Transitions Cardiac Flashcards
(130 cards)
1
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Mid sternal chest pain is an emergency
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2
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MI- Pain that lasts longer than 15 minutes and typically does not go away.
Jaw pain and shoulder pain are common symptoms
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3
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Pericarditis- substernal chest pain and radiate towards the back and is intermittent. Position changes help.
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4
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Anxiety chest pain- sudden midsternal chest pain, doesn’t radiate and is usually relieved upon relaxation
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5
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Cardio physical assessment
- look for generalized edema
- any O2 impairment- clubbing, cyanosis, pallor
- bp low or up BP and orthostatic hypotension
- pulses bounding or weak and thready.
- fluid overload is typically right sided HF
- juggular vein distention
- bruit
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6
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Have the client lean forward or lay in Left side if trouble hearing sounds
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7
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Troponin I and troponin T look for cardiac necrosis or if client is experiencing a MI
Creatine Kinase (CK) used to see if there is muscle damage.
Myoglobin- if increased issue with oxygenation to the tissues
Serum lipids- to see if lipid is high
Homocysteine- if increased could be clots
C reactive- inflammation
Microalbumin- protein in urine
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8
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PTT/INR
ABG- tissue oxygenation
Fluid and electrolyte- K+
Erythrocytes- if increased heart disease.
H&H- if low anemia and w fluid overload
Leukocyte- infection
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9
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Diagnostics:
PA & LA chest x ray- cardiac enlargement
Angiography, arteriography, cardiac cath
Anytime going into an artery: must have consent form, no anticoagulant prior
No allergy to iodine and she’ll fish
Renal function, NPO 8hr prior
Aftercare:
Wear weight or sand bag to prevent bleeding for 4-6 hour
Decrease fat and sodium diet
Anticoagulant after procedure up to 8 weeks
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10
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Stress test: stress on the heart to see how it responds (adenosine or dabutamine if med stress test)
Don’t eat 2-4 hour prior
No stimulant prior- tobacco etc
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11
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Sinoatrial node “pacemaker” of heart
Responsible for atrial contraction
Electrical wave impulses 60-100 bpm
P wave on ECG
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12
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Atrioventricular junction
Activates after SA node “atrial kick”
40-60 bpm
PR segment on ECG
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13
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Bundle of his- works for ventricular contractions
Right bundle branch
Left bundle branch
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14
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Automaticity- electrical impulse
Excitability- heart cell response
Conductivity- action potential of SA node sending a message to AV node to start pumping
Contractility- actual contraction
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15
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EKG- you can delegate to UAP to obtain the EKG.
Make sure skin is clean and dry
If excessive hair shave as needed
Do not add gel to electrodes
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16
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V1 placement:
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4th R sternal edge
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V2 placement:
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4th L sternal edge
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V4 placement:
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5th midclavicular line
19
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V3
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Between 2&4
20
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V5 placement:
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Anterior axillary
21
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V6 placement
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Midaxillary
22
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EKG
The small tiny squares inside bigger squares is .04 seconds
Usually 5 tiny squares in one big square
5 big squares is one second of time
30 boxes is 6 seconds
Count the Rs to calculate the pulse
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23
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Represents atrial depolarization
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P wave
24
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Represents the time required for the impulse to travel through the AV node where it is delayed and through the bundle of his, bundle branches, and purkinjie fiber network, just before ventricular depolarization
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PR segment
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Represents the time required for atrial depolarization as well as impulse travel through the conduction system and purkinjie fiber network, inclusive of the p wave and PR segment- it is measured from the beginning of the p wave to the end of the PR segment
PR interval
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represents ventricular depolarization and is measured from the beginning of the Q or (R) wave to the end of the S wave
QRS complex
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Represents the junction where the QRS complex ends and the ST segment begins
J point
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Represents early ventricular repolarization
ST segment
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Represents ventricular repolarization
T wave
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Represents late ventricular repolarization
U wave
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Represents the total time required for ventricular depolarization and repolarization and is measured from the beginning of the QRS complex to the end of the T wave
QT interval
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EKG rhythm
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Determine the rate
Determine the rhythm
Analyze p wave
Measure PR interval
Measure QRS duration
Interpret rhythm
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Normal sinus rhythm
Rate: 60-100
Regular rhythm
P waves present consistent configuration, one p wave before QRS complex
PR interval: 0.12 to 0.20 second and constant
QRS duration: 0.04 to 0.10 second and constant.
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Permanent pacemaker: internal but programmed externally: battery is good for 10 years.
Avoid magnetic fields
Report dizziness, sob, weight gain, fatigue, and excessive hiccups
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__ __ __ is ectopic focus of atrial tissue fired an impulse before next sinus impulse is due.
Caused by stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, certain drugs
Premature atrial complexes
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___ __ rapid stimulation of atrial tissue occurs at rate of 100 to 280 bpm with mean it 170 bpm (adults)
Paraoxymal supraventricular tachycardia rhythm is intermittent, terminated suddenly with or without intervention
Treatment: vagel maneuver- massage carotid arteries and see if it slows HR. If it doesn’t work they can use beta blockers or calcium channel blockers. Or a cardio version and given adenosine
Supraventricular tachycardia
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__ __ is chaotic rhythm, no clear p wave, irregular ventricular response
Most commonly diagnosed*
Etiology and genetic risk:
Fatigue, SOB, syncope, palpitations, or asymptomatic
Atrial fibrillation
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Atrial fibrillation
Assessment:
Signs of poor perfusion: anxiety, SOB, fatigue, syncope
Chest pain
12 lead ECG.
If left untreated: embolus due to irregular cardiac rhythm.
Potential for heart failure due to altered conduction pattern.
Anticoagulants used
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How to treat atrial fibrillation
Electrical cardio version
Left atrial appendage closure
Radio frequency catheter ablation
Bi ventricular pacing
Digoxin assess apical pulse for one min
Beta blocker pulse for one minutes
If less than 60 for either hold and call doc
Surgical intervention: maze procedure
Education:
Medication therapy
Anti dysrhythmia
Anticoagulants
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Ventricular dysrhythmia is more concerning. They are responsible for getting blood out to the body
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___ ___ ___ is a result if increased irritability if ventricular cells.
Seen as early ventricular complexes followed by a pause
Premature ventricular complexes
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__ __ also called V tach- repetitive firing of irritable ventricular ectopic focus; usually at 140 to 180 bpm
Adenosine to block responses
Beta blocker and calcium channel blockers to reduce pulse
cardiovert- shock into normal rhythm
First step follow cpr skills
Can kill you
Ventricular tachycardia
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__ __ also called v fib- result of electrical chaos in ventricles
Ventricular fibrillation
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___ ___ is also called ventricular standstill- complete absence of any ventricular rhythm
Ventricular Asystole
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Asynchronous counterstock that depolarizes critical mass of myocardium simultaneously to stop re entry circuit and allow sinus node to regain control of heart
When doing this people need to stay clear
Know how to document that you had to and document follow up ekg, how many energy setting used, called jewels that we’re used and skin condition afterwards
Defibrillation
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Automated external defibrillaton
Battery powered device placed under skin to monitor heart rate, acts as a pace maker
Allows for earlier defibrillation
When used, there is a greater chance of successful rhythm conversion and patient survival
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Implantable cardioverter/defibrillator
Indicated for patients who have experienced one or more episodes of spontaneous sustained VT or VF not caused by MI.
They can take it off for a shower.
Wearable cardioverter defibrillator is a external west like device worn 24 hours a day except when showering or bathing
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Heart failure also called pump failure; Inability of heart to work effectively as a pump.
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Left sided heart failure:
Formerly known as congestive heart failure. Not enough oxygenated blood to body. Back up of blood in lungs**
Typical causes: hypertension, coronary artery disease, valvular disease.
Not all cases involve fluid accumulation
Two types:
Systolic
Diastolic
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Right sided heart failure:
Causes;
Left ventricular failure, right ventricular MI, pulmonary hypertension
Right ventricle cannot empty completely.
Increased volume and pressure in venous system and peripheral edema.
You see a lot of fluid volume overload, blood backed up to the body, decreased amount of blood going to lungs
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High output failure:
Cardiac output remains normal or above normal.
Body has higher demand for cardiac function.
Caused by increased metabolic needs or hyperkinetic conditions. Like;
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Septicemia
High fever
Anemia
Hyperthyroidism
Symptoms:
Fatigue, chest pain, enlarged heart
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Usually dietary restriction: minimize salt and water intake to prevent fluid overload.
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When heart is failing
Compensatory mechanisms
Sympathetic nervous system stimulation> renin angiotensin activation> chemical responses> myocardial hypertrophy
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Left sided heart failure:
Weakness
Fatigue
Dizziness
Acute confusion
Pulmonary congestion- wet lung sounds, frothy pink sputum
Breathlessness
OLIGURIA
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Shortness of breath w activity **
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Right sided heart failure:
Jugular vein distention
Increased abdominal girth
Dependent edema
Hepatomegaly
Hepatojugular reflux
Ascites
Weight most reliable indication of fluid gain/ loss
Polyuria
Swelling of liver
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Assessment for HF
lab:
Electrolyte: potassium
Hematocrit and hemoglobin is decreased w fluid over load
BNP: compensatory mechanism going into effect
Chest x ray and ekg is huge to get if suspected HF
echo is also done
Urinalysis (proteinuria/high specific gravity
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Treatment for Hf
Ace inhibitors and diuretic is used to help with pumping of heart
Digoxin is used to help contractility
Calcium channel blockers or beta blockers to help with pulse
Diet: low fat low sodium
Surgery: mechanical heart transplant or heart transplant
Know.
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Stable angina: chest pain that usually occurs with stress and goes away with rest
Unstable: increased frequency and severity. Still goes away with rest. Has anxiety nausea; chest pain and dizziness. Less than 15 minutes. Rest helps:
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Peripheral venous disease
Circulatory disorder where the veins become damaged or blocked: venous insufficiency
Thrombus formation
Defective valves
Skeletal muscle that do not contract to help pump blood in the veins
Check: neuro assessment; pulse, color of extremities and pulse, capillary refill. Tend to complain of legs when legs are dependent when standing.
Blood usually pools in lower extremity: edema and skin will be dark in color like sunspots
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Venous thromboembolis (VTE)
Thrombus- a clot
Phlebothrombosis is a clot in vein
Thrombophlebitis- clot in vein now led to inflammation
DVT: deep vein thrombosis in lower extremities
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Peripheral venous diseases
1. Virchows triad- have blood pooling
2. Blood flow stasis
3. Endothelial injury
4. Hypercoagulability
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Peripheral venous disease
History:
History of VTE
risk factors: cancer patient, obesity, bed rest,
Padua prediction score: asks questions if they answer yeah it increases risk of clot
Physical assessment signs and symptoms:
May be asymptomatic
Calf or groin pain (one. Not both) warm to touch
Sulfide onset of unilateral leg swelling
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Peripheral venous disease
Venous duplex ultrasonography
Doppler flow studies
Impedance plethysomography- measure blood volume in body
MRI
D dimer was elevated- found in blood after blood clot developed
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Peripheral venous disease
Potential for injury due to complications of VTE and anticoagulant therapy
No surgical management
Surgical management
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Shock:
Any problem impairing oxygen delivery to tissues and organs can precipitate shock. Do not have enough oxygen delivering to body. Emergency
Widespread abnormal cellular metabolism
Oxygenation and tissue perfusion needs not met
Whole body response; “syndrome”
Lead to life threatening emergency
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Hypovolemic- low volume, body has decreased volume of fluid or blood. Adverse effect to surgical procedures or injury.
Cardiogenic- heart pump insufficiency.
Distributive- widespread vasodilation, increased capillary permeability- decreased oxygen
Obstructive- heart pump insufficiency caused by obstruction of blood flow leadin to pump issue
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Anaphylactic shock: related to histamine release, allergic response:
Wheezing, edema, erythema, when airway becomes obstructed.
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Stages of shock
Initial- not many s/s, you have decent o2 to vital organs, you may see increase HR, slight increase in respiratory rate. Stable
Nonprogressive- decrease o2 to non vital organs. Cooler temp extremities. Decreased urinary output, HR elevated, change in BP, restless
Progressive: non vital organs getting no oxygen and vital organs becoming hypoxic. Mental status change, fatigue, impending sense of doom, elevated HR bigger decline in BP, decline urinary output.
Refractory: almost too late. Non vital and vital is anoxic too much cell death and tissue injury. Multiple organ failure.
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Multiple organ dysfunction syndrome
Sequence of cell damage caused by massive release of toxic metabolites and enzymes.
Micro thrombi form
Occurs in liver, heart, brain, kidney
Myocardial depressant factor from ischemic pancreas
Liver: use all of available platelets and clotting factor. DIC
Heart: cardiac failure
Brain: mental status change
Kidney: OLIGURIA
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Hypovolemic shock
Low circulating blood volume
Causes mean arterial pressure (MAP) decrease; inadequate total body oxygenation
Commonly caused by hemorrhage (internal or external) and dehydration
- plasma loss through burns
- diuresis
- diabetes insipidus
- gi loss bleeding, diarrhea, vomiting
Look for: increased systemic vascular resistance poor skin turgor, OLIGURIA, thirst, low systemic and pulmonary pre-loads, and rapid heart rates
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Hypovolemia can be prevented
Avoid trauma and hemorrhage
Proper safety equipment
Seat belts
Awareness of hazards in home and workplace
Drink plenty of fluids
Secondary prevention
Assess for early manifestations
Risk:
Individuals who have altered mobility
Decreased thirst response
Someone who is malnourished
Signs of dehydration:
Start becoming thirsty no matter how much they drink
Decreased urinary output
Dizziness
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S/s for hypovolemia
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Increased pulse
Decreased bp
Narrowed pulse pressure
Delayed capillary refill
Postural hypotension
Low central venous pressure
Flat neck and hand veins in dependent positions
Slow capillary refill
Diminished peripheral pulses
Confusion
Anxiety
Increased RR
Shallow breathing
Decreased Paco2
Decreased P
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Treatment for hypovolemia
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Oxygen
IV therapy
Fluid*
Drug therapy- vasoconstrictors or dabutamine for BP
Hemodynamic monitoring
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Patient teaching for hypovolemia
Increased thirst
Decreased urine output
Light headed
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Sepsis and septic shock
Complex type of distributive shock- bacterial/ fungal infection processes to dangerous conditions within days
Sepsis- a life threatening organ dysfunction resulting from a dysregulated host response to infection
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Septic shock
Stage of sepsis and SIRS- multiple organ failure evident; uncontrolled bleeding occurs
Death rate for patients in this stage is very high.
Begins:
Local infection >
Systemic infection (early sepsis)
SIRS (systemic inflammatory response syndrome)
Organ failure (severe sepsis)
Multiple organ failure (MODS) (septic shock)
Death
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Septic shock:
Prevention is the best management strategy
Evaluate risk: malnourished people, immuno suppressed, cancer patients
Use aseptic technique
Early detection of sepsis
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S/S of septic shock
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Increased HR**
Increased RR
hypotension
Decreased urinary outputs
Increased WBC- early indicator
Mental status change or DIC signs
Clammy skin/ flushed in appearance
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Treatment:
Oxygen therapy
The most common causative agents are gram negative bacteria- multiple antibiotics, vasoconstrictors, and agents to enhance myocardial perfusion and contractility.
Blood replacement therapy. ABX IS PRIORITY
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Antigens: blood type A develop antigens for A.
Antibodies: Blood type A develop antibodies to people with blood type B.
ABO system: AB develops antigens for both with no antibodies. O develops antigens for O and has antibodies against A and B.
AB and A and B can take blood from type O.
O is universal donor.
AB can receive blood from anyone- universal recipient
People with negative RH factor need to receive blood from other negative people.
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Donor: giving blood
Recipient: getting blood
Directed donation: specific donations of blood
Autologous donation: donate your own blood to themself if your having a procedure
Blood preservation: store blood in a freezer for like 3 weeks on stock then it becomes bad blood.
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Transfusion responsibility
Have to get a consent prior
Review agency policy.
Verify prescription with another RN
get a blood typing for client
Use two identifiers for patients who receive transfusions and verify with another RN
Examine blood bag Label, attached bag, and requisition slip for ABO and Rh compatibility with the client
Check expiration date and time with another RN
Inspect blood for discoloration, gas bubbles, cloudiness
Blood ignitated within 30 minutes as it arrives to the floor
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Transfusion responsibilities
Administer the blood product using the filtered tubing to remove aggregates and possible contaminates
Unless directed otherwise infuse blood products only with IV normal saline solutions because some other IV solutions can cause hemolysis
Stay with patient for the first 15-30 minutes of the infusion because this time severe reactions occur
Infuse the blood product at the prescribed rate for the transfusion type to avoid the possible complication of fluid overload
Monitor vital signs at least as often as agency policy ab the patients condition indicated to identify early indications of adverse transfusion reactions
Normal Saline 0.9% is the only fluid you can run with the blood. Usually connected with a V tube. Prime tubing with blood before you get started.
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RBC transfusion: replaces cells lost from trauma or surgery
Platelet transfusions: given low platelet counts, active bleeding, schedule for invasive procedure
Plasma transfusions: replaced blood volume and clotting factors
Granulocyte (WBC) transfusions: given rarely to neutropenic clients
Massive transfusion protocol: given when H&H levels are low
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Transfusion reactions
Febrile- elevated temperature within first 2hr. Hold transfusion give NS and contact physician.
Hemolytic- damaging to blood cells. Fever, chills, low back pain, flushing, low bp, hr goes up- stop transfusion give NS and contact physician
Allergic- hives, wheezing, itching, flushing- stop infusion, flush with NS, give antihistamine usually prior to prevent this
Bacterial- something in the blood(contaminated) usually wheezing, low bp high HR, dyspnea. Stop blood, NS, call physician
Circulatory overload- sob, jugular vein distention, bounding pulse, increased HR and RR. Stop infusion and call physician
Transfusion associated graft versus host disease- rare, almost always fatal. Lymphocytes found in transfusion donor blood attack the host tissues and cells. Usually happens later then has reaction.
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Autologous blood transfusions
Collection and infusion of patients own blood
Eliminated compatibility problems
Reduces risk for transmitting blood borne disease
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Transient ischemic attack
Warning sign
Transient focal neurologic dysfunction
Brief disruption in cerebral blood flow
Diabetes increases risk for stroke and diet.
Prevention would also be anticoagulant therapy to prevent development of the stroke. I
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Stroke
Change in normal blood supply to brain
Types: all affect blood supply to brain
Ischemic- caused by inclusion of cerebral or carotid artery. Obesity or elevated cholesterol
Thrombolic- most common. A clot developed in cerebral or carotid artery
Embolic: dislodged clot that has been transported to cerebral or carotid artery
Hemorrhagic: a bleed. Typically called aneurysm. Caused by HTN and advanced age.
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Stroke assessment:
Priority: ABCs.
S/S: facial dropping, slurred speech, extremity numbness and extremity is not working, vision changes, confusion
Right side affected: more likely to see a client who has trouble with dizziness (proprioception)and ataxia and disoriented more
Left side affected: reading, writing, arrhythmic. More issue with speech, math, writing, analytical thinking
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High risk people for stoke:
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Obese
HTN
Diabetes
Cholesterol
Drug use- hemorrhage stroke
Smoker
Birth control
Age
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Treatment:
Hemorrhage stroke: go in and cartarize bleed and maybe plasma
Thrombolic: anticoagulants, thrombolytic(given 3 hours of stroke onset) don’t give thrombolytic if older than 80 and prior history of stroke.
Anxiety meds
Stool softeners
Calcium channel blockers
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Medical management of stroke;
Thrombolytic therapy
Neuroprotective drugs
Surgery:
- carotid artery angioplasty with stenting
- endarterectomy
- extracranial-intracranial bypass
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Traumatic brain injury (TBI)
Blow or jolt to head
May be result of head penetration by foreign object
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Two types of injury related to TBI
Acceleration: when external force come in contact with head and causes it to go in a certain motion head goes back.
Deceleration: head is moving then it gets stopped.
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Brain injury:
Primary brain injury:
Open versus closed head injury
Mild, moderate, severe classification
Fractures
Secondary:
Any processes that occur after the initial and worsen patient outcomes
Damage occurs because delivery of oxygen and glucose to the brain is interrupted
Examples: intracranial hypertension, cerebral edema
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Nursing care for TBI
Spine precautions: can develop herniation that leads to more impairment
Neuro assessment: glascow coma scale. Signs of mental status change* watch for light sensitivity, hypotension, shock, monitor VS, watch for headache thats getting more severe.
Bed rest, no neck flexion, log roll, bed pan,
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Treatment for TBI:
Prevent and detect secondary brain injury
Drug therapy: mannitol
Maintain cognition, sensory perception, and mobility: cognitive rehab.
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GERD
Risk factors: NSAID, pregnancy,
, obesity, age, apnea, NG tube
Contributing factors; spicy food, fried foods, tight clothing, caffeine, coffee, eating or drinking before bed, tobacco use
S/S: chest pain, reflux, pyrosis- heart burn, throat irritation, loss of tooth enamel
Medication: antacids- magnesium or calcium- kills off acid, proton pump inhibitors, end in azol. Histamine to antagonists- end in dine. For Frequent gerd.l
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Peptic ulcer disease
Cause: to much acid, organism called by h pylori.
Ulcer formation: acid produced will irritate intestinal lining causing ulcers
S/s gi bleeds are common, can lead to perforations or tears. Can cause peritonitis
Pyrosis-heart burn, tarry stools or melena. Coffee ground emesis.
Treatment is same as gerd. Antacid, PPI, histamine antagonist, mucosal Protectants like surfactant.
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Intestinal obstruction:
Occurs in the small (more common) or large intestine (sigmoid colon most common)
Can be partial or complete
Severity depends on the region if the bowel, degree of the occlusion, and the degree of vascular disruption.
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Types of intestinal obstruction
Non mechanical: usually related to paralytic lieus when post op and have an obstruction bc bowels are still asleep. Or a muscular disturbance like Parkinson’s or muscular dystrophy
Mechanical: physically blocked. Hernias, tumors or intussusception- where intestines start to telescope within itself. More common in children. Can resolve on its own. Volvulus- twisting of intestine
Complications: perforation- rupture. Requires surgery: and colostomy. And peritonitis- inflammation around stomach lining and worry for sepsis. Fever chills abdominal pain, bloating, decreased urinary output.
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S/S of small bowel obstruction:
Crampy abdominal pain (usually seen in small bowel obstruction)
Reflux, vomiting, if obstruction is complete.
Fecal smelling breath
Dehydration signs: thirst, drowsiness, malaise, acchiness, parched tongue, and mucous membranes, anorexia
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S/S of large bowel obstruction
Develop and progress slowly
Constipation may be the only symptom for months
Weakness, weight loss, and anorexia
Marked abdominal distention
Crampy lower abdominal pain.
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Physical assessment
Obstipation- small bowel, constipation with large
Abdominal distention with both
Peristaltic waves: small
Bobborygmi: increased bowel sounds proximal to obstruction. Usually abdominal scan to find obstruction
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Intestinal obstruction treatment
Main one is NG tubes-
IV fluid replacement
Surgical management:
Exploratory laparotomy- to look for specific cause like mechanical construction or tumor.
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NG tube insertion:
For measurements: NEX measurement- measure from nose to ear to xiphoid process and add an inch. Wrap tape around the end to now where to stop.
To confirm placement after initial x ray is done, a combination of three methods is combined.
- measure the length of the exposed portion of the tube every shift and compare it with the original measurement. An increase in length of exposed tube may indicate dislodgment or a leaking or ruptured balloon if the tube has a balloon.
- visually assess the color of the aspirate to help distinguish between gastric and intestinal placement.
- measure the pH of aspirate, which is a more accurate method of confirming tube placement than measuring the exposed tube length or assessing tube aspirate
Have patient lean forward for better tube placement.
Ask client if they had any nasal injury.
Assess nares. Once you hit resistance have client swallow and it will guide to correct placement:
If shortness of breath or excessive coughing stop it could go into lungs.
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Patient teaching about NG tube:
Increased risk for hypokalemia
Discuss bowel regimen with patient, including avoiding laxative use, increasing fluids, and increasing fiber.
Teach personal care to a patient who has undergone surgery with an patient who has undergone surgery with a ileistomy or colostomy, and dietary changes to help reduce gas production.
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Colorectal cancer:
Colorectal- refers to colon and rectum, which together make up large intestine.
Most are are adenocarcinomas
Etiology: age >50 years
Heavy alcohol use, genetic predisposition, personal family history of cancer, familial adenomatous polyposis
Drinking increases risk
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With colorectal cancer:
Physical assessment: bleeding and change in stool (most common signs)
Psychosocial assessment:
Fecal occult blood test: usually two within 3 days.
Carcinoembryonic antigen; lab work to see if there is cancer markers in blood.
Sigmoidoscopy or colonoscopy biopsy is main to diagnose
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Treatment: prevent/control metastasis
Radiation, chemo, surgical management
Assist: assist with grieving process
Care: care coordination an transition management.
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Hep A: fecal oral transmission: contaminated food and water
Hep: B blood transmission, sex, infected blood
Hep C: blood transmitted, sex, needles
Hep D: coinfection with hep B.
Hep E is fecal oral and contaminated food and water
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Hepatitis treatment:
Vaccines for hep a and hep b.
Healthcare workers- standard precautions, needless systems
Hep a recommendation:
Proper hand washing after handling shell fish
Avoid contaminated food and water
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Heptatitis s/s
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Flu like symptoms
Fatigue
Anorexia
Abdominal pain
Nausea
Joint pain
Dark colored urine
Clay colored stool
Jaundice
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Dx: US and liver biopsy
And labs to see if antibodies are present
Liver function test: ALT AST are increased
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With hep A they will let it run its course usually give immunoglobulins and encourage use of vaccinations
B&D- antiviral meds
interferon to treat
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Hepatitis treatment diet
High calorie
High carb
Low fat
Low protein diet
Small frequent meals
Promote hepatic rest
Avoid OTC meds and herbal supplements
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Pancreatic cancer:
Converts food to fuel and glucose regulations
Difficult to diagnose
Treatment has limited results
Low survival rate
Drug therapy: radiation or chemo, biliary stent insertion
S/S clots
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Surgical management for pancreatic cancer
Whipple: 5 year survive rate goes goes up by 20% they remove the head of the pancreas, dedunum, jejunum, and part of the stomach if not all. Gallbladder, common bile duct and some of the spleen.
NG given afterwards
TPN typically began
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Pancreatic cancer: whipple surgery complications
Hemorrhage or hypovolemic shock and hepatorenal failure.
Monitor labs and urinary output. And signs for hypovolemia
Monitor bowel sounds
Watch for hypokalemia bc of NG tube
Glucose monitoring
Monitor electrolytes and mental status
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Risk factors for under nutrition
Chronic conditions/ illness
Constipation
Decreased appetite
Dentition drugs
Dry mouth
Failure to thrive impaired eyesight
Pain that is acute or peristant
Weight loss
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Psychosocial risk factors for under nutrition
Ability or inability to make their own meals due to functional decline, fatigue, or memory
Decrease in enjoyment of meals
Depression
Income(ability to afford food)
Loneliness
Transportation access
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Administering total enteral nutrition
Nasoenteric tube is short term (NET)
Nasogastric the
Nasoduodenal and nasojejunal tube is what physician will place.
Enterostomal feedings tubes- long term
Gastrostomy performed
PEG and PEG/J
Physicians placed these
Verify placement before Feeding
Done with pH typically
Pull back contents and measure gastric residual for delayed emptying.
Most feedings are room temp, HOB 30 degrees or higher when feeding. If bolus only 30 to an hour after. Flush with water before and after feedings.
Flush tubs four to 6 hours
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Types of tube feedings
Bolus: you will just connect it and give the feeding and disconnect after flushed
Continuous: continuous on a feeding
Cyclic: faster than continuous and slower than a bolus and over a period of time.
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Complications of TEN
Priority is always safety
Obstructed clogged tube is most common prob
Tube misplacement, dislodgment
Abdominal distention and nausea vomiting
Fluid and electrolyte imbalance
Crackles or coughing you will stop feeding
Refeeding syndrome- body goes into starvation. Fatal shift in fluid and electrolyte. Decreased glucose and electrolyte. Mental status change, HTN, signs of HF
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Peripheral parenteral nutrition means there less than 10% of dextrose in the nutrition itself and is used when gI tract isn’t function. PPN can be by a peripheral vein.
Total parenteral nutrition TPN
Has greater than 10% dextrose and has to be given through central line or peripherally inserted catheter or PIC line.
* You can add insulin and heparin to prevent fibrin build up.
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Complications for routes for TPN administration
At risk for
Sepsis: wash hands before you use it, use sterile technique with dressing changes every 3-7 days. Mask on yourself and client. NewTubing every 24hours
Pneumothorax: watch for shortness of breath, inhale and exhale and one side not move, pain.
Embolism: most pic lines have occlusion to catheter so that’s why we use heparin sometimes. Turn them on left side to trendelinburg and use anticoagulants
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Monitoring TPN administration
Flow rate and tubing
Standard TPN blood work: electrolyte, urea, creatine, Ca, PO4, Alb, TG, glucose, ALP, AST, ALT, cholesterol, bilirubin, platelets, INR, PTT
Glucometer BID*
Patients weight daily
Intake and output
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TPN administration
Double check physicians orders with Tpn pharmacy labels
Document how client is tolerating and glucose level and vital signs
Aseptic technique for IV therapy
Clean ports with 2% chlorhexidine gluconate with alcohol wipes
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TPN administration
Always infuse TPN With an infusion pump
Change TPN tubing every 24 hours
Monitor for S/S of complications- back up banana bag so you can change to next one. If you don’t have one hang 10% dextrose and water until you get banana bag or TPN.. if you don’t hang something then you stop it it increases risk of hypoglycemic event
TPN room temp one hour prior to administration, no cracks in bag, if it has oily appearance or layer of fat then throw it out. If you discontinue TPN then do it slowly because to rebound hypoglycemia
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Hyperglycemia s/s nausea, thirst, blurred vision, headache, polyuria.
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Calcium level 8-10
Affect brain kidney and Neuro status
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Bowel Elimination
Diet: increase fluid, fiber and wheat, fresh fruit, increase activity
Ostomies: stoma should be beefy red/pink color if it’s purple or black it’s not getting blood supply
Ostomy care: assess skin for irritation or breakdown. Empty bags when they are a half or 1/4 way full.
Assess stoma and discuss avoiding odorous foods that cause gas.
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right sided is fluid overload, like fluid backs up to abdomen, ankles, legs and left is when it backs up to your lungs
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