Week 7 Study Guide Flashcards
1
Q
General Assessment: Tachycardia/Bradycardia
A
-Tachycardia is normal with exertion and exercise but abnormal at rest
-Could indicate weak heart muscle, pain, fever, inadequate fluid volume
-Bradycardia at rest can be normal in those with good physical condition.
- Can also indicate low CO, be aware of dizziness, SOB, chest pain
2
Q
General Assessment: Blood pressure
A
- Reflection of the pressures generated during cardiac cycle.
*Postural hypotension can be indicative of poor CO or decreased blood volume - Influencing factors: amount of blood ejected during systole or CO, resistance to flow in the peripheral vessels, or peripheral vascular resistance
3
Q
General Assessment: Poor Peripheral Perfusion
A
Can be noted by pallor (light) or cyanosis (blueish grey) and capillary refill
4
Q
General Assessment: Edema
A
- Can indicate a heart problem when it is noted bilaterally (affecting two sides).
- Can be a sign of cardiac or liver issues.
5
Q
General Assessment: Gender- related concerns
A
- For awhile it was considered difficult, time consuming, and not worth it to research/investigate problems equally for men and women
- Research was based off of men and then assumed to be the same for women.
- Heart attack: Men S&S= crushing chest pain, radiation down left arm and back. Women S&S= indigestion, jaw pain, fatigue, SOB
6
Q
General Assessment: Age-related Changes
A
- Stenosis, stiffening of arterial walls, and fibrotic changes of heart chambers can result in hypertension
- Atherosclerosis (buildup of fats and cholesterol on artery wall) plagues, narrowing of arterial walls can increase the risk of stroke and MI.
- Heart diseases is #1 cause of death in older adults.
- Physical deconditioning can result in atrophy of left ventricle, decreased elasticity of the aorta, rigidity of the valves
- Common cardiovascular age-related changes: hypertension, coronary artery disease, congestive heart failure, aFib.
7
Q
Labs: Brain Natriuretic Peptide (BPN)
A
- Less than 100 pg/mL
- measures degree of stretch in the ventricles- indicates heart failure
8
Q
Labs: Cardiac Panel
A
- Contains CK (creatine kinase), CKMB (creatine kinase myocardial bands 0-3 ng/mL), *TROPONIN (< 0.4 ng/mL) (order from least specific to most specific for heart damage, opposite for speed)
- Troponin is specific to heart damage.
- “Serial cardiac panels”: several in a row to determine trends. Usually drawn q4 hrs.
9
Q
Procedure: Stress Testing
A
- Evaluating the heart function during increased workload
- No eating or drinking for 4 hours before procedure, no smoking, no caffeine.
10
Q
Procedure: Angiography & Catheterization
A
- Advancing catheter through the radial or femoral artery to the heart to directly visualization the vessels of the heart and remove any blockages.
- Risks: Infection & bleeding, clot formation, dysrhythmias
11
Q
Procedure: Pacemaker Placement
A
- Surgically implanted device under the skin, near the collarbone to generate electrical signals for the heart
- After surgery: Avoid lifting L arm above shoulder level, keep arm in sling as ordered, no lifting > 5 lbs, monitor for infection, avoid magnetic fields (heavy duty electrical equipment, radio towers), take pulse at least once daily. Usually inserted to treat low heart rate.
- Other considerations: medical-alert bracelet and carry pacemaker information card, report pulses < pacemaker set rate, report and cardiac issues to primary care provider (PCP)
12
Q
Cardioversion
A
- Used to electrically correct arrhythmias
- Synchronized shock at peak of R wave of QRS complex.
- Patient is awake and aware: shocking is painful. Treat with with anxiolytics, sedatives, or pain meds prior if possible.
- Pads placed anterior/posterior on clean, dry, hair-free skin
13
Q
Defibrillation
A
- Unsynchronized shock that resets a non-perfusing rhythm and brings back a stable, perfusing rhythm
- Used on pulseless patients (cardiac arrest)
- Pads placed on anterior/posterior on clean,, dry, hair-free skin
- Steps in defibrillation: turn on machine, place the paddles/pads select energy level, ALL CLEAR, deliver shock
- AED is similar, choose energy, announces on its own all clear, delivers shock automatically
14
Q
Transcutaneous Pacing
A
- Using the same pads of our defibrillator machines to provide external pacemaking triggers to a patients heart
- Typically used for symptomatic bradycardia and heart blocks
15
Q
Telemetry
A
- Constant monitoring of rhythm with a 5-lead EKG monitor.
- Provides rate and rhythm information, but not detailed electrical and conduction information like a 12-lead EKG
- Nurse delegates to a tele tech (CNA with training)
16
Q
EKG
A
- 12-lead snapshot of the heart. A quick picture of the electrical conduction of the entire heart from multiple ‘angles’
17
Q
EKG Interpretation: Normal Sinus Rhythm
A
18
Q
Pulseless Electrical Activity
A
- Electrical system working fine at the moment, but the heart isn’t responding to it
- Potential causes: hypoxia, hypovolemia, altered potassium levels, Tamponade, MI
- Cardiac arrest, no pulse> CPR, Epinephrine, treat underlying cause
19
Q
Asystole “Flatline”
A
- Flat line of electrical activity (no electrical activity)
- Can we defibrillate this rhythm? No.
- Provide CPR
20
Q
Sinus Bradycardia
A
- NSR that is slower than 60 BPM
- Asymptomatic= monitor but it can be normal in athletes & sleep
- Symptomatic= give atropine, transcutaneous pacing, or place a pacemaker
21
Q
Sinus Tachycardia
A
- NSR that is faster than 100 BPM
- Treat underlying causes: infection, caffeine, exercise, anxiety, certain drugs, fever
- Beta blockers or calcium channel blockers can be given to reduce the rate
22
Q
Premature Atrial Contractions (PACs)
A
- Non-life-threatening out-of-rhythm beat when the atria cause a full contraction. After PAC, normal conduction returns
- Causes: stimulant ingestion (caffeine, illegal drugs), CAD, Hypoxia
- Treatment:
23
Q
Atrial Fibrillation
A
- No P-waves, atria just quivering, fibrillation
- AV node gets chaotic signals, transmits some of them down the line to ventricles. Less than 100 bpm (controlled A-fib.), Greater than 100 bpm (noncontrolled a-fib).
- Causes: age, cardiomyopathy, pericarditis, valve disease, obesity, diabetes, CAD
- Complications: clot formation & loss of atrial kick (reduces pts. cardiac output)
- ## Treatment: Controlled <100 bpm= rhythm control with medications or cardioversion. Uncontrolled >100 bpm= first control rate, then rhythm control
24
Q
Atrial Flutter (Aflutter)
A
- Not driven by SA node= no P wave. Flutter waves (F waves) with sawtooth pattern waves between QRS complexes
- More symptoms than Afib: hypotension, dizziness, lightheadedness, fainting, feeling palpitations
- Treatment, same as Afib: rate control, rhythm control with meds or cardioversion
25
Supraventricular Tachycardia (SVT)
- Rapid heart rhythm, narrow QRS complex (150-250 bpm)
- Can be symptomatic or asymptomatic
- Symptoms: hypotension, dizziness, fainting, palpations, anxiety- heart disease/failure, a lot of caffeine/alcohol, lung disease
- Treatment: slow down HR with vasovagal maneuvers, administer Adenosine, cardioversion
*Adenosine= FUN, fast push medication that causes a brief period of asystole (flat line 3-4 sec.) before recapture and slowed HR. Ensure a transcutaneous pacemaker, a DR. and code card is on hand.
26
Vasovagal Maneuvers
1. Sit/ lie down
2. Take a deep breath and hold it
3. Pinch nose shut
4. Close your mouth
5. Bear down hard as if trying to pass a BM
27
Premature Ventricular Contractions (PVCs)
- Wide, weird-looking QRS complexes that fire randomly from within the ventricles themselves
-Like PACs, a brief pause at the end allows normal electrical conduction to happen after
-Only concerning when frequent or semi-rhythmic -> bigeminy, trigeminy, couplets
-After 3 PVCs in a row, we are V-tach
-Causes: typically stimulant usage, electrolyte issues, hypoxia, MI, HTN
-Treatment: fix underlying causes and potentially use anti-arrhythmic
28
Ventricular Tachycardia (Vtach, VT)
- Wide, weird-looking QRS complexes, all the time
- Potential causes: altered potassium
- CHECK A PULSE FIRST
29
Ventricular Fibrillation (V-fib, VF)
- Pure chaos, non-perfusing (no blood moving), LETHAL
- Potential causes: altered potassium levels, toxins,
30
1st Degree Heart Block
- NSR with a long PR interval (time between P wave and QRS complex)
- Caused by a delay in conduction in the AV node
31
2nd Degree Heart Block
- NSR with an increasing PR interval until a beat drops (longer, longer, longer, drop)
-
32
2nd Degree Type 2 Heart Block
- NSR with a regular/normal PR interval until a random beat drops.
33
3rd Degree Heart Block (complete heart block)
- No communication between atria and ventricles- completely
34
Medication: Atropine
- When to use:
-What the do:
- Way they work:
35
Dysrhythmia Synmptoms
- VS changes = drop related to cardiac output decreases
- LoC changes
- Chest pain
36
1. S3 Ventricular Gallop
2. S4 Atrial Gallop
1. - Ventricular dysfunction when heard in adults
- Gallop-like sounds
- Early diastole
2. - Decreased ventricular compliance
- Gallop like sounds
- Late diastole after atrial systole
37
1. Systolic Murmur
2. Diastolic Murmur
1. - Valvular disease such as aortic stenosis
- Turbulent flow heard
- Systole between S1 and S2
2. - Valvular disease such as aortic or pulmonic
regurgitation
- Turbulent flow heard
- Diastole after S2
38
1. Click
2. Friction Rub
1. - Mitral valve stenosis
- High-pitched sound
- Early diastole
2. - Pericarditis
- Harsh, scratching sound
- Anywhere during the cardiac cycle
39
1.Systole (Contraction)=
2.Diastole (Relaxation) =
3.Stroke Volume=
4.Contractility=
1-the squeeze that moves the blood out of the ventricles. "Pumping part of the pump".
2-Allows blood to fill up the ventricles. Myocardial tissue perfusion happens.
3-amount of blood ejected from ventricles with each contraction of heat
4- the force of the 'squeeze' that the heart produces
40
1. Preload=
2. Afterload=
1- amount of blood in the ventricles at the end of diastole
*Increased in: hypervolemia, regurgitation of cardiac valves, heart failure
2- Resistance that the left ventricle must overcome to circulate blood (push it OUT).
*Increased in: Hypertension and cardiac output, vasoconstriction
41
Heart Electric Pathway
SA Node -> atrial myocardium causing contraction (inter-nodal pathway) -> AV Node (impulse is delayed) -> Bundle of His -> Branches into the R and L (branches even further), branches -> Purkinje fibers of each ventricle -> ventricle contraction
42
Inherent Rates of the Conduction System
- Sinoatrial node (SA node) = 60-100 bpm [default]
- Atrioventricular node (AV node) = 40-60 bpm [AV takes over when SA isn't working]
Ventricular pacemaker cells = 20-40 bpm
Purkinje fibers = 20 bpm
43
EKG Basics and their Associations
P Wave
QRS Complex
T Wave
- P Wave: ATRIAL DEPOLARIZATION produced by the SA node through atria. Atria contract milliseconds after depolarization.
- QRS Complex: VENTRICULAR DEPOLARIZATION. Ventricular contraction occurs after QRS complex in the ST segment.
- T Wave: VENTRICULAR REPOLARIZATION. Atrial repolarization occurs during ventricular contraction.
44
Cardiac Output = HR x SV
- SV effected by Preload: Increased preload increases stroke volume. Too full decreases the contraction which decreases CO.
- SV effected by Afterload: Hypertension is implicated by increased afterload which decreases stroke volume.
- SV affected by Contractility: Contraction can increase with stimulation or calcium release. Decrease from hypoxia or acidosis. Increase contractility can increase SV
45
RAAS (Renin - Angiotensin - Aldosterone System)
- Activated by low blood pressure noted by baroreceptors
- RAAS increases blood pressure by causing vasoconstriction, telling the kidneys to increase sodium reabsorption
46
Cardiac Monitoring
- EKG, telemetry, cardioversion/defibrillation units
- Skin must be clean, dry, and hair-free for good conduction
