate red blood cells to B negative and AB negative recipients.

Donate platelets to B positive and O positive recipients.

Donate plasma to B negative, B positive, O negative, and O positive recipients.

(B-) B negative is a very rare blood type. These clients can:

Receive B negative and O negative blood only.

Donate red blood cells to B negative, B positive, AB negative, and AB positive recipients.

Donate platelets and plasma to B negative, B positive, O negative, and O positive recipients.

(AB+) AB positive blood type is rare but is called the “universal recipient”. These clients can:

Receive blood from any other type.

Donate red blood cells to AB positive recipients only.

Donate platelets to AB positive, A positive, B positive, and O positive recipients.

Donate plasma to any blood type.

(AB-) AB negative blood type is the rarest of all blood types. These clients can:

Receive AB negative, A negative, B negative, and O negative blood.

Donate red blood cells to AB negative and AB positive recipients.

Donate plasma or platelets to any blood type.

(O+) Almost half of the population has O positive blood type. These clients can:

Receive O positive and O negative blood.

Donate red blood cells to O positive, A positive, B positive, and AB positive clients.

Donate platelets to O positive recipients.

Donate plasma to O positive and O negative recipients.

(O-) Donors with O negative blood type are called the “universal donor” because these red blood cells can be transfused into any client, regardless of the client’s blood type. Even though O negative blood has the highest demand, only a small percentage of the population has this very important blood type. When there is no time to determine a client’s blood type, such as in an emergency, O negative blood can be used to save a life.

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The correct blood product is given based on the prescription​.

The blood product is compatible with the client’s blood type​.

The correct client identification is confirmed based on using two identifiers.​

The blood bank identification number on the blood product matches the client’s armband​.

The expiration date has not past.​

The nurse must verify that no bubbles, cloudiness, sediment, or clots are in the blood product bag​.

REMEMBER!!!!!!

Medications should never be added to blood products or piggybacked into a blood transfusion.​

Vital signs before and throughout a blood or blood product transfusion are an essential nursing assessment.

There are four distinct times that vital signs should be assessed:​

1. Before the transfusion begins​

2. After the first 15 minutes of a transfusion​

3. Every 30 minutes – 1 hour during the transfusion​

This may vary based on facility policy. ​

4. Approximately 30 minutes – 1 hour after the completion of the transfusion ​

Once the infusion is complete, flush the intravenous line with normal saline to administer any blood remaining in the tubing, then properly discard the blood tubing and bag. ​

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The word hemodynamics refers to the measurement of pressure, flow, and oxygenation within the circulatory system, as well as the forces and mechanisms that cause blood to circulate within the body

assessing the client for decreased cardiac output (e.g., diminished peripheral pulses, hypotension)​

identifying cardiac rhythm strip abnormalities (e.g., sinus bradycardia, premature ventricular contractions, ventricular tachycardia, atrial fibrillation, ventricular fibrillation)​

applying knowledge of pathophysiology to interventions in response to client abnormal hemodynamics​

providing a client with strategies to manage decreased cardiac output (e.g., frequent rest periods, limit activities)​

intervening to improve client cardiovascular status (e.g., initiate protocol to manage cardiac arrhythmias, monitor pacemaker functions)​

monitoring and maintaining arterial lines​

managing the care of a client with a pacing device​

managing the care of a client on telemetry​

managing the care of a client receiving hemodialysis or continuous renal replacement therapy​

managing the care of a client with alteration in hemodynamics, tissue perfusion, and hemostasis (National Council of State Boards of Nursing, 2023, p. 51)

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The arterial line has a port that can be used for arterial blood sample collection so as not to have to do excess arterial punctures to draw samples. An arterial line is used in a critical care environment when caring for clients who need ongoing hemodynamic monitoring as well. Hemodynamic monitoring is done to evaluate how a client responds to the treatments that are initiated in the plan of care, such as fluid therapy. Calibration of the arterial line should occur at least every 4 hours and at the change of shift. Additionally, the nurse should zero (calibrate) the line after blood draws are completed.

A non-invasive blood pressure should be checked on a routine basis and be compared to the reading from the arterial line. If the nurse finds that there is a 20 mmHg difference (or greater), then the arterial line needs to be recalibrated as a 20 mmHg or more pressure difference indicates an issue with the line that needs investigation. Routine neurovascular checks are needed, but they are conducted on the area distal to the line insertion site rather than proximal. The nurse must ensure that the arterial line’s transducer is kept in proper alignment so accurate readings are maintained. The phlebostatic axis is estimated as the 4th intercostal space at the mid-axillary line and this is where the transducer needs to be kept aligned. The nurse needs to make sure that each time the client is repositioned, that the height of the transducer is checked.

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The client with cardiac tamponade may report chest pain and is often confused, anxious, and restless. As the compression of the heart increases, there is decreased cardiac output, muffled heart sounds, narrowed pulse pressure, tachypnea, and tachycardia. Neck veins are markedly distended because of increased jugular venous pressure. Pulsus paradoxus, if present, is a significant decrease in systolic blood pressure (BP) during inspiration. Dyspnea may be the only manifestation in a patient with a slow onset of cardiac tamponade. ​

Beck’s Triad​

Beck’s triad refers to the three key clinical manifestations of worsening cardiac tamponade:​

distant heart sounds​​

distended jugular veins​​

decreased arterial pressure​

When present in a client at risk for cardiac tamponade, they indicate a medical emergency. ​

When left untreated, cardiac tamponade is likely to result in death or disability resulting from decreased oxygenation and perfusion. The primary treatment is to remove the fluid from the pericardium using a needle decompression.

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Blood is best given during dialylsis to prevent fuid over load

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Symptoms: headaches, visual changes, palpitations, chest pains, lightheadedness​Acute signs: flushing, bounding pulse, edema, irregular pulse, tachycardia/bradycardia​

Chronic signs: retinopathy, cardiomyopathy, nephropathy​

Environment: chaotic situation, recent emotional trauma​

History: family or personal history of hypertension, taking antihypertensive medication​

Serial blood pressures: consistently measured high blood pressures over days or weeks

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BLOOD ETTIQUETTE

Blood products should not be left at room temperature for >30 minutes before a transfusion is started. Leaving blood out at room temperature for a prolonged period increases the likelihood of bacterial growth.

If the start of the transfusion is delayed, the blood should be returned to the blood bank, where it can be refrigerated at a precise temperature.

If the client has symptoms related to low hemoglobin level (<12 g/dL  in females and <14 g/dL in male clients), such as low blood pressure, the healthcare provider should be notified.

This would occur after the blood is sent back to the blood bank and attempts to restart the IV have occurred. Blood products should not be placed in the unit refrigerator as the temperature cannot be precisely regulated.​

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Neutrophils have vesicles that stain neither distinctly acidic or basic (neutr-: "neutral"; -phile: "loving"). Neutrophils are also commonly called polymorphonculear (PMN) leukocytes (poly-: "many"; -morph-: "shape"; -nuclear: "nucleus") are so named because they have 2-7 lobes on their nucleus and can phagocytize pathogens and cellular debris. They also can release large quantities of oxidizing agents and cell-lysing enzymes. Neutrophils are found in the greatest numbers, constituting 3,000-7,000 per cubic millimeter or 60-70% of circulating leukocytes. During bacterial infection, rapid proliferation of these cells takes place in a process called neutrophilia. They are highly mobile and engage in phagocytosis to protect the body.​

​Eosinophils form 100-400 per cubic millimeters or 2-4% of circulating WBCs and are abundant in the mucus membranes of the digestive and lower respiratory tracts. They have a bi-lobed nucleus that stains a vibrant red (due to the acidic stain eosin). They secrete chemicals that destroy parasitic worms which are too big to be phagocytized by WBCs. They also play a key role in inflammation by releasing histaminase that breaks down histamines released by basophils. Eosinophils also phagocytize antigen-antibody complexes.​

​Basophils are rarest of all WBCs with less than 0.5% circulating in WBC s or 20-50 per cubic millimeter in blood. Their nucleus is also bi-lobed; however, their vesicles stain dark bluish-purple. These cells help promote inflammation by migrating to already inflamed tissues and releasing histamine (a vasodilator), heparin (an anticoagulant), and serotonin (a chemical that attracts neutrophils and eosinophils thus intensifying the inflammatory response).

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Monocytes lack visible granules in their cytoplasm and form 100-700 per cubic millimeter or 3-8% of the WBC count in blood. Monocytes are the largest of all leukocytes and are often two to three times the diameter of a RBC. The nucleus of the monocyte is said to resemble a horseshoe or kidney bean in shape. Their count rises during inflammation and viral infection. They migrate into the tissues where they are known as macrophages and phagocytize microbes and cellular debris. They are also one of the antigen presenting cells which process foreign antigens and display fragments of them on the cell surface to T helper cells during adaptive or specific immune response.​

Lymphocytes make up 25-35% of circulating leukocytes and are one of three different specific cells (but we cannot distinguish between them in a normal slide): B lymphocytes, T lymphocytes, and natural killer (NK) cells.​ Most common are B and T lymphocytes, which are important for adaptive immunity. B lymphocytes are responsible for producing antibodies once they mature into plasma cells while T lymphocytes help coordinate the overall adaptive immune response (Helper T cells) and cell-mediated immunity (Cytotoxic T cells). NK cells are important for the innate immune response, especially dealing with virally infected or cancerous cells. We will investigate the functions of these cells in more detail in the coming weeks.

WBCs, specifically the phagocytic cells, leave the blood stream by a process called diapedesis or emigration into the interstitial fluid where they can dispose of pathogens and other dead cells.​

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Angiotensin II. This is a potent vasoconstrictor that raises the blood pressure. Its synthesis and action are depicted in figure 23.15. Its synthesis requires angiotensin-converting enzyme (ACE ). Hypertension is often treated with drugs called ACE inhibitors, which block the action of this enzyme, thus lowering angiotensin II levels and blood pressure.

Aldosterone. This “salt-retaining hormone” primarily promotes Na+ retention by the kidneys. Since water follows sodium osmotically, Na+ retention promotes water retention, thereby supporting blood pressure.

Natriuretic peptides. These hormones, secreted by the heart, antagonize aldosterone. They increase Na+ excretion by the kidneys, thus reducing blood volume and pressure. They also have a generalized vasodilator effect that helps to lower blood pressure.

Antidiuretic hormone. ADH primarily promotes water retention, but at pathologically high concentrations it is also a vasoconstrictor—hence its alternate name, arginine vasopressin. Both of these effects raise blood pressure.

Epinephrine and norepinephrine. These adrenal and sympathetic catecholamines bind to α-adrenergic receptors on the smooth muscle of most blood vessels. This stimulates vasoconstriction and raises the blood pressure.

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Ammonia is produced by the deamination of amino acids

Urea is synthesized from ammonia and carbon dioxide

Uric acid is produced from nucleic acids; Creatinine is produced from creatine phosphate.

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The primary functions of the kidneys are to

(1) regulate the volume and composition of extracellular fluid (ECF)

(2) excrete waste products from the body.

**** The kidneys also function to

A. control BP,

B. make erythropoietin,

C. activate vitamin D

D. regulate acid-base balance

The urinary system excretes a broad variety of metabolic wastes, toxins, drugs, hormones, salts, hydrogen ions, and water.

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Hyperkalemia serum potassium level greater than 5 mEq/L, is caused by impaired renal excretion, a shift in potassium from the intracellular to extracellular fluid (massive cell destruction), or a massive intake of potassium. The most common cause of hyperkalemia is renal failure.

he most clinically significant problems associated with hyperkalemia are the changes in cardiac conduction, including impaired cardiac depolarization. This results in:​​

loss of P wave​​

prolonged PR interval​​

ST segment depression​​

widened QRS complex​​

tall T wave​​

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serum potassium level less than 3.5 mEq/L, is caused by the increased loss of potassium or an increased shift of potassium from the extracellular to the intracellular fluid (treatment of diabetic ketoacidosis, catecholamine release in stress, coronary ischemia). The most common cause is potassium loss through the kidneys (diuresis) or the gastrointestinal tract (diarrhea, laxative use, vomiting, ileostomy drainage).

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HYPOCALCEMIA

weakness, fatigue​​

depression, irritability, confusion​​

hyperreflexia, muscle cramps​​

hypotension​​

numbness, tingling (extremities and around mouth)​​

Chvostek’s sign​​

Trousseau’s sign​​

laryngeal and bronchial spasms​​

tetany, seizures ​

HYPERCALCEMIA

lethargy, weakness, fatigue​​

decreased memory​​

depressed reflexes​​

hypertension​​

confusion​​

anorexia, nausea, vomiting​​

bone pain, fractures​​

polyuria, dehydration​​

nephrolithiasis​​

seizures, coma ​

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​ Neurological: weakness, visual changes, paresthesia, altered levels of consciousness (ALOC), seizures​ Gastrointestinal (GI): ascites, increased motility, acute weight gain Renal: increased urine output​ Respiratory: crackles, cough, dyspnea (pulmonary edema)​ Other: peripheral edema, distended neck veins, skin cool with pallor​ ​

LABS

Hemoglobin and hematocrit: decreased
Blood urea nitrogen (BUN): decreased
Urine specific gravity: decreased​
Serum sodium: decreased

DEFECIET

hyperthermia​

tachycardia​

weak, thready pulses​

hypotension​ ​

tachypnea​ ​

eurological: dizziness, syncope, confusion, weakness, fatigue, seizures​
Gastrointestinal (GI): thirst, dry mucous membranes, nausea, acute weight loss​
Renal: oliguria​
Respiratory: hypoxia​
Other: diminished capillary refill, cool clammy skin, diaphoresis, sunken eyeballs, flat neck veins, poor skin turgor

Hemoglobin and hematocrit: increased​
Blood urea nitrogen (BUN): increased
Urine specific gravity: increased​
Serum sodium: increased
Blood osmolality: increased

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SODIUM AND POTASSIUM

CALCUIM AND PHOSPHATE

MAGNESIUM AMD PHOSPHATE

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A mediport is an implanted central venous access device (CVAD) located on the upper chest. This device contains a port underneath the skin that can be accessed and de-accessed between uses with a specialized needle (such as a Huber needle). All connections to the port must be sterile when it is being accessed.​

When the port is not in use, the client can shower without covering the port area since the intact skin is the barrier.

Each type of central venous catheter requires different care. The nurse should remain knowledgeable about the different types and care required to prevent complications.

Non-Tunneled Percutaneous Central Venous Catheter (CVC): CVC is a short-term catheter that is placed by a provider for acute infusion therapy. They are commonly placed in the subclavian or jugular veins.​

Peripherally Inserted Central Catheter (PICC): PICC catheters are small and more fragile. They are long-term catheters that are placed by specially trained nurses. A 10 mL syringe is recommended to prevent the rupture of the fragile catheter.​

Implanted Port: Implanted ports are long-term catheters surgically placed under the skin. Once the incision has healed, a specially trained nurse can access the site using a non-coring needle. A dressing is not required at the site once it has healed.​

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long-term IV therapy​

administration of rapid IV fluids during an emergency​

multiple blood samples per day​

inability to initiate or maintain a peripheral intravenous (IV) site​

total parental nutrition (TPN)​

hemodialysis​

vesicant IV medications​

MAINTENENCE

Dressings must be changed per policy, usually every 7 days. ​

Dressings must be changed if they become wet, loose around the edges, or soiled (even if before the next dressing change is due).​

Most facilities have sterile dressing change kits that include most of the required materials.​

Dressing changes are a sterile procedure. Any break in a sterile procedure may contaminate the CVAD and lead to infection.​

Stat locks are used to secure the device to the skin and prevent pulling on the catheter.​

When removing the old transparent dressing, don clean gloves and pull in the direction of the catheter, not against it, to prevent accidental catheter displacement and minimize skin irritation.

FLUSHING

Change caps and apply disinfecting caps per policy, and ensure the connections are tight and secure.​

Wipe the access port with an antimicrobial swab for a minimum of 30 seconds and allow it to dry prior to accessing it.​

Flush the line before and after every intravenous (IV) medication, blood draw, cap change, or dressing change.​

Only flush a CVAD with a large volume syringe (at least 10 mL).​

Only use sterile 0.9% normal saline to flush the line.​

Use a firm, push-pause-push motion when flushing to clear the line and prevent any thrombosis or fibrin sheath formation.

It is important to remember that all connections to central venous access devices CVADs must remain sterile to prevent infection! Some facilities may require special bathing procedures or specialized disinfecting caps to prevent the risk of infection.

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Infections are caused by biofilms that stick to the catheter line and eventually spread within the bloodstream, which can lead to septic shock.​

Manifestations include redness, swelling, warmth, and drainage

Pneumothorax is caused during insertion when the guidewire needle advances into the pleural space. The size of the pneumothorax depends on the injury (Patel et al., 2019).​

Manifestations include shortness of breath, unequal chest expansion, and an abnormal X-ray.

Thrombosis is caused by a blood clot within or around the catheter line.​

Manifestations include redness, warmth, and swelling of the neck, arm, and face.

DEVICE MALFUNCTION

Tip migration occurs when the tip of the catheter is no longer in the proper placement. Therefore, confirmed x-ray placement is essential prior to use. Manifestations of time migration include the catheter length being increased or decreased and an abnormal x-ray.

Catheter obstruction occurs when a fibrin sheath is formed inside the catheter line, blocking the lumens. Manifestations of tip migration include being unable to flush the line, excessive resistance when flushing, and no blood return.

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Parenteral nutrition (PN) is nutrition that is administered through the intravenous route to bypass the gastrointestinal (GI) tract. Parenteral nutrition can be classified as total parenteral nutrition (TPN) or partial (or peripheral) parenteral nutrition (PPN). The purpose of parenteral nutrition is to prevent or correct nutritional deficiencies and avoid the dangerous adverse effects of malnutrition while also bypassing the GI tract. ​

When transitioning, a slow, gradual reduction in TPN rate is expected. Do not stop the TPN suddenly or adjust the dose without a healthcare provider’s prescription. Sudden discontinuation of TPN may lead to severe hypoglycemia which may lead to coma or death.

When starting on foods, begin with clear liquids then advance as tolerated to a soft diet. A regular diet would not be appropriate at the beginning of the transition.

The nurse should closely monitor the client’s calorie counts, daily weight, BMI, and daily labs including electrolytes and prealbumin to evaluate how the client is tolerating the transition and ensure they are not falling behind on their nutrition requirements.

The following data is consistent with enteral nutrition support:

Prescription for nasogastric tube placement

Assessment includes diarrhea or cramping

Prescription for intermittent boluses

The following data is consistent with parenteral nutrition support:

Chest x-ray confirms central line placement

Assessment includes bowel sounds absent

Your response is correct!

Partial (or peripheral) parenteral nutrition (PPN) is provided for short-term, supplemental nutritional support.

It can be delivered in a peripheral intravenous (IV) site because it contains a lower dextrose content and is less of a vesicant to the vein. However, PPN is not as common as TPN due to multiple complications including infiltration and extravasation of the peripheral veins. PPN may also be used when no central IV line is available and for short-term supplemental nutrition in smaller dosages for those with poor oral intake. ​

Total parenteral nutrition (TPN) is used for those requiring intense nutritional support for extended periods or for those with high caloric requirements providing 100% nutritional support. (Examples include cancer, bowel disorders, critical illness, trauma, and extensive burns.)

Parenteral nutrition contains nutrients that are already broken down to a microscopic level so that the body can absorb them directly into the bloodstream and bypass the gastrointestinal (GI) system. ​

Our bodies use these nutrients as well as water, minerals, and vitamins to perform all functions in the body. Each of these nutrients is necessary for basic survival but is also required for wound healing, increased metabolic needs during illness or injury, and boosting immunity.

What are the chemical components of proteins, fats, and carbohydrates? Proteins break down into amino acids, fats break down into fatty acids, and carbohydrates break down into glucose.

​Components of parenteral nutrition:

Main components include amino acids, dextrose, vitamins/folic acid, minerals/electrolytes/trace elements, and water​.

Other add-ins may include insulin and heparin.

Total parenteral nutrition (TPN) includes higher tonicity/concentrations (up to 70%), and partial (or peripheral) parenteral nutrition (PPN) includes lower tonicity/concentrations (2.5%–10%)​.

Lipids may be included in concentrations of 10%, 20%, or 30%​.

Note: Parenteral nutrition must be prepared by a pharmacist due to the many serious incompatibility reactions.

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UNSTABLE AND ACUTE

Unstable Angina​

Signs and Symptoms: acute chest pain​

chest pain > 10 minutes​

radiating pain​

dyspnea​

syncope or presyncope​

palpitations​

Non-ST elevation MI (NSTEMI)​

Signs and Symptoms: acute chest pain​

and​

+ cardiac biomarkers​

Troponin I or T​

ST elevation MI (STEMI)​

Signs and Symptoms: acute chest pain​

and​

+ cardiac biomarkers​

and​

+ ST elevation on electrocardiogram (ECG)​

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Classes of Diuretics​

Carbonic Anhydrase Inhibitors (CAIs)​

Glaucoma​

Loop Diuretics​

Hypertension​

Renal failure​

Heart failure ​

Osmotic Diuretics​

Cerebral edema​

Glaucoma ​

Potassium-Sparing Diuretics​

Congestive heart failure​

Thiazides and Thiazide-Like Diuretics​

Hypertension​

Congestive heart failure​

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Anemia is measured by looking at three different values: the red blood cell count, hemoglobin, and hematocrit. If one of these three values is below normal, the client has a condition called anemia. This is not a diagnosis; it is a condition caused by an underlying problem.​

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A sickle cell crisis occurs when inadequate oxygenation or hydration exacerbates sickling and causes red blood cells (RBCs) to clump together in the capillaries (vasoocclusion).​

Vasoocclusion causes severe ischemic pain, hypoxia, and possible organ dysfunction if left untreated. Adequate oxygenation and hydration may reverse the acute sickling response. In a sickled state, RBCs cannot carry enough oxygen from the lungs to the tissues, even with supplemental oxygen. The priority intervention is the administration of intravenous (IV) fluids to reduce blood viscosity and restore perfusion to the areas previously affected by vasoocclusion. Only after IV rehydration reverses vasoocclusion can non-sickled RBCs effectively carry supplemental oxygen to the tissues. Bed rest improves oxygen use and reduces energy consumption during the sickle cell crisis but does not directly resolve vasoocclusion. Blood transfusions provide the client with nonsickled RBCs, increasing the oxygen-carrying capacity of the blood. However, this therapy is generally reserved for clients with sickle cell disease who do not respond to rehydration with IV fluids.​

Sickle cell crisis results from vasoocclusion of sickled red blood cells in the microcirculation, resulting in severe ischemic pain. The administration of IV fluids reduces blood viscosity and restores perfusion to the areas previously affected by vasoocclusion.

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Blood sampling for arterial blood gases (ABGs) can be collected through this system without repeated arterial punctures​.

It allows for more accurate titration and monitoring of blood pressure when titrating vasoactive medication to allow more rapid intervention.​

MAINTENCE

Assess the neurovascular status of the extremity distal to the arterial line​.

If arterial occlusion is present, the extremity will be cool, pale, and have >3 seconds capillary refill.​

Maintain line patency by keeping the system under high pressure and flush per agency protocol​.

RISKS

There is an increased risk of hemorrhage (high-pressure system), infection, and sepsis.​

Circulatory impairment can occur due to thrombus formation, embolus, spasm, or occlusion of the circulation by the catheter​.