Tuesday, August 26, 2008

- ADVANCED ASSESSMENT

The Formula for Learning Success in Class

- Disorder
- Anatomy
- S/S seen
- What will I, as the nurse, do?
- How will I evaluate my care?

Does this look at all like the Nursing Process? ADPIE

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- ADVANCED/FOCUSED ASSESSMENT

- Managing many
- Prioritize
- Ask
- What was in report?
- What additional information do I need for care?
- Where do I need to look?
- What are the important signs?
- What do I need to do as the nurse?
- Who comes first?

ABC's first!

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- DON'T DIMINISH THE IMPORTANCE

- Full assessment is still needed
- But with the load
- Importance of critical thinking
- Define critical thinking
- Give an example
- Scenarios

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- HOW DO YOU ASSESS EACH SYSTEM?

- Cardiac-equipment used
- Where do you hear the apical pulse?
- What part of the stethoscope allows you hear dull sounds on auscultation?
- Respiratory-where to put stethoscope?
- What do the breath sound mean?
- Where would you hear each sound?
- What about percussion?
- CONSIDER:

- Take a health history - what risks?

- Look at B/P, pulses. +HR/-BP = shock. Add volume back.

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Tuesday, September 2, 2008.

Realizing the Assessment of the Cardiac System, Focusing On Action

Now that we have focused on what the problem is?

- How do we do it and what anatomy do we need to review. What equipment will we
use and what are our cues from our assessment?
- What does the relevent data tell us?
- How do we fit it into our nursing process?

Reviewing how to do a cardiac assessment?

- Pulse
- Assess blood pressure for; equality on right and left arm; pulse pressure; postural
hypotension.
- Inspect neck veins for distension. pressure too high or too low?
- Assess temperature by appropriate method.
- Palpate chest to locate point of maximal impulse of heart.
- Palpate chest to determine presence of heaves of lifts.
- Auscultate heart sounds for:
- Palpate skin for temperature.
- Palpate dependent areas and extremities for edema and determine grade if
applicable. Include inspection of facial edema. feet up?
- Inspect nailbeds for clubbing. hypoxia.
- Inspect and palpate digits for capillary refill.
- Review chart and assess: drugs that effect the cardiovascular system, and
diagnostic tests.

Assessment of the Cardia System with Nursing Implications

- Ask health history. Why?
- Know anatomy and physiology. How does the heart work?
- Use assessment skills. Assessing the cardiac system - hemodynamics. measuring
blood and functions.
- Swan Ganz - hemodynamic monitor - CVP - central venous pressure - fluid
volume - CHF - burn patients (fluids). LVEDP - left ventricular end diastolic
pressure. *level with atrium.
- arterial pressure monitor

Know the Anatomy and Physiology

Heart Beat
- The heartbeat cycle consists of two components: diastole and systole
- explain diastole - LVEDP - CVP - phlebostatic access - *level with atrium.
- explain systole - heart at work - pump blood.
- Systole and diastole continuously alternate as long as the heart continues to beat.

Blood Pressure - Measurement and Implications for Client Care

- Define Blood pressure

- Regulation
- Short Term and Long Term
- Mean Arterial Pressure - Define and delineate
- Mean Measurement - Hemodynamics
- Short Term - Baroreceptors (aorta and carotid)
- Sympathetic (Flight or Flight) and Parasysmpathetic (Calm) Effects
- Shock
- Long Term - Humoral Factors
- Regulation of Na+ and Water.

Teaching Point
- The valsalva maneuver is a simple test of the baroreceptor reflex
- The patient tries to breathe out forcefully against a closed larynx -
"straining" - resulting in an increased intrathoracic pressure.
- This causes decreased venous return, cardiac output and a fall in blood
pressure leading to reduced baroreceptor discharge to the vasomotor centre.
- This then causes peripheral constriction, and an increase in heart rate which
is the normal response.
- This has the effect of maintaining systolic pressure, althought the pulse
pressure is reduced due to vasoconstriction.

Mean Arterial Pressure - As a Regulator of BP

- Mean Arterial Pressure
- Cardiac Output
- System Vascular resistance and
- Central Venous Pressure
- MAP = (CO X SVR) + CVP
- MAP = diastolic + 1/3 of pulse pressure
*SVR = systemic vascular resistance (atherosclerosis)

Pulse Pressure - Affects BP

- Difference between systolic and diastolic pressure.
- Increases when stroke volume (SV = 70+) increases or vascular compliance
decreases.
- Calculation of - pg. 760 text (systolic - diastolic).

Bounding Pulse?
- Pulse is reflective of volume and pressure. high BP.
- How do we have and why do we have a bounding pulse. What makes it
bound? How do you tell?
- fluid volume overload.
- fever.
- heavy exercise

Thready Pulse?
- Dehydration.

Contractility
 - Strength of contraction (automaticity = sense to beat)
- SV X HR = CO
- No direct measure of contractility
- Increase it with catecholamines - Epi, Norepinephrine - SNS
- first line drug (epi, atropine).
- fools heart to beat faster.
- primary concern: HR first. contractility second.
- Decreased contractility
- negative inotropics, acidosis, barbiturates, alcohol, calcium channel & beta
blockers.
- chronotrophs = timing.

Cardiac Output
- stroke volume is determined by three main factors: preload, afterload and
contractility.
- preload: filling (right side)
- afterload: pushing

Hemodynamics
- Defined
- Machines (blood pressure machine)
- What do they tell
- Swan Ganz
- Afterload
- Preload
- CVP - Fluid volume
- Pressures in left side - LVEDP

Preload
- Volume of blood in the right chamber at rest.
- Pressure within the cardiac chamber at diastole
- Also known as right or left ventricular end-diastolic pressure-LVEDP
- Dependent on:
- venous return to the heart
- An increased preload leads to an increased stroke volume.
- Starling's Law: The relationship between ventricular end-diastolic volume
and stroke volume is known as the Starling's Law of the Heart (the more
you stretch it the harder it pumps)
- CVP - Rt., PCWP (pulmonary capillary wedge pressure) - Lt. - Swan Ganz or
CV monitor - good way to measure fluid.
PCWP = pressure in pulmonary artery and contractility (CHF)
- +venous return = +preload, +stroke volume

Teaching Point-Machines vs. Man

- A pulmonary artery catheter can measure pressures in the right heart as it
is floated into position.
- the catheter includes a small balloon which is transiently inflated to wedge it
into a small pulmonary artery.
- the catheter can also be used to measure cardiac output.
- in the absence of a PAC, what physical assessment could you make to
determine cardiac output? (BP and pulse).

Afterload
 - Peripheral resistance against which the left ventricular must pump to
evacuate it's content. (atherosclerosis, arteriosclerosis)
- Resistance ventricular ejection
- Involves size of ventricles, wall tension and arterial pressure - systemic
circulation.
- Increase usually means increased workload.
- Lessens it with antihypertensives (diuretics, etc.), vasodilators
(nitroglycerin, dilantin).
*heart attack = not enough blood to the heart.

Cardiac Output
- Cardiac Output
- Formula: CO = SV X HR
- 4-8 liters/min.
- Factors affecting
- Preload
- Afterload
- Contractility
- Perfusion!
- digoxin toxicity (decreases HR)
- CO affects toxicity.

Cardiac Conduction
- Action potential
- causes heart to beat.
- specialized muscle (automaticity)
- depolarization
- contraction
- repolarization
- gathering back action potential
- the ECG (electrocardiogram)
*today's lecture on basic ECG is all you need for 1st exam.
*never shock asystole. you CPR asystole

ECG
- P-wave: SA node fires depolarization of atria (can be longer or shorter)
- QRS: depolarization of atria through ventricles
- T-wave: repolarization of ventricles
- U-wave: could represent delay in ventricles repolarization.
- isoelectric line: baseline
- ventricular tachycardia: shock!

The P-Wave
- 0.04x5 = 0.2x5 = 1 second
- should be one in front of each QRS
- represents atrial depolarization
- measures normally rounded to 0.11 seconds or less in duration (can fit 2-3
0.04 in each 0.11)
- for a normal ECG reading the P wave should be:
- in front of each QRS
- regular meaning same space between each in distance
- and all look alike (no irregular-oadd shaped p-waves)
PR interval
- represents the amount of time taken for electrical impulse to travel from the
SA node the ventricular musculature
- measured from the beginning of the p-wave to the beginning of the QRS
complex
- PR interval has a duration of usually (normally) 0.12-0.20 seconds. (3-5
blocks)

QRS complex
- represents depolarization of ventricles
- QRS complex has a normal duration of 0.05-0.12 (2-3 blocks)
- CO affected, action potential decreased = measured by swan ganz.

ST segment
- represents the earliest phase of ventricular repolarization
- depicted from the end of the S fo the QRS complex to the beginning of the
T-wave.
- is normally isoelectric or slightly elevated or depressed (0.5-1mm)

*know for exam: sinus rhythm, sinus tachycardia, sinus bradycardia

Rate
- look at a 6-second strip.
- to determine the ventricular rate, count the number of complete QRS
complexes within a 6-second time period then multiply by 10. This is your
rate. This can be used for regular and irregular rhythms.

Rhythmn - Regular or Irregular

- Rhythm is used to indicate the site of origin in an electrical impulse, e.g.
sinus rhythm, junctional rhythm.
- To determine if the rhythm is regular or irregular:
1. ventricular: to determine if the ventricular rhythm is regular or
irregular measures the distance between two consecutive R-R intervals
and compare taht distance with the R-R intervals. If the ventricular
rhythm is irregular, the R-R intervals will be the same.
2. atrial:

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Fluids and Electrolytes: Part of the Ongoing Assessment

Fluids and Electrolytes, Acids & Bases: Their importance Hyper, Hypo, Iso,
Related to the Client

What is an electrolyte?
- solutes found in body fluids ICF and ECF.
- electrolytes include:
- needed for life process, conduct electricity across cell membranes
- maintain osmolality of body fluid compartments (what is osmolality).
- regulate acids and bases.
- sources:
- foods, fluids, medications, iv solutions, hyperalimentation
ECF-ICF
- ECF: this includes intravascular and insterstitial fluids.
- ICF electrolytes are found in the intracellular space and are not measurable.
They can only be measured by their ECF values.
- electrolytes are regulated by the kidneys and the endocrine system.

Osmolality
the movement of water between the ICF and ECF compartments is largely
controlled by each compartment's osmolality, because most cell membranes
are highly permeable to water.
- ECF-blood osmolality (290mOsm/kg water)
- IV solutions
- isotonic: 240-340
- hypertonic: above 340
- hypotonic: below 240
- dextrose, sodium fluids, and electrolyte replacement fluids.
- Lactated Ringers

IV Fluid Replacement
- Isotonic: same osmolar concentration as plasma.
- NS
- LR = low electrolytes, burn patients

Hypotonic Fluids
- Lower osmolar concentration than plasma
- Solutions is more dilute
- More water than particles
- Infuse this solution then fluid shifts from ECF to the intracellular space
- Swelling, water logging, cell eventually ruptures
- Examples: 5% dextrose, D5W, 0.45NS, 0.33% sodium chloride

Hypertonic Fluids
- More solutes than water
- Higher concentration of particles in solution
- Fluid shifts out of the cell causing cellular crenation (shrinkage)
- FVE = out of the cells into the ECF.
- 3% NaCl, protein solution, hyperalimentation solutions of 10%, 50%
- albumin = volume expander (+ oncotic pressure)
- separate tubing due to viscocity.

Assessing the Status

- Look at the Primary Problem.
- What electrolytes are relevent?
- Think of the body systems.
- What solutions are running?
- What do lab tests reveal?

Electrolyte Deficiencies
- Do you know the S&S of each electrolytes?
- What happens if you have too much? Too little?
- Chvostek and Trousseau - Hypocalcemia!
- Chvostek: cheek spasms when touched.
- Trosseau: BP cuff to systolic. Hand forms a duck-shape.
 - Other electrolyte hyper, hypo
- How about diet teaching?
- NEVER PUSH IV POTASSIUM!

Questions?

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Define Delegation
- The reassigning of responsibility for the performance of a job to another...
- Can be direct or indirect

Benefits to Effective Delegation

- Rapid change in healthcare environment
- Nursing shortage
- Health Care Reform
- Increasing Need
- Demographic Trends

Barriers to Effective Delegation

- Some nurses have difficulty in delegatin:
- Reasons may be:
- Experience Issues
- Licensure Issues
- Quality of Care Issues
- Assigning Work to Others

Safe Delegation
- Informed Judgement
- Education and experience of assignee
- Individual competence and qualification
- Legal definitions
- Orientation to task

- Be well acquainted with state's nurse practice act

- Acquainted with institution policies for delegation

Accepting Rules of Delegation

- Delegated activity involves the:
- right task
- right circumstances
- right person
- right communication
- right feedback - did i tell them what they did wrong AND right?

Red Flags for Delegation

- Lack of experience relevant to task assigned
- Inability to effectively accept or understand direction
- Fairness
- Compatibility - right person. right patient.
- Maintain Responsibility

What Can Be Delegated?

- frequently occur
- are considered technical by nature
- are considered standard and unchanging
- have predictable results and
- have minimal potential for risks

Nursing Responsibilities That Can Not Be Delegated

- Assessment
- Planning
- Educating
- Evaluating

*Assessments can not be delegated to LPN.

*Education can not be delegated to LPN.

Florida Nurse Practice Act

- Specifically provides for the delegations of nursing activities
- Nurse must know the competencies of the delegates
- Consequences if nurse knows the delegate lacks skill and knowledge
- Disciplinary action if fail to supervise

Some Principles To Remember

RN
- RN's can take care of unstable patients. (VTAC, post-op, etc.)
- Can do teaching needs.
- Various procedures. (IV start, push)
- Admissions
- Unpredictable conditions

LPN
- Dependent on RN to assess, analyze and establish a plan of care-shared liability for
harm; stable patients.

CNA/NT
- ADL's, I&O, VS, nothing invasive or sterile.

Problems After Delegation

- Develop a plan for corrective action when assistive personnel do not perform a task
as delegated.

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Tuesday, September 9, 2008

PQRST: What do we do with it?

Review Lead Placement: Pg. 844-845

Remember: Time Intervals

- Small Box = 0.04
- Large Box = 5 small boxes = 5 x 0.04 = 0.20 seconds
- PR Interval = 0.12-0.20 seconds
- QRS = 0.08 seconds
- Rate = 3 segment marks

Dysrhythmias
- Hypoxia
- Ischemia (vascular remodelization)
- Sympathetic Stimulation (Fight Or Flight) and Parasympathetic (Relax)
- Drugs
- Electrolyte Disturbances
- Bradycardia
- will eventually lead to asystole
- Stretch (contractility/hypertrophy)

website: "http://www.skillstat.com/ECG_Sim_demo.html"
sinus bradycardia: R/T vagus stimulation
sinus tachycardia: narrow QRS. -> supraventricular tachycardia (above ventricles).
- differentiates from A-TACH in that A-TACH has no P-wave.
- adenosine IV push.
- ablasion: burning part of muscle to introduce vascular remodelization.

Sinus Tachycardia
- particulars
- rate
- rhythm
- why?
- caffeine
- drugs
- stress
- hypovolemia
- treat with?
- diagonoses?

Atrial Rhythm Disturbances

- When electrical impulses originate in the atria, atrial activation (P-wave, flutter
waves, etc.) always precedes the QRS complex
- premature beats (PACs).
- supraventricular tachycardia
- atrial fibrillation
- AV junctioinal rhythm distrurbances
- ventricular rhythm distruvances
*atrial depolarization
*will be on heparin due to coagulation and clot precautions. coumadin for life.
*edema, venous congestion, JVD.
*do not elevate feet due to CHF.
*A-Flutter (shark/saw teeth) and A-Fib have no P-waves. Has electrical impulse other
than the P-wave. Possible stroke. (-) CO and eventual organ failure. thin blood
(heparin).

Atrial Activity
- Since atrial events are primary and ventricular response is secondary, atrial rates
equal or exceed ventricular rates during atrial arrhythmias.
- QRS source is generally similar to that of sinus beats since the impulses travel over
the same route, the AV nodes and His bundles branch-perkinje fibers.
- chronotropics (beta-blockers -> slows HR/parasympathetic)
- calcium channel blockers (rate)

PAC = Premature Atrial Complex

- It is not an entire rhythm. It is a single beat.
- Arises before the expected snius beats.
- Premature atrial beats generally depolarize.
- Premature beats may be produced by the atria, AV junction or the ventricles.
- Identified by site of original, ex. atrial, junctions or ventricles
- If irritability is close to SA note the atrial P-wave will look similar to the P-wave that
are initiated by the SA node.
- The P-wave of a PAC can look flat, notched, pointed, partly negative (downward
deflection).
- Identify the underlying rhythm first!
- Ectopic beats.
- So it could be a sinus bradycardia with 46beats/min with PAC.
*A-Flutter/A-Fib = clots/stroke/heparin.
*patient complains of chest pain = ECG strip!
*pathological Q-wave = previous MI/stays with you.
*women/diabetics silent MIs
*close T-wave and P-wave = (-) contractility
*lidocaine/digoxin
*shock/defib: vtac/vfib (unconscious)
*cardiovert: conscious (cardiovert)

Supraventricular Tachycardias Includes atrial flutter and atrial fibrillation

- Another atrial beat.
- Supra-above the ventricles in the atria.
- Includes atrial fibrillation (an atrial dysrhythmias)
- 150-250 beats/minute.
- QRS: normal duration unless bundle brach block is present.
- P waves: When P-waves are identifiable, the P-wave morphology is often different
from sinus P-wave morphology, and the P-wave may precedie, coincide with or follow
the QRS complex.

Atrial Fibrillation (FIB=lie, no P-wave)

- Atrial fibrillation may result from multiple areas of reentry within the atria or from
multiple ectopic foci.
- Atrial fibrillation may be associated with sick sinus syndrom, hypoxia, increased
atrial pressure, pericarditis and many other conditions.
- The atrial electrical activity is very rapid (approximate 400-700 beats/min) but
each electrical impulse results in the depolarization of only a small islet of atrial
myocardium rather than the whole atrium. (P-wave absence. Not visible)
- As a result, ther is no contraction of the atria as a whole. Since there is no uniform
atrial depolarization, there is no P-wave. The chaotic electrical activity produces
deflection on the ECG, referred to as fibrillatory wave.
*PUMPKIN DRY!
*heart may continue functioning without brain stimulation via ventilation.
*NO atrial kick.
*venous thrombus risk high after A-Fib.
Atrial Fibrillation Summary
- Total disorganization of electrical activity.
- 300-600 atrial chaotic, irregular-ventricular rate 50-180
- Thrombi may form - coumadin, heparin
- Cause: heart disease, can lead to thrombus and stroke, (-) CO.
- Rhythm: P-wave - not discernible, see tiny, erratic spikes on EKG - these are not
pacer spikes.
- PR-Interval - not measurable
- QRS-complex = normal
- Atrial fibrillation leads to ineffective atrial transport and the loss of the atrial
contribution to cardiac output.
- Treatment: cardioversion, digoxin, calcium channel blockers, amiodarone, will be
put on coumadin prophalactically.
*Acute Coronary Syndrome/MI: fatigue

Ventricular Concerns
- PVC = premature ventricular contraction
- (+) 3-5 = VTAC
- lidocaine drip
- monitor respiratory status
- Ventricular tachycardia
- sustained PVC's (+5)
- shockable rhythm
- tombstone
- hemodynamic compromise
- PVC-landing on a T-wave (R-on-T).
- no blood!
- PUMPKIN DRY! :]
- SHOCK! NOT CARDIOVERT!
- PRECORDIAL THUMP (APPLIED AT PMI!)
- Ventricular fibrillation
- SHOCK!
- no blood! NO CO!
- Asystole (DO NOT STOCK! BEGIN CPR!)
- CPR: COMPRESSIONS ACT AS HEART CONTRACTIONS
- ET-Tube: must be administered twice dosage strength for absorption.
*BRASLOW TAPE: color coded tape apply next to baby's length will determine drawer
and dose.

PVCs
- Premature ventricular contractions (PVCs), also known as "extrasystole", are
"extra" heartbeats.
- They arise from an irritable area in the heart's lower pumping chambers (the
ventricles)
- PVCs interrupt the normal rhythm and cause an irregular beat.
- This is often felt as a "missed beat" or a "flip-flop" in the chest
- PVCs are often harmless, but when they occur very often or repetitively, they can
lead to more serious rhythm disturbances.
- Ventricular bigeminy is one example of a PVC. In it, a regular hearbeat is coupled
with an irrugular beat.
-PVCs are characterized by premature and bizarrely shaped QRS complexes usually
wider than 120msec on with the width of the ECG.
*bigeminy: IRREGULAR PVC with every 2 REGULAR.
*trigeminy: IRREGULAR PVC with every 3 REGULAR.

Heart Blocks
- Classified as SinoAtrial exit blocks
- Cause they occur in the atrial part of the conduction system
- Many reasons for blocks
- Many types of blocks
- Pacemakers
- Cause
*ALWAYS HAS TO DO WITH P-WAVE! There, not there, etc.
*1st degree, 2nd degree, 3rd degree (WORST).
*pacemaker required with heartblock

Recall
- The heart's "natural" pacemaker is called the sinoatrial (SA) node or sinus node.

1st Degree Heart Block

- 1st degree heart block or , 1st degree AV block, is when the electrical impulse
moves through the AV node more slowly than normal. elongated or prolonged PR-
Interval.
- people can live with 1st degree heart block. watch & wait.
- cause: vagal stimulation, MI, drugs, etc.
- Normal time for the impulse to get from the atria to the ventricals (PR-Interval)
should be less than about 0.2 seconds.
*Digoxin may cause this!
*check pulses, medications (digoxin) and call physician.

What is 2nd-degree heart block

- Some signals from the atria don't reach the ventricles. This causes "dropped
beats."
Type 1 (Mobitz Type 1, or Wenckebach's AV block)
- electrical impulses are delayed more and more with each heartbeat until a
beat is skipped. This condition is not too serious but somtimes causes dizziness
and/or other symptoms. (PR-Interval gaps extend longer and longer until beat
skipped = going, going, gone syndrome!).
*calcium channel blockers, digoxin, betablockers may cause!
*caused by enhanced vagal tone
Type 2
- This is less common than type 1.
- PR-Interval does not change (there, there, gone syndrome!)

TYPE 2 MAY LEAD TO TYPE 3!

3rd Degree Heart Block (COMPLETE HEART BLOCK)

- Means taht the heart's electrical signal does not pass from the upper to the lower
chambers.
- When this occurs, an independent pacemakers in the lower chambers takes over.
- The ventricles can contract and pump blood, but at a slower rate than that of the
atrial pacemaker.
- These impulses are called functional or ventricular scope beats. They're usually
very slow and can't generate the signals needed to maintain full functioning of the
heart muscle.
*needs pacemaker
*hemodynamic compromise
*DO NOT SHOCK! SIMILAR TO ASYSTOLE! CARDIOVERT WILL NOT HELP!
*ensure atropine at hand (bradycardia also indicated).

PEA (Pg. 856)

- Pulseless Electrical Activity.
- Activity on ECG with no pulse.
- No mechanical activity.
- NO HEARTBEAT!
- volume problem, metabolic acidosis, hypokalemia, etc.
Treatment:
- CPR
- bicarbonate
- (+) volume

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When Discussing Delegation

- You must also discuss supervision and assignment (Pg. 123)
- Supervision defined - "the provision of guidance or direction, evaluation, and
follow up by the licensed nurse for accomplishments of a nursing task
assigned to an unlicensed assitive personnnel."

- Assignment
- Defined-Defined
- Designating nursing activities to be performed by an individual
consistent with his/her licensed scope of practice.

- Coordinating Assignments (Pg. 127)

- The Transfer
- Note the delegator when assigning a task retains...
Scenario:
- When a nurse is told to care for a group of patients, by the
nurse manager. This is assignment.
- In this example, the nurse manager is accountable only for
making the assignment and selecting who will be responsible
for caring for the patient.
- The staff nurse is accountable and responsible for actually
providing care or ensuring that it is provided.
- In turn the staff nurse can only delegate work to
others, such as UAPs but can not assign work.
- In comparison, delegation is the partial transfer of
authority and responsible regarding care activities, while
accountability for completion and outcomes remains with
the delegator.
*REVIEW SECTION 68-9 IN NPA!

RELATE TO YOUR NURSE PRACTICE ACT

- Think critically:
- What questions should the registered nurse ask when learning about their
state laws pertaining to delegation?
 - Does it permit delegation?
- How is the delegation defined?
- Does the nurse practice act specify certain tasks for delegation or list
any that can not be delegated?
- Does it authorize delegation based on certain circumstances?
- What does supervision mean in the state?
- Does the nurse practice act indicate the consequences of
inappropriate deletation?
- Does it provide guidelines for reducing delegation tasks?
*REVIEW PG. 98 - DELEGATION TO UNLICENSED ASSISTIVE PERSONNEL!

*"RNCEU.COM" - 30 CEUs for $30

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Tuesday, September 16, 2008

So looking at these concepts

- If we look at the patient whether it be in one dysrhythmias, or another how will the
failure of the electrical system of the heart affect the patient?
- How will the overall concept of perfusion be affected by:
- 1. A change in the anatomy of the heart? MI, tissue damage?
- 2. A change in the rhythmic conduction system of the heart?
- 3. A change in the complete filling of the heart?

*afib = heparin, coumadin at home

What is a pacemaker?
- A pacemaker is a small, battery-operated device.
- "Artificial pacemaker"
- Some are permanent (internal) and some are temporary (external).
- A defective natural pacemaker or blocked pathway.
- The anatomical, built-in pacemakers provide what's called the "intrinsic" rhythm.

How does the electronic pacemaeker work?

- The pacemaker does two things: it senses the patient's own rhythm using a
"sensing circuit" and it sends out electrical signals using an "output circuit".
- If the patient's intrinsic rhythm becomes too slow or goes away completely, the
electronic pacemaker senses that, and starts sending out signals along the wires
leading from the control box to the heart muscle.
- The signals, if they're "capturing" properly, provide a regular electrical stimulus,
making the heart contract at a rate fast enough to maintain the patient's blood
pressure.
*all patients should carry a pacemaker card including manufacturer, contact
information and type.

Temporary
- Lead placement
- Epicardial
- Most seen post-op heart
- Transvenous
 - Threaded through large vessels
- Emerge through skin
- Transcutaneous
- Emergency situation
- Electrode patches
- Pg. 878 for larger version

Permanent
- Those totally in the body
- Permanent pacemaker is inserted under the skin just above the left nipple and is
used in patients whose electrical activity of the heart is ineffective, intermittent or
weak.
- Refer to picture page 877, 860 text
- Table 35-10
- Table 35-11
- Table 36-27

Normal Pacer Spikes

Single Wire Pacers
Failure To Sense

Failure To Capture (Catch)

- The basic idea is that the pacing box sends an impulse to the heart at the right
time, but the heart doesn't respond. The box is sensing that the intrinsic heart rate is
too slow, but the output signal isn't making the myocardium respond.
- You see this on a rhythm strip when there are clear pacing spikes coming from the
box - at the right time after either an intrinsic beat or a paced one - but they're not
followed by a QRS response.
Two pacing functions
- The first spike is generating atrial kick, and the second is kicking the ventricles: two
spikes, two wires.

How much electricy does the pacemaker use to actually pace the heart?
- The output of the pacemakers is measured in two ways:
- "signal amplitude" and "pulse width".
Paced beats generated by a ventricular wire look like PVCs.

What does "asynchronous" mean and what does "demand" mean?

S/S of malfunctioning pacemaker include:

- dizziness
- syncope
- change in mental status
- difficulty breathing
- prolonged weakness or fatigue
- decreased heart rate
- irregular heart rhythm
- decreased blood pressure
- increased respiratory rate

Nursing Diagnosis
- Cardiac Output Decreased
- Impaired Tissue Perfusion
- Gas Exchange Impaired
- Anxiety

Nursing Interventions
- ABC's.
- Assess for capture, sensing, pacing.
- Observe for changes in vital signs.
- Assess for chest pain (tissue damage).
- Assess heart and lung sounds.
- Teach patients to carry pacemaker identifications cards.

What is an AICD?
- AICD stands for Automatic, Implantable, Cardioverter-Defibrillator. This is a
variation on the idea of a pacemaker - the device has a sensing circuit and an output
circuit, but instead of acting as a pacer, it spends its time waiting for the onset of
some nasty tachyarrhythmia, like VT, or SVT - which it then atries to shock the
patient out of it. Apparently they will also sometimes try to override-pace a patient
out of a rapid rhythm.

-----------------------------------------------------------------------------------------

MYOCARDIAL INFARCTION

Definitions
- Ischemia
- Injury
- Infarct-death of injured myocardial cells - can happen within minutes to hours
*give O2 to relax heart = (-)O2 -> (+)HR

Types of Infarct
- Anterior
- Inferior
- Lateral
- Posterior
- Septal
- Combo of above
- Transmural
*knowing type and where will allow recognition of treatment (type of medication).

Show Me A Picture
- certain leads will depict area of heart

Anterior Wall Infarct (MI)

- signifies LAD occlusion
- May involve the RCA or circumflex occlusion
- ECG changes in V1 and V4
- if it extends to the lateral wall shows in V5, V6, lead 1 and AVL.
*assess patient pain scale and appearance (relaxed? anxiety?)

ECG Changes Post Myocardial Infarction

"http://www.nlm.nih.gove/medlineplus/imagepages/18030.htm"

Angina Versus Myocardial Infarction

- Angina-cellular injury can be reversed
- MI-cellular damage not reversible. (remodeled)
*Assess -> IV -> Draw Blood -> Morphine -> Aspirin -> Nitro ->
Oxygen(MANO/MONA) *Nitroglycerin (SL) = 1 every 5 minutes for total of 5.
*Angina = pain goes away from nitro via vasodilation.
*MI = pain is sustained. Adminsiter thrombolytic (2 hour window). CT -> R/O
pregnancy, stroke, multiple abdominal surgeries, hemorrhage.

The Patient Picture

- Symptomology
- Patient Reports
- What you can see
- The nervous system
- Sympathetic - catecholamine
- Diaphoresis - cold sweats
- Nausea (vaso-vagal response)

MI and Vital Signs

- BP and HR can be initially elevated but
- BP may drop later due to decreased CO.
- Crackles (pulmonary edema)
- Urine (decreased urine output do to decreased CO)
- Constipation (decreased motility/peristalsis)

More Complications of MI
- arrhthmias (VFIB most common)
- CHF
- Cardiogenic Shock
- PE
- Dresslers (Review)
- Pericarditis

Diagnostics
- H&P
- Risk Factors
- ECG-STEMI greater than 1mm or more in 2 leads.
- No definite diagnostic test -> look at many.

Cardiac Markers-Diagnostic
Page 805/806
- Proteins
- Cardiac serum enzymes - CK (rises 2nd)
- Troponin (rises 1st)
- Myoglobin
- BNP
*review chart 34-13.

Diagnostics
- Echocardiogram
- TEE (Trans Esophageal Echocardiogram)
- Thallium Scan (adenosine-thallium stress test)
*patient NPO.
Some Measurements
- Ejection Fraction - fraction of blood pumped out of a ventricle with each
heartbeat
- End Diastolic Volume - volume of blood within a ventricle immediately before
contraction.
- volume of blood left in a ventricle at the end of a contraction is known as End
Systolic Volume

EF Explained
- Fraction of blood pumped out of a ventricle with each heart beat.
- Applies to both L and R ventricles.

Coronary Circulation and Collateral Circulation

"http://www.jdaross.cwc.net/heart6.htm"

- Collateral Defense Mechanism

- Blood bypasses normal routes to supply the heart.
- Refer to page 801, figure 33-5 for further discussion (page 786).

Treatment
- thrombolytics (clot busters)
- cardiac cath
- PTCA (angioplasty)
- "http://www.ptca.org/videos.html"
- "http://www.hgcardio.com/ptca.htm"
- CABG (coronary artery bypass graft)
-
"http://www.sts.org/sections/patientinformation/adultcardiacsurgery/cabg/index.htm
l"
- athlerectomy (removal of plaque/artery)

Nursing Diagnoses
- perfusion
- pain
- cardiac output
- anxiety
- infection (lack of perfusion, tissue necrosis)
- activity intolerance
- knowledge deficit
- ineffective coping
- diet
- family
*5 small meals after MI.

Nursing Goals
- increase oxygenation to the myocardium
- monitor oxygenation (O2 sat, ABGs)
- decrease anxiety and workloud - NTG (nitroglycerin)/bed rest
- thrombolytics - watch the window
- prepare for PTCA or CABG

More Goals
- Decrease the workload of the heart
- Continuous ECG monitoring
- VS
- inotropic drugs - increase contractility
- beta blockers - block the action of endogenous catecholamines (epinephrine,
adrenaline) and norepinephrine (noraderenaline) in particular, on B-adrenergic
receptors, part of the sympathetic nervous system which mediates the fight or flight
response.
- decrease afterload.
- patient educations - stool softeners, diet

Knowledge of Drugs
- Important terms to know
- Beta Blockers
- Calcium Channel Blockers
- Chronotropic
- Inotropic (digoxin)
- Dromotropic
- Ejection Fraction

Treatment/Medications
- Heparin (aPTT?)
- Nitroglycerin (assess relief chest pain?)
- Morphine Sulfate (pain scale)
- Positive Inotropic (CO = CVP/swan ganz)
- Beta-Blockers (-) HR / (-) BP
- Calcium Channel Blockers (-) HR -> relax / (-) BP

Nurse Also
- pain relief-pain = lactic acid
- MONA - First Line
- In the hospital, oxygen, aspirin, nitroglycerin and analgesia (usually
morphine, hence the popular mnemonic (MONA), are administered as sson as
possible.
- IV-KVO - only 1? MORE THAN 1!
- enzymes and ECG with pain

Patient and Family Knowledge

- exercise and diet
- smoking cessation
- decrease alcohol intake
- meds
- stress reduction
- medical follow-up
- disease process and risk factors

Assess
- prevent common complications
- assess for dysrhythmias
- assess for increased damage-how? pain returns/increases, ECG change
- administer antidysrhtymics (lidocaine)
- assess for CHG and cardiogenic shock
- intra aortic balloon pump (IABP)
IABP
- beneficial effects
- reduces cardiac work by decreasing afterload.
- increases coronary blood flow
- basic mechanism
- placed in the thoracic aorta
- balloon inflated during diastole, thus increasing aortic pressure diastole and
increases coronary blood flow
- balloon deflated prior to and during early left ventricular ejection thus
reducing aortic pressure and thus afterload
*TEMPORARY HELP AT HOSPITAL. DOES NOT GO HOME WITH. HELPS AFTERLOAD.

-----------------------------------------------------------------------------------------

CHF (CONGESTIVE HEART FAILURE)

- Congestive Heart Failure
- The pump is not efficient any longer

Opening Statement
- LEFT OR RIGHT SIDE
- typically, heart failure begins with the left side - specifically the left ventricle, your
heart's main pumping chamber.

Systolic Or Diastolic
- Can be systolic heart failure (when the left ventricle loses its ability to contract
vigorously) or diastolic heart failure (when the left ventricle loses its ability to relax
or fill fully) or a combination of both.
- Right sides usually caused by left sided.

CHF - pathophysiologic process

- Heart is unable to pump enough blood to meet the metabolic needs of the body's
tissue.
- Characterized by: left ventricular failure
- reduced exercise tolerance
- diminished quality of life
- shortened life expectancy

Etiology
- Caused by the interference with normal mechanism that regulates CO.
- preload - venous return
- afterload-chamber must pump against this force to eject blood during
systole
- myocardial contractility
- heart rate
- metabolic rates

Heart Failure
- NOT A DISEASE. IT IS A DISORDER!
- Not able to pump enough blood to the body's other organs. Causes:
- narrowed arteries
- past MI (scar tissue)
- high blood pressure
- heart valve disease
 - etc.

Compensatory
- dilation
- hypertrophy
- sympathetic response (+) HR
- neurohormonal (ADH, renin-angiotensin)

Types of CHF

-----------------------------------------------------------------------------------------

Tuesday, September 23, 2008

Heart Disease
- Not a disease.
- Most commonly caused by MI. Leads to cardiogenic shock.
- Not able to pump enough blood to the body's other organs. Causes:
- Narrowed arteries.
- Past MI (scar tissue).
- High blood pressure.
- Heart valve disease.
- Primary disease of the heart muscle itself.
- Congenital heart defects.
- Infection of the heart valves and/or heart muscle itself.

Pulmonary Edema a manifestationi of Acute Heart Failure.

- Life threatening situation.
- Alveoli = Gas exchange.
- Lung alveoli become filled with serous or serosanguineous fluid.
- Most common factor of Pulmonary Edema is LV failure caused by CAD.

Compensatory
- dilate.
- hypertrophy.
- sympathetic response.
- neurohormonal. (renin/angiotensin response = retain sodium/water)

Types of CHF
- Left Sided-Forward Failure-Pulmonary Edema
- What does patient look like?
- Pink/Frothy
- Right Sided-Backward Failure-Peripheral Edema
- What does patient look like?
- Sacral/Dependent edema.
- Tell me what patient looks like. S/S. What would be important to report to
physician?
*The most common signs of congestive heart failure are swollen legs or ankles or
difficulty breathing. Another symptom is weight gain when fluid builds up.

*LEFT SIDE CAN CAUSE RIGHT SIDE

Left Side Failure
- Failure-blood back up=Left sided failure
- When this occurs, the lungs become congested with fluid (called pulmonary
edema)
- Causing difficulty breathing, fluid in lungs and interfering with the
movement of oxygen from the lungs into the bloodstrea, causing fatigue
- What does this client look like?
- What would you do for this client?
- Name one nursing diagnosis?
- Name one medication that might help this client? lasix.
*renal dose dopamine.
*vasopressors?

Right Side Failure

- When an abnormality or condition affects the flow of blood through the right
ventricle.
- pressure in the blood vessels increases and fluid is forced from the blood
vessels into body tissues.
- This "right-sided" heart failure casuses swelling (edema), usually in the feet
and legs and sometimes the abdomen.
- Anasarca = weeping edema.

To Diagnose?
- A&P
- ABGs, CXRs, XR shows enlarged.
- LABS (BNP)
- hemodynamic monitoring
- 12-lead ECG
- echocardiogram-key technique
- nuclear studies
- cardiac catheterization
- dye retains in system = induce fluids.
- dye retention = 6-12 hours. (24 hours recommended)
- hold glucophage prior to cardiac catheterization.

Medical Management
1. oxygen therapy - N/C, mask, intubation.
2. pharmacology
- diuretics, nitrates (vasodilators), inotropic (contractility)
3. fluid retention
4. dietary restrictions
- 2gm, Na diet.

Medication Modalities
- ACE inhibitors and vasodilators expand blood vessels and decrease resistance.
- Beta blockers can improve how well the heart's left lower chamber (left ventricle)
pumps.
- Digitalis increases the pumping action of the heart.
- Diuretics.
- Valve replacement
- Mitral valve prolapse
- regurgitation
- stenosis (hardening)
- Transplant.

Nursing Interventions
- Cardiac & respiratory assessment (diminished heart sounds, murmurs, S3,
crackles)
- Monitor EKG
- Monitor hemodynamic parameters
- Monitor lab values (dilutional, low H&H)
- Maintain nutritional status (high protein unless renal failure)
*cacexic.
- Provide bed rest / semi-fowlers position
- Monitor I&O's closely.
- Daily weights
- Assure patient safety
- Prevent complications
- Provide psychological support
- Patient teaching / discharge planning.

Nursing Diagnosis
- Alteration in CO R/T impaired ventricular contractility
- Impaired gas exchange R/T ventricular perfusion inequality secondary to pulmonary
vascular congestion.
- Activity intolerance R/T decreased CO.

Focus On Cardiogenic Shock: Concepts of Shock of the Heart (CHAPTER 67)

(Page 804)
Focus on definition of cardiogenic shock (PUMP FAILURE)
- Cardiogenic shock is sustained hypotension with inadequate tissue perfusion in
spite of adequate left ventricular filling pressure.
- This is manifested with organ dysfunction such as oliguria, confusion, cool
extremities and lactic acidosis (muscle breakdown).
- Strict definitions are:
- a systolic BP of <90mmHg for greater than 30 minutes
- a cardiac index of <2.2/min/m2 in the presence of a pulmonary wedge
pressure of >15mmHg.
*MI = MOST COMMON CAUSE!
*V-TACH = CPR, shock!

-----------------------------------------------------------------------------------------

Endocarditis
- Vegetation Around The Valves / Sub-Acute / Acute Stages

ANATOMY & PHYSIOLOGY

- Recall the layers of the heart.
- What are the functions of the valves in the heart?
- Why do we care about the valves when talking about endocarditis?
- Review

Ineffective Endocarditis
- Defined as bacterial or fungal infection of the endocardium that includes the valves-
infection of the heart chambers or valves.
- heparin protocol = prevent clot embolus
 - causes: cardiac catheter, EP study, rheumatic fever (pericarditis), IV drug
use (infected needles, cardiac surgeries, pulmonary artery catheter,
abdominal surgery, immunosuppression, infections, dental procedures (deep
cleaning), pacemakers.

Infectious Cardiovascular Disorders

- Infectious cardiac disorders can alter the structure and functions of the heart.
- The endocardium is contiguous with the valves of the heart.
- Etiology: viruses, vacteria, or inflammation.
- Acute and sub-acute.

How Does Ineffective Endocarditis Happen?

- What are some causes?
- endothelial lining?
- vegetation?

Pathophysiology
- Turbulent blood flow resulting from valvular diseases.
- Invasive procedures.
- Dental procedures.
- Causes vegetation on the valves.

Clinical Manifestations
- splinter hemorrhages
- What causes splinter hemorrhages in ineffective endocarditis?
- blood vessel damage / rupture = from valvular failure (+) pressure.
- microembolism.

Predisposing Factors
- What kind of clients are at risk for this?
- Name some interventions.
- Teach client about what?
- antibiotics, control fever.
- bedrest.
- cultures.
- anti-platelets, anti-coagulants.
- meticulous aseptic technique
- foley catheter insertion.
- V/S, cardiac monitoring
- TED hose.
- sequentials.
- hygiene, dental, etc.

Diagnostics for Ineffective Endocarditis

- Name and explain them.
- ECHO.
- EKG (1st/2nd degree heart block).
- Cardiac Catheter.
- Health history.
- Labs / CBC / Culture
- CRP
- BNP
* STENOSIS AND REGURGITATION CAN CAUSE ENDOCARDITIS. MOBILIZATION OF
INFECTOUS VEGETATION.

Nursing Diagnoses R/T Endocarditis

- Risk for decreased CO R/T mechinical changes in heart valves.
- Risk for altered cardiopulmonary, cerebral, and peripheral perfusion R/T
thromboembolus.
- Risk for Injury
- Anxiety.
- Safety.

PERICARDITIS: Peri-Around, Card-Heart, Itis-Inflammation

Etiology
Common cause is unknown, Non-infectious-MI, trauma, uremia, radiation,
autoimmune-dressler's syndrome (late pericarditis), lupus, rheumatic disease, TB.

Pathophysiology of Pericarditis (Page 871/872)

- Layers are inflamed and roughened.
- May be dry or effusive
- Influx of neutrophils, increasing peripheral vascularity.
- leads to fibrin deposition on visceral pericardium.

Assessing Pericarditis
- Pericardial Pain
- Dyspnea
- Pericardial Friction Rub
- Pericardial Effusion
- Cardiac tamponade
- fluid build-up causes compression of the heart. (-) cardiac output.

Pathophysiology: Side-By-Side
Acute
- increased cap permeability R/T inflammatory conditions.
- leakage of plasma proteins into pericardial sac.
- can result in scar tissue formation.
Chronic
- same basic process as with acute form with addition of:
- scar tissue contracts and decreases cardiac filling.
- cardiac output decrease
- Right atrium unable to expand to receive venous blood so clinical SS
of Right sided heart failure.
*HEPARIN, COUMADIN AT HOME!

DIAGNOSIS: CXRAY, MRI, WBC, ECHO, ECG, ENZYMES?

Managed By:
- antibiotics
- anti-inflammatories
- corticosteroids
- pericardiocentesis (volume expanders, inotropes) (Page 873)

-----------------------------------------------------------------------------------------
Cardiomyopathy: Primary - Secondary
- A group of diseases that affect structur of heart.
THINK: perfusion, CO, pain.
- A diagnosis is made by clinical manifestations.

Causes
- Primary = unknown cause (idiopathic)
- Secondary = secondary to another disease process (3-types)
- dilated (congestive)
- hypertropic
- restrictive

Dilated
- most common.
- cardiomegaly with ventricle dilation and atrial enlargement
- walls of ventricle do not hypertrophy due to rapid cell destruction.
- often follows infectious myocarditis
- S/S of CHF.
- thrombus = heparin.

Diagnose And Treat

- CXRAY, ECHO, cardiac catheterization
- treatment to decrease preload and afterload
- antidysrhythmics
- anticoagulants
- heart transplant
- high mortality within one year after transplant.

Hypertropic (BIG HEART)

- massive ventricular hypertrophy.
- rapid, forceful contraction of the left ventricle.
- impaired relaxation.
- obstruction to aortic outflow.
- thickened septum and LV wall.

Signs And Symptoms

- dyspnea
- fatigue
- perfusion
- angina
- dysrhythmias
- PVC

Diagnose And Treat

- Diagnose with echocardiogram
- Treat with:
- Beta and CCB
- AICD
- Ventriculomyotomy and myectomy
- Surgical treatment of the hypertrophied section. Involves incision and
resection of some of the hypertrophied muscle.

Restrictive (Page 889)

- Rare
- Cardiac muscle stiffness
- Impairs diastolic volume and stretch
- Etiology: UNKNOWN!

SIGNS & SYMPTOMS

angina, orthopnea, syncope, palpitations, fatigue, dysnpea, activity intolerance, JVD,
dependent, peripheral edema, ascites, hepatomegaly.

DIAGNOSIS
- ECHO, CXRAY

TREAT WITH:
- restrictive cardiomyopathy
- treat with?
- no treatment exists.
- can treat symptoms of CHF.
- treat the dysrhythmias
- heart transplant?

-----------------------------------------------------------------------------------------

Valvular Disorders: Incompetent Valves (Page 878)

Defined By:
- The valve involved.
- Stenosis or regurgitatioin
- Which is which?
- Defined
- Involves most often mitral and aortic valves.

Caused By:
- History of rheumatic fever - scarring and deformity of all layers of valve.
- Endocarditis - vegetation on leaflets, fusion and calcification of chordae tendonae
- Review anatomy.
- Beta hemolytic strep.
- Upper respiratory infections.
*NORMAL = PRESSURES EQUAL ON BOTH SIDES OF VALVES. STENOSIS =
PRESSURES IMPEDES FORWARD FLOW = REGURGITATION.

A MURMUR
- Murmurs defined:
- Series of vibratory sounds caused by turbulent blood flow through a stenotic
valve or as a result of incompetent valve.
- Produces regurgitant flow form a high pressure chamber to a low pressure
chamber.
- These sounds are heard during the systole, diastole, or both phases of the
cardiac cycle.

Mitral Stenosis
- Rheumatic Heart Disease
- Congenital
- Systemic Lupus
 - Pathophysiology - thickening and scarring

SIGNS & SYMPTOMS

dyspnea, palpitations, hemoptysis, crackles, S3 sounds, chest pain (perfusion), AFIB
(incomplete conduction system)

MANIFESTATIONS
emboli
- heparin
- TED hose
- aPTT
- SCD
seizures
- padded siderails
- dilantin
- dilantin levels
CVA
- clot busters
- blood thinners
- O2
- stool softeners
- decrease ICP

MITRAL VALVE REGURGITATIONS

Pathophysiology:
- backward flow from Left ventricle to Left atrium.
- pulmonary edema.
- assess: weakness, fatigue, dyspnea, S3 and loud murmer.
CAUSE:
mitral valve prolapse, damage to chordae tendonae, ischemic papillary dysfunction,
RHEUMATIC FEVER.

MITRAL VALVE PROLAPSE

- displacement of leaflet toward lt. atrium during systole
- causes: unknown
- most common valve disorder in U.S.

ASSESSING MITRAL PROLAPSE

- wide variety from asymptomatic to severe.
- murmer which increases through systole.
- dysrhythmias.
- chest pain-possible.
- recommend prior prophylactic antibiotic treatment for dental or surgical cases.

AORTIC STENOSIS
- congenital
- rheumatic fever
- pathophysiology:
- obstructs blood flow from left ventricle to aorta.
- left ventricle hypertrophy eventually leads to decreased contractility.
- decreased cardiac output.
- pulmonary hypertension.
ASSESSING AORTIC STENOSIS
- angina
- syncope
- heart failure
- murmur

SUMMARY
- Heart Valve Incompetence
- stenosis
- regurgitation
- prolapse
- end results of severe defects - CHF

*TREATMENT: O2, inotropics, valve replacement, safety, antibiotics.

COLLABORATIVE THERAPY FOR VALVE INCOMPETENCES

- prophylactic antibiotics
- digitalis (inotropic)
- diuretics
- sodium restrictions
- anticoagulants
- antidysrhythmics
- nitrates and beta blockers

-----------------------------------------------------------------------------------------

Tuesday, September 30, 2008

AORTIC ANEURYSMS: OUTPOUCHINGS OR DILATIONS (page 896)

Types: abdominal, cerebral, etc.

- Most common: abdominal.

- can involve many structures of the aorta.

- most found in abdomen.
- larger aneurysm the greater the risk of rupture.
- exact cause not known.
- could be atherosclerosis.
- plague causes degenerative changes in middle layer of wall.
- loss of elasticity, weakening, eventual dilation of aorta.
- AAA = hypovolemic shock.

1. true - wall of artery forms the aneurysm. at least 1 layer intact.

2. false - not an aneurysm but disruption of all layers.

DX: pain, CO, tissue perfusion, pain R/T tissue necrosis, risk for injury.

- manifestations: pain similar to MI, lateral BP variance.

Asymptomatic to varied:
- deep diffuse chest pain.
- dysphagia depending on location.
 - decreased venous drainage with superior vena cava pressure.
- AAA most often asymptomatic - this is dangerous, no warning, death?
- pulsatile mass in periumbilical area.
- or on physical exam for other problems.

peritoneal bleeding towards liver = gray-turner's sign and flank ecchymosis.

rupture:
- retroperitoneal - gray turners sign.
- flank ecchymosis.

rupture:
- abdominal-survival
- hypovolemic shock tachycardia.
- abdominal tenderness.
- treat shock and repair bleeding site.
- grafting.

what tests?
diagnostic tests: XRAY, CT (most accurate: size, location), MRI (location),
angiography.

nursing care for those tests?

XRAY: client consent.
CT: IV line 20 gauge, allergies.
angiography: invasive, allergies.

what diagnoses?
nursing DX: anxiety.

what about collaborative care?

- after the hospital what?
- low sodium diet.
- protein.
- physical therapy.
- meds: heparin, coumadin.
- lab tests: aPTT, PT/INR.

what to do?
12-lead, monitor, obtain patent IV, good bp, assess pain, CVP.

-----------------------------------------------------------------------------------------

DIC: Disseminated Intravascular Coagulopathy: Confusion In Coagulation.

(page 710)

what happens?
- DIC occurs when the antagonis systems of coagulation and anticoagulation are not
balanced.

body realizes bleeding. starts coagulation. too much clotting. factors are used up.
continued bleeding.
basically a state of increased propensity for clot formation...

triggered by:
- a variety of stimuli related to such diverse disorders.
- as sepsis, endothelial cell damage (heat stroke, shock), obstetrical
complications (abruptio placenta, anmiotic fluid embolism) and neoplasias
(tumor).

pathophysiology of DIC
- normally the response to tissue damage is a regulated, contained explosion of
thrombin at the injured site.
- this results in coagulation of blood in the surface of damaged microvessels
and stops blood loss.

BUT WITH DIC...

- unregulated thrombin explosion.
- widespread microvascular thrombosis produces.
- in an attempt to maintain vascular patency, excess plasmin is...
- this generation of free thrombin and plasmin within the circulation leads to the
clinical feature of DIC...

clinical manifestations
- no well defined sequence.
- bleeding should be questioned.
- weakness.
- malaise.
- fever (inflammatory response).
- bleeding and thrombotic manifestations
- refer to page 710 and review.
- spleen issues.
- microemboli?

diagnose by:
- while many laboratory tests are available to detect excess thrombin and plasmin
generation, only a few simple tests are required to confirm the diagnosis.
- thrombocytopenia due...
- production of platelets by the bone marrow is increased.
- tests of the capacity to generate thrombin may show prolonged thrombin
times (PT) and activated partial thromboplastin times (aPTT) because of
consumptive deficiency of coagulation factors.
- however, PT and aPTT are prolonged in only 70% and 50& of patients
respectively.
- all these tests reflect excess thrombin generation.

collaborative care
- quick care, quick diagnosis.
- resolve the underlying issues.
- what is the suitable means is up for research.
- treat the primary diseases, the causative factors.

medications
- heparin
- blood products
 - platelets
- cryoprecipitate
- amicar-inhibits fibrinolysis
- chronic DIC - no oral anticoagulants = no coumadin.

nursing of DIC
- look for complications that may lead to DIC in all clients.
- DIC is secondary to underlying.
- look for outward signs of bleeding.
*ADMINISTER BLOOD PRODUCTS CORRECTLY!

-----------------------------------------------------------------------------------------

SHOCK: shock, SIRS, and MODS - they are interrelated but first shock.

clinical presentation, patient care, treatment and drug therapy.

*shock always involves hypovolemia!

shock syndrome.
- shocks is condition in which the cardiovascular system to perfuse tissues directly.
- types: an impaired cardiac pump, circulatory system, and/or volume can lead to
compromised blood flow to tissues.
- inadequate tissue perfusion can result in:
- generalized cellular hypoxia (starvation).
- widespread impairment of cellular metabolism.
- tissue damage - organ failure.
- death.

*cardiogenic shock, neurogenic shock.

pathophysiology of shock syndrome.

- impaired tissue perfusion occurs when an imbalance develops between cellular
oxygen supply and cellular oxygen demand.
- all types of shock eventually result in impaired tissue perfusion & the development
of acute circulatory failure or shock syndrome.

diagnosis of shock.
MAP < 60
- average pressure during a cardiac cycle. normal 70-90mmHg.
- clinical s/s of hypoperfusion of vital organs
- capillary refill.
- 5P's
- urine output.
- vomiting large amounts of food hours after eating.
- hypoactive bowel sounds.
- digoxin toxicity.
- dizziness.

pathophysiology systemic level

- net results of cellular shock:
- systemic lactic acidosis (lack of circulatory oxygen).
- decreased myocardial contractility.
 - decreased vascular tone.
- decreased blood pressure, preload and cardiac output.
- table 67-2 page 1774 and hymodynamics: let's review the table.
(neurogenic shock = stimuli to regulate hemodynamics is disrupted).

shock syndromes
- hypovolemic shock
- blood VOLUME problem
- cardiogenic shock
- blood PUMP problem
- distributive shock - referred to as maldistributive (text)
(septic, anaphylactic, neurogenic)
- blood VESSEL problem

hypovolemic shock
- loss of circulating volume "empty tank"
decrease tissue perfusion > general shock response.
- etiology:
- internal or external fluid loss
- intracellular and extracellular compartments
- most common causes:
- hemorrhage
- dehydration

hypovolemic shock : external loss of fluid

fluid loss: dehydration
- nausea, vomiting, diarrhea, massive diuresis, extensive burns.

- blood loss:
- trauma: blunt and penetrating
- blood you see
- blood you don't see.

hypovolemic shock: internal fluid loss

- loss of intravascular integrity (vasogenic shock)
- increased capillary membrane permeability
- decreased colloidal osmotic pressure (third spacing)

hypovolemic shock presentation depending on volume loss amount

s/s vary depending on severity of fluid loss:
- 15% (750ml) = compensatory mechanism maintains CO.
- 15-30% (750-1500ml) = hypoxemia, decreased BP & UOP.
- 30-40% (1500-2000ml) = impaired compensation & profound shock along with
severe acidosis.
- 40-50% = refractory stage: loss of volume = death.

pathophysiology of hypovolemic shock

- decreased intravascular volume leads to...
- decreased venous return (preload, RAP) leads to...
- decreased ventricular filling (preload, PAWP) leads to...
- decreased stroke volume (HR, preload & afterload) leads to...
- decreased CO leads to (compensatory mechanisms)...
- inadequate tissue perfusion!
clinical presentations hypovolemic shock
- tachycardia and tachypnea.
- weak, thready pulses.
- hypotension.
- skin cool & clammy.
- mental status change.
- decreased urine output: dark & concentrated. (lack of dilution)

initial management: hypovolemic shock

management goal: restore circulating volume, tissue perfusion, & correct
cause
- early recognition - do not delay on BP (30% fluid loss).
- control hemorrhage.
- restore circulating volume.
- optimize O2 delivery.
- vasoconstrictor if BP still low after volume loading.

more types of shock

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Tuesday, October 7, 2008

hypovolemic shock: hemodynamics
changes correlate with volume loss
- low CO
- decreased RAP (preload)
- decreased PAD, PAWP (swan ganz)
- increased SVR (afterload)
- low volume = vasoconstriction to sustain BP.

anaphylactic shock
- may lead to DIC.

clinical presentation: hypovolemic shock

- tachycardia and tachypnea.
- weak, thready pulses.
- hypotension.
- skin cool & clammy.
- mental status changes. (cardinal sign of hypoxemia)
- decreased urinary output: dark & concentrated.

*infuse large bore IV fluids!

initial management: hypovolemic shock

management goal: restore circulating volume, tissue perfusion & correct cause.
- early recognition - do not rely on BP (30% fluid loss).
- control hemorrhage.
- restore circulating volume. (plasma expanders = albumin. check H&H for blood
volume.)
- optimize oxygen delivery.
- vasoconstrictor if BP still low after volume loading.

*foley catheter.
*pain due to poor oxygenation and tissue ischemia.

vasogenic / distributive shock

- etiologies
- septic shock (most common).
- anaphylactic shock.
- neurogenic shock. (spinal injury = communication between brain and body
inhibited).

maldistributive shock - still a volume problem BUT...

- inadequate perfusion of tissues through maldistribution of blood flow.
- intravascular volume is maldistributed because of alterations in blood vessels.
- cardiac pump & blood volume are normal but blood is not reaching the tissues.

*blood clots.
*ascites = albumin, dialysis.

anaphylactic shock
- a type of maldistributive shock that results from widespread systemic allergic
reaction to an antigen.
- this hypersensitive reaction is LIFE THREATENING.

*atropine, epinephrine = adrenergic, increases HR and vasodilator.

clinical presentation: anaphylactic shock

- almost immediate response to inciting antigen.

- cutaneous manifestations.
- urticaria (hives), erythema, pruritis, angioedema (shock = jugular veins).
- respiratory compromise.
- stridor (crow-like sound, common in asthma and children), wheezing,
bronchorrhea (excessive bronchial secretions), respiratory distress.
- circulatory collapse.
- tachycardia, vasodilation, hypotension.

anaphylactic response
- vasodilation.
- increased vascular permeability.
- bronchoconstriction.
- increased mucus production.
- increased inflammatory mediators.
- recruitment to sites of antigen interaction.

management anaphylactic shock

- early recognition, treat aggressively.
- airway support.
- iv epinephrine (open airways).
- open IV wide open.
- antihistamines, diphenhydramine 50mg IV.
- corticosteroids.
- immediate withdrawal of antigen if possible (blood, insect, snake, etc.).
- prevention.
- judicious crystalloid adminsitration - page 1786, table 65-8)
- isotonic and hypertonic.
- albumin - all types of shock except cardiogenic and neurogenic shock.
- vasopressors to maintain organ perfusion.
- positive inotropes.
- dobutamine?
- patient education.
- prevention.

pathophysiology of neurogenic shock

- disruption of sympathetic nervous system.
- loss of sympathetic tone.
- venous and arterial vasodilation.
- decreased venous return.
- decreased stroke volume.
- decreased cardiac output.
- decreased cellular oxygen supply.
- impaired tissue perfusion.
- impaired cellular metabolism.
*no increases with neurogenic shock.

explanation
- neurogenic shock causes disruption of blood flow because of the damage to the 5th
thoracic vertebrae or above causing massive vasodilation = (-) BP/CO.
- you have blood but it is not where it should be and cannot get there.
*medulla oblongata near brain stem (cervical vertebrae) = controls
breathing.

assessment, diagnosis and management of neurogenic shock (page 1789,

table 67-10)
patient assessment
- hypotension
- bradycardia (due to interruption of impulse)
- hypothermia
- warm, dry skin
- RAP (-)
- PAWP (-)
- CO (-)
- flaccid paralysis below level of the spinal lesion

MEDICAL MANAGEMENT: goals of therapy are to trat or remove the cause &
prevent cardiovascular instability & promote optimal tissue perfusion.

*feet first, first time = diving.

management neurogenic shock

- alpha agonist to augment tone if perfusion still adequate.
- dopamine at alpha doses (>10mcg/kg per minute)
- ephedrine (12.5-25mg IV every 3-4 hours)
- treat bradycardia with atropine 0.5-1mg doses to maximum 3mg.
- may need transcutaneous or transvenous pacing temporarily.
sepsis - related to shock (page 1802)
- systemic inflammatory response to a documented or suspected infection.
- in as many as 10-30% of patients with sepsis, the causative agent is not identified.
- septic shock is the presence of sepsis with hypotension despite fluid resuscitation
along with the presence of tissue perfusion abnormalities.
- parasites, fungi and viruses can also lead to the development of sepsis and septic
shock.

*sepsis -> endothelial damage -> mods -> DIC

sepsis - systemic inflammatory response (SIRS) to INFECTION manifested by two or

> of following:
- temp > 38 or <36 centigrade
- HR > 90
- RR > 20 or PaCO2 < 32
- WBC > 12,000/cu mm or > 10% bands (immature WBC)
*SED rate? c-reactive protein?

septic shock
sepsis with:
- hypotension (SBP < 90 or > 40 reduction from baseline) and...
- tissue perfusion abnormalities invastion of the body by microorganisms & failure of
body's defense mechanism.

risk factors associated with septic shock

- age
- malnutrition
- general debilitation
- use of invasive catheters
- traumatic wounds
- drug therapy

clinical presentatioin septic shock

two phases:
- "warm" shock - early phase
- hyperdynamic response, vasodilation.
- "cold" shock - late phase
- hypodynamic response
- decompensated state

pathophysiology of septic shock

- initiated by gram-negative (most common) or gram-positive bacteria, fungi, or
viruses.
- cell walls of organisms contain endotoxins.
- endotoxins release inflammatory mediators (systemic inflammatory response)
causes...
- vasodilation & increase capillary permeability leads to...
- shock due to alteration in peripheral circulation & massive dilation.

nursing diagnoses
- altered tissue perfusion.
- impaired C/O
- anxiety
- infection
- decreased fluid
- thermoregulation

clinical manifestations - septic shock

early-hyperdynamic state-compensation
- massive vasodilation.
- pink, warm, fluished skin.
- increased HR = full bounding pulse.
- tachypnea.
- decreased SVR.
- increased CO & CI.
- SVO2 will be abnormally high.
- crackles.

clinical manifestations
late-hypodynamic state-decompensation
- vasoconstriction.
- skin is pale & cool.
- significant tachycardia.
- decreased BP.
- change in LOC.
- increased SVR.
- decreased CO.
- decreased UOP.
- metabolic & respiratory acidosis with hypoxemia.

collaborative management - septic shock.

- prevention.
- find & kill the source of the infection.
- fluid resuscitation.
- vasoconstrictors.
- inotropic drugs = contractility -> CO -> perfusion.
- maximize O2 delivery support.
- nutritional support.
- comfort & emotional support.

sequelae of septic shock

- the effects of the bacteria's endotoxins can continue even after the bacteria is
dead.

-----------------------------------------------------------------------------------------

compensatory mechanisms: sympathetic nervous system (SNS) - adrenal

response.
- SNS -> hormonal: renin-angiotensin system (RAAS)
- decreased renal perfusion.
- released renin > angiotensin I
- angiotensin II > potent vasoconstriction &
- releases aldosterone adrenal cortex
- sodium & water retention
SNS - hormonal: antidiuretic hormone
- osmoreceptors in hypothalamus stimulated
- ADH released by posterior pituitary gland
- vasopressor effect to increase BP
- acts on renal tubules to retain water.

in summary, treatment of shock

- identify the patient at high risk for shock.
- control or eliminate the cause.
- implement measures to enhance tissue perfusion.
- correct acid base imbalance.
- treat cardiac dysrhythmias.

vasodilation: ANP, BNP, nitric oxide

reflections
- what have you seen?
- experiences
- other

-----------------------------------------------------------------------------------------

multiple organ dysfunction syndrome (MODS) (page 1794, 1796 table 67-
11)
- presence of altered organ function in an acutely ill patient such that homeostasis
cannot be maintained without intervention.

- PERRLA
- urinary system
- >30cc urine q1h
- skin
- dry and intact
- cardiac output
- 4-6L/minute

MODS defined
- SIRS can progress to MODS.
- multiple organ dysfunction syndrome.
- failure of more than one organ in an acutely ill client.

pathophysiology of MODS
- at a local site of injury - balance between mediators (DIC).
- sepsis-pro-inflammatory state starts.
- body launches anti-inflammatory to control pro-inflammatory.
- when the balance ceases the sequelae start
- reduced circulating volume - massive vasodilation.
- reduced oxygenation and tissue perfusion - state of hypotension.

systems to show dysfunction by SIRS and MODS

- respiratory first to show.
- cardiac shows myocardial depression.
- neurologic - mental status changes with SIRS and MODS.
- renal failure.
- compensatory mechanisms enhanced.
- GI - early shunt blood away - causing less perfusion resulting in possible ischemic
injury. (paralytic ileus).
- metabolic exchanges - glycogen, amino acids converted.

mortality
- mortality increases with increase in number of SIRS symptoms and in severity of
the disease process.

the goal is to prevent

- prognosis poor.
- mortality increases the more organs affected.
- prevent progression of SIRS to MODS.
- vigilant assessment and ongoing monitoring.

know clinical manifestations - think nursing diagnoses

- altered cerebral function
- fluid volume deficit.
- safety.
- liver dysfunction - caused by a hyper metabolic state - inflammatory response
- risk for injury.
- anasarca - what is this?
- albumin.
- impaired renal function.

nursing interventions
- assess all systems.
- ventilator support.
- patent airway.
- cardiovascular and renal status - monitor (swan ganz, H&H)
- fluid and medication administration - name some meds - name some fluids.
- fluids
- N/S
- LR
- prevent further sepsis.
- aseptic technique.
- no aspiration.
- labs.
- teaching.

so what do i do as a nurse, critically think this through...

- if it is an infection then...
- if fever is present then...
- what tests will this patient have done...
- if an H and H what do the resutls mean...
- if the patient needs an antibiotic think...
- if the patient has oliguria what are my intervention?
- if the patient is receiving antibiotics then what?

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Tuesday, October 14, 2008
Acute Respiratory Failure (ARF)
- Failure to exchange oxygen with carbon dioxide in a normal respiratory cycle.

rhonchi
wheezes
crackles
bronchovesicular

terms to explain - basic anatomy

total lung capacity
vital capacity (500mL) - total volume exchanged with each inspiration AND
expiration cycle
tidal volume
residual volume
expiratory reserve volume
inspiratory reserve volume
functional residual capacity
inspiratory capacity
anatomical dead volume

clinical states
- those that interfere with adequate oxygen transfer result in hypoxemia - give
oxygen
- those that result in insufficient CO2 removal result in hypercapnia.
- normal blood gases? review normals on your own.
- CO2, PaCO2, PaCO2, SaO2.

define - ARF
- when client is unable to maintain ventilation and gas exchange at rest.
- PO2 less than 50 and/or PaCO2 greater than 50.
- pH less than 7.3 (acid)
- acute dyspnea
- exception - COPD
- high risk

two categories of ARF

- type 1 - hypoxemic RF
- oxygen failure
- low PaO2 (normal 80-100) + normal PaCO2
- type 2 - hypercapnic RF
- ventilation failure
- high PaCO2 (normal 35-45) + low PaO2
*CO2 in tidal indicator

mismatch
- ventilation/perfusion - (V/Q) mismatch
- abnormal ratio of CO to ventilation
- there is a blood flow to areas of decreased or absent ventilation.
- pneumonia, pneumothorax, atelectasis.
- there is ventilation to areas of decreased or absent blood flow - P.E.
hypoxemic respiratory failure
- oxygen failure
- V/Q mismatch
- shunting - anatomic and intrapulmonary
- diffusion limitations
- alveolar hypoventilation (cystic fibrosis)

hypercapnic respiratory failure

- or also called ventilatory failure
- ventilation failure - is inadequate to remove CO2.
- imbalance between ventilatory supply and demand.
- in normal respiratory system the supply exceeds the demand.
- however when ventilatory demand exceeds supply PaCO2 no longer
sustained...and hypercapnia occurs.
- many different causes.
- decreased dead space.
- ventilation supply vs. demand.
- tissue oxygen needs.
- diagnosis. (ABGs)

*Multiple Sclerosis = "the great crippler of young adults!"

remember
- PaO2 and PaCO2 determine the definition of respiratory failure.
- the major threat of respiratory failure is the inability of the lungs to meet the O2
demand of the tissues.

manifested by:
- over minutes or hours.
- decrease ini PaO2 - sudden or a rapid increase in PaCO2 implies a serious
condition.
- gradual changes compensation can occur.

look for:
- understand them.
- tachy and mild hypertension - early
- rapid shallow breaths (hyperventilation) can be inadequate resulting in non-
removal of CO2.

look at: consequences

- hypoxemia - how do we treat?
- O2 in blood is less than normal...
- how to treat?
- hypoxia is the PaO2 fallen enough to cause signs and symptoms of
inadequate oxygenation.

collaborative care
- oxygen therapy
- respiratory therapy
- managing secretions
- ventilation

drug therapy
- bronchodilators - how do you give? what are some types? (alupent / albuterol)
- anti-inflammatories - how would you know they work?
- (corticosteroids: atrovent / solumedrol) wait 2-5 minutes
- weight gain, high sugar, immunosuppression, drug compatibility.
*DO NOT ABRUPTLY STOP.
- diuretics - LASIX (works on LAST SIX INCHES of LOOP OF HENLE.
- antibiotics
- sedatives - increases O2 supply, decreases O2 demand.

-----------------------------------------------------------------------------------------

Acute Respiratory Distress Syndrome

ARDS - acute respiratory distress R/T insult

defined
- sudden.
- progressive.
- capillary membrane damaged.
- results in the alveoli filling with fluid...no gas exchange.
- remember the inflammatory response.
- resulting in no oxygen perfusion.

alveoli fill
- when the alveoli fill with fluid.
- no gas exchange.
- despite oxygen - no gas exchange.
- hallmark sign

it is an emergency

ventilation-perfusion studies
- know that the predominant pathogenesis of hypoxemia in ARDS is related to
intrapulmonary shunts.
- recall and review the term VQ scan.
- recall and review the term intrapulmonary shunts.

pathophysiology (page 1813-1814)

- 3 phases:
- injury or exudative phase.
- reparative or proliferative phase.
- fibrotic phase.

*major cause of death in ARDS patients is MODS.

treatment
- preventive measures
- treat the underlying cause
- adequate oxygentation-primary goal correct hypoxia
- mechanical ventilation
- fluid balance
- positioning-debatable

medications
- diuretics
- anti-inflamatory
- bronchodilators
- epinephrine
- theophylline (bronchodilates)
- propofol (diprovan) = ramsey scale (matching dosage with BP)
- ketamine = tranquilizer
- TOF (train-of-four) = page 1766 / 1766.

prioritize
- what is the most important intervention for this client? oxygentation.
- what medications might you see?
- what patient care will be important?
- what can you tell the family in their language?
- how do you tell the family what you want to tell them. how is communication
important in this disease?

critical thinking
in a client with ARDS, what is the common early clinical manifestations than a nurse
caring for the client will observe?
1. dyspnea and tachypnea.
2. cyanosis and apprehention.
3. hyptension and tachycardia.
4. respiratory distress and frothy sputum.

-----------------------------------------------------------------------------------------

pulmonary embolus

embolus
- an undissolved mass that travels in the bloodstream - occlusion of blood vessel.
- PE can be venous thromboemboli, air, fat or catheter emboli.
- PE - an obstruction of one or more pulmonary arteries.
- originated in venous system or right side of heart.

thrombophlebitis
three factors- virchow's triad
1. stasis of venous flow
2. damage of endothelium (DIC?)
3. hypercoagulability of blood

pathophysiology
- RBCs, WBCs, platelets and fibrin adhere to form a thrombus.
- collect at valve cusps of veins.
- occlude or moved with blood flow.
- other contributing factors?

other types of emboli

- air
- fat
- catheter emboli

thromboemboli
- small emboli
- large emboli
- multiple
- "wasted ventilatioin"
- deadspace - result of lack of perfusion of ventilated alveoli
- hypocarbia
- hypocapnia

results in:
- increase in pulmonary vascular resistance.
- increase in PAP pressures.
- pulmonary hypertension.
- right ventricular failure without left failure. (cor pulmonale)

resolved by:
- absorption and fibrosis.
- intrinsic fibrinolytic system.
- thrombolytics (streptokinase / tPa)

diagnostic studies:
- V/Q scan - 2 components
1. perfusion scan - pulmonary circulation.
2. ventilation scan - distribution of gas through the lung.
- ABGs
- pulmonary angiography.

nursing management
- prevention - sequentials, activity, etc.
- treatment - anticoagulants, clot lysis.
- surgery - pulmonary embolectomy.
- intracaval "umbrella" or "filter" - greenfield filter.

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Tuesday, October 21, 2008

acute and chronic renal failure: nursing management of the client with
impaired renal function.

3 types of acute renal failure (page 1198):

pre-renal
intra-renal
post-renal

arterial-venous shunt (a/v shunt)

asses for function: presence of bruit (auscultate) and thrill (palpate)

terms:
1. nephron
2. GFR
3. acute/chronic
4. dialysis
5. CRRT (continuous renal replacement therapy)
- patient goes beyond dialysis.
- patient cardiac function unable to tolerate dialysis
6. NSAIDS
8. BUN
9. creatinine (muscle metabolism)

drugs to learn:
lasix
potassium chloride
sodium bicarb
epoiten (epogen)
k-exelate (potassium excreted via stool)

periteal dialysis: peritoneum used as a filter.

question: is a patient with hemodialysis worst than peritoneal dialysis? yes.

anatomy and physiology

- function unit is nephron. the nephron has a glomerulus, bowman's capsule and
tubular system.
- tubular system has proximal convoluted tubule, loop of henle and distal
convoluted tubule.

the urinary system

- the urinary system consists of two kidneys that filter the blood, two ureters, a
urinary bladder and a urethra to convey waste substances to the outside.
- the kidney is a reddish brown, bean-shaped organ 12 centimeters long; it is
enclosed in a tough, fibrous capsule.
- the kidneys are positioned retroperitoneally as either side of the vertebral column
between teh twelfthe thoracic and third lumbar vertebrae, with the left kidney
slightly higher than the right.

FIND OUT WHERE LIVER IS! 2 POINTS ON EXAM! :]

liver failure = predominant with diabetes!

diabetes (hyperglycemia) affects perfusion to kidneys.

functions to:
- the kidneys function to regulate the volume, composition, and pH of body fluids
and remove metabolic wastes from the blood in the process.
- the kidneys also help control the rate of red blood cell formation by secreting
erythropoietin (procrit, epogen), and regulate blood pressure by secreting renin.

function of the urinary system:

1. excretion of metabolic waste and foreign chemicals from blood.
- urea
- creatinine
- uric acid
 - uremic frost (amonia on skin = turns into frost in atmospheric contact).
- skin care.
2. maintenance of water-salt
3. maintenance of acid-base balance
4. secretion of hormones
- antidiuretic hormone (ADH) = retains urine!
- aldosterone

5. help activate vitamin D precursors in skin promoting calcium reabsorption from

the digestive tract.

urine formation
- glomerular filtration rate-fluid and solutes.
- tubular reabsorption.
- tubular secretion.

GFR: constant < 60 = chronic kidney disease.

role of ADH (antiduretic hormone)

- ADH is secreted to increase water reabsorption.
- osmoreceptors in the hypothalamus of the brain.
- this stimulates the pituitary to increase the secretion of ADH into the blood.
- ADH is transported everywhere throughout the body in the blood.
- ADH causes these parts of the nephron to become more permeable to water.
- extra water is now reabsorbed into the blood reduction its concentration back to
normal.
- the loss of extra water from the nephron reduces the volume but increases the
concentration of the urine.

mechanism of kidneys
recall: renin-angiotensin mechanism
- how does it vasoconstrict?
- how does it increase plasma volume?
- how does ADH control water reabsorption?

renal failure terms

- acute = rapid onset
- chronic = insidious onset
- azotemia: accumulation of nitrogenous waste products - (+) BUN and creatinine.
- uremia-azotemia progresses to signs and symptoms
- ATN: acute tubular necrosis (intra-renal)

impaired of kidney function

- results when the kidneys are not able to regulate water and chemicals in the body
or remove waste products from your blood
- partial
- complete

acute renal failure (ARF)

- acute renal failure is a sudden and almost complete loss of kidney function with
azotemia - an accumulation of nitrogenous wastes in the blood.
- this accumulation is not due to extra renal factors.
- REVERSIBLE!
can it be reversed?
- ARF can be acute or chronic-the acute syndrome, unlike the chronic syndrome is
usually reversible.
- the creatine clearance which is a measure of glomular filtration rate (GFR)
drops suddenly.

types of acute renal failure

prerenal (most common)
- due to ischemia
intra-renal
- damage to renal parencymal tissue-malfunction of nephrons.
post-renal

pre-renal
- hypovolemia
- decreased CO
- vasodilation
- all above lead to decreased renal blood flow, decreased perfusion, renal ischemia,
decreased GFR.

intra-renal
- circulatory infections
- nephrotic agents
- glomerular lesions
- vascular disease
- infections

pathophysiologic processes and manifestations (page 1199)

- conditions that most commonly cause ARF is ATN (acute tubular necrosis):
- can be grouped in five phases:
- onset
- oliguric-anuria
- early diuretic phase
- late diuretic
- convalescent phase

onset phase
- the period from the precipitating events to the onset of oliguric-anuric phase

oliguric phase
- toxins accumulate
- urinary changes - daily output (usually 8-15 days is usually less than 400ml/day,
rising BUN and creatinine.
- fluis volume excess.
- metabolic acidosis - accumulation of acid end products.
- sodium balance - what happens?
- increases.
- retention of fluid.
- lack of urination.
- RAAS (renin-angiotensin-aldosterone-system)
- potassium excess:
- why?
 - potassium is retained.
- kayexelate/sodium polystyrene sulfonate (page 1202)
- give insulin.
- sodium bicarb.
- calcium gluconate.
- dialysis.
- calcium deficit and phosphate excess
- k-phos/phos-lo (removes phosphate)

diuretic phase
- early diuretic phase extends from the time daily output is greater than 400 to the
time the BUN stops rising.
- late diuretic phase extends from the first day the BUN falls to the day it stabilizes
or is in the normal range.
- what is the normal BUN and creatinine range?

testing...
- healthy kidneys removes wastes and excess fluid from the blood.
- blood tests show whether the kidneys are failing to remove wastes.
- urine tests can show how quickly body wastes are being removed and whether the
kidneys are leaking abnormal amounts of protein.

blood tests = show kidney failure

kidney tests = show how fast failure occurs
BUN = blood test
creatinine clearance = urine test

blood tests - serum creatinine (page 1147)

- serum creatinine. is a waste product that comes from meat protein in the diet and
from the normal wear and tear on muscles of the body.
- creatinine levels in the blood can vary and each laboratory has its own normal
range. in many labs the normal range is 0.6-1.2mg/dL (text: 0.5-1.5mg/dL)
- higher levels may be a sign that the kidneys are not working properly.
- as kidney disease progresses, the level of creatinine in the blood increases.

BUN normal and what is it?

- blood urea nitrogen (BUN). is produced from the breakdown of food protein.
- a normal BUN level is between 10-30mg/dL.
- as kidney function decreases, the BUN level increases.

recovery phase
- BUN and creatinine stabilize.
- GFR begins to increase.
- may take up to 12 months for complete recovery.

collaborative care and therapeutic management

- correct hypervolemia and maintain CO.
- I&O.
- daiily weights.
- dialysis: hemodialysis and peritoneal.
- CRRT: hemodynamically unstable patients.
- nutritional therapy.
- replace protein.
nurses
- intervene by:
- prepare the client for dialysis (monitor V/S).
- NPO hours prior to dialysis.
- monitor fluids, electrolytes and acids and bases.
- monitor cardiac status
- salt plays a vital part in the sodium/potassium pump.
- administer medications to control symptoms as ordered.

-----------------------------------------------------------------------------------------

Tuesday, October 28, 2008.

kidney key points: renal

review: elsevier/evolve website and cd.

distended neck veins? why? kidney failure = right-sided heart failure.

high phosphate? give phos-lo. given during meals. excreted in feces.

do not give excessive protein!

SYSTEM EFFECTS

MUSCULOSKELETAL: muscle cramps, loss of strength, bone fractures, lumps in

skin, calcium phophate.

GI: stomatitis, ulcerations, GI bleed, vomiting, weight loss or gain. LABS: increased
BUN and creatinine.

RESPIRATORY: crackles, coughing, rapid deep respirations (acidosis). a potential

for congestive heart failure.

CARDIOVASCULAR: hypertension, dysrhythmias, increased potassium, potential for

pericarditis, and or congestive heart failure. LABS: increased potassium, decreased
or increased sodium, increased phosphorus, decreased calcium, decreased total
proteinn and albumin.

MOUTH/NUTRITION: anorexia, uremic fetor.

GENERAL APPEARANCE: weakness (erythropoietin), fatigue and edema.

PERIORBITAL EDEMA

GU: decreased urinary output, potential for all complications of dialysis, potential for
metabolic acidosis, amenorrhea.

SACRAL EDEMA

MUSCLE CRAMPS, PITTING EDEMA

FOOT DROP, SENSATION

most common cause of death: cardiac and infection.

collaborative management: eliminate cause, manage signs and symptoms,

manage complications.

catabolic: breakdown
anabolic: build

peritoneal dialysis principles: filtration, osmosis, diffusion, oncotic pressure.

CNA/NT: florida nurse practice act states they "SHOULD NOT" insert foley catheters.

-----------------------------------------------------------------------------------------

DIALYSIS

CRRT (page 1224):

- alternative/adjunctive treatment.
- electrolytes are adjusted slowly.
- not hemodynamically stable enough to remove 200ml/hr.
- vascular access: double lumen. femoral. subclavian.

kidney transplant

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BURNS (chapter 24/page 483)

risk related groups, anatomy of the body r/t burns, incidence, education and
nursing management of the burn client.

- hemodynamically unstable

types: radiation, chemical, electrical, heat, etc.

statistics and incidence

- latest numbers
- article
- where does it happen?
- incidence (home)
- etiology
- groups at risk (children and elderly)

anatomy and physiology: a review

- function of skin
- protection from infection
- conservation of body fluids
- you name the rest please
- layers
introduce and define thermal burn injury
- types- depth of skin destruction - ABA
- partial thickness (page 485) - first degree - second degree
- full thickness - third degree
- classification of burns
- calculation of the extent of the burn
- rules of nine
- lund-browder
- pts. hand = 1% TBSA

pathophysiology
- two stages
- immediate hypovolemic
- diuretic state

phases of burn management (page 489-491)

- prehospital
- emergent phase
- fluid and electrolyte shifts
- complications
- respiratory
- renal: acute tubular necrosis

*airway, fluid, wound care, infection control

analgesics and pain management

- morphine
- tetanus shots
- antimicrobial agents

*test 4: heavy on diet and drugs!

acute phase
- mobilization of fluid and subsequent diuresis

diagnostics
- 24 hour urine collection: creatine clearance, renal function.
- ABGs - metabolic acidosis - what can we do about this? sodium bicarb (IV push).
- blood chemistries - increased k+ and decreased sodium, electrolytes, WBCs.
- hematologic studies - hematuria, myoglobinuria.
- urine chemistry

emergent
- airway: oxygen management (always first! except safety!)
- circulatory management
- fluid: formula (page 497)
- fluids to use: why colloids?
- body systems
- GI, renal
- pharmacology
- what about electrolyte losses, metabolic acidosis with betadine. how about
sulfamylon/silvadine metabolic acidosis?
- acid-base balances: why in a burn client?
nutritional therapy: goal: provide calories and protein.

decrease anxiety! pain management!

stigma with burn patients. body image.

JOBST: garment/stocking used on burn victims.

diagnoses:
- fluid
- pain
- risk for infection
- body image
- skin integrity
- imbalanced nutrition
- anxiety

to treat:
- biological dressings
- diet
- early excisionial therapy
- escharotomy
- IV therapy
- protective isolation
- splints
- transfusion therapy
- hydrotherapy

drug management:
- pain (morphine)
- stomach (curlings: zantac, nexium, protonix)
- anxiety
- antibiotic
- colloids
- diuretic
- histamine antagonists
- mucosal barrier
- vitamins (may be given TPN)

teach:
- explain disorder and treatment
- medicationis
- dietary
- avoid restrictive clothing (skin sensitivity)
- use of splints and Jobst clothing
- community agencies

summary of burns
- how
- classifications: area, thickness, etc.
- phases
- nursing care for each phase
- systems approach
- nutritional needs - collage lab
- check for signs of stress ulcer? how?
- check continuing respiratory status
- check for infection - death

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Tuesday, November 11, 2008.

the significance of cancer
- change of life
- people's thoughts
- change of life impact
- it is always a death sentence
- nurses can have an impact
- some types of cancer are more prevalent

defined and introduced-cancer

- uncontrolled growth
- unregulated growth
- group of diseased
- progress, still exist
- second common cause of death
- more prevalent in African Americans
- feared more than heart disease
- health care workers must be trained to change attitudes

immune system in cancer

"it is generally agreed that regardless of the cause of cancer, a properly functioning
immune system will attach and attempt to destroy it."
http://www.purlife.com/immune.htm

immune system
- normal cells differentiate into cancer cells
- cancer cells were once normal cells
- suppressor cells congrol growth, directioin, adhesive of normal cells
- only one cell has to undergo malignant transformation for cancer to begin

the cell cycle animated

http://www.cellsalive.com/cell_cycle.htm

two factors regarding cell growth

- proliferation: growth factors simulate new tissue to grow
- differentiation: stem cells commit
- cancer cells
- have rapid or continous cell division
- do not respond to signals for adoptosis (cell death)
- perform no special functions
- have a different shape - large nuclear cytoplasm
- etc. more difference between cancer cells and regular cells
- review your immunology - self study
tumor cell markers
- substance producted by cancer cells found on tumor plasma membranes or in the
blood, spinal fluid or urine
- include hormones, enzymes, genes, antigens and antibodies.

best method cancer diagnosis: biopsy

metastasis
- implantation
- serosal bleeding
- surgical manipulation

- lymphatic system
- lymph nodes

- vascular system
- emboli formation

treating cancer - with radiation therapy

- radiation therapy: principle is to attack and destroy cells in rapid growth (mitosis)
- attacks all rapidly growing cells
- gi mucosa, esophagus, oral cavity, bone marrow, skin, hair
- internal radiation: brachytherapy
- external radiation: teletherapy

assess and treat local reactions to internal radiation

- oral/oropharyngeal
- stomatitis
- loss of taste
- difficulty swallowing
- gentle mouth care
- soft foods

look also to assess and treat (internal radiation)

- reproductive problems (drying of cells)
- effects determined by dose
- reduced sperm count, dysfunction
- cessation of menses, sloughing of cells
- loss of vaginal lubrication
- discuss potential problems
- lubricants, analgesics, force fluids

gastrointestinal and internal radiation

- highly susceptible
- radiation gastritis
- decrease mucous, HCl, pepsin
- N/V
- diarrhea
- assess for dehydration
- low residue diet
- calorie count
external radiation
- think of where the patient is being beamed
- and what lies beneath that area
- fatigue: during 3-4 weeks of treatment
- anorexia: nausea/vomiting
- weight twice weekly
- assess nutritional status and give appropriate supplements
- augment nutrition with supplements

external radiation can cause - treat with

- skin reactions
- erythema followed by desquamation
- lubricate dry skins, aloe, ivory soap
- antibiotic creams
- protect from traumas such as heat and cold
- no constricting garments
- avoid exposure to the sun-drying effect

chemotherapy history
- mustard gas
- wartime
- low white blood cell counts
- maybe work on cancer
- 1940s, several patients with advanced lymphomas (cancer of certain
white blood cells) were given the drug by vein, rather than by
breathing the irritating gas.

chemotherapy treatment
- systemic treatment
- often first choice of treatment
- it differs from surgery or radiation in that it is almost always used as a systemic
treatment

chemotherapy
- mechanism of action
- the faster cells are growing more likely that cytotoxic drugs are to "catch" them
- also accounts for toxicity on rapidly growing normal tissues (eg. GI mucosa, bone
marrow)
- large tumors are relatively unresponsive to chemotheray
- more cells are in G0 and drug penetration is reliable
- most drugs kill a fixed proportion of cells rather than fixed number
- different drugs act at different phases of the cell cycle
- as a result, combinations of drugs are more likely to be effective

non-phase dependent drugs

- non-phase dependent drugs
- kill cells exponentially with increasing dose
- equally toxic for cell within the cell cycle or G0 phase
- examples include:
- alkylating agents - cyclophosphamide, cisplatin
- 5-flurouracil
- anthracyclines - doxoruvicin
phase dependent drugs
- phase dependent drugs
- kill cells at a lower dose
- act within a specific phase of the cell cycle

chemotherapy administration
- IV administration is very dangerous
- need to be chemo-certified
- extravasation-infiltration into tissue
- vesicants: severe local tissue reactions & necrosis
- know the safe administration protocols
- teach client to report any buring and or stinging

side effects
- chemotherapy is given to kill cancer cells, it also can damage normal cells
- recall from earlier: most likely to be damaged are normal cells that divide rapidly:
- bone marrow/blood cells
- cells of hair follicles
- cells in the reproductive and digestive tracts
- damage to these cells accounts for many of the side effects of chemotherapy drugs.
- side effects are different for each chemotherapy drug
- also differ based on the dosage
- differ according to the route the drug is given
- how the drug effects the patient on an individual basis

side effects of chemo

- similar to radiation
- cachexia (malnutrition)
- fatigue (plan activities)
- anorexia (small frequent)
- N/V (zofran, phenergan)
- bone marrow suppression
- risk for fractures
- demineralization
- calcium imbalance
- anemia
- leukopenia: WBC less than 2,000
- thrombocytopenia: less than 50,000 platelets
- anemia: hgb less than 10

nursing care for the anemic client

- assess H&H
- blood transfusion
- epogen for RBCs
- food diary
- assess the degree of hypoxia

thrombocytopenia and care

- assess for bleeding tendencies
- monitor the PT and APTT, platelets
- plasma and platelet infusion
- thrombopoetin
- rate: as fast
- assess the mental status
- assess GI and GU status

nursing for leukopenia/neutropenia

- leukopenia: total WBCs
- granulocytopenia: all granulocytes, including neutrophils, eosinophils and basophils
- neutropenia: neutrophils
- assess immune response
- early identification of infectious source
- neupogen, leukine, prokine

oncologic emergencies
- obstructive
- superior vena cava syndrome
- spinal cord compression
- third space syndrome
- infiltrative
- cardiac tamponade
- intestinal obstruction
- metabolyic
- SIADH
- hypocalcemia
- tumor lysis syndrome
- septic shock and
- DIC
- carotoid artery rupture

alopurinol: removes urea

radical neck
why
indications for
- lymphatic metastasis is the most important mechanism of spread in head and neck
squamous cell carcinoma

the candidate for

- a client who has a cancerous tumor in the lymph nodes in the neck and upper
airway

involves
- radical neck dissection is an operation that was created in 1906 to solve the
problem of metastatic neck disease
- classical radical neck dissection is still the optimum standard today for surgical
control of a neck metastasis

several forms (page 552)

- there are several forms of neck dissections
- ranging from the radical neck dissection to a less extensive selective neck
dissection
- differ by the amount of tissue removed from the neck
- goals are to remove lymph nodes proven or likely to contain
metastatic cancer
- amount of tissue to be removed depends on the size and extent of
 the metastatis

presentation
- unilateral or bilateral neck mass
- lesion known to patient
- or is found by physical examination of the upper esophagus and digestive
pathway
- in about 10-15% of patients a metastatic neck mass is present without an
obvious primary lesion
- making every effort to identify the primary lesion is difficult
- require careful evaluation of all mucous membranes, airway, digestive tract,
close examination of mouth, tonsil, esophagus

head and neck cancer

- affects mucosal surface
- typically squamous cell
- disfiguring in nature

what could prevent it

- what are some preventative measures for head and neck cancer?

collaborative care:
- early care before radical neck could be:
- radiation
- depends on staging and how far advanced
- radical neck depends on extent of cancer

clinical manifestations:
- vary with tumor location
- remember how a tumor is staged
- early stages vary and often undetectable
- late stages

indications of
- tumor growth
- sore throat
- hoarseness
- pain is late symptom
- ulcer that does not heal
- review nursing assessment head and neck cancer table 26-9 page 585

detect by:
- detect airway involvement
- laryngeal mirror
- CT scan
- biopsy
- MRI

nursing care after surgery

- keep in mind the anatomy affected
- know the anatomy and what its functions are
- vocal cord: nurse will implement what
- aspiration risk after surgery: nurse will implement what
post-op
- maintain NPO for at least first 24 hours
- if the radical neck dissection has been combined with mroe extensive
surgical procedures, a longer period may be needed
- maintain head elevation at a 30 degree angle
- monitor vital signs, intake and output every 4 hours
- maintain constant humidification
- suctioning and cleansing of the tracheostomy tube
- administer pain medications PRN
- ensure that the hemovacs or drains
- are functioning properly

more post op care

- administer antibiotics
- monitor for fever, bleeding, or hematoma formation in the postoperative period
- avoid atelectasis
- move the patient out of bed the day after surgery with assistance.
encourage deep breathing and early ambulation with assistance
- monitor for possible fistula if the oral or upper digestive tract was opened,
particulary during the 3rd or 4th postoperative day

nutrition
- parenteral-why?
- tube feedings-is this possible?
- before advancing to food what nursing interventions is required mandatory and
why?
- patient can still speak due to true vocal cords

how about other complications

- speech
- body image
- perfusion: why might this be a problem?
- pain
- exercise what parts
- in this diagnosis: therapeutic regimen compliance with is a big problem and issue to
deal wiith
- airway: tracheostomy
- semi-fowlers, edema can compromise the airway

summarize
- review

FINAL EXAM: thrombolytics, pancreatitis, whipple procedure

liver CA discussed today!

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liver and liver cancer

- regeneration
- the liver is among the few internal human organs capable of natural regeneration of
lost tissue
liver location and appearance
- the liver is shaped like a pyramid and is divided into right and left lobes. unlike
most other organs
- it has its own blood supply - why?

- the liver receives blood from two sources

- the hepatic artery supplies the liver with blood that is rich in oxygen
- the portal vein carries nutrient - rich blood from the intestines to the liver

functions of the liver

- carbohydrate metabolism
- glycogenesis, glycogenolysis, glucogenesis
- protein metabolism
- synthesis of non essential amino acids, plasma proteins, clotting factors
- ammonia conversion
- lactalose (removes ammonia)
- urea formation from ammonia
- fat metabolism
- steroid metabolism
- conjugation and excretion of gonadal and adrenal steroids
- coagulation

the liver also

- detoxifies
- acts as a home for enzymes: LFT's - what does that stand for, when would it
get ordered
- AST/SGOT, ALT, GGT, alkaline phos
- bilirubin metabolism (RBCs)

what is liver cancer

- because the liver is made up of severeal different types of cells
- several types of tumors can form in the liver

appear as
- benign tumors
- hemangioma: is the most common type of benign liver tumor. it
starts in blood vessels
- malignant tumors: while there are other types of liver cancer, the
most common form in adults is called hepatocellular carcinoma

cancer of the liver

- major manifestations:
- jaundice: how do you see this in a patient? how would you document
- portal hypertension: why is it called portal?
- ascites: what is this?
- hepatic encephalopathy: what are signs and symptoms of this?
change in volume, color, BP, mental status, urine output

risk factors
- certain types of liver disease:
- too much iron in the liver
- tobacco use:
 - aflatoxins:
- vinyl chloride and thorium dioxide (thoroclast): dry cleaning
- anabolic steroids
- arsenic
- birth control pills
- alcohol

symptoms of liver cancer

- weight loss (for no known reason and without your trying to lose weight)
- on-going lack of appetite
- feeling very full after a small meal
- liver swelling or a mass taht can be felt in the area of the liver
- ongoing stomach pain
- swelling in the area of the stomach
- yellow-green color to the skin and eyes (jaundice)
- becoming sicker if you have chronic hepatitis or cirrhosis

tests: how to detect?

- medical hx and doing a complete physical exam
- ultrasound
- CT scan
- MRI (magnetic resonance imaging)
- angiography
- laparoscopy provides a view of organs that can help the doctor in planning surgery
or other treatment
- LFT
- biopsy

treatment / treatment modality

- surgery offers only chance to cure liver cancer
- liver transplation
- tumor ablation or embolization
- chemoembolization involves combining with chemotherapy
- radiation therapy
- chemothereapy vein or by mouth. once the drugs enter the bloodstream, they
spread throughout the body

failure
- liver failure results in impairment
- liver failure mostly arises slowly
- it can happen from infections, cancer, alcohol and toxic substances
- much of the treatment of liver failure is focused upon salvaging whatever liver
function is left and avoiding overtaxing the liver

diet? nutrition? what drugs metabolized?