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