Exam 2 ppt Flashcards
Insensate loss:
fluid loss that you can’t measure. (sweat and breathing) These things are always going on
Electrolytes: cations and anions
Cations (+) Sodium: outside the cells Potassium: mostly inside the cells Calcium Magnesium Hydrogen
Anions (-) Chloride Bicarbonate phosphate sulfate proteinate
How does the body regulate fluids and electrolytes ?
Kidney function Heart and blood vessels Lungs Pituitary Adrenal glands Parathyroid gland Baroreceptors Renin-angiotensin-aldosterone ADH and thirst Osmoreceptors BNP/ANP
Fluids, electrolytes and aging
Physiologic changes
↓Cardiac, renal, respiratory function
-Decreased thirst mechanism
-Alterations in ratio of body fluids to muscle mass
-Increased sensitivity to changes in fluids and electrolyte levels
-Frequent medication use that affects
-Renal function
-Cardiac function
-The elderly are particularly at risk for electrolyte imbalances
-Thirst mechanism doesn’t work as well
-Check skin turgor on forehead and sternum
Hypovolemia: Fluid volume deficit causes
Occurs when loss of ECF volume exceeds the intake of fluid
Mild – 2% of body weight loss
Moderate – 5% of body weight loss
Severe – 8% or more of body weight loss
Hypovolemia: Fluid volume deficit signs and symptoms
- Acute weight loss/flat neck veins
- Decreased skin turgor-lost elastin in the skin. Check for turgor in elderly on forehead and sternum
- Oliguria/concentrated urine
- Postural hypotension
- Weak, rapid, heart rate/circulatory collapse
- Increased temperature
- Decreased central venous pressure
Hypovolemia: Fluid volume deficit treatment
-First, find the cause (vomiting, diarrhea) then replace fluids. If someone is low because they fell, IV then push fluids orally. Vomiting excessively will also change pH, electrolytes, and fluid volume.
-Mild hypovolemia: use oral route if possible
-Acute or severe: Isotonic or hypotonic IV solutions
-Nursing: I & O, daily weights, vital signs, urine output, skin turgor, LOC
-Normal Hb: 12-14 in women 14-16 in men
drop in Hb could be bleeding, concentrated blood can skew results, dehydration
30 mls (avg) is normal urine output
Hypervolemia: Fluid volume excess contributing factors
People most at risk: pts with renal failure (can’t eliminate fluid) and Heart failure (can’t pump fluid)
An isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF
Contributing factors: CHF Renal Failure Cirrhosis of the liver Excess sodium intake Our job is to frequently assess to be able to treat these things. Measure weight daily: 1L of fluid=1kg
System Specific assessment Fluid Volume Excess : assessment findings
↑ pulse ↑ B/P ↑ weight ↑ edema ↑ ascites ↑ crackles in lungs ↑ dyspnea ↑ confusion JVD
Normal/desired expected Outcome – Fluid Balance
Pulse within client norm - B/P within client norm Weight within client norm ↓ edema ↓ ascites ↓ crackles in lungs ↓ dyspnea ↓ confusion
“Third spacing”
-Fluid is trapped in the interstitial space.
-Trapped in a space that is not beneficial to the body. (ie: ascietes from liver failure)
-Remember that fluids shift
-Anytime theres an inflammatory response, fluid is sent to that area. You can start third spacing small amounts
L-oss of albumin or protein leads to decreased oncotic pressure, causing fluid to “leak” from the intravascular into the interstitial space.
Normal albumin in the body:
3.5-5.0 (know the low end.)
When albumn is 1.7 or less you develop
anasarca: total body edema. handprint in the middle of their back if you try to turn them.
extremely malnourished patients (like those in the hospital) have reduced albumin
Most of the proteins are carrying things
ie transthyroiretin transports thyroid hormone
Examples of what can cause decreased albumin
Burns Peritonitis Cirrhosis Alcoholism Malnutrition Long/complex surgeries
causes of hyponatremia: Na+
- Caused by active losses or by dilution hyponatremia
- We need Na for nerve stimulation and muscle contraction
Hyponatremia manifestations
Clinical manifestations depend on the cause, magnitude, and speed of the deficit but are primarily neurological :
- Nausea and malaise
- Lethargy, headache
- Decreased level of consciousness: confusion
- Seizure, coma, death (cerebral edema)
- Brain herniation and death
changes can be from: n/v, diarrhea, suctioning, diuretics, fluid overload, etc
Fatal levels at 115/severe at 125
HYPONATREMIA: FIRST - Priority Nursing Interventions
S odium intake , Seizure precaution especially in high risk levels (125)
O verload—restrict water intake
D aily weight, diuretics, drugs (what are we doing that might cause it?)
I ntake & Output
U se isotonic fluids to restore ECF
M onitor: blood pressure, N/V, HR, dry mucous membranes / LOC
Look for CNS changes Increase sodium IV fluids (not 3% because its so hypertonic you risk damaging myelination in neurons)
Priority nursing intervention for hyponatremia
Protect airway:
suctioning: due to N/V and LOC
to get emesis out for aspiration risk reduction
in case of seizure
Hypernatremia: Na+>145 mEq/L overview
This is rare. But if you have a patient who can’t respond to their thirst mechanism or their thirst mechanism is impaired: dehydration=sodium level increases.
Can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium
Fluid deprivation in patients who cannot perceive, respond to, or communicate their thirst.
Diabetes insipidus
Acute: associated with rapid decrease in intercellular water and brain volume and causes an osmotic shift of free water out of the cell
Hypernatremia: Na+>145 mEq/L dangerous levels
ICU pts. increased mortality of 38-48% if their sodium reaches or exceeds 150.
Hypernatremia: Na+>145 mEq/L manifestations
Decreased urine output, Dry mouth dehydration, swollen tongue
Restless, irritable, confusion, delusions, hallucinations, seizures
Increased heart rate, temp, and flushed skin
Edema (peripheral and pulmonary)
Deep muscle reflexes increased
Hypernatremia: Na+>145 mEq/L treatment
I & O, daily weights Oral hygiene Monitor sodium intake Monitor vitals and neurological symptoms Monitor urine output
Normal potassium levels
3.5-5.0
Hypokalemia: serum K+ causes
Caused by active losses of potassium or insufficient intake
Needed for nerve stimulation and muscle contraction
Main sources of losses are:
Urinary loss
Gastrointestinal loss
Redistribution from extracellular to intracellular space
diuretics like lasix
starvation
trauma
alkalosis
laxative use and abuse (especially the elderly)
Hypokalemia: serum K+ s/s
low potassium will cause a flat or inverted T wave (nicknamed U wave)
Muscle weakness
Severe hypokalemia can cause DEATH through cardiac or respiratory arrest
Skeletal muscle weakness, cramping
U Wave EKG changes, arrythmias, inverted T waves
Constipation, ileus, hypoactive bowel sounds, N/V
Toxicity of digitalis glycosides
Irregular, weak pulse
Orthostatic hypotension
Numbness and tingling (paresthesia)
Hypokalemia: serum K+ treatment
Be very careful when administering potassium! It burns! Either slow it down or dillute it more
Potassium is NEVER administered by IV push or IM! Their heart stops and they die
IV potassium must be administered using an IV pump
Concentrations of potassium >20 mEq/100 mls should be administered through a central line
No more than 10-20 an hour. Ex if you need to give 40ml, that will take 4 hours typically.
Run alongside something else so it doesn’t burn
Potassium supplements are extremely dangerous for patients who have impaired renal function
know heart rate and rhythm
Hyperkalemia: K+ >5 mEq/L causes
Caused by decreased renal excretion, increased intake, medication effects, or a shift of potassium out of the cells as seen in acidosis or musculoskeletal injury muscle weakness paralysis nausea/vomiting colic
Hyperkalemia: K+ >5 mEq/L manifestations
Clinical manifestations are cardiac, nervous system, and GI
Hyperkalemia: K+ >5 mEq/L treatment
Mild- Restrict potassium intake and/or potassium sparing medications.
Serious- Cation exchange resins (e.g. Kayexelate. can be enema. Sticky and constipating. Tries pushing K into cells)
Emergent- Intravenous bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate
False readings of potassium levels
Random draw reveals random 7.2 potassium level. If this occurs, redraw and recalculate. False positives can occur from clotted blood. When you look at a patient’s labs, notice the trends to see where the patient is headed (upward or downward)
Hypocalcemia: causes
Inadequate intake, increased loss, malabsorption or increased binding of calcium
Most of our calcium is in our bones.
Calcium is carried by albumin
Needed for bone structure,…………….list she listed too fast
Normally 8.5 to 10.5 mg/dL circulates:
40% bound to protein
10 % chelated (attached to other electrolyetes)
50% “free” or “ionized”-this is what moves into and out of cells.
Need vitamin D. Add picture from ppt.
Hypocalcemia: s/s
Tetany- ↑ neural excitability, spasms Paresthesia- tingling Refractory hypotension Arrythmias Seizures
Hypocalcemia: treatment
Calcium replacement ! Don’t give with phosphorus because it will precitate
Seizure precautions!
Hypercalcemia: >10.5 mg/dL causes
Malignancy
Hyperparathyroidism
Hypercalcemia: >10.5 mg/dL: manifestations
↑ Calcium →↓neuromuscular excitability: Anorexia, N/V, constipation Muscle weakness/incoordination Confusion, lethargy, coma Bone pain Kidney stones/diuresis/thirst Cardiac arrest If your calcium is above 16, youre in trouble
Hypercalcemia: >10.5 mg/dL
Treatment:
Treat the underlying cause Increase fluids Restrict intake of calcium Mobilize the patient Monitor cardiac and neurological status Calcitonin: forces Ca into the bone
Magnesium normal ranges and overview
Magnesium travels with Potassium Also associated with Calcium Most ICU patients will experience depravation. Normal 1.3-2.3 1/3 bound to protein the rest is free
Hypomagnesemia causes
Helps maintain normal muscle and nerve activity
Major causes:
Chronic alcoholism
↓intake, especially TPN/PPN or tube feeding that lacks Mg (esp. after starvation)
Lower GI loss (Mg. absorbed in small intestines)
Diabetic ketoacidosis: has effect on potassium, so has an effect on Mg
Hypomagnesemia s/s
Neuromuscular Neuropsychotic Cardiac dysrhythmias deep tendon reflexes start to really see problems if levels are below 1 We really worry about heart block
Hypomagnesemia treatment
-Magnesium replacement: diet, PO supplement or IV (if severe)
-Patient education: on diet, DKA, diabetic control, and alcohol consumption
Replace gradually because it acts as a laxative. (milk of magnesia)
Hypermagnesemia >2.3 mEq/L causes
Most common cause: renal failure or laxative addicted/taking too much Mg.
If blood drawn with hemolyzed, you see a false high
Peripheral vasodilation
Don’t push magnesium
Excessive intake, Lithium therapy, untreated DKA
Hypermagnesemia >2.3 mEq/L manefestations
CNS depression
Muscle weakness/paralysis
N/V, flushed skin
Cardiac: bradycardia, heart block, arrest
Hypermagnesemia >2.3 mEq/L treatment
IV fluids: with or without calcium
Hold magnesium
Dialysis
Hypophosphatemia overview
Phosphate binds with Ca+ which pulls it out of the bone, giving these two an inverse relationship. If given to fast: tetany. We try to give it by mouth. Seen in: Refeeding syndrome: malnutrition, alcoholism, anorexia. Hyperparathyroidism Malignancies, severe burns Vit. D deficiency Overuse (binds with) of antiacids Post organ transplant
Hypophosphatemia s/s
Nonspecific, and depend on cause/duration/severity
Muscle weakness, numbness, fatigue
Bone pain/fractures
Altered mental status: anxiety, irritability, confusion, seizures, coma
Often dehydrated
decrease function of platelets=bruising
Hypophosphatemia treatment
-Education on diet
-Oral supplementation
-IV replacement- GO SLOW
Watch the site
Monitor Ca + and Phosphorus levels
Hyperphosphatemia >4.5 mg/dL causes and s/s
Common causes:
Renal failure
Hypoparathyroidism
Excessive intake &/or Vit. D toxicity
Chemotherapy
Acidosis
*Signs and symptoms are mostly related to hypocalcemia because they are inversed.
Treatment focuses on the underlying disorder, diet and patient education.
Hypochloremia overview, s/s, and treatment
Tend to travel with Na and K. Normal 97-107. Usually attached to another electrolyte. If there’s a problem, like an electrolyte imbalance,
Signs and symptoms are associated with hyponatremia, hypokalemia, and metabolic alkalosis
Chloride needed to make hydrochloric acid in the stomach
Treatment involves correcting the cause and replacing the electrolyte involved
Hyperchloremia >107 mEq/L causes
Doesn’t have its own warning signs:
Related to hypernatremia, bicarbonate loss, metabolic acidosis, and hypervolemia
Related to hypernatremia, bicarbonate loss, and metabolic acidosis
pH regulators
Lungs and kidneys control pH, but lungs are faster.
Metabolic Acidosis
Low pH (increased H+ concentration) and a low plasma bicarbonate concentration (
Metabolic acidosis manifestations
tachypnea
confusion
hypotension
decreased cardiac output
Metabolic acidosis treatment
Treatment focuses on the underlying metabolic disorder
Less than 7: decreased cardiac output
Respiratory rate speeds up
Metabolic Alkalosis overview
High pH (greater than 7.45) (decreased H+ concentration) and a high plasma bicarbonate concentration (26 ml of bicarb) Can be produced by a gain of bicarbonate or a loss of H+ (usually by vomiting or suction)
Metabolic alkalosis overview
Often accompanies hypokalemia; manifestations are similar to hypokalemia and hypocalcemia
Treatment addresses underlying disorder as well as K+ replacement and fluid volume replacement
Respiratory Acidosis
Always due to inadequate excretion of CO2 with inadequate ventilation
Respiratory alkalosis
pH is >7.45 and PaCO2 is
Hypotonic solutions
Provide salt and water to replace cellular fluid. We don’t give water because it’s so hypotonic cells take it in so fast, the cells burst
Examples:
1/2 normal NS (0.45% normal saline)
1/3 NS (0.33%)
Hypertonic solutions
3% or 5% NaCl
Given for increasing intervascular volume. The problem (like with D5NS) it starts as hypertonic, but gets metabolized so quickly that it becomes hypotonic. Not used for emergent critical situations …... talks too fast
ISOTONIC SOLUTIONS
Closest to osmolality of blood itself. Diffuses into extracellular space. Used a lot to give meds because it doesn’t interact with meds. Also with burns
0.9% NS
Lactated ringer’s solution: Used a lot in burns! Contains small amounts of calcium, potassium, ….talks too fast.
never use in a patient that’s alkalotic because it can be made worse
Never use in liver disease
5% dextrose in water-very quickly metabolizes into isotonic solutions
DEXTROSE
What happens when you add dextrose to a solution?
D5- metabolizes too fast
D10 - weaning off of something
D50-hypoglycemia
Troponin I or T (cTnI or cTnT):
peak
There are variations (I: cardiac specific/T:more sensitive)
will peak between 4-24 hours. Will peak early and stay peaked up to 24 hours. Will remain elevated after the event
Creatinine Kinase-MB (CK-MB):
this form is more Cardiac specific. Peaks at 4-24 hours, but doesn’t stay peaked
Myoglobin:
not cardiac specific at all. Rules out MI. Peaks 1-3 hours. If this is not elevated, it is unlikely there is a cardiac event
*at no time will these labs be the deciding diagnostic factor in MI
Fasting Lipid Profile pg.399.
Goals will vary. A general set of numbers can act as a guideline, but goals vary according to number of risk factors. Pt specific. Instruct pt that they need to be fasting! No eating or drinking at least 4 hours preferably 12 hours. NPO after midnight, draw first thing in the morning.
Total Cholesterol: should be less than 300 ish
LDL: bad. Range for CAD pts-you want it less than 70
Triglycerides: go hand in hand with LDLs… less than 150
HDL: good: go in opposite direction of LDL. Varies with sex and CAD. In general remember you want it above 40
cholesterol
*Your body needs cholesterol, just the right kind. Different cholesterols are different sizes. LDL are the big sticky ones. HDL is a dumptruck that comes around to pick up cholesterol trash… you want a big, fat dumptruck
Brain Natriuretic Peptide (BNP):
released when the heart is stretched too much due to heart failure. You want it less than 100.
Pro-BNP:
quickly becoming something drawn along with BNP. Targets heart failure a little more specifically. Want less than 300
Pro-BNP of more than 300 correlated with an ejaction fraction of less than 40%
C-Reactive Protein (CRP):
not cardiac specific, shows if there’s inflammation in the body. Elevated with muscular trauma or statin medication. (statins can cause muscle aches. Doc might have them stop statin then retest in two weeks to see if that’s the cause)
Coagulation Labs: I&R will be on test***
PT/INR/aPTT: usually all drawn together “coag panel”
normal values depend on hospital’s equipment. Changes according to location.
Prothrombin Time (PT):
Norm 11.0-12.5
how many seconds for blood to clot
clotting is easy at less than 11
Activated Partial Thromboplastin Time (aPTT):
Norm 21-35
thicker sticker blood with low number
high number thinner blood
International Normalized Ratio (INR):
Norm 0.8-1
regulated values from powers that be
Normal person not on Warfarin should be in this normal range
pt on warfarin, the target ratio is adjusted. Cardiologists will set range in general between 2-3.5. These patients take longer to clot than a normal person
5 would be an awfully long time: they take a long time to clot
dangerous bleeding
easy bruising
Electrocardiogram (ECG)
Noninvasive way to look at electrical activity of the heart. Doesn’t assess pt symptoms, just looks at trends. Telemonitors are portable ways to measure electric activity. Continuous reading. As this patient walks around, you still see what they’re doing. Tele tech watches it all the time. Hardest part is practicing where to place the leads.
Difference between this and 12-lead: 12 lead is just a snapshot of what a patient does in a limited point of time.
Prepping patient:
try to pick a spot without much hair. NO RAZORS. use clippers
Stress Test
We’re talking about regular, treadmill stress test. Important to understand what patient needs to know ahead of time.
wear shoes with traction
comfy clothes
can’t have anything that altars your heart rate: coffee, tea, beta blockers, chocolate
No bed rest afterwards
results need to be read by cardiologist “they may be nervous, so you can say if we saw anything immediately dangerous, we wouldn’t let you leave here today.”
The treadmill increases speed and incline every three minutes. Will measure blood pressure and rate how hard they feel like they’re working. All is recorded. If at anytime, they complain of dizziness, nausea, or chest pains. We are trying to recreate the symptoms they came into the clinic in the first place. Can be fasting, but depends on the doctor and the kind of stress test they’re doing.
Cardiac labs
Cardiac biomarkers -Troponin -Myoglobin -Creatinine Lipid panel -LDL -HDL -Triglycerides -Total cholesterol Brain Natriuretic Peptide (BNP) -Pro-BNP C-Reactive Protein (CRP) Coagulation tests -a-PTT -INR* -PT
Echocardiogram
Ultrasound of the heart. Estimates ejection fraction. Some involve injecting radioactive isotope to show the blood. Can be bubbles pumped through the heart to see if there are holes in the heart. Required at Research.
Transesophageal Echocardiogram (TEE)
Another kind of invasive ultrasound. A long tube goes down pts esophagus. Gives you an electrocardiogram closer to the heart. Might do a shock to see heart blocks.
Nursing considerations for transesophageal echocardiogram
They will have to sign informed consent conscious sedation pt monitored all the way through recovery for at least an hour. Sedative + something down their throat=NPO for the first hour. ice chips first, then clear liquids, then food. Can't drive themselves home or take a taxi. someone needs to be in charge
Lab tests are performed for the following reasons
- To assist in identifying the cause of cardiovascular signs and symptoms
- To identify abnormalities in the blood that effect the prognosis of a patient with CVD
- To assess the degree of inflammation
- To screen for risk factors associated with CAD
- To determine baseline values before initiating therapeutic interventions
- To ensure that therapeutic levels of medications are maintained
- To assess the effects of medication
`Biomarkers-overview
plasma levels of cardiac biomarkers are used to diagnose acute MI in conjunction with the history, physical examination, and ECG. These substances leak into the bloodstream after injured myocardial cells rupture their cell membranes.
Lipid profile-overview
Helps evaluate a person’s risk for developing atherosclerosis or to diagnose a specific lipoprotein abnormality
Contains:
- cholesterol
- HDL
- LDL
- Triglycerides
Nursing considerations for PAD
• Assist patient to develop exercise routine: we want them to be active! They might complain of numbness or of leg tingling. Work with PT to walk a little further each day. Helps develop collateral circulation.
• Prevent anything that causes vasoconstriction: cold, crossing legs, up and moving every hour or so.
• No heat on numbness because they wouldn’t know when they’re getting burned.
• Educate patient
○ Avoid crossing legs
○ Avoid exposure to cold
○ Never put heat on extremity
○ Inspect skin daily for breakdown
○ Avoid smoking
○ Take medications as prescribed
○ Elevation of lower extremities may decrease blood flow and increase pain. A dependent position (dangling feet) may improve flow and decrease pain.
Buerger’s disease assessment and considerations
• Assess: ○ pain, ○ color, ○ temperature, ○ sensation, ○ pulses • Nursing Management and Patient Education ○ Monitor pulses ○ Smoking cessation ○ Avoid injury to extremities ○ Vasodilators
Raynaud’s assessment and considerations
• Assess: ○ color, ○ temperature, ○ sensation, ○ edema • Nursing management and patient education ○ Monitor pulses ○ Administer vasodilators ○ Assist patient to ID/avoid triggers (stress) ○ Instruct to wear warm clothing during cold weather ○ Avoid smoking ○ Avoid injuries to hands: wear gloves
Aneurysms
outpouching of arteries. If found early enough, monitor the size. Once its big enough for surgery, they’ll correct. If it’s not big, make sure they don’t aggrevate it. (monitor BP daily, blood pressure meds taken correctly)
Abdominal aneurysms
S/S: Pulsating abdominal mass with bruit. Don’t push on it!
• Imminent rupture: Severe Low back/abdominal pain
Thoracic abdominal aneurysms
S/S: Cough, dyspnea, dysphagia
• Imminent rupture: Constant/Boring down pain when supine
Dissecting aneurysms
*medical emergency. Needs to be repaired if possible.
Sudden Tearing/ripping pain
SOA, diaphoresis, tachycardia
Nursing management of aneurysms
Prevent Rupture
Monitor: VS, aneurysm size
DVT prevention
Prevention (TJC Core Measure) • Movement: up and moving as much as possible as soon as possible. • SCD’s • Compression Stockings • Anticoagulants
DVT s/s
Signs and Symptoms: most common at knee or below • Redness, spot • Edema • Warm, red skin • Pain
DVT management
If present
• Bed rest
• Avoid massage
• Measure calf/thigh circumference because we want it to get smaller, not bigger.
○ Swelling can cause circulation problems in leg
○ Thrombolytics: risk it will travel to the lungs or somewhere else you don’t want it to be.
DVT patient education
- Avoid prolonged sitting: for every hour, get up and walk.
- Avoid crossing legs: compresses artery behind the knee.
- Progressive walking program
- Avoid smoking
- Elevate feet ~20 min every few hrs daily
- Wear antiembolism stockings as prescribed
lymphedema overview and s/s
Edema in extremities d/t accumulation of lymph
Risk Factors: congenital lymphedema, node dissection
S/S
• Pitting edema
• Firm/thick skin (late)
lymphedema management
• Decrease edema
• Compression garments
Diuretics
Nursing interventions for lymphedema
• Avoid BP cuff/needle sticks on affected limb: could push fluid someplace where it can't drain • Report redness/pain/heat/rash/fever • Elevate affected limb • Skin clean/dry • Education ○ Lifestyle modification ○ Medication
patient care during defibrillation
UNSYNCHRONIZED (untimed) delivery of high voltage shock
• Tx: Lethal dysrhythmias like VF and pulseless VT
Nursing: Never defibrillate a conscious pt with a pulse
• Doesn’t matter when you shock them: unsynchronized
Is it true that we should NEVER shock someone with a pulse, both unsynch and synch? Don’t we stop their heart, then shock?
I addressed some of this in the thread talking about VT from the ECG packet.I guess it is misleading to say “never shock a patient with a pulse”. Really, we care about stablity of the patient (are they perfusing with their rhythm) and we care about timing of the “shock”. My apologies for confusing you with that.
If the patient has a pulse then you’re more likely going to do synchoronized cardioversion because you dont’ want to risk shocking the patient on the T wave (think of theVT patient with a pulse or afib patient; we sometimes do synchronized cardioversions for those patients). If the patient does not have a pulse and is in ventricular fibrillation (where there is NO perfusion happening), then it’s a lethal rhythm. You MUST defibrillate as soon as possible and it won’t be synchronized (because there isn’t anything to synchronize with).
So, it’s not that you’ll NEVER “shock” a patient with a pulse. It’s more that you’ll want to determine when to do a synchronized cardioversion vs defibrillation (which is not synchronized).
Synchronized cardioversion
SYNCHRONIZED (Timed) with QRS, no shock on T wave
• Tx: tachyarrhythmias like afib
Nursing Considerations:
• Consent
• NPO prior
• r/o thrombus
• pt take anticoagulants
• O2
• sedation & pain control provided
• assess VS
• LOC during & post
More considerations:
• Be sure no one touching bed during electrical discharge.
• Cannot shock during the T wave. Synch to the top of the QRS.
○ A-fib: atria are quivering and occasionally toss out a beat. Blood swirls around risking blood clots. Once it does pump, the clot can be pushed through to create pulmonary embolism or stroke.
▪ These patients need an anticoagulant
▪ If medications don’t work, we will check to make sure there are no clots before trying a synchronized cardioversion
Temporary pacemakers
Temporary
• Tx: after open heart surgery
Nursing:
• Wear gloves when handling leads/connecting cables
• Don’t touch pacemaker components on first entering room
• Keep dressings dry
Permanent pacemakers
• Tx: symptomatic bradycardia, 3rd degree blocks, sick sinus syndrome
Nursing
• Device programmed when inserted/checked by HCP
• Educate patient
• Insertion site initial care
• Report s/s infection
• Immobilization of arm until cleared by cardiologist
• Avoid electromagnetic fields (notify airport security)
• Avoid contact sports
• Wear medic alert bracelets
Implantable cardioverter defibrillator (ICD)
May be combined with pacemaker • Tx: lethal dysrhythmias Nursing: • Same as pacemaker • Do not place defib pads on/near generator • Address concerns r/t shock delivery
Clinical Manifestations of Hypertension
- HA
- Vision Changes
- Numbness/tingling in extremities
- SOA
- Fatigue
- Epistaxis: nose bleeds
- May have some shortness of air
Nursing considerations of hypertension
- assess for manifestations
- patient education
- –weight reduction
- –diet changes (DASH and Mediterranean)
- –Sodium reduction/ alcohol reduction
- –regular exercise
- –sugar reduction
- –smoking cessation
- –medications
Hypertensive crisis signs and symptoms
Acute and life threatening: risk of stroke Signs and Symptoms • BP usually > ~ 180/120 • HA • Confusion/change in neuro status • Blurred vision • Tachycardia and tachypnea • Dyspnea
Hypertensive crisis interventions
• Maintain patent airway:
○ Airway problems would come from pulmonary edema
○ Have emergency equipment ready (tubes, suction)
• Administer antihypertensive medications IV:
○ start slowly! Could be on these for hours-days
• Assess for hypotension or fluid volume overload
• Slowly reduce BP (over hours/days)
• Monitor VS and I&O’s
• Bed rest, HOB ~ 45 degrees. Being up and around can increase pressure.
• Keep the head of the bed up to keep ICP down.
• Must have emergency equipment available
Stable Angina
predictable. occurs with activity. Better at rest or with nitroglycerin.
Unstable Angina
unpredictable and doesn’t get better with rest or nitro.
Nursing Management of angina
• Assessment-COLDSPA
• Medication history
• Treat as emergency until determined otherwise
• Correct O2 supply/demand
• Control Comorbidities /Prevent Disease Progression
○ Hypertension
○ Diabetes: blood is sticky. Damage to blood vessels
○ Hyperlipidemia: cholesterol buildup causes atherosclerosis and causes hypertension
▪ Life Style modifications/Reduce Risks of the comorbidities are all very similar
• Patient Education
• Disease process
• Risk Factor Modification/Prevention
• Medications
• Nitroglycerin-Pg 403
Angina lifestyle and medication education
• teach on angina patho and risk factors ○ angina ○ diabetes ○ lifestyle • Medication teach (pg. 403) ○ place under tongue, wait 5 minutes. If the pain doesn't go away, take a second one and call 911. If they're still in pain, take a third. ○ Nitro can cause a headache ○ Nitro makes the BP drop
Myocardial Infarction overview
We can tell with cardiac markers whether this is a risk.
• STEMI: tissue injury happening (fire hat=emergency)
• ST depression: ischemia occurring in the tissue. Injury has not occurred yet.
• Non STEMI: We could have a pt with elevated lab values, with no ST change. Collateral circulation could be a cause.
Myocardial infarction manifestations
• Chest Pain/discomfort • Palpitations • Fatigue • ECG and BP changes • Limb numbness/tingling • SOA/tachypnea • Diaphoresis • Anxiety/restlessness • Dizziness/Lightheadedness • Backpain (women, diabetics, and elderly) • N/V (women, diabetics, and elderly) ○ look in book for differences between manifestations of men and women
MI acute stage interventions: first 10 minutes
○ labs: CBC, BMP, BNP, BUN/creat, PTT, INR, Cardiac enzymes (CPP, Myoglobin, troponin)
○ VS
○ 12 Lead ECG: If it comes back showing ST elevation, its an emergency. ST depression means there is ischemia with no injury yet.
MI treatments in acute setting
• Oxygen (if indicated): Administering oxygen won’t hurt, but it is not always indicated. Keep saturation above 94%
• Aspirin: 325 mg chewed to absorb faster. If all you have are baby aspirin, tell them to chew 4.
• Nitroglycerin (if indicated) or Morphine (if indicated): if the pt has taken nitro and their BP is low, you won’t give morphine
• Start 2 IVs: 18 gauge. One in each Antecubital (elbow bend)
• If a candidate for TPA, they need it within 30 minutes of walking in the ED.
• If not a candidate for TPA, they get PCI
○ consent needed. Explain they might go straight from cath lab to surgery
○ Assess for allergy to dye or shellfish to see if Benadryl is needed before cath lab
• bed rest/semi-fowlers
• IV
Labs for someone with MI-acute setting
○ BNP
○ BMP
○ Triponin
○ Coagulation labs
○ CBC-to look at other factors of the body
○ Hb and Hct
○ BUN/Creat: to make sure they can take contrast dye. If greater than 1, they might have trouble with the contrast dye
Once in cath lab after MI
• Conscious sedation
• Angioplasty or a stint
• CABG: coronary artery bypass graft
• percutaneous
• peripheral entry
○ They’ll cut a vessel from another part of the body: saphenous vein of the leg most likely or mammary vein
○ Valves will be stripped of the valves so it could be used as an artery
Post cath lab after MI
• Straight from OR to ICU
• 1:1 for a while until they’re off the ventilator.
• Looking for hemostatic stability
• Docs might not want systolic BP over 120 at any time. Drips will be ordered ahead of time.
○ that graft is weak and needs time to heal. High BP will push it out of place.
• Fluid volume overload will be a risk
• Pain from surgery
• ICU to telemetry
• Patient education
• identify risk factors that got them there
Eval for reperfusion therapy
Tissue Plasminogen Activator (t-PA)
• If candidate for TPA, door to drug time
Coronary Artery Bypass Graft
Nursing management
• Hemodynamic Stability • Adequate gas exchange • Fluid-volume balance • Pain management • Sternal precautions/Wound care ○ sternum is wired together. We have to help them move. ▪ We put them on sternum precautions • can't drive • can't pull or push • Brace with a pillow during movement ○ Infection control: ▪ hand washing ▪ keep area clean
Cardiac rehab after CABG
• Progressive activity: Phase I of cardiac rehab in the hospital
○ goal is sitting up and dangling within 24 hours. Up for meals within 24 hours. Up and walking as soon as possible.
○ Ambulation is progressive and measured in feet in the hallway
• Cardiac rehab: phase II of cardiac rehab outside the hospital
○ telemetry monitoring during progressive exercise
○ education on diet, medication, and exercise
• Phase III cardiac rehab
○ vitals monitored
○ further education
Discharge after CABG
○ diet plans
○ make sure theres an intent for cardiac rehab
○ meds in addition to the drugs they started getting at the hospital
▪ nitro: teach that they go bad, how to take it, and that it might cause burning under the tongue and headache. May cause drop in BP.
▪ metoprolol-extended release: beta blocker. Teach that it causes fatigue, but it will go away in about 30 days. They can take it at night. Orthostatic hypotension.
▪ lisinopril: ACE inhibitor. If this doesn’t work, they can take an ARB. He needs to record if there’s a dry hacking cough. Must keep BP log
○ Medication reconciliation
○ Education: all must be documented
▪ teach back on lifestyle changes, medications
▪ sternal precautions
▪ when to call doc or 911
Prevention of complications after surgery
- DVT
- anticoags/lovonox
- stockings/SCDs
- leg movement
- Pneumonia
- incentive spirometer: act like it’s a giant straw. suck in as much as they can. Measured how much air is inhaled.
- deep breathing
Fall risk
Patient education after surgery
- Determine what likely got them in that situation
- Smoking Cessation Counseling (TJC Core Measure) Every single person gets smoking cessation education
- Meds (SAAB-TJC Core Measures) Start on the lowest dose. They will be on a:
- Statin or if they can’t handle that, document some other anti-cholesterol medication
- Aspirin: to thin blood
- Ace Inhibitor or ARB: for BP
- Beta Blocker: for BP
- Risk Factors & life style modifications that need to be made
- When to call physician and/or 911
- Psychological factors
Heart failure
Inability of heart to pump effectively. They will think their heart doesn’t work anymore.
TJC Core Measure r/t high readmission
• Discharge Instruction/Education material documented
• Evaluation of ejection fraction (EF) on chart
• Document Medications
Risk factors for heart failure
- Genetics
- Lifestyle Factors: diet, exercise, alcohol or tobacco usage
- Psychological stress
- Low socioeconomic status: less likely to eat healthy foods or exercise regularly
- Complications from disease processes
Clinical manifestations of right sided heart failure
Peripheral Congestion • JVD • Dependent Edema • Ascites • Hepatomegaly • Splenomegaly • Anorexia/Nausea • Weight Gain-occurs with both sided heart failure, but more common with right
Clinical manifestations of left sided heart failure
Pulmonary Congestion Dyspnea/tachypnea Orthopnea/PND Wheezing/crackles Cough with pink, frothy sputum Anxiety Dizziness/confusion Tachycardia
Medical Management
Diagnostic testing for heart failure
- ECG to find distortions
- Echocardiogram
- BNP to know if it’s sending out warning signals
- Pro-BNP
- Measure ejection fraction
Medical management
Lifestyle modification for heart failure
- same as CAD/hypertension/MI
* they’ll have activity limitations, but we want them to be as active as possible
Pharmacologic Treatment for heart failure
• will center around diuretics to get the extra fluid out of the body
• Either strengthen the beat, or decrease the workload of the heart
○ diuretics: track daily weights to make sure the drugs are working. Put the weights on the same spreadsheet as their daily BPs. Have them weigh at the same time every day. More than 3-5 lbs in a day or 7 lbs in a week. If so, it will be due to fluid.
Nonsurgical treatment for heart failure
• Ultrafiltration: IV dose of diuretic that forces the fluid out
Surgical treatment for heart failure
- if heart remodels and stretches electrical pathways, they may need surgical repair
- Cardiac resynchronization
- Pacemaker/defibrillators
- Ventricular access device
- Transplant
Nursing Management for heart failure
- High Fowler’s position
- Oxygen administration
- Rapid assessment
- VS, lung sounds, LOC, perfusion, wt, etc.
- Ask about cough. Dry/wet. Sputum color and character
- IV; prepare to administer medications
- ACE inhibitor/ARB
- diuretics
- I&Os
- Prepare for administration of medications
- Diuretics (furosemide), ACE/ARB, digitalis (Digoxin), etc.)
- Labs:
- ABGs,
- electrolytes, especially potassium
- BNP
- Psychological support
Complications for heart failure
Cardiogenic Shock: Signs and Symptoms • Cerebral hypoxia (restlessness, anxiety) • Hypotension (fatigue/dizziness) • Tachycardia, poor peripheral pulse • Urinary output
s/s of pulmonary edema
- Cyanosis
- Pink, frothy sputum
- Restlessness, anxiety
- Cool, moist skin
- Cyanotic nail beds
- Tachycardia
Wheezing, crackles
management of pulmonary edema
- Priority is oxygenation
- O2 administration
- Rapid assessment
- IV; prepare to administer meds
- Bronchodilator
- Foley as prescribed
Pericardial effusion and cardiac tamponade
Causes: Pericarditis: inflammation get inflammation down to prevent fluid buildup around the heart that would compress it advanced HF, trauma
S/S of pericardial effusion and cardiac tamponade
Fullness in chest CP Dyspnea Muffled heart sounds Distended neck veins Pulsus paradoxus
Nursing management of pericardial effusion and cardiac tamponade
Hemodynamic Monitoring
IVF
Prepare for CXR or Echo
Prepare patient for interventions
MEDICAL management of pericardial effusion and cardiac tamponade
- Pericardiocentesis
- Pericardiotomy
Pericardiocentesis:
needle to draw out fluid around the heart
Pericardiotomy:
cut window of tissue around pericardial sack
PR interval
In this step you should measure the interval from where the P wave begins until the beginning of the QRS complex. Calipers, marked paper or counting small boxes methods can be used to determine PR Intervals. Normally this interval is 0.12 to 0.20 seconds (3 to 5 small boxes) in adults, longer in elderly people. This interval shortens with increased heart rate.
Also evaluate if PR Intervals are constant or varying across the EKG strip. If they vary, determine if the variations are a steady lengthening until the point where an expected QRS does not appear.
QRS complex
In this step, measure the QRS interval from the end of the PR interval to the end of the S wave. Use calipers, marking paper or by counting small boxes. Normally this interval is 0.06 to 0.12 seconds (1.5 to 3 boxes).
QT Interval
It is measured from the beginning of the QRS complex to the end of the T wave. Normally, the QT interval is 0.36 to 0.44 seconds (9-11 boxes). The QT interval will vary with patient gender, age and heart rate. Another guideline is that normal QT Intervals is less than half of the R-R Interval for heart rates below 100 bpm.
ST segment
The ST segment is the line that from the end of the QRS complex to beginning of the T wave. Normally the ST segment is flat relative to the baseline.
Cardiac Arrest and Pulseless electrical activity causes
Causes
Hypoglycemia, hypoxia, hypothermia, hyper/ hypokalemia, hypovolemia
Thrombosis (PE/MI), toxins, trauma, tension pneumothroax, Tamponade
s/s of cardiac arrest and pulselessness
Loss of consciousness No pulse Decreased blood pressure Ineffective/absent respirations Seizures
management for cardiac arrest or pulselessness
CPR
Causes of Valve Disease/Dysfunction
Rheumatic Fever
Infectious Endocarditis
Congenital abnormalities
Other disorders that cause inflammation (Rheumatoid arthritis, systemic lupus erythematosis)
s/s of valve problems
May not be s/s until significant damage CP/palpitations Dyspnea on exertion/orthopnea/Paroxysmal nocturnal dyspnea Lightheaded/syncope Fatigue Anorexia Nausea/Vomiting Murmur (sound depends on type of valve issue, location and severity)
diagnosis of valve problems
Auscultation (Murmur) Echocardiogram Electrocardiogram (ECG) CXR Possible Cardiac Cath
Treatment options for valve problems
No treatment if asymptomatic Treat underlying issue Eradicate infection Treat HF Valve Repair Stenosis Valvuloplasty Commissurotomy Prolapse Leaflet Repair Annuloplasty Chordoplasty Options for Repair/Replacement Open heart surgery Transcatheter Valve Replacement
Valve replacement types
- mechanical
- bioprosthetic
advantages of mechanical valves
durable; long lasting
Disadvantage:
Lifelong anticoagulation
Wouldn’t want for someone in whom anticoagulants are contraindicated.
advantages/disadvantages of bioprosthetic valves
No Anticoagulation, but not as durable and more prone to infection
Nursing management of someone with artificial valves
Post op care same as CABG or PCI
Prevent Complications
Antibiotics as prescribed
