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201A > Final cardiac > Flashcards

Final cardiac Flashcards

1
Q

What is the conduction pathway in the heart

A
  1. SA node
  2. Intra atrial pathways
  3. AV node
  4. Bundle of His
  5. Left and right bundle branches
  6. Purkinje fibers
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2
Q

Does the parasympathetic nervous system increase your SA node or decrease? What about the sympathetic nervous system?

A

The parasympathetic system slows the SA node (it’s like the brake)
The sympathetic system increases the SA node (it’s like the gas)

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3
Q

What do the waves and the intervals stand for on an ECG

A

P wave = depolarization of the atria
PR interval = time for the impulse to spread through the atria
QRS = depolarization of the ventricles
ST = time between ventricular depolarization and repolarization
T wave = repolarization of the ventricles
QT interval = time for entire depolarization and repolarization of the ventricles

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4
Q

How many seconds is a typical strip

A

6 seconds

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5
Q

How many seconds is a big box and how many seconds is a little box

A

Big box = 0.2 seconds
Little box = 0.04 seconds

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6
Q

What is the rate of the SA node and the atria

A

60-100

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7
Q

What is the rate of the AV node and bundle of His

A

40-60

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8
Q

What is the rate of the bundle branches and purkinje

A

20-40

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9
Q

How many seconds should the PR interval be?

A

0.12-0.20 seconds (about 3-5 little boxes)

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10
Q

How many seconds should the QRS complex be

A

Less than 0.12 seconds (less than 3 little boxes)

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11
Q

What is artifact

A

Artificial ECG info - maybe a lead is lose, pt is up walking around, etc…

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12
Q

What is the absolute refractory period? Why is it important? What part of the ECG wave is it?

A

When excitability is zero and the heart cannot be stimulated (important with cardioversion - we don’t want to shock the heart when it’s doing something). It’s from Q to the T wave.

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13
Q

How do we diagnosis dysrhythmias? (probably don’t need to memorize - just be familiar just in case)

A
  • Holter monitoring (usually only worn for 24 hours)
  • ZIO Patch (usually worn for 14 days)
  • Event recorder monitoring (you can control when it records)
  • Exercise treadmill testing
  • Signal-averaged ECG (multiple ECG’s use averages for dx)
  • Electrophysiologic study (“EP Study” with the use of catheters to study the origin of the dysrhythmia)
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14
Q

What are the steps when we look at a rhythm?

A
  1. Is the rate regular or irregular? Is it regularly irregular?(R wave to R wave)
  2. Rate? (multiply the R waves by 10)
  3. Is there one P wave in front of every QRS? Do they all look the same?
  4. Is the PR interval normal and consistent?
  5. Is the QRS narrow or wide?
  6. Is there a T wave?
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15
Q

How do we know someone is in sinus bradycardia

A

Rate is less than 60

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16
Q

What can cause sinus bradycardia 9

A
  • Carotid sinus massage
  • Hypothermia
  • Hypothyroidism
  • Increased intracranial pressure
  • Obstructive jaundice
  • MIs
  • Increased vagal tone (when a pt is bearing down and passes out on toilet)
  • Administration of parasympathomimetic drugs
  • Drugs like beta blockers and CCBs.
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17
Q

What are symptoms of bradycardia

A
  • Hypotension
  • Pale, cool skin
  • Weakness
  • Angina
  • Dizziness or syncope
  • Confusion or disorientation
  • Shortness of breath
    (anything that you would see with decreased cardiac output)
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18
Q

What is our tx for bradycardia 4

A
  • Stop offending drug (like beta blocker or CCB)
  • IV atropine (1mg) (may or may not work depending on what’s causing the bradycardia)
  • Pacemaker
  • Dopamine or epinephrine infusion
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19
Q

How do we know someone is in sinus tachycardia

A

Their HR is over 100

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20
Q

What things can cause sinus tachycardia

A

Yes - here are the signs
- Exercise
- Pain
- Hypovolemia (Heart is working faster and faster to try and increase cardio output because volume is low)
- Myocardial ischemia (with any kind of ischemia, heart works harder to get blood to that area)
- Heart failure (HF)
- Fever
- Anxiety
- Hyperthyroidism
- Effects of drugs: Levophed, atropine, caffeine, theophylline, hydralazine, pseudoephedrine

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21
Q

How can we treat sinus tachycardia 2

A
  • Treat the underlying cause! (such as pain, fever, hypovolemia (someone is really dehydrated, give them fluids, heart rate goes down)
  • Vagal maneuver (have them bear down, blow into a straw)
  • Drugs (beta blockers, adenosine, CCBs)
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22
Q

What do (premature atrial contraction) PACs look like

A
  • Caused by ectopic focus (starting from somewhere other than the SA node)
  • The p wave looks different, because it is firing prematurely from a different place in the heart (not the SA node), and then it will be followed by a narrow QRS
  • This beat occurs sooner than the next expected beat
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23
Q

How can we tell the difference between a PAC and PVC

A

Since the PAC is coming from the atrium, the QRS will be narrow, versus a PVC, which is coming from the ventricle, the QRS will be wide

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24
Q

If someone has PACs or another dysrhythmia, how would we describe their rhythm

A

Describe the underline rhythm, like sinus tachycardia, with PACs

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25
Q

What can cause PACs

A
  • Emotional stress
  • Physical fatigue
  • Caffeine
  • Tobacco
  • Alcohol
  • Hypoxia
  • Electrolyte imbalances
  • COPD
  • Valvular disease
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26
Q

If someone is healthy, are we worried about isolated PACs

A

No, not really

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27
Q

When would we be worried about someone with PACs

A

If they have heart disease, because it may be a warning sign of a more serious dysrhythmia like a-fib

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28
Q

What might PACs feel like

A
  • Palpitations
  • Heart “skips a beat”
    (shouldn’t have dramatic symptoms)
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29
Q

What might PACs feel like

A
  • Palpitations
  • Heart “skips a beat”
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30
Q

What are tx options for PACs

A
  • Get off caffeine
  • Beta blockers
  • Monitor for more serious dysrhythmias
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31
Q

What does paroxysmal supraventricular tachycardia mean

A
  • Paroxysmal = abrupt onset and termination
  • Supraventricular = occurs above the ventricles (bund of His)
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32
Q

What will a PSVT look like

A
  • Rate 150-220
  • Regular
  • Sometimes you can’t even see your P waves because it’s going so fast
  • QRS narrow
  • Has an abrupt onset and end (doesn’t gradually get faster and faster, all of a sudden it’s just really fast - ie you were in 80 and now you’re in 220)
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33
Q

What can cause paroxysmal supraventricular tachycardia

A
  • Overexertion
  • Stress
  • Deep inspiration
  • Simulants
  • Disease
  • Digitalis toxicity
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34
Q

Why would we be worried about paroxysmal supraventricular tachycardia

A

Well a HR of 180 or greater can lead to a decreased cardiac output and stroke volume leading to hypotension, palpitations, dyspnea and angina.

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35
Q

If a patient is stable, what techniques can we use to help treat PSVTs

A
  • Vagal stimulation (ie beardown, blow through a straw)
  • Coughing
  • IV adenosine (6mg IV push - fastest IV push ever - because its half life only lasts seconds)
  • Beta blockers
  • CA channel blockers
  • If these do work, move to cardioversion
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36
Q

Would we expect to see a pause in someone’s rhythm when we give adenosine? Why?

A

Yes, the pause may even last 6 seconds, because we’re stopping the electricity in the heart (might have asystole)

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37
Q

If a patient is in paroxysmal supraventricular tachycardia rhythm and they’re unstable, what do we do

A

Synchronized cardioversion

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38
Q

How does synchronized cardioversion work

A

Hit sync on your cart, it will find your QRSs and puts lines above them, so that way you won’t shock them in the wrong spot of their rhythm

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39
Q

What does atrial flutter look like

A

Recurring, regular, sawtooth-shaped flutter waves, but eventually you’ll have a ventricular get through.
- Big key = it’s regular and fast (usually 75-150bpm) (Little flutter waves, and then every 4th beat, for example, you’ll have a beat get through and create a QRS complex)
- P wave = looks sawtooth-shaped

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40
Q

What typically causes a-flutter

A

Disease, like coronary artery disease, hypertension, heart failure, etc…

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41
Q

What is the one of the big things that we worry about with atrial flutter

A

A clot developing, because the blood flow is not moving out of the atrium (it’s just swirling there)

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42
Q

If a pt is tolerating a-flutter well, will we treat it

A

No, probably not (pt might just live with it)

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43
Q

What is our tx goal for atrial flutter

A

Slow the atrial response by increasing AV block

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44
Q

How can we treat atrial flutter

A
  • Beta blockers, CCBs
  • Anticoagulants
  • Cardioversion if unstable
  • Radiofrequency ablation
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45
Q

What is a-fibrillation

A

Total disorganization of atrial electrical activity due to multiple ectopic foci (basically firing everywhere), resulting in an ineffective contraction

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46
Q

What is the most common dysrhythmia

A

A-fib, prevalence increases with age

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47
Q

How can we tell if someone is in a-fib on their ECG

A

The rhythm is irregularly irregular (a bunch of random looking little p waves, and then random QRSs

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48
Q

What can cause atrial fibrillation

A

*Caused by a disease (not by taking a med or caffeine, etc)
- Valvular heart disease
- HTN
- CAD, acute MI
- Cardiomyopathy
- HF
- *Pericarditis - big risk for developing a-fib
- Obesity
- Hyperthyroidism
- Cardiac surgery (Common after a CABG)
- ETOH

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49
Q

What can a-fib lead too

A
  • Decrease in cardiac output
  • Increased risk of stroke
  • Increase risk of rapid ventricular response (going into tachycardia)
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50
Q

What are the different classifications of a-fib

A

Recurrent- 2 or more episodes
Paroxysmal- terminates spontaneously
Persistent- sustained greater than 7 days
Permanent- lasts longer than 1 year
Lone AF young adults with no causative reason

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51
Q

What are our tx goals for atrial fibrillation

A
  • Decrease ventricular rate to less than 100
  • Prevent embolic stroke using an anticoagulation
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52
Q

What drugs can we give to help stop atrial fibrillation

A
  • *Calcium channel blockers
  • *Beta blockers
  • Amiodarone
  • Digoxin
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53
Q

What is interesting about amiodarone

A

It has a long half life, 40-55 days, which means that it’s going to stay in your system for a long time, so really make sure that you want to give it.

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54
Q

What txs can we do to help treat atrial fib

A
  • Pacemakers
  • Cardioversion if unstable
  • AV ablation possibility
  • Long-term anticoagulation if in chronic a-fib
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55
Q

What is the big thing with a-fib and cardioversion

A

*They don’t want you to throw a clot if they cardiovert you
- So if they know that you have been in a-fib more than 48 hours or if they don’t know when your a-fib started, the n they won’t cardiovert you until you have been on anticoagulants for 3-4 weeks

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56
Q

What tool can they use for anticoagulant decision making

A

CHAD-SVASC score

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57
Q

What are our different anticoagulants, and what are the benefits

A
  • Coumadin: cheap, can be reversed easily, can spike blood levels, have to have INRs drawn (vitamin k is the antidote)
  • ASA
  • Novel oral anticoagulants (dabigatran (Pradaxa), apixaban (Eliquis), rivaroxaban (Xarelto)): no INR testing, keep blood levels smooth, expensive
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58
Q

What interval are we looking at with heart blocks

A

The PR interval

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59
Q

Is a first-degree a big deal

A

No not usually, people tolerate these pretty well, can live their whole lives with these.

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60
Q

What can cause first-degree AV blocks

A
  • MI
  • CAD
  • Rheumatic fever
  • Hyperthyroidism
  • Vagal stimulation
  • Drugs: Digoxin, β-adrenergic blockers, calcium channel blockers, flecainide
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61
Q

What does first-degree AV blook look like

A

They have a long PR interval (greater than 0.2)

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62
Q

What are the 2 different types of second degree AV blocks type 1

A
  1. Mobitz 1
  2. Wenckebach
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63
Q

What is happening in a second degree AV block

A
  • The PR interval gets longer and longer, and then the QRS complex is blocked (you won’t have a QRS complex (you’ll have a missed ventricular contraction)
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64
Q

Are we worried about second degree type 1?

A

Yes and no, usually people are fine, but it can progress into a type 2 or type 3.

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65
Q

How do we treat a second degree type 1 if the patient is symptomatic or asymptomatic?

A
  • Asymptomatic: just observe
  • Symptomatic: treat with atropine or pacemaker
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66
Q

What can cause a second degree AV block type 2

A
  • Heart disease
  • Drug toxicity
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67
Q

Why are we worried about a second degree AV block type 2

A

It is often progressive and can result in a decreased cardiac output

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68
Q

How do we treat a second degree AV block type 2

A

Pacemaker

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69
Q

What is the difference between a type 1 and a type 2 second degree AV block

A

In type 1 we will see the PR interval progressively get longer and longer, while in type 2 the PR interval is the same

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70
Q

What is happening in a third degree AV heart block (complete block)

A

The atrium and ventricles are not coordinated at all. There are random p waves and random QRSs (they are firing at different rates and not talking to each other) (rhythm is very slow)

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71
Q

What can a third degree block lead too

A
  • Decreased cardiac output
  • Ischemia
  • HF
  • Shock
  • Syncope
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72
Q

How do we treat a third-degree AV heart block

A

With pacemaker

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73
Q

What is a big way to tell if someone is having PVCs

A

They have wide QRSs and no P waves

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74
Q

How can we tell if someone is having premature ventricular contractions (PVCs) based on the ECG

A

We will find a premature, wide, crazy big looking QRS and no P waves (because they’re coming from the ventricles

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75
Q

What is causing a PVCs

A

A contraction is originating in ectopic focus in the ventricles

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76
Q

What is important to remember about PVCs?

A

We get really worried when PVCs start going together in a row, because it can lead to ventricular tachycardia

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77
Q

What can cause PVCs (probably don’t need to know)

A

Anything that can increase the workload on the heart
- Exercise
- Fever
- Hypervolemia
- HF
- Tachycardia
- Caffeine
- Stress
- Pain

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78
Q

Do PVCs cause a pulse

A

No, not usually (this is why we can feel/hear a pulse difference when listening to the apical pulse and feeling the radial pulse)

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79
Q

After what procedure do we commonly see PVCs

A

After someone has had an angiogram or stent placement and the coronary artery is getting perfused again

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80
Q

What is the tx for PVCs

A
  • Oxygen
  • Fix electrolytes
  • Drugs: beta blockers, procainamide, amiodarone, lidocaine
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81
Q

What is ventricular tachycardia V-tach

A

Run of three or more PVCs and the ventricles take over

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82
Q

Can someone live with V-tach

A

No, not for very long - it’s life-threatening and they will not live very long in this rhythm

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83
Q

What is a good way to remember what v-tach looks like

A

It looks like tombstones (very wide QRS - can’t really see any other waves)

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84
Q

What can cause v-tach

A
  • Long QT syndrome (big one)
  • Electrolyte imbalances
  • Heart disease
  • Drug toxicity
  • CNS disorders
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85
Q

What can sustained v-tach cause

A

Severe decrease in cardiac output, which can lead to:
- hypotension
- pulmonary edema
- decreased cerebral blood flow
- cardiopulmonary arrest

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86
Q

What rhythm are we worried about our patient’s going into if they have v-tach

A

V-fib

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87
Q

What can cause v-tach

A
  • MIs
  • Electrolyte imbalances
  • Digoxin toxicity
  • Stimulants like caffeine and meth
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88
Q

How do we treat v-tach if the pt is stable

A
  • Antidysrhythmic, like amiodarone
  • Cardioversion
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89
Q

Will a pt have a pulse with v-fib

A

No

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90
Q

What does v-fib look like

A

Basically you can’t tell anything from the ECG, it just looks like little irregular waves

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91
Q

Why is it important to catch someone in v-fib

A

It’s the last shockable rhythm before they go into asystole

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92
Q

What does a person in v-fib look like

A
  • No pulse
  • No BP
  • No respirations
  • Unconscious
  • Pretty much dead
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93
Q

Do we do cardioversion or defibrillation with v-fib

A

Defibrillation, because they don’t have a pulse

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94
Q

What big things can cause v-fib 2

A
  • When someone gets shocked
  • Coronary reperfusion after fibrinolytic therapy
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95
Q

Will asystole always look like a flatline

A

No, not always. It may have a little bit of movements

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96
Q

Is there any electrical activity in asystole

A

No - there isn’t anything going on

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97
Q

What is the rule when determining if someone is in asystole

A

They have to be in asystole in more than one lead

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98
Q

Can you defibrillate someone in asystole

A

No - because there isn’t any electrical activity going on in the heart

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99
Q

What is our tx for asystole

A
  • CPR
  • Epinephrine
  • Treat the underlying cause
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100
Q

No matter the rhythm, if someone doesn’t have a pulse, what are we doing

A

CPR

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101
Q

What is happening in pulseless electrical activity

A

You have a rhythm (can be anything) on the ECG, but you’re not getting a pulse

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102
Q

What mnemonic can we use to think about what is causing someone to go into cardiac arrest

A

Hs and Ts (what is causing the problem and how can we reverse it)

Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hyper-/hypokalemia
Hypoglycemia
Hypothermia

Toxins
Tamponade (cardiac)
Thrombosis (MI and pulmonary)
Tension pneumothorax
Trauma

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103
Q

What is the treatment for pulseless electrical activity

A
  • CPR
  • Intubation
  • Epi
  • Fix the underlying cause
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104
Q

What is the issue with peripheral artery disease (PAD)

A

Their arteries are pretty far occluded before they start having symptoms (so it’s difficult to catch early)

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105
Q

What causes most sudden cardiac deaths

A

Ventricular dysrhythmias like v-tach and v-fib

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106
Q

What is prodysrhythmia

A

Where antidysrhythmic drug can actually cause life-threatening dysrhythmias (so they are given to try and treat dysrhythmias, but end up causing them)

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107
Q

What two rhythms do we use defibrillation on

A
  • V-fib
  • V-tach
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108
Q

Do we do defibrillation for a pulseless electrical activity rhythm

A

No - start CPR and fix the underlying cause

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109
Q

When is defibrillation most effective

A

Within 2 minutes of dysrhythmia onset

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110
Q

What is happening in defibrillation

A

You’re sending an electrical shock through the heart to depolarize the cells, and hopefully help the AS node resume the pacemaker role

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111
Q

What 4 things should I remember about synchronized cardioversion

A
  • Done on a pt with a pulse
  • Synchronizer switch must be on
  • There should be little lines above the R wave
  • It will shock on the R wave
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112
Q

Can a pt have a combination of a defibrillator and a pacemaker

A

Yes - important to know what kind they have

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113
Q

Why would a pt get a defibrillator in

A

Have survived SCD
Have spontaneous sustained VT
Have syncope with inducible ventricular tachycardia/fibrillation during EPS
Are at high risk for future life-threatening dysrhythmias

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114
Q

If someone’s defibrillator is shocking them more than once, what should they do

A

Call 911 because the could be in a lethal dysrhythmia

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115
Q

What are pacemakers used for

A

To pace the heart when the normal conduction pathway is damaged

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116
Q

What do we want to see after a pacemaker spike

A

We want to see something, like a QRS, so we know that it’s doing something

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117
Q

How do pacemakers work

A
  • They can pace either the atrium, ventricle and/or both
  • They can start working with a HR drops below a preset rate
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118
Q

What is cardiac resynchronization therapy

A

Where they have a pacemaker that is pacing both ventricles, which is called biventricular pacing. It’s used to treat pts with HF

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119
Q

What are big complications that we should watch for with pacemakers

A
  • Infection
  • Hematoma formation
  • *Pneumothorax (puncturing a lung)
  • Atrial or ventricular septum perforation
  • Lead misplacement
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120
Q

What should you teach your pt to avoid if they have a pacemaker, because these things can either deactivate the pacemaker or rip the pacemaker out with a magnet

A

Power-generating equipment
Welding equipment
Anti-theft stuff
Certain pieces of equipment used by dentists
Magnetic resonance imaging (MRI) machines
Radiation machines for treating cancer
Heavy equipment or motors that have powerful magnets

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121
Q

What is our pt teaching for pacemakers

A

Follow-up appointments for pacemaker function checks
Incision care (keep incision dry for 4 days - report signs of infection)
Arm restrictions (don’t raise arm on pacemaker side above shoulder until approved by your cardiologist)
Avoid direct blows
Avoid high-output generator
No MRIs unless pacer approved
Microwaves are OK
Avoid anti theft devices
Travel not restricted
Monitor pulse
Pacemaker ID card
Medic Alert ID

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122
Q

What are indications for pacemakers

A

Pretty much anything
- AV blocks
- A-fib
- Bundle branch blocks
- Cardiomyopathy
- HF
- SA node dysfunction
- Tachydysrhythmias, like v-tach

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123
Q

What is radiofrequency catheter ablation therapy

A

They can go into an ectopic area of the heart that is causing an issue and “burn” or ablate that area so it hopefully stops causing problems

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124
Q

What are noncardiovascular causes of syncopeobably not super important)

A

Stress
Hypoglycemia
Dehydration
Stroke
Seizure

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125
Q

What are cardiovascular causes of syncope (probably not super important)

A

Cardioneurogenic or “vasovagal” syncope (Carotid sinus sensitivity)
Dysrhythmias (tachycardias, bradycardias)
Prosthetic valve malfunction
Pulmonary emboli
HF

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126
Q

What are the 3 layers of the heart, starting with the inner most layer

A
  • Endocardium
  • Myocardium (muscle)
  • Pericardium (also has the pericardial space with 10-15mLs)
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127
Q

What is infective endocarditis 2

A
  • Disease of the endocardial layer of the heart
  • Most often affects the aortic and mitral valves
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128
Q

How is infective endocarditis classified

A
  • Cause (like from IV drug use, fungal, etc)
  • Plus the site of involvement (like a valve)
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129
Q

What is the difference between subacute and acute infective endocarditis

A
  • Subacute: when there is a preexisting valve disease
  • Acute: when the valves are healthy
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130
Q

What 3 organisms can cause infective endocarditis

A
  • Bacterial (most common)
  • Viruses
  • Fungi
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131
Q

What is the issue with bacterial caused infective endocarditis

A

These bacteria make biofilms, which can make it hard for us to kill

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132
Q

What are risk factors for infective endocarditis

A
  • Aging
  • IV drug use
  • Prosthetic valves
  • MRSA in your blood
  • Hemodialysis
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133
Q

What are the 3 stages of infective endocarditis

A
  1. Bacteremia (bacteria floating around in the heart)
  2. Adhesion (adhere to heart valves)
  3. Vegetation (start growing - create biofilms)
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134
Q

What is a big risk with infective endocarditis

A

Things can get stuck in these biofilms like fibrin, leukocytes, platelets and microbes, and create clots, which can break off and cause a stroke
(30% of people develop embolization)

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135
Q

What are the nonspecific symptoms of infective endocarditis

A
  • Fever
  • Chills
  • Weakness
  • Malaise
  • Fatigue
  • Anorexia
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136
Q

What are subacute symptoms of infective endocarditis

A
  • Arthralgias
  • Myalgias
  • Back pain
  • Abdominal discomfort
  • Weight loss
  • Headache
  • Clubbing
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137
Q

What are vascular symptoms of infective endocarditis

A
  • Splinter hemorrhages in the nail beds (look like little splinters)
  • Petechiae
  • Osler’s nodes on fingertips or toes (red and painful lesions)
  • Janeway’s lesions on pads of the fingers and toes (not painful)
  • Roth’s spots
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138
Q

If someone has infective endocarditis, what might we hear when listening to the heart

A

Murmur

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139
Q

Besides a risk for an embolism, what is another complication caused by infective endocarditis

A

HF

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140
Q

How do we diagnosis infective endocarditis

A
  • History is SUPER important (anything that can introduce bacteria into the blood)
  • Labs: *blood cultures (from 3 different sites), CBC with diff (look at WBCs) , ESR and c-reactive protein (see if there’s inflammation)
  • *Echo (look at the valves to find vegetation/disfunction)
  • Chest x-ray
  • ECG
  • Duke criteria
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141
Q

If someone is at risk for infective endocarditis, what should they do before having a procedure done (think of Kaleb and the dentist)

A

Need to be on prophylactic antibiotics before having tx

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142
Q

What is our tx for someone with infective endocarditis 7

A
  • Long-term IV antibiotics (4-6 weeks)
  • Repeat blood cultures to see if the antibiotics are working
  • Valve replacement if needed
  • Follow up echo and inflammatory markers (1, 3, 6, 12 months)
  • Antipyretics (acetaminophen)
  • Fluids
  • Res
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143
Q

What type of infection is a big risk for infective endocarditis

A

Staph or strep

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144
Q

What is some nursing care for someone with infective endocarditis 2

A
  • Moderate activity (don’t want to cause chest pain while they’re fighting the infection)
  • Deep breath and cough every 2 hours
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145
Q

What is happening in myocarditis

A

There is inflammation going on

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146
Q

What things can cause myocarditis 6

A
  • Viruses
  • Bacteria
  • Fungi
  • Radiation
  • Pharmacological factors
  • Chemical factors
  • Autoimmune
  • Idiopathic
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147
Q

What can myocarditis lead too

A
  • Cellular damage
  • Necrosis
  • Cardiomyopathy
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148
Q

What is interesting about the symptoms of myocarditis

A

The symptoms can range from benign to life threatening symptoms like HF, dysrhythmias or sudden cardiac death

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149
Q

What are symptoms of myocarditis

A
  • Fever
  • Fatigue
  • Malaise
  • Myalgias
  • Pharyngitis
  • Dyspnea
  • Lymphadenopathy (swollen lymph nodes)
  • N/V (early symptom of viral illness)
  • Cardiac symptoms usually 7-10 days after viral illness
  • Pericarditis
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150
Q

What are early and late symptoms of pericarditis

A

Early: pleuritic chest pain, pericardial friction rub, effusion
Late: HF symptoms - s3 heart sounds, crackles, JVD, syncope, peripheral edema, and angina

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151
Q

How do we diagnosis myocarditis

A
  • ECG
  • *Endomyocardial biopsy (provides conclusive diagnosis)
    (a lot of other lab findings might show that something is wrong, but aren’t inconclusive)
152
Q

What is our tx for myocarditis

A

Basically anything we would do to treat HF
- Drugs: ACEs, Beta blockers, diuretics, nitroprusside, milrinone
- If caused by autoimmune: can treat with immunosuppressants

153
Q

What is pericarditis

A

Inflammation of the pericardial sac (where there is 10-15mLs of fluid), often with fluid accumulation

154
Q

What are common causes of pericarditis

A
  • Infectious (like from bacterial, fungal, viral, etc)
  • Non-infectious (from MIs, cancers, dissecting aortic aneurysm, radiation, trauma, renal failure)
  • Hypersensitive or autoimmune (like rheumatic fever, RA, lupus, etc)
155
Q

What are the 3 different types of pericarditis

A
  1. Acute
    - Develops rapidly
    - Causes pericardial sac to become inflamed and leak fluid = pericardial effusion
    - Characteristic pathological finding is inflammation, neutrophils, increased pericardium vascularity, fibrin deposits on epicardium
  2. Subacute
    - Occurs weeks to months after the event
  3. Chronic
    - Lasts more than 6 months
156
Q

Why is pericardial effusion bad

A

The fluid leaking can compress the heart, decrease your cardiac output and lead to cardiogenic shock

157
Q

What are the symptoms of pericarditis

A
  • *Progressive, sever, sharp chest pain that is worse when taking in a breath or when laying flat, and is improved when sitting or leaning forward
  • *Pericardial friction rub
    • Pain that is referred to the trapezius muscle (shoulder, upper back)
158
Q

Where can we best hear a pericardial friction rub and how do we tell the difference between it and a pleural friction rub from the lung

A

Listen at the lower left sternal border with the patient leaning forward. Have the pt hold their breath, if you can still hear it, then it’s a pericardial friction rub

159
Q

What are the two big complications of pericarditis

A
  1. Pericardial effusion
  2. Cardiac tamponade
160
Q

What are signs that someone may be having a large pericardial effusion

A

The build up of fluid can compress other nearby structures causing:
- Cough
- Dyspnea
- Tachypnea
- Hoarseness

161
Q

What does a pericardial effusion make the heart sound like

A

Heart sounds will be distant and muffled

162
Q

As the pericardial effusion becomes bigger and bigger, what can it lead too

A

Cardiac tamponade

163
Q

What are symptoms and findings in cardiac tamponade

A
  • Confusion
  • Anxiety
  • Cardiac output will decrease
  • Heart sounds will be muffled
  • JVD
  • Narrowed pulse pressure
  • Tachypnea
  • Tachycardia
  • Pulse paradoxes (large decrease in systolic BP during inspiration)
164
Q

How can we treat effusions and tamponade

A

Pericardial paracentesis

165
Q

How can we diagnosis pericarditis

A
  • *ECG - we would see diffuse widespread ST elevation in lots of leads (different than in an MI, where we don’t see it in a lot of leads)
  • Echo - helps determine the amount of fluid
  • Labs - leukocytosis, increased CRP and ESR, and increased troponin
166
Q

What are the different txs for pericarditis

A
  • NSAIDs for the pain and inflammation (these pt can be in serious pain)
  • Pericardiocentesis (using an echo)
  • Pericardial window (cut a little window so that the fluid can drain out)
167
Q

What is some nursing care for these pts

A
  • Provide a table if needed for them to lean on to help with the pain
  • Keep HOB elevated above 45 degrees
  • NSAIDs for pain (give with food to prevent upset)
168
Q

What is chronic constrictive pericarditis

A

Can happen after acute pericarditis, where fibrin deposits into that space causing scarring and thickening, which results in a destruction of that space

169
Q

Why is chronic constrictive pericarditis bad and what can it lead too?

A

It’s bad because it can prevent the heart from adequately streatching and can mimic HF and cor pulmonale

170
Q

What is the tx of chronic constrictive pericarditis

A
  • Pericardiectomy (reconstruct the pericardium)
171
Q

What type of infection can lead to rheumatic fever/rheumatic heart disease

A

Complications from strep A

172
Q

Basically what is strep A doing if left untreated

A

Can cause acute inflammation involving all layers of the heart (rheumatic fever), which can then lead into chronic scarring and deformity of the heart valves (rheumatic heart disease)

173
Q

What is the key with rheumatic fever/rheumatic heart disease

A

Prevention is key - once they have strep A, we want them to take abx so it doesn’t turn into rheumatic fever/rheumatic heart disease

174
Q

What are our 4 valves

A
  • Two atrioventricular valves (sperate the atriums and ventricles) Mitral and tricuspid
  • Two semilunar valves - Aortic and pulmonic
175
Q

What are the 2 types of valve dysfunctions

A
  1. Stenosis
  2. Regurgitation
176
Q

What is happening in a stenosis

A
  • Valves thicken and fuse together
  • Narrows the opening, which requires more pressure for blood to get through the valve
  • Does not fully open or close
  • Causes blood to backflow to the preceding chamber
  • Disease can be pretty progressed before you get symptoms
177
Q

What is happening in regurgitation

A

Incompetent valves that are not closing completely, which causes blood to flow backwards

178
Q

What is the most common cause of mitral valve stenosis

A

Rheumatic heart disease

179
Q

What is happening in mitral valve stenosis

A
  • Scarring of the valve leaflets and chordae tendineae
  • Contractures develop with adhesions
  • Results in an increased left atrial pressure and pulmonary vasculature pressure
  • Risk for a-fib
180
Q

What is a good way to describe what a mitral valve stenosis looks like

A

Looks like a “fish mouth”

181
Q

What is the pathway affected by mitral valve stenosis

A
  • Oxygenated blood is coming from the left atrium
  • The mitral valve stenosis does not let enough blood pass through from the left atrium to the left ventricle
  • This causes a backup in the left atrium, which causes an increase in pressure in the left atrium
182
Q

What are symptoms of mitral valve stenosis

A

(like left sided HF - blood is backing up into the lungs)
- *Exertional dyspnea caused by reduced lung compliance
- Loud s1
- Diastolic murmur
- Fatigue
- Palpitations
- Hoarseness
- Hemoptysis
- A-fib with risk for stroke

183
Q

What 4 things do we need to have intact in order to prevent mitral valve regurgitation

A

Functioning:
- mitral leaflets
- mitral annulus
- chordae tendineae
- papillary muscles

184
Q

What might cause mitral valve regurgitation

A
  • MI
  • Chronic rheumatic heart disease
  • Mitral valve prolapse
  • Ischemic papillary muscle dysfunction
  • Infectious endocarditis
185
Q

What can acute mitral valve regurgitation cause? What are the symptoms?

A
  • Pulmonary edema
  • Symptoms: thready peripheral pulses and cool, clammy extremities, possible cardiogenic shock
186
Q

What can chronic mitral valve regurgitation cause

A
  • Left atrial enlargement
  • Ventricular dilation
  • Eventual ventricular hypertrophy
  • Decrease in cardiac output
187
Q

What are symptoms of chronic mitral valve regurgitation

A

(pts can be asymptomatic for years)
- Weakness, fatigue, palpitations, dyspnea
- Progress to orthopnea, paroxysmal nocturnal dyspnea
- Peripheral edema
- S3, murmur

188
Q

What is the tx for mitral valve regurgitation

A
  • Valve replacement
189
Q

What is happening with mitral valve prolapse

A

There is some sort of abnormality with the leaflets, papillary muscle or chordae that is causing the leaflets to prolapse back into the left atrium during systole

190
Q

Is mitral valve prolapse serious

A

Actually, no, not really. Not a lot of people will be impacted by it if they have it. (most people are asymptomatic for life)

191
Q

What doe the aortic valve separate

A

The aorta and left ventricle

192
Q

What are the causes of aortic valve stenosis

A
  • Congenital
  • Rheumatic fever
  • Degenerative (progressive deterioration)
193
Q

What will an aortic valve stenosis cause

A
  • Obstruction of blood flow from the left ventricle to the aorta
  • Causes an increase in left ventricle pressure
  • Left ventricle will become hypertrophy
  • Leads to poor cardiac output
194
Q

What are some symptoms of aortic valve stenosis

A
  • Angina
  • Syncope
  • Exertional dyspnea
195
Q

Should we treat aortic valve stenosis

A

YES! - very poor prognosis if symptomatic and it’s not corrected

196
Q

What drug do we want to use cautiously with someone with an aortic valve stenosis? Why?

A

Nitroglycerin
- It can cause severe hypotension
- Can worse the patient’s chest pain

197
Q

What can cause acute aortic valve regurgitation

A
  • Infectious endocarditis
  • Trauma
  • Aortic dissection
    (acute is usually a life-threatening emergency)
198
Q

What can cause chronic aortic valve regurgitation

A
  • Rheumatic heart disease
  • Congenital bicuspid aortic valve
  • Syphilis
  • Connective tissue problems
  • Post-surgical causes
199
Q

In chronic aortic valve regurgitation, what will happen to the left ventricle

A

It will dilate and hypertrophy to try and compensate for what is going one

200
Q

What are the symptoms of acute aortic valve regurgitation

A
  • Severe dyspnea
  • Chest pain
  • Hypotension
  • Cardiogenic shock
201
Q

What are symptoms of chronic aortic valve regurgitation

A

(may be asymptomatic for years)
- Exertional dyspnea
- Orthopnea
- Paroxysmal dyspnea
- Angina
- *“water-hammer” pulse (strong quick beat that collapses immediately)
- Soft or absent S1
- S3 or S4
- Murmur

202
Q

Where is your tricuspid valve located

A

Between right atrium and right ventricle

203
Q

What almost always causes tricuspid valve stenosis

A

Rheumatic fever

204
Q

What are symptoms of tricuspid valve stenosis

A
  • Fluttering discomfort in the neck
  • Fatigue
  • Right upper quadrant pain
205
Q

What almost always causes pulmonic valve stenosis

A

It’s congenital

206
Q

What will pulmonic valve stenosis cause

A

Right ventricular hypertension and hypertrophy

207
Q

What are the symptoms of pulmonic valve stenosis

A
  • Syncope
  • Dyspnea
  • Angina
208
Q

How do we diagnosis valvular heart disease (all of these valves diseases)

A
  • Get a good pt history and exam
  • Echo (we can look at the valves on these)
  • Chest xray (show us the heart size)
  • ECG (catch hypertrophy)
  • Heart catheterization
209
Q

What is our conservative therapy tx for valvular heart disease

A
  • Prevent HF exacerbations (vasodilators (ACEs, ARBS), positive inotropes (digoxin), diuretics, beta blockers)
  • Prevent pulmonary edema (sodium restrictions)
  • Prevent thromboembolism (anticoagulation)
  • Use antibiotics to prevent rheumatic fever and infectious endocarditis
210
Q

What is a percutaneous transluminal balloon valvuloplasty

A
  • Put in a new valve through a balloon-tipped catheter in the femoral artery
211
Q

Would we rather repair or replace a valve

A

Repair (has a lower mortality rate)

212
Q

Will repairing a valve restore total function?

A

No, it might not always

213
Q

What are the two different types of valves that we can put in when replacing

A
  • Mechanical (artificial)
  • Biologic (tissue)
214
Q

What are the benefits and drawbacks of a mechanical valve replacement

A
  • More durable
  • Last longer
  • However, there is a risk of thromboembolism, so they require long-term anticoagulants
215
Q

What is the benefit and drawback of a biologic valve (like Kaleb’s)

A

Don’t need anticoagulants, but they are less durable (so they won’t last as long)

216
Q

What is happening with a transcatheter aortic valve replacement (TAVR)

A
  • Used for severe aortic stenosis
  • Takes a transfemoral approach
  • Two different types of valves that they can use
  • Even if they get a biological valve, they may still need anticoagulants if they have a-fib
217
Q

What is peripheral artery disease

A

Thickening of the artery walls, which leads to the progressive narrowing of the arteries in the extremities

218
Q

Is it easy to catch peripheral artery disease early?

A

No, it’s usually underdiagnosed and hard to catch early (usually advanced when you start to have symptoms)

219
Q

What are the risk factors for PAD

A
  • Tobacco use
  • Atherosclerosis
  • Diabetes
  • HTN
  • High cholesterol
  • Age greater than 60
220
Q

How do they think PAD starts

A

Getting a lesion someone in the arteries

221
Q

Basically what is happening in PAD

A

Atherosclerosis

222
Q

If you have PAD, will the lesions be generally in one spot?

A

No, it’s more likely that you’ll have lesions in multiple different spots, it’s not just localized.

223
Q

What is interesting about men and women who have PAD

A

Women actually have worse outcomes, progress much and have a higher mortality rate than men with PAD

224
Q

What is the process of developing atherosclerosis

A
  1. Injury to the endothelium (can be from HTN, tobacco, etc).
  2. Develops into a fatty steak
  3. Forms a fibrous plaque, vessel becomes narrowed from this
  4. Complicated lesions form (total occlusion can occur or the clot can break off and go to other parts of the body)
225
Q

Where are diabetics more likely to have atherosclerotic lesions form

A

Below the knee, while non-diabetics have lesions that develop above the knee

226
Q

What is a classic symptom of PAD? What is it?

A

Intermittent claudication - ischemic muscle pain that is caused by a constant level of exercise, due to a build up of lactic acid from anaerobic metabolism.
- It resolves within 10 minutes or with rest.
- It’s reproducible.
- Acts like angina but in the extremities

227
Q

Does everyone with PAD present with the same symptoms?

A

No, only 1/2 have classic symptoms like intermittent claudication, but the others may have no symptoms at all or they may have atypical symptoms.

228
Q

Is paresthesia a common symptom of PAD? What is it? What can it cause?

A

Yes it is.
- Numbness and tingling in the toes or feet from nerve tissue ischemia
- Decreased in healing
- Can cause shooting pain (neuropathy)
- Skin is going to be thin and shiny
- Injuries can go unnoticed
- Have reduced sensations

229
Q

What is an early sign of PAD? What does this mean?

A

Reduced blood flow to limbs causing:
- Thin, shiny, and taut skin
- Loss of hair on the lower legs
- Diminished or absent pedal, popliteal, or femoral pulses
- Pallor of foot with leg elevation
- Reactive hyperemia of foot with dependent position (when you put your legs up you have pain and they go pale, when you put them down they feel better and turn red)

(NO EDEMA!)

230
Q

If someone has PAD, should you put their feet up?

A

NO! It’s going to hurt.

231
Q

Why does it hurt to put someone’s feet up if they have PAD

A

Because they have poor blood flow, so it’s harder for blood to get to the extremities if the extremity is elevated

232
Q

When is pain with limb elevation more likely to occur with PAD

A

At night, because our BP and cardiac output gets a little slower at night (these guys want to sleep with their feet more down)

233
Q

What is critical limb ischemia? Can PAD cause this? What can it lead too?

A
  • It’s chronic ischemic rest pain lasting more than 2 weeks
  • Yes, it can be caused by PAD
  • Can lead to non healing ulcers or gangrene
234
Q

What is the most serious complication resulting from PAD

A

Non healing arterial ulcers and gangrene

235
Q

What do many non healing arterial ulcers and gangrene result in

A

Amputation

236
Q

What are diagnostic studies for PAD 4

A
  • Doppler ultrasound
  • Duplex imaging
  • Ankle-brachial index (ABI)
  • Angiography and MRI (can use contrast to see how much blood is getting through your arteries)
237
Q

What are ways to treat PAD

A
  • Get BP under control (DASH diet can help to reduce sodium)
  • Tobacco cessation
  • Hemoglobin A1C under 7%, optimally near 6
  • Aggressive tx of hyperlipidemia using diet and statins
238
Q

What types of drugs can help reduce the symptoms of PAD? How?

A

ACE inhibitors like ramipril - they can:
- Decrease cardiovascular morbidity
- Decrease mortality
- Increase peripheral blood flow
- Increase blood flow
- Help increase your walking distances

239
Q

If you have PAD - Are they worried about clots? What drugs will they give you?

A

Yes, but they actually give it more to help thin your blood so it can pass more easily in the clogged arteries! You’ll get antiplatelet agents like:
- Aspirin (low dose)
- Clopidogrel (Plavix) - if allergic
- Usually not recommend to give coumadin

240
Q

What two drugs can be given for the tx of intermittent claudication

A
  • Cilostazol (Pletal) - inhibits platelet aggregation and increases vasodilation (except you can’t give it if they have HF)
  • Pentoxifylline (Trental) - improves flexibility of RBCs and WBCs and decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity
241
Q

When it comes to exercise with pts with PAD, what is important to remember

A

It needs to be supervised by the provider

242
Q

What is the most effective exercise for pts with claudication? Why?

A

WALKING - they should walk 30 minutes daily or 45 minutes 3 times/week (helps increase circulation and slow down the disease progression)

243
Q

For what gender is it really important to encourage walking to treat claudication

A

Women, because they have a faster decline with PAD and a faster decline in mobility

244
Q

What are BMI and waist circumference goals for individuals regarding nutritional therapy and PAD

A
  • BMI <25
  • Waist circumference less than 40 for men
  • Waist circumference less than 35 for women
245
Q

What are our txs for a leg with critical limb ischemia

A
  • Bypass surgery (bypass the clotted artery)
  • Not a good candidate for bypass, they can do a percutaneous transluminal angioplasty and put in something like a stent
  • Atherectomy (remove the plaque with a catheter)
  • Endarterectomy (open surgery to remove the plaque)
  • Cryoplasty
  • Amputation
  • Not a good candidate for these, they can go on a drug called iloprost
246
Q

Compared to men, do women who have a hospital procedure done for the tx of PAD do better or worse in the hospital

A

Women actually do worse, regardless of the disease severity or procedure being done.

247
Q

When a pt is recovering from a procedure, like a bypass, how often are we checking their vitals, sensations, pulses, cap refill, temperature, etc?

A

Every 15 minutes initially, then eventually every hour

248
Q

If someone has just had a bypass or a stent, should we put their knee in a flexed position

A

No

249
Q

After a surgical procedure, like a bypass, should the pt have an increase or decrease in circulation compared to their baseline

A

They should have an increase in circulation

250
Q

Should people with PAD use heating or ice packs?

A

No, because they might not be able to feel that it is burning or getting too cold.

251
Q

Should a pt who has PAD, who just had a procedure like a bypass, exercise through their pain

A

NO! We want them to stop exercising when they have pain, so we can avoid the lactic acid buildup, but once the pain stops, they should continue with their exercise (they shouldn’t cut back on their exercise plan)

252
Q

If a pt has a stent placed or an amputation, what kind of med are they going to be on

A

Long-term antiplatelet therapy

253
Q

What is acute arterial ischemia

A

When arterial blood supply is suddenly cut off from a tissue, organ or extremity

254
Q

What can cause acute arterial ischemia

A
  • Embolism (from infective endocarditis, mitral valve disease, atrial fibrillation, cardiomyopathies, and prosthetic heart valves)
  • Thrombosis
  • Trauma
    (basically anything that can stop blood supply)
255
Q

What are the 6 P’s of compartment syndrome and acute ischemia (signs that there is a blockage)

A
  1. Pain (going to be very severe pain, and is not relieved)
  2. Pallor
  3. Pulselessness
  4. Paresthesia (at least decreased sensation, does not have to be a complete loss)
  5. Paralysis (late sign)
  6. Poikilothermia (the limb takes on the temperature of the atmosphere, so its getting cold)
256
Q

What is our tx for compartment syndrome (acute ischemia)

A
  • Anticoagulant (IV heparin)
  • Remove the clot (ie surgically, bypass, etc)
257
Q

What are the surgical interventions for compartment syndrome (acute ischemia)

A
  • Percutaneous catheter-directed thrombolytic therapy (go into the artery and put in alteplase or urokinase (TPA) to dissolve the clot at the site)
  • Surgical revascularization (fix the artery, like if it was damaged from a trauma)
  • Amputation
258
Q

What is thromboangiitis obliterans (Berger’s disease)

A

Recurrent inflammatory disorder of the small and medium arteries and veins in the arms and legs, which is not caused by atherosclerosis, where a thrombosis will block the vessel.

259
Q

Who most commonly has thromboangiitis obliterans

A

Men younger than 45 who have a history of tobacco and/or marijuana use with other CVD risk factors like HTN, hyperlipidemia, diabetes, etc.

260
Q

What are the symptoms of thromboangiitis obliterans

A
  • Intermittent claudication of feet, hands or arms
  • Ischemic ulcers
  • Changed in color and temperature (ie having purple, white and red fingertips)
  • Paresthesia
  • Cold sensitivity
261
Q

How do we diagnosis thromboangiitis obliterans

A

Really not a lab or diagnostic test that we can do, mostly base it off of symptoms

262
Q

What is the tx for thromboangiitis obliterans

A
  • Stop smoking tobacco or marijuana (*don’t replace with nicotine)
  • Avoid cold exposure
  • IV iloprost to promote vasodilation
263
Q

What are the symptoms of Raynaud’s

A

Changes in color and pain to the fingers, toes, ears and nose

264
Q

What is happening in Raynaud’s phenomenon

A

Vasopastic disorder most commonly affecting the small cutaneous arteries (vasospasms happening)

265
Q

What can trigger Raynaud’s

A
  • Exposure to cold
  • Emotional upset
  • Tobacco use
  • Caffeine use
266
Q

How can we treat Raynaud’s

A

Avoid temperature extremes; wear appropriate clothing
No tobacco products; avoid caffeine
Submerging fingers in warm water may decrease vasospasm
No vasoconstrictor drugs
Can be placed on long acting calcium channel blockers to stop the vasospasms

267
Q

What is an aortic aneurysm

A

Permanent, localized, outpouching, or dilation of wall of aorta

268
Q

What can cause aortic aneurysms

A
  • Degenerative (age, etc)
  • Congenital
  • Mechanical (penetrating or blunt trauma)
  • Inflammatory
  • Infections
269
Q

What are risk factors for aortic aneurysms (a lot)

A
  • Age
  • Male gender
  • *HTN
  • *Coronary artery disease
  • *Family history (a lot of congenital things can cause this to happen)
  • *Tobacco use
  • High cholesterol
  • Lower extremity PAD
  • Carotid artery disease
  • Previous stroke
  • *Excess weight or obesity
270
Q

What are some congenital anomalies that can increase your risk of an aortic aneurysm

A

Bicuspid aortic valve
Coarctation of aorta
Turner’s syndrome
Autosomal dominant polycystic kidney disease
Ehlers-Danlos syndrome (connective tissue disorder - lose skin)
Loeys-Dietz syndrome
Marfan’s syndrome

271
Q

What are the two classifications of Aoritc aneurysms

A
  • True
  • False (don’t worry about this one)
272
Q

What is happening in a true aortic aneurysm

A

The wall of the artery forms the aneurysm and at least one vessel layer is still intact

273
Q

What are the 2 different types of aortic aneurysm

A
  • Fusiform: where you have the aneurysm forming into a uniform shape
  • Saccular: where the aneurysm forms a sac on one side
274
Q

What are the symptoms of a thoracic Aoritc aneurysm (TAA) (anything above the diaphragm)

A
  • Often asymptomatic, but…
  • Might have diffuse chest pain
  • Pain might extend to interscapular area (*pain radiating to their back or shoulder - we start to think that it might be an aneurysm)
275
Q

What are symptoms if the aneurysm is in the ascending aorta/aortic arch

A
  • Angina
  • Transient ischemic attacks
  • Coughing
  • SOB
  • Hoarseness
  • Dysphagia
  • If it presses on your superior vena cava it can cause distended neck veins and edema of the face and arms
276
Q

How do we detect an abdominal aortic aneurysm (AAA)

A
  • On physical exams (we can hear a bruit or feel a mass)
  • When a pt is examined with a scan for another problem
    (it’s usually an incidental finding)
277
Q

What are symptoms of an abdominal aortic aneurysm

A
  • Pain that may look like it’s caused by abdominal or back disorders
  • Epigastric discomfort
  • Altered bowel elimination
  • Intermittent claudication
  • May spontaneously embolize plaque leading to “blue toe syndrome”, where the feet and toes turn patchy blue with a palpable pulse
278
Q

What is the biggest complication of an aortic aneurysm

A

RUPTURE into the retroperitoneal space
- Bleeding may be tamponaded by surrounding structures, thus preventing exsanguination and death.
- Severe back pain
- May/may not have back/flank ecchymosis (bruising - takes several hours to develop) (Grey Turner’s sign)
- Will lead to hypovolemic shock (most do not survive long enough to get to the hospital - very high mortality 53%)

279
Q

What can we do to diagnosis an aortic aneurysm

A
  • X-ray
  • ECG (to rule out MI)
  • *Echo
  • Ultrasound (don’t want to be pushing if someone is bleeding)
  • CT or MRI (CTs are nice and quick)
  • Angiography
280
Q

What is the tx for aortic aneurysm

A

Depends on how big it is - if it’s small they might just wait and watch

281
Q

If an aortic aneurysm is considered small (under 5.4cm) what is the tx?

A

Conservative therapy used
- Risk factor modification
- ↓ blood pressure, tobacco cessation, optimize lipid profile, gradual 🠕 physical activity
- Size 4 to 5.4 cm—ultrasound, CT scan monitoring every 6 to 12 months
- Size < 4cm—ultrasound every 3 years

282
Q

What is the aortic aneurysm is larger than 5.5cm? What is the tx?

A

Surgical repair

283
Q

What pre-op care do we want to do for our pt before they have surgery on their aneurysm

A
  • *Keep BP low
  • Rest
  • Keep stress level down (have them chill)
284
Q

What are the 2 types of surgical repairs that they can do on aortic aneurysms

A
  • Open aneurysm repair
  • Endovascular graft procedure
285
Q

What are the 2 types of surgical repairs that they can do on aortic aneurysms

A
  • Open aneurysm repair (very risk - high death)
  • Endovascular graft procedure (minimally invasive - go through the femoral artery - lower risk of death)
286
Q

What are potential complications with an endovascular graft procedure

A

Endoleak—most common - Seepage of blood into old aneurysm
Aneurysm growth at either end
Aneurysm rupture
Aortic dissection
Bleeding
Renal artery occlusion caused by stent migration
Graft thrombosis
Incisional site hematoma
Surgical site infection

Graft dysfunction may require surgical repair
Need for life-long follow-up

287
Q

During a AAA repair, what is a complication that can occur? What is it? What is the tx?

A

Intra abdominal hypertension (similar to abdominal compartment syndrome)
- Blood flow is reduced to viscera
- Leads to multisystem organ failure

TX: decompress the belly

288
Q

What are the symptoms that an aneurysm has ruptured

A
  • Severe pain (feels like a tearing or ripping)
  • Hypovolemic shock (low BP, diaphoresis, tachycardia, changes in LOC, pulsating abdominal mass)
289
Q

What is a big thing to watch with these aneurysms

A

Renal status (watch urine output, etc)

290
Q

What would be helpful to do with pedal pulses and skin lesions

A

Mark them before surgery

291
Q

After an open repair on a aneurysm, what will the care be like

A
  • Go to the ICU for 24-48hrs
  • They’ll have all of these lines:
    Arterial line
    Central venous pressure (CVP) or pulmonary artery (PA) catheter
    Endotracheal tube and mechanical ventilation
    Peripheral IV lines
    Urinary catheter
    NG tube
    Chest tube (possible)
    Lumbar drain (possible)

ECG—continuous monitoring
Pulse oximetry
Pain medication
Keep BP low, but not low enough that it’s going to clot off
Monitor urinary output hourly
Check neuro

292
Q

What do you do if your pt after post-op for an aneurysm has Absent pulses + cool, pale, mottled, or painful extremity

A

Report immediately - it may mean that there is a clot or occlusion

293
Q

After post-op for an aneurysm, what should we tell our pt about exercise and lifting

A

Gradually increase exercise and avoid heavy lifting for 6 weeks

294
Q

Is an aortic dissection a “dissecting aneurysm”

A

No - it’s not a type of aneurysm

295
Q

What is an aortic dissection

A

Where a false lumen forms between the inner and middle layer of the blood vessel

296
Q

What is the difference between an aneurysm and a dissection

A

In an aneurysm the layers of the blood vessel are still intact, while in a dissection the layers have split

297
Q

How do we classify aortic dissections? What are the two types?

A

We classify by either type A or type B (based on location)
- Type A: affects the ascending aorta and arch and requires emergency surgery
- Type B: begins in the descending aorta and can be treated with conservative therapy

298
Q

What is happening in a nontraumatic dissection

A
  • Caused by weakened elastic fibers in the arterial wall
  • Chronic hypertension hastens the process
  • Tear in inner layer allows blood to surge between inner and middle layer
  • Can lead to rupture through outside wall can cause death
299
Q

How can your heart make the dissection worse

A

As the heart contracts, each systolic pulsation increases pressure on the damaged area, which can make it worse

300
Q

Besides rupturing, what else are we worried about with dissections

A

That they may occlude major branches of the aorta - cutting off blood supply to the brain, abdominal organs, kidneys, spinal cord and extremities

301
Q

What is the most important risk factor for dissection

A

HTN

302
Q

What are other risk factors for dissection

A
  • Drug use (meth)
  • Blunt trauma
  • Tobacco use
  • Connective tissue disease
  • Pregnancy (bc connective tissue gets looser)
303
Q

What are type A aortic dissection symptoms

A

Abrupt onset of severe (very, very painful) anterior chest pain or upper back pain (where your ascending aorta is)

304
Q

Why is a type A more emergent than a type B

A

Because if a type A ruptures, it can cut off blood supply to the whole body (these is why we check for neuro status, because blood supply to the brain could be impacted

305
Q

What are type B aortic dissection

A

Pain in the back, abdomen, or leg (pain is very severe)

306
Q

How can we tell the difference between an aortic dissection or MI

A

Usually a dissection pain is very abrupt onset, where an MI pain might be a more gradual

307
Q

What is interesting about MIs and dissections

A

It’s hard to tell the different between the two - this is why we would do a diagnostic confirmation like with a CT scan, because we don’t want to treat them for an MI when they might actually have a dissection (they’ll die)

308
Q

What are the symptoms of an aortic dissection

A

(depends on where it is located)
If aortic arch involved - Neurologic deficits may be present
Type A - Causes disruption of blood flow in coronary arteries and aortic valve insufficiency
Subclavian artery - BP and arterial pulses different between arms
Aortic progression - Decreased tissue perfusion to abdominal organs and lower extremities

309
Q

What is a cardiac tamponade

A

When you have blood leaking from the aorta due to a dissection and into the pericardial sac

310
Q

What are symptoms of cardiac tamponade

A
  • Hypotension
  • Narrowed pulse pressure
  • Distended neck veins
  • Muffled heart sounds
  • Pulsus paradoxus (> 10 mmhg difference)
311
Q

How can we diagnosis an aortic dissection

A

H & P
ECG
Chest x-ray
CT scan (pretty easy to do - seems like the go to)
MRI
Transesophageal echocardiography

312
Q

What is our tx for an aortic dissection (besides surgery)

A
  • Control HR and BP (can use beta blockers and CCB) - want to get HR less than 60 and/or BP to 100-110
  • Pain management with morphine (want to help keep them calm)
313
Q

Why do we want to keep a pts BP down if they have an aortic dissection

A

Because we want to decrease the pulsating forces within the aorta

314
Q

What type of dissection can we do conservative therapy on

A

Acute or chronic type B without complications (can’t do on type A, as type A is an emergency)

315
Q

What is our conservative therapy for type B without complications

A

Pain relief
HR and BP control
CVD risk factor modification
Close surveillance with CT or MRI

316
Q

What is the standard to treat acute and chronic type B dissections with complications

A

Thoracic endovascular aortic repair (TEVAR)

317
Q

What is the tx for type A

A

Emergency surgery

318
Q

What is good to know about surgery to fix a dissection

A
  • Put a graft in to fix the spot
  • The aorta is very fragile though and it can be hard to get sutures to stick
  • Before surgery, they like to make sure that edema is decreased and blood is able to clot
319
Q

What is our goal for preop before surgery for an aortic dissection

A
  • Semi-Fowler’s position & quiet environment to ↓ HR
  • Goal HR around 60 BP around 100-120-lowest possible that will still perfuse organs
  • Anxiety and pain management (using Opioids and sedatives)
  • Titrate IV antihypertensive agents (like a beta blocker drip)
  • Continuous BP and ECG monitoring
  • Frequent VS ( every 2 to 3 minutes)
  • Feel peripheral pulses
  • Monitor for increasing pain, restlessness or anxiety
320
Q

If a patient had surgery for an aortic dissection, what medication will they probably be on for the rest of their life

A

Beta blockers

321
Q

What are the 2 types of venous thrombosis

A
  1. Superficial
  2. Deep vein (DVT)
322
Q

When someone says venous thromboembolism (VTE), what are they talking about

A

Spectrum from DVTs to pulmonary embolisms

323
Q

What is virchow’s triad 3 factors that put you at a high risk for VTE

A
  • Venous stasis (laying in bed, issues with valves, can’t move your extremities)
  • Damage to the endothelium (Chemo, diabetes)
  • Hypercoagulability of blood (sepsis, smoking, cancer)
324
Q

What are signs of a VTE

A
  • Pain
  • Redness
  • Area is warm
  • Edema
    (can be painless)
325
Q

What are signs of a superficial VTE

A
  • You can feel a palpable, firm, cordlike vein
  • Area is itchy, painful, red and warm
  • May have a mild fever and leukocytosis
326
Q

How do we diagnosis superficial VTE

A

Ultrasound

327
Q

What tx do we do for a smaller clot less than 5cm and not near the saphenofemoral junction

A

Oral (or topical) NSAIDs
Graduated compression stockings
Warm compresses
Elevate limb above heart
Mild exercise

328
Q

What are symptoms of lower extremity DVTs

A

Unilateral edema (usually only one leg)
Pain, tenderness with palpation
Dilated superficial veins
Sense of fullness in thigh or calf
Paresthesias
Red, warm
Fever greater than 100.4° F (38° C)

329
Q

How can we diagnosis a VTE

A
  • Ultrasound
  • D-dimer (if it’s elevated - it may indicate a clot in the body) should be less than 250
330
Q

For VTE, who is at a super high risk for hypercoagulability of blood

A

Women who smoke and are on oral contraceptives

331
Q

If someone is on warfarin, what labs do we want and what should those levels be

A

INR (2-3) and PT (20 seconds)

332
Q

What is the antidote for warfarin

A

Vitamin k

333
Q

What lab do we look at for heparin? What should it be?

A

aPTT 47-70 seconds

334
Q

What is the antidote for heparin

A

protamine

335
Q

What two labs besides aPTT do we want to monitor if they are on heparin

A
  • H&H (12-18, 36-54%)
  • Platelets (150,000-450,000)
336
Q

What are serious complications from VTEs

A
  • PE
  • Chronic thromboembolic pulmonary hypertension
  • Post-thrombotic syndrome (PTS)
337
Q

What is happening in post-thrombotic syndrome

A

Basically have chronic inflammation and hypertension that can lead to these symptoms:
Pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, and venous claudication

Persistent edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, white scar tissue, and lipodermatosclerosis (bottle neck shape of leg)

Signs may occur in a few months or years

338
Q

What are our 3 measures to prevent VTEs

A
  1. Early and progressive mobilization
  2. Graduated compression stockings
  3. Intermittent pneumatic compression devices (IPCs)
339
Q

If your pt has VTE already (a clot) should you put their ted hose or SKUDs on?

A

NO

340
Q

Should you wear SKUDs with ted hose

A

Yes

341
Q

What is the issue with warfarin

A

It takes 48-72 hours before it’s up to therapeutic levels, so they will give heparin or lovenox in the meantime

342
Q

What is the antidote of warfarin

A

Vitamin k

343
Q

What lab should we monitor for warfarin

A

INR (should be 2-3)

344
Q

What is a serious side effect with heparin

A

Heparin-induced thrombocytopenia (HIT)

345
Q

What is our direct thrombin inhibitor? What is it used for? What is the antidote? What are the advantages over warfarin?

A

Dabigatran (Pradaxa)
Used for VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE
Antidote: idarucizumab
Advantages over warfarin: rapid, no monitoring, few drug-food interactions, fewer risks of bleeding
But… it’s much more expensive than warfarin

346
Q

What are our factor Xa inhibitors? What are they used for? What is the antidote?

A

Fondaparinux, Rivaroxaba (Xarelto), apixaban (Eliquis), edoxaban
Used for VTE prophylaxis and tx
Antidote is andexant alfa

347
Q

If a pt is having abdominal or pelvic surgery for cancer or a major orthopedic surgery, should they receive VTE prophylaxis

A

Yes

348
Q

Will they do thrombolytic therapy for VTEs

A

yes - they can go in there with tPA and administer it through a catheter to dissolve the clot directly

349
Q

How many seconds should the QRS complex be

A

Less than 12 seconds

350
Q

How do we know someone is in sinus bradycardia

A

Rate is less than 60

351
Q

What should you teach your pt to avoid if they have a pacemaker, because these things can either deactivate the pacemaker or rip the pacemaker out with a magnet

A

Power-generating equipment
Welding equipment
Anti-theft stuff
Certain pieces of equipment used by dentists
Magnetic resonance imaging (MRI) machines
Radiation machines for treating cancer
Heavy equipment or motors that have powerful magnets

352
Q

What is happening in myocarditis

A

There is inflammation going on

353
Q

Is paresthesia a common symptom of PAD? What is it? What can it cause?

A

Yes it is.
- Numbness and tingling in the toes or feet from nerve tissue ischemia
- Decreased in healing
- Skin is going to be thin and shiny
- Injuries can go unnoticed
- Have reduced sensations

354
Q

What are BMI and waist circumference goals for individuals regarding nutritional therapy and PAD

A
  • BMI <25
  • Waist circumference less than 40 for men
  • Waist circumference less than 35 for women
355
Q

What are our two surgical options for VTE

A
  1. Open venous thrombectomy (where they open up the vein to remove the clot)
  2. Inferior vena cava interruption devices, like a filter, where they can trap clots
356
Q

What objective data might we see if someone has a VTE

A
  • General: fever, *anxiety, pain
  • Integumentary: increased size of the extremity, taut shiny skin, redness, tenderness
  • Cardiovascular: edema, cyanosis
  • Possible diagnostic findings: d-dimer, positive duplex ultrasound or venogram, CT
357
Q

If someone has an acute VTE, do we want them up and moving around

A

NO! This can cause the clot to move

358
Q

For someone that is on blood thinners, what is good pt teaching

A
  • Wear medical ID braclet
  • Avoid falls and trauma
  • Apply pressure to bleeding sites for 10-15 minutes
  • No ASA or NSAIDs
  • Limit alcohol
359
Q

If you are on blood thinners due to VTE risk, what reasons should you report/call EMS

A
  • Bleeding (urine, stool, vomit, nose, gums, skin)
  • Severe headache
  • stomach pain
  • Chest pain
  • SOB
  • Palpitations
  • Cold, blue or painful feet
  • mental status changes (may indicate cerebral bleeding)
360
Q

What is good pt teaching for someone going home with VTE risk

A

Know the signs of a PE
- Chest pain
- Dyspnea
- Tachypnea

361
Q

If you are on warfarin, what foods should you avoid

A

Foods high in vitamin k, like broccoli, spinach, kale, greens)

362
Q

What is happening in varicose veins

A

Valves are working in the legs, so blood isn’t flowing properly, which leads to veins in the legs becoming dilated and tortuous from the increase in pressure

363
Q

What are risk factors for varicose veins

A

Family history of venous problems, female, tobacco use, aging, obesity, multiparity, history of VTE, venous obstruction, phlebitis, leg injury, prolonged sitting or standing

364
Q

What two risk factors are the highest for varicose veins

A

A woman with a lot of pregnancies, being obese and prolonged sitting or standing, where we’re putting a lot of pressure on those veins

365
Q

What are the most common symptoms of varicose veins

A

heavy, achy feeling or pain after prolonged standing or sitting; relieved by walking or limb elevation

366
Q

What is the most common complication from varicose veins

A

Superficial venous thrombosis (since the blood is just sitting in the veins, it can lead to a clot)

367
Q

What is conservative tx for varicose veins

A
  • Rest with limb elevation
  • Graduated compression stockings
  • Leg-strengthening exercises
  • Weight loss
368
Q

What are some surgical therapy that we can do on someone with varicose veins

A
  • Sclerotherapy (take concentrated saline and inject it into the vein) (pretty severe pain)
  • Transcutaneous laser therapy or high-intensity pulsed light therapy (can cause burns)
369
Q

What is chronic venous insufficiency

A

When you have trouble getting blood back up to the heart

370
Q

What are the symptoms of chronic venous insufficiency

A
  • Pain: especially in the dependent position (pain when legs are down)
  • Lower legs look “leathery”, brown, thick, hard, dry
  • Eczema with itching and scratching
  • May have ulcers
371
Q

Do we treat ulcers for arterial and venous disease the same?

A

No - not so much

372
Q

What can help treat leg pain for someone who has chronic venous insufficiency

A

Put the legs up

373
Q

Should we put compression stockings on someone who has PAD? What about chronic venous insufficiency?

A

NO - because this will reduce blood flow for PAD. We should put them on for chronic venous insufficiency to help return blood flow.

374
Q

What are activity guidelines and limb positioning for chronic venous insufficiency

A

Avoid prolonged sitting or standing
Elevate legs above heart
Daily walking
Avoid trauma
Daily foot and leg care

375
Q

What are the 2 biggest things to promote wound healing for chronic venous insufficiency

A
  • Keep the area moist and wear the compression stockings or have the area wrapped
376
Q

When someone has an ulcer, what should you tell them to do

A

Monitor for infection - in the beginning, they might not be infected, so be on the lookout for signs of infection like changes in odor, drainage, induration and cellulitis

377
Q

Does it take a really long time for ulcers from PAD and chronic venous insuffiency to heal

A

Yes

201A (5 decks)

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