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GEN MED II Final EXAM > Study For Final > Flashcards

Study For Final Flashcards

1
Q 
No Trauma
Severe Stabbing Unilateral Chest Pain
Worse on Inspiration
Radiates to shoulder - same side
Lung Sounds Reduced/Absent in comparison
A

Primary Spontaneous Pneumothorax

A “Bleb” arises & goes unnoticed in a healthy Pt until it bursts, air rushes in and increasingly compresses the lung tissue

Often young tall wiry males, Often they are smokers - Sometimes 2nd to pneumonia

IV atavan and phenobarbitol for anxiety and pain relief, clean & dry shaved area mid claviclular @ 2nd intercostal space. Draw up lidocaine into 1.5” syringe, lidocainwheal, slip cannula over needle & reinsert needle w/cannula thru wheal, injecting lidocaine on the way down - you know you’ve pierced the pleura when bubbles form in the lidocaine syringe. Remove needle, leave catheter in place, attach one way valve, tape in place, open valve, bandage. Take serial X-rays to ensure lung is slowly re-inflating.

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2
Q

Bachman’s Bundle

A

SA Node tracts to Left Atrium

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3
Q

Internodal Tracts

A

Transmit impulses from SA Node thru Right Atrium

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4
Q

Right Vagus depresses

Left Vagus depresses

A

Sinoatrial Node

AV Node

Persistent bouts of bradycardia caused by SA and/or AV block can be rectified by vagotomy

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5
Q

Fastest cardiac conduction tract

A

Purkinji Fibers, then His then SA then AV

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6
Q

SA generated impulses

A

Usually 60-80 bpm

SA pacemaker intrinsic rate is 100-110 but is slowed by the Right Vagus to 60-80. Ectopic pacemakers are not under the control of Vagus though, so they can be much faster and, in the absence of epinephrine, are likely the cause of tachycardia, especially if irregular.

Generate a P-Wave on the EKG

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7
Q

AV Node generated impulses

A

Usually 40-60 bpm

Controlled by Rt Vagus, which may be responsible for AV Block.

Waves initiating below the Rt Atrium

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8
Q

P-Waves

A

0.12 seconds or less from Beginning of P to R (really its the Q point), if longer we have heart block shaping up, first degree

Ps are upright in AVF and II and BiPhasic in V1. They are Inverted in AVR as is the QRS

Ps are normally only 2.5 mm high

Elevation or Depression of the normally flat space between the hump of the P and the Q point indicates atrial infarction or pericarditis

Enlarged Ps = Enlarged Right Atrium

Biphasic Enlarged Ps = Enlarged Left Atrium

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9
Q

P-Waves

A

0.12 seconds or less from Beginning of P to R (really its the Q point), if longer we have heart block shaping up, first degree

Ps are upright in AVF and II and BiPhasic in V1. They are Inverted in AVR as is the QRS

Ps are normally only 2.5 mm high

Elevation or Depression of the normally flat space between the hump of the P and the Q point indicates atrial infarction or pericarditis

Enlarged Ps = Enlarged Right Atrium

Biphasic Enlarged Ps = Enlarged Left Atrium

Inverted P waves originate from either an ectopic atrial pacemaker or the AV Node. Below the AV node, there are NO P-Waves at all.

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10
Q

QRS Complex

A

Represents Ventricular Contraction.

Should be no more than 0.6 - 0.12 or
1.5 - 3 boxes wide

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11
Q

Hyper-Kalemia/ Digoxin Toxicity

A

Increased [K+] in the blood depolarizes the ventricles very quickly, giving rise to
1. “Peaky” T-Waves.

However, the increased K+ also depresses Na+ channels, slowing conduction of cardiac impulses through the heart and leading to

  1. Smaller P-Waves
  2. Wide QRS complexes (if you see this, the Hyper K+ is severe, think Dig Toxicity)
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12
Q

Hyper K+/ Dig Toxicity

A

Peaky T
Tiny P
Wide QRS

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13
Q

Hyper K+/ Dig Toxicity

A

Peaky Ts
Tiny Ps
Wide QRS

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14
Q

Normal Serum Potassium

A

3.5 - 5.5 mEq/L

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15
Q

HypoKalemia

A

Below 3.5 mEq/L

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16
Q

Hyper-Kalemia/ Digoxin Toxicity

A

Increased [K+] in the blood depolarizes the ventricles very quickly, giving rise to
1. “Peaky” T-Waves.

However, the increased K+ also depresses Na+ channels, slowing conduction of cardiac impulses through the heart and leading to

  1. Smaller P-Waves
  2. Wide QRS complexes (if you see this, the Hyper K+ is severe, think Dig Toxicity)
  3. R may slope right into the T, the smiley
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17
Q

Hyper K+/ Dig Toxicity

A

Peaky Ts
Tiny Ps
Wide QRS

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18
Q

Hyper Kalemia

A

Above 5.5 mEq/L

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19
Q

Hypo-Kalemia

A

Below 3.5 mEq/L

But EKG changes don’t appear until 2.7 isn

Often seen with Hypo Mg so watch out for Torsades and give MgSO4 empirically with our K+

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20
Q

Hypo K+ EKG Findings

A

Inverted T or Flat

Presence of big “U” waves between Inverted T and P-Wave

ST Depression

Taller Wider P Waves

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21
Q

Axis Deviation

A

The electric vector, the mean direction of all current moving through the heart, will point toward the thickest tissue.

Normally the vector begins at the AV node and proceeds down and to the left toward the apex of the left ventricle, the thickest part of the heart.

If there is Left ventricular Hypertropy, the thickest part of the heart shifts somewhat, and the vector moves left of where it normally is. This is called Left Axis Deviation.

If there is Right Ventricular Hypertropy, the vector moves to the right of normal. This is called Right Axis Deviation.

We assess Axis Deviation on the EKG by tracking lead I and lead AvF. In normal axis, both leads show +QRS complexes.

In Left Axis Deviation, The QRS in AvF will deflect downward but the QRS in lead I will still be positive. I(+) AvF(-) = Left Axis Deviation

In Right Axis Deviation, the QRS complex in lead I will be downward (-) and the QRS in lead AvF will be upward (+) or normal.
I(-) AvF(+) = Right Axis Deviation

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22
Q

JNC-8 HTN for 60 & over

A

over 150/90

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23
Q

JNC-8 HTN for under 60yrs

A

over 140/90

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24
Q

Primary HTN

A

Cause unknown but not due to comorbitity

The most common kind of HTN

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25
Q

Most Common Cause of Secondary HTN

A

Kidney Disease

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26
Q

Coarctation of the Aorta

A

A congenital narrowing of the Aorta in the arch or thoracic area which leads to a lower blood pressure below the coarctation (femoral) than above (brachial).

Presents as delayed or absent Femoral Pulses & Failure to Thrive

Rx is resection of the Aorta w/ stent. Sarah’s sister had this. Followed annually by CT for life.

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27
Q

Metabolic Syndrome

A 
Truncal Obesity
Triglycerides over 150
HDL under 40 (m) under 50 (f)
Bp 130/85 and over
Fasting Blood Sugar over 100
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28
Q 
BP Cuff Sizes
Infant
Child
Small Adult 
Adult
Lg Adult
Thigh
A 
7
9
10
11
12
13
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29
Q

Copper Wiring, Cotton Wool Spots &

Papillodema

A

Retinal Effects of HTN

Cu Wiring - Retinal arterial atherosclerosis

Cotton Wool Spots - Retinal Nerve Damage. Exploded ganglia

Papilladema - Optic Disc Swelling from increased intracranial Pressure, late consequence of atherosclerosis / HTN

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30
Q

Dx Studies to order if you Dx HTN

A

UA for urine protein

BUN/Cr for Renal Function - impaired if over 20 for BUN and over 1.5 m/1.2 f in Cr. If these values are high, order a Renal Ultrasound or Renal Artery Doppler to assess for Renal Stenosis

Lipid Panel
Electrolytes

Fasting Blood Sugar

EKG

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31
Q

Dx Studies to order if you Dx HTN

A

UA for urine protein

BUN/Cr for Renal Function - impaired if over 20 for BUN and over 1.5 m/1.2 f in Cr. If these values are high, order a Renal Ultrasound or Renal Artery Doppler to assess for Renal Stenosis

Lipid Panel
Electrolytes

Fasting Blood Sugar

Plasma Renin Test - if low, may indicate high salt ingestion, Steroid Use, Cushing Syndrome or other mechanisms by which the RAAS is being suppressed

EKG

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32
Q

Dx Studies to order if you Dx HTN

A

UA for urine protein

BUN/Cr for Renal Function - impaired if over 20 for BUN and over 1.5 m/1.2 f in Cr. If these values are high, order a Renal Ultrasound or Renal Artery Doppler to assess for Renal Stenosis

Lipid Panel
Electrolytes

Fasting Blood Sugar

EKG

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33
Q

Plasma Renin Test Results

A

Low: may indicate high salt ingestion, Steroid Use, Cushing Syndrome or other mechanisms by which the RAAS is being suppressed

High: Chronic Renal Failure

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34
Q

Widened Pulse Pressure

A

Systolic and Diastolic diverge over serial Bp

Aortic Regurge/Aortic Dissection

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35
Q

Test for Cushings Syndrome

A

Dexamethasone Test: Give Dexamethasone (essentially hydrocortisone) which should suppress cortisol production. If it doesn’t, there is a tumor, likely pituitary, pumping out ACTH and causing override of the feedback loop and continuous Cortisol release by the Adrenals

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36
Q

Target BMI

A

25

Overweight is 26
Obese in the 30s

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37
Q

Diabetes over 60, Bp goal is?

DM Triglyceride Goal is?

A1C goal is

A

150/90

Under 100 for Triglycerides in DM

Under 7

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38
Q

First Line HTN Rx:

A

ACEs & ARBs exp in DM
Thiazide Diuretics
Calcium Channel Blockers

Second line, increase doses of these

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39
Q

Thiazide Diuretics MOA

A

Block the Na/Cl symporter in the Distal Tubule

Also increase Ca+ retention and Lowers K+ retention

Don’t give to:
Hypokalemia - stop Thiazide if this develops
Renal Failure
Lithium for BiPolar, may increase serum levels
Nursing Mothers
Gout Pts (increase Ca XL formation)

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40
Q

THIAZIDES

vs

LOOPS

A

Use Thiazide in healthier Pts with GFR over 30
and if Ca+ retention is a plus and loss of
K+ is not a concern

Use Loops in more elderly Pts with GFR under
30, significant Renal Damage and where
Ca+ loss is desirable or where K+ loss is
not a concern. Use Loop for CHF edema

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41
Q

African Descent HTN Rx

A

CCB (Ca+ Channel Blocker) + Thiazide

DON’T use ACE Inhibitors for African Decscent UNLESS there is comorbid CKD

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42
Q

Never Combine ACEs with

A

ARBs

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43
Q

Thiazide Diuretics MOA

HCTZ

Triamterine

Chlorthiazide

A

Block the Na/Cl symporter in the Distal Tubule

Also increase Ca+ retention and Lowers K+ retention

Don’t give to:
Hypokalemia - stop Thiazide if this develops
Renal Failure
Lithium for BiPolar, may increase serum levels
Nursing Mothers
Gout Pts (increase Ca XL formation)

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44
Q

Post MI Rx

A

Beta Blocker ALWAYS ALWAYS

ACE Inhibitor

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45
Q

Loop Diuretic MOA

A

Inhibit the Na/K/Cl co-transporters in the thick ascending loop of hence

Furosamide

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46
Q

ACEI dangerous side effects:

Lisinopril

A

Lymphadenopathy - swollen face, tongue, neck

Cough

Both due to blocking of Bradykinin degradation and the bradykinin causes the effects

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47
Q

Lisinopril Std Dose

A

20-40 mg/day

Work up from 10mg

5 mg in MI if not already on ACE

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48
Q

ACEI benefits

A

Long Term ACEI use reduces albuminaria and protects kidney function in HTN, DM and renal disease

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49
Q

ARBs

Valsartan “Sartans”

A

Same benefits as ACE

No bradykinin Cough

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50
Q

Diltiazem
Verapamil
Amlodipine
Nifedipine

A

Calcium Channel Blockers

Nifedipine for Reynauds

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51
Q

Diltiazem
Verapamil
Amlodipine
Nifedipine

A

Calcium Channel Blockers

Nifedipine for Reynauds

Prolongs AV pause by blocking Ca+ channels and slowing depolarization

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52
Q

Beta Blocker MOA

Metropolol B1/B2 Selective
Carvedilol B1/B2 & A2

A

Beta 1 receptors in heart bind Epi/Nor and increase Rate & Contractility

Beta Blockers block Beta 1s (everywhere) and reduce cardiac rate and contractility, saving energy for a tired heart That’s why we always give them post MI

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53
Q

Beta Blocker MOA

Metropolol B1/B2 Selective
Carvedilol B1/B2 & A2

A

Beta 1 receptors in heart bind Epi/Nor and increase Rate & Contractility

Beta Blockers block Beta 1s (everywhere) and reduce cardiac contractility, saving energy for a tired heart That’s why we always give them post MI

Also slows AV node conduction, this is how it slows rate.

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54
Q

Use Esmolol (BBlock) in

A

SVT

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55
Q

Alpha Receptor Antagonists:

The ZOSINS

A

Prevent vessel constriction and thereby bring down Bp

Also good for relaxing Prostate in BPH and relaxes detrusor muscle in urine retention

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56
Q

Beta Blocker MOA

Metropolol B1/B2 Selective
Carvedilol B1/B2 & A1

A

Beta 1 receptors in heart bind Epi/Nor and increase Rate & Contractility

Beta Blockers block Beta 1s (everywhere) and reduce cardiac contractility, saving energy for a tired heart That’s why we always give them post MI

Also slows AV node conduction, this is how it slows rate.

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57
Q

Direct Vasodilators

A

Nitroglycerine

Hydralazine (use in pregnancy for eclampsia)

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58
Q

Central Alpha 2 Agonists

A

Clonadine & Methyl Dopa

These lower Bp by preventing sympathetic stimulation of Adrenal Epi/Nor release

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59
Q

Hypertensive Urgency: Get Bp down 20mmHg in 24 Hrs

vs

Hypertensive Emergency: Get Bp down 20% in 1 Hr

A

Urgency:
Bp of 180/120 WITHOUT signs of end organ damage like Copper Wiring or Papillodema & without CHF, Renal Damage, Stroke, Ecclampsia or Unstable Angina.

Emergency:
Bp of 180/120 WITH signs of end organ damage

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60
Q

Hypertensive Urgency Rx

A

Lasix

Clonadine (central A2 Agonist - reduce Epi/Nor from the Adrenals)

Captopril (ACE) instead of Lisinopril

get it down by 20 mm Hg in 24 hrs then get Bp stabilized on an outpatient basis. You might give first doses in the office and ensure they’re working before allowing Pt to leave, return next day - no work.

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61
Q

HTN End Organ Damage:

A 
Stroke
Vision Changes
       Cu Wire Nicking   Papilledema
Seizure
Chest Pain
SOB
Azotemia - BUN over 20
Edema
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62
Q

HTN End Organ Damage:

Very High Bp??
DO A FUNDOSCOPIC EXAM!!

A 
Stroke
Vision Changes
       Cu Wire Nicking   Papilledema
Seizure
Chest Pain
SOB
Azotemia - BUN over 20
Edema
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63
Q

HTN End Organ Damage:

Very High Bp??
DO A FUNDOSCOPIC EXAM!!

Check for JVD and take Bp in both arms, more than a 20mm Hg difference could be aortic dissection.

A 
Stroke
Vision Changes
       Cu Wire Nicking   Papilledema
Seizure
Chest Pain
SOB
Azotemia - BUN over 20
Edema
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64
Q

Hypertensive Urgency: Get Bp down 20mmHg in 24 Hrs

vs

Hypertensive Emergency: Get MAP down 20% in 1 Hr

A

Urgency:
Bp of 180/120 WITHOUT signs of end organ damage like Copper Wiring or Papillodema & without CHF, Renal Damage, Stroke, Ecclampsia or Unstable Angina.

Emergency:
Bp of 180/120 WITH signs of end organ damage

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65
Q

MAP

Normal MAP is 70 - 110

A

Mean Arterial Pressure- Average Arterial Bp in one cardiac cycle

Best measure of perfusion

MAP= Diastolic+ 1/3 (Systolic - Diastolic)
This is an approximate not the actual formula

So, to calculate the target MAP for HTN Emergency w/Bp of 180/120:

MAP= (120+ 1/3(180-120) = 140
bring that down by 20% to MAP of 112.

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66
Q

HTN Emergency Rx

A

DO use:

Esmolol, Labetolol & Nicardipine (a CCB)

DO NOT use:
Nitroprusside
Nitroglycerine
Hydralizine These lower MAP too quickly

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67
Q

Stroke, Intracerebral Hemorrhage HTN Emergency Rx

A

DO use:

Labetolol & Nicardipine (a CCB)

DO NOT use:
Nitroprusside
Nitroglycerine
Hydralizine These lower MAP too quickly

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68
Q

General Hypertensive Emergency Rx (no stroke/bleed)

A

Nitroprusside

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69
Q

Orthostatic Hypotension Definition

A

Drop of at least 20 mm Hg Systolic and/or 10mm Hg diastolic upon rising from supine to standing

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70
Q

Rx causes of Orthstatic Hypotension

A

Alpha Blockers (the Zosins for BPH)
Diuretics
Nitrates
Calcium Channel Blockers

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71
Q

Rx causes of Orthstatic Hypotension

Tilt Table Tests for Orthostatic Hypotension

A

Alpha Blockers (the Zosins for BPH)
Diuretics
Nitrates
Calcium Channel Blockers

prolonged bed rest

Autonomic Impairment - evaluated by Rectal tone & urinary continence

fluid loss

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72
Q

Rx for Orthostatic Hypotension

A

Fludrocortisone/Florinef, increases Na+ retention and bumps up blood volume

Midodrine (+ inotrope) constricts vasculature

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73
Q

Most Common Artery Occluded by Peripheral Artery Dz

A

Superficial Femoral Artery

Numbness/tingle burn on lateral superficial thigh

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74
Q

Most Common Artery Occluded by Peripheral Artery Dz (PAD)

PAD = atherosclerosis in limb arteries (legs)

A

Superficial Femoral Artery

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75
Q

Signs of PAD

A

Abnormal Hair Distribution on legs
Ulcers
Atrophy of limbs
Thin Skin - is not being fed!!!

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76
Q

Risks of PAD

A

Smoking #1
DM
Hyperlipidemia

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77
Q

Signs of PAD

A 
Dependent Rubor
Claudication (cramping on walking)
Abnormal Hair Distribution on legs
Ulcers
Atrophy of limbs
Thin Skin - is not being fed!!!
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78
Q

PAD foot pain vs DM foot neuropathy

A

PAD pain is due to lack of blood flow. If dangling foot over side of bed relieves pain, its due to PAD/ischemia. If not, think DM neuropathy (also ultimately caused by poor blood flow…)

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79
Q

PAD encourages Infection due to Stasis

A

Cellulitis - usually strep progenies/epidematis or staph aureus

Leg will be warm/hot, painful, may have ulcers and be swollen in comparison to the other leg

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80
Q

PAD Diagnostic Testing

A

ABI - Ankle Brachial Index
Best Initial Test, can do in office
Duplex Ultrasound/aka Wave Velocity Form
Can pinpoint location of PAD blockage

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81
Q

Arteriogram - CT w/Contrast

A

Pinpoints stenosis and catheter used to stent the artery

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82
Q

PAD Rx

A

Cilostazol (Pletal)
Not in CHF
Phosphodiesterase Inhibiter

+

ACE Inhibitors for all PAD Pts

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83
Q

Thrombus vs Embolus

A

Stationary vs On The Move

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84
Q

5 P’s of Arterial Occlusion (of limb)

A 
Pulseless 
Pallor
Pain
Parasthesias
Paralysis

If you see these, get Angiography to confirm location and set up Thromectomy/Emboli removal via catheter or emergency Bypass of the blockage

You might use TPA to lyse the blockage if its less than 2 weeks old and amputation is not already in order

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85
Q

Polycystic Kidney Disease is weirdly comorbid with

A

Cerebral Aneurysm

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86
Q

Thunderclap Headache or Pain behind the eye, bleeding into the eye

A

Ruptured Cerebral Aneurysm

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87
Q 
Abdominal Ripping/Tearing
Searing Pain in the lumbar back
Hypotension
Tachycardia
Shock
A

Aortic Aneurysm - most common in Lumbar

Intervene surgically @ 5.5cm w/stent or, more invasive, an aortic graft

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88
Q

Ripping/Tearing pain between scapula

A

Thoracic Aneurysm Rupture

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89
Q

Gold Std for Aortic Aneurysm Imaging

A

MRI is gold for DX & following but

CT is image of choice in emergency- do thorax AND abdomen as most thoracic aneurysms also have AAA

even CXR is can help… enlarged aortic arch a clue or widened Mediastinum (tamponade)

Can also do TEE

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90
Q

Gold Std for Aortic Aneurysm Imaging

A

MRI is gold for DX & following but

CT is image of choice in emergency- do thorax AND abdomen as most thoracic aneurysms also have AAA

even CXR is can help… enlarged aortic arch a clue or widened Mediastinum (tamponade) You might just see a HUGE mediastinum

Can also do TEE

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91
Q

Nitroprusside for Malignant HTN should never be given alone as it causes rebound tachycardia. Always give with

A

A Beta Blocker

Lobetalol or Esmolol are IV Beta Blockers

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92
Q

Nitroprusside for Malignant HTN should never be given alone as it causes rebound tachycardia. Always give with…

A

A Beta Blocker

Lobetalol or Esmolol are IV Beta Blockers

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93
Q

Temporal Arteritis

A

Inflammation of the Internal & External Carotids

Multi-Nucleated Giant cells infiltrate the walls of the arteries perpetuating inflammation and that’s why we call it Giant Cell Arteritis

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94
Q

Temporal Arteritis

Giant Cell Arteritis

A

Inflammation of the Internal & External Carotids

Multi-Nucleated Giant cells infiltrate the walls of the arteries perpetuating inflammation and that’s why we call it Giant Cell Arteritis

Biopsy confirms Dx but you might SEE the swollen Temporal Artery & Pt may have Headache, Visual Disturbances, Tenderness, Pain on Chewing and Elevated ESR.

Rx is high dose oral corticosteroids ( 40-60 mg/day X 4 weeks) then taper slowly over 2 + years, back peddling if sxs reappear.

If visual disturbances on presentation, start on IV corticosteroids ASAP

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95
Q

Temporal Arteritis

Giant Cell Arteritis

A

Inflammation of the Internal & External Carotids

Multi-Nucleated Giant cells infiltrate the walls of the arteries perpetuating inflammation and that’s why we call it Giant Cell Arteritis

Biopsy confirms Dx but you might SEE the swollen Temporal Artery & Pt may have Headache, Visual Disturbances, Tenderness, Pain on Chewing and Elevated ESR.

Rx is high dose oral corticosteroids ( 40-60 mg/day X 4 weeks) then taper slowly over 2 + years, back peddling if sxs reappear.

If visual disturbances on presentation, start on IV corticosteroids ASAP

Start Rx immediately, Biopsy up to 14 days later

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96
Q

Most Common Vein for Varicosities

A

Great Saphenous aka Long Saphenous

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97
Q

Peripheral Arterial Disease

Vs

Chronic Venous Insufficiency

A

PAD: Rubor & Claudication
Pain relieved by dangling foot off bed

CVI: Sxs relieved by foot elevation and compression stockings and venous sclerosis with saline or venous removal/stripping

98
Q

Stasis Dermatitis

A

Bronzing of lower legs in Chronic Venous Insufficiency with/wo pruritus and dry thin skin or ulcerations

99
Q

Diagnostic Study of Choice to confirm clinical diagnosis of Chronic Venous Insufficiency or Varicose Veins AND to plan treatment

A

Doppler Ultra Sound

100
Q

Gold Std Varicose Vein Therapy

A

Sclerosing with FOAM

101
Q

+ Homan’s Sign

Pain in calf when foot is flexed

A

Suggestive of Superficial Thrombophlebitis

little clot in vein causes inflammation

102
Q

Palpable nodular cord and (+) Homan’s sign

recent IV catheter or PICC line

A

super ficial thromboplebitis

Rx is: Heat NSAIDS Compression Stocking

Serious if extends up near Great Saphenous junction with Femoral Vein

103
Q

Virchow’s Triad

A 
Stasis
Vascular Injury
Hypercoagulability
       Factor V Leiden Mutation
       Polycythemia
       Thrombocythemia
104
Q

Most Common Sites for DVT

A

Superficial Femoral
Popliteal
Posterior Tibial

105
Q

Homan’s sign is unreliable for

A

DVT, keep it for varicose veins and thrombophlebitis and venous insufficiency

106
Q

Test for DVT

A

D-Dimer is a product of fibrin breakdown so if
D-Dimer is (+) there is clotting
somewhere - just not sure where. If
it’s negative, you don’t have a DVT or
clotting anywhere.

Doppler Ultra Sound to locate the DVT

107
Q

Test for PE

A

Spiral CT of the Chest to ID PE

108
Q

Rx DVT/PE

A

Anticoagulation

Usually outpatient w/LMWH X 5 + days while initiating coumadin therapy and getting INR where you want it. Coumadin/Warfarin for life if you’ve had a DVT/PE

Thrombolytic Therapy if a 911
TPA

109
Q

Rx DVT/PE

A

Anticoagulation

Usually outpatient w/LMWH X 5 + days while initiating coumadin therapy and getting INR where you want it. Coumadin/Warfarin for life if you’ve had a DVT/PE that was not due to some reversible risk like protracted bed rest.
Could use Xaralto or Pradaxa instead of
Coumadin

Thrombolytic Therapy if a 911
TPA

110
Q

Acute
Coronary
Syndrome

A

Unstable Angina
Stemi
N-Stemi

111
Q

Cardiac Injury Panel

A

Troponins rise within 3 hrs, stay elevated 7-14
days post MI depending on whether you
are testing Troponin T or I. T stays up
longer

CKMB rises in 6 hrs, peaks @ 12-24 back to
baseline in 24-48 hrs

112
Q

Substernal pain and Dyspnea on Exertion but Cardiac Enzymes are not elevated

A

Unstable Angina

Nitro, stabilize for 24 hrs & send to the cath lab the next day.

113
Q

Pain, SOB, Nausea… MI symptoms and Cardiac Enzymes are elevated and ST-elevations on EKG

A

Stemi- Full thickness infarction 911

Stabilize, heparinize and send to cath lab in ambulance

114
Q

MI sxs, Cardiac Enzymes ARE elevated but EKG does not show ST elevations, may show ST Depression though or TWave Inversion

Enzymes up
No ST Elevations
ST Depressions present
Inverted T waves

A

Non-Stemi MI - only a partial thickness MI 911

Stabilize, heparinize/anticoagulate and send to cath lab in ambulance

115
Q

ST Elevations/Depression in II III & AvF

A

Inferior MI

116
Q

ST Elev./Depression in I, AvL, V5 & V6

A

Lateral MI

117
Q

V1 & V2 elevation/depression

A

Anteroseptal

118
Q

V1, V2 V3 V4

A

Anterior MI

119
Q

V4 V5 V6

A

Antero-Lateral MI

120
Q

MI Rx:

A

324 mg Aspirin
300 mg Plavix/Clopidrogel
Glycoprotein IIb IIIa antigoagulant
The Mab Reopro abciximab
very pricy, save for 1 hr before cath
IV Nitroglycerine for PAIN unless He took Viagara

121
Q

PICA

A

Percutaneous
Intervention
Coranary
Arteriography

aka - Catheterization to locate blockage and place stent

122
Q

MI Rx:

A 
324 mg Aspirin
300 mg Plavix/Clopidrogel
Glycoprotein IIb IIIa antigoagulant
      The Mab   Reopro  abciximab
      very pricy, save for 1 hr before cath
IV Nitroglycerine for PAIN unless He took 
       Viagara
Metropolol PO
123
Q

Angina occurs at rest and in clusters

A

Prinzmetal Angina

Caused by vasospasm

124
Q

Typical MI EKG progression

A

Peaky T w/in minutes = ischemia

ST Elevation & Inverted T w/in hrs = necrosis

Q-Wave w/in days when scar is formed

125
Q

Pain, SOB, Nausea… MI symptoms and Cardiac Enzymes are elevated and ST-elevations on EKG

A

Stemi- Full thickness infarction 911

Stabilize, heparinize and send to cath lab in ambulance

If cath lab not an option, Thrombolytic Therapy w/TPA or Reopro, the MAB

126
Q

MI sxs, Cardiac Enzymes ARE elevated but EKG does not show ST elevations, may show ST Depression though or TWave Inversion

Enzymes up
No ST Elevations
ST Depressions present
Inverted T waves

A

Non-Stemi MI - only a partial thickness MI 911

Stabilize, heparinize/anticoagulate and send to cath lab in ambulance

If cath lab not an option, Thrombolytic Therapy w/TPA or Reopro, the MAB

127
Q

MI Dx Studies

A

Serial EKG q 6 hrs
Cardiac Injury Panels q 6 hrs
Bedside Echo

128
Q

Pain, SOB, Nausea… MI symptoms and Cardiac Enzymes are elevated and ST-elevations on EKG

A

Stemi- Full thickness infarction 911

Stabilize, heparinize and send to cath lab in ambulance

If cath lab not an option & w/in 3-12 hrs, Thrombolytic Therapy w/TPA or Reopro, the MAB

129
Q

MI sxs, Cardiac Enzymes ARE elevated but EKG does not show ST elevations, may show ST Depression though or TWave Inversion

Enzymes up
No ST Elevations
ST Depressions present
Inverted T waves

A

Non-Stemi MI - only a partial thickness MI 911

Stabilize, heparinize/anticoagulate and send to cath lab in ambulance

If cath lab not an option & w/in 3-12 hrs Thrombolytic Therapy w/TPA or Reopro, the MAB

130
Q

Most serious risk of fibrinolytic therapy like TPA or ReOpro

A

intracranial hemorrhage

131
Q

TPA aka:

A

Alteplase

132
Q

Abciximab aka:

A

Reopro

133
Q

If MI pt also has Heart Failure (10%)

A

start on ACEI

134
Q

VTach 911 Rx

A

Lidocaine IV Bolus if VTACH is stable (i.e.
no signs of hypoperfusion/hypoxia)

Cardioversion if VTACH is unstable (signs
of hypoxia present)

135
Q

VFib 911 Rx

A

Defibrillate

Amiodarone IV

136
Q

Pacemaker req if:

A

2nd degree Heart block does not resolve spontaneously- might use temporary

Third Degree Heart block, permanent & implanted

137
Q

Hypotension SBP less than 90 Rx

A

IV Fluids -

Vasopressors: Dopamine & Dobutamine IV

138
Q

Stable Angina

A

Pain on exhertion, goes away with rest

Nitroglycerine SL spray, tabs patch paste

139
Q

Levine’s Sign

A

Clenched Fist over Mediastinum

Classic Heart Attack sign

140
Q

(+) Stress Test REsult

A

1mm ST depression/Slope on exertion

Refer for Catheterization

141
Q

Hypotension SBP less than 90 Rx

A

IV Fluids -
Vasopressors: Dopamine & Dobutamine IV

Dobutamine increases heart rate & contraction
Dopamine can do that too but also constrict vasculature

142
Q

Don’t use Dobutamine in

A

Wolf Parkinson White

LBBB or permanent pacemaker - use Adenosine instead

143
Q

Adenosine

A

Nucleoside that Dilates Coronary Arteries

Only lasts 6 seconds from IV injection so push hard with saline and place high up on arm

144
Q

Electron
Beam
CT EBCT

A

Quantifies Coronary Artery Calcificaton

145
Q

Definitive Diagnostic Imaging and Treatmetn for Coronary Artery Disease

A

Coronary Angiography

CATH

146
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG
Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)
147
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG its like an MI EVERYWHERE but doesn’t present like an MI and cardiac enzymes may or may not be elevated

Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)
148
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG its like an MI EVERYWHERE but doesn’t present like an MI and cardiac enzymes may or may not be elevated

Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)

RX is Indomethacin
Colchecine
Aspirin
Prednisone

149
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG its like an MI EVERYWHERE but doesn’t present like an MI and cardiac enzymes may or may not be elevated

Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)

RX is Indomethacin
Colchecine X 3 mo
Aspirin
Prednisone

150
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG its like an MI EVERYWHERE but doesn’t present like an MI and cardiac enzymes may or may not be elevated

Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)

If Tamponade develops - 911 procedure is a “pericardial window”

RX is Indomethacin
Colchecine X 3 mo
Aspirin
Prednisone

151
Q

10mm decline in SBp during inspiration

A

Pulsus Paradoxis

Due to impaired LV filling - Tamponade

152
Q

Males over 50
Pericardial Friction Rub- like a stenotic murmur throughout the entire cardiac cycle

Diffuse ST elevations throughout EKG its like an MI EVERYWHERE but doesn’t present like an MI and cardiac enzymes may or may not be elevated

Muffled Heart Sounds

Sharp Chest Pain Thru to the Back is relieved by sitting forward, exacerbated by lying down

Had a cold or URI a week ago

A

Pericarditis

Likely with Percardial effusion that is compressing the heart muscle in the same way as early tamponade may.

Most often Viral or 
Dressler Syndrome (w/in 2 days of an MI)

If Tamponade develops - 911 procedure is a “pericardial window” if SBp drops or Pulsus Paradoxis develops

Echo is study of choice in pericarditis to rule out tamponade and ensure heart is not compressed CXR will show enlarged mediastinum though

RX is Indomethacin
Colchecine X 3 mo
Aspirin
Prednisone

153
Q

This shock will have hypotension WITHOUT an increase in heart rate to compensate

A

Neurogenic Shock

154
Q

The depth of the S wave in V1 added to the height of the R wave in V5 is greater than 35mm in this cardiac development

A

Left Ventricular Hypertrophy

We get larger deviations from baseline when conduction has to pass through thicker tissue

155
Q

Imaging of choice for Aortic Dissection

A

CT Chest & CT Abdomen

156
Q

IV insertion or PICC lines cause this venous disease

A

Superficial venous thrombophlebitis

157
Q

Petechiae, Splinter hemorrhages, Osler’s Nodes, Janeway Lesions & Roth Spots are signs of this disease

A

Bacterial Endocarditis

Osler’s Nodes: painful red lesions hands/feet
Janeway: Nontender lesions palms/soles
Splinter Hemm: tiny red streaks in nailed
Roth Spots: Retinal lesions w/white centers

158
Q

Diagnostic NonInvasive Image of choice for claudication (PAD)

A

ABI

Ankle Brachial Index - do it first, then doppler to locate problem and plan treatment

159
Q

Marfan’s Syndrome (and smoking and overweight/HTN and old age and trauma) are risks for this CV development

A

Aortic Aneurysm

intervene at 5.5

Stent it

160
Q

PAD Risk Factors

A

Smoking, age, DM, Renal Failure, HTN, lipids

161
Q

Giant Cell Arteritis is 50% comorbid with

A

Polymyalgia Rhumatica

This is muscle & joint pain
ESR will be up, cause not understood
Rx is corticosteroids, high then long taper as with Giant Cell Arteritis

162
Q

1 Risk Factor for Dissecting Aortic Aneurysm

A

Uncontrolled HTN

163
Q

PAD maintenance regimen, once urgent risks/ulcers and/or infections are managed:

A

Smoking Cessation
Anticoagulation: coumadin, plavix, xaralto
HTN Control:
ACEI + Thiazide Diuretic

Might also add a peripheral CCB like
Amlodipine or Nifedipine (diltiazem/verapamil
are more cardiac focused and too strong
for mere hypertension control)

Alpha/Beta Blockers

Hydralazine in pregnancy for ecclampsia

164
Q

Hydralazine as HTN medication

A

Not a good mono therapy for a compromised heart as it causes reflex tachycardia but ok in pregnancy so long as the heart is strong.

If used with a beta blocker and a diuretic (usually thiazide), Hydralazine can be used for HTN mgt in the setting of CAD but why not just go with the ACEI and a thiazide and maybe amlodipine?

165
Q

Garment Rx for Orthostatic Hypotension

A

TED Stockings:

More compression @ ankles, easing as they go up often all the way to the thigh. Good for PAD and also varicose veins and venous insufficiency. Come made w/silver for antimicrobial effect..

166
Q

Dressler Syndrome

A

Pericarditis & Post MI symptoms of:

Fever
Chest Pain (usually pleuritic)
Friction Rub on heart eval

Usually resolves in a few days BUT…
Need to sort this pericardial situation from a PE with a spiral CT and need to ensure heart is pumping adequately/no tamponade with a bedside echo.

167
Q

PAD maintenance regimen, once urgent risks/ulcers and/or infections are managed:

A

Smoking Cessation
Anticoagulation: coumadin, plavix, xaralto
HTN Control:
#1 is a Thiazide Diuretic
ADD ACEI if DM or BUN/Cr show renal issue

Might also add a peripheral CCB like
Amlodipine or Nifedipine (diltiazem/verapamil
are more cardiac focused and too strong
for mere hypertension control)

Alpha/Beta Blockers

Hydralazine in pregnancy for ecclampsia

168
Q

1 Go To HTN Monotherapy if no Comorbidities

A

Diruetic, usually Thiazide

Add ACEI if DM or Renal Damage

Add CCB like Amlodipine and/or Beta Blockers if any Heart Failure

Add Statins in CAD or otherwise control lipids

169
Q

1 Go To HTN Monotherapy if no Comorbidities

A

Diruetic, usually Thiazide

Add ACE/ARB if DM or Renal Damage

Add CCB like Amlodipine and/or Beta Blockers if any Heart Failure

Add Statins in CAD or otherwise control lipids

170
Q

HTN & BPH??? Easy, use

A

Alpha Blockers
The Zosins

Up to Date likes Tamulosin (FLOMAX) as it doesn’t react with Viagara/Cialis, which many of these pts are also taking.

171
Q

Drug of Choice for Perioperative HTN prep

A

Nitroprusside

Dilates arteries & veins decreasing both preload and after load. It works fast and clears fast and Deb likes it but…

My research indicates that it shouldn’t be used if there is CAD or Renal compromise or if there is any sort of issue with intracranial pressure as it is SUCH a vasodilator it steals blood from these vital organs. ALSO it contains lots of Cyanide??? Which is released into the blood so you need to control dose carefully and use it only for “quick” surgeries - not 2-3 hrs or CN toxicity develops

Clavidipine and Nicardipine, 3rd & 2nd Gen dihydropyridine CCBs are more in vogue than any of the other HTN drugs peri and postop as they are

172
Q

Drug of Choice for Perioperative HTN prep

A

Nitroprusside

Dilates arteries & veins decreasing both preload and after load.

It works fast and clears fast and Deb likes it but…

My research indicates that it shouldn’t be used if there is CAD or Renal compromise or if there is any sort of issue with intracranial pressure as it is SUCH a vasodilator it steals blood from these vital organs. ALSO it contains lots of Cyanide??? Which is released into the blood so you need to control dose carefully and use it only for “quick” surgeries - not 2-3 hrs or CN toxicity develops

Clavidipine and Nicardipine, 3rd & 2nd Gen dihydropyridine CCBs are more in vogue than any of the other HTN drugs peri and postop as they are highly selective for vessels in the brain, heart and kidneys and therefore protect those organs from HTN damage and maintain a good blood flow there while not letting the systemic Bp fall too low. They allow the coronary arteries to stay open while not decreasing atrial filling from low systemic Bp.

173
Q

First drug on board in an aortic dissection?

A

IV Labetolol

Get that BP DOWN FAST!!! to relieve pressure on the aortic walls!!!

174
Q

Heart Murmur Study of Choice?

A

Echo

Also MI to eval damage to wall
Peri/Endocarditis & Tamponade

175
Q

Endothelial injury and fatty streak formation occur early in

A

Atherosclerosis

176
Q

Don’t do a stress echo if

A

Resting Angina
Severe Aortic Stenosis
Unstable Rhythm
Duh…

177
Q

Study to monitor a KNOWN abd aneurysm

A

Abdominal Ultrasound

To Diagnose it - CT

178
Q

1 Most Common cause of orthostatic hypotension

A

Dehydration/ hypovolemia

179
Q

Drugs that commonly cause Hypotension

A

diuretics (via hypovolemia)
nitroglycerine (via vasodilation)
CCBs (via vasodilation & reduced contractility)

180
Q

Fludrocortisone std Rx for

A

Orthstatic Hypotension,

Mineral corticoid stimulates the RAAS system to retain more salt

181
Q

Midrodine MOA

A

Alpha 1 agonist

Promotes peripheral vascular constriction

182
Q

When to use Dobutamine?

A

Best for cardiogenic Shock or Heart Failure not for Hypovolemic shock.

Dobutamine is a B1 Agonist with weak B2 Agonist properties. It is mainly an inotrope, causing increased contractility.
B2 receptors in the heart dilate the coronary arteries but as Dobutamine’s B2 effects are weak, it doesn’t do too much for coronary repercussion but at least it doesn’t block it

It is also a weak Alpha 1 agonist and Alpha 1 stimulation effects vasoconstriction so Dobutamine contributes a smidge to peripheral vasoconstriction but not enough to help in hypovolemic shock

183
Q

Beta Receptor

Agonists: Epi, Dobutamine, Isoproteronol, albuterol

Antagonists: Beta Blockers

A

Stimulation increases contractility and cardiac output

B1= contractility in heart

B2= Coronary Artery Dilation AND bronchiole relaxation

Agonists increase Contractility & Blood Supply to the heart and relax bronchioles

Antagonists reduce contractility and unfortunately coronary blood supply and also constrict the bronchioles.

You can counter the bronchiole bit by choosing carvedilol which also blocks A1, which also has activity on bronchiole smooth muscle, blockage of which can counteract any B2 blockade in bronchi.

184
Q

Alpha Receptors

A1 Agonists: Midrodrine, Phenylepherine
A2 Antagonists: Tamulosin (Flomax)
Prazosin (MiniPress

A2 Agonists: Clonadine, Methyl Dopa
A2 Antagonists: Yohimbe not much used

A

Carry out Fight or Flight!

A1 Dilates pupils, shuts down GI, Skin & Renal, Constricts vasculature to conserve blood to heart, lungs & brain.

A2 Shuts down Pancrease & induces contraction of Alpha islets to secrete glucagon and increase blood sugar.

We agonize Alpha1 receptors to increase blood pressure in orthostatic hypotension and

We agonize Alpha 2 receptor to do the opposite, ultimately to reduce HTN but via the CNS as there are A2 receptors in the vasomotor area of the brain which somehow inhibits Nor Epi release at the adrenals.

185
Q

grades IV, V & VI will have a thrill:

A

Heart Murmurs

186
Q

Standing Manuver in Murmur MOA

A

Increases Venous Return to the heart, increasing preload while simultaneously decreasing after load. Overall it accentuates all murmurs …

EXCEPT Mitral Valve Prolaps, because the increased preload works against the prolapse

187
Q

Standing/Squatting/Valsalva Manuver in Murmur MOA

Double Bp Cuff Inflation manuver:

A

Standing & Valsalva are good but Squatting THEN standing is better:

Both Increase Venous Return to the heart, increasing preload while simultaneously decreasing after load. Overall it accentuates all murmurs …

EXCEPT Mitral Valve Prolapse (MVP), because the increased preload works against the prolapse

To accentuate MVP inflate Bp cuffs on both arms simultaneously & listen after 20 seconds. Need to transiently block both brachia’s.

188
Q

These Murmurs are ALWAYS pathologic

A

Diastolic only murmurs

189
Q

Most common cause of mitral stenosis

A

Rhumatic Fever

Now likely only in older adults in US due to antibiotic treatment

Abnormal valve or impaired papillary muscles or short thick chordae tendinae can also cause it.

190
Q

Opening Snap in early Diastole best heard over Apex in decubitus

A

Mitral Stenosis

Valve “snaps” open once pressure builds enough in the atrium to overcome the built up “hinges” on the stenosed valve. Its hard to open with all that buildup!

Opening snap then a mid/late diastolic rumble as the blood rushes in to the left ventricle

191
Q

Opening Snap in early Diastole best heard over Apex in decubitus

A

Mitral Stenosis

Valve “snaps” open once pressure builds enough in the atrium to overcome the built up “hinges” on the stenosed valve. Its hard to open with all that buildup!

Opening snap then a mid/late diastolic rumble as the blood rushes in to the left ventricle

Since the left atrium has to work extra hard to push the blood through this gunky valve, you might actually see an enlarged Left Atrium on CXR or rather the aortic arch will not stick out so much.

As with all murmurs, you’ll see this one best with an ECHO and you’ll see if there’s any backup to the lungs as well. If there is, this left sided problem can eventually cause backup into the right ventricle and effect right sided heart failure sxs like dependent edema and pulmonary edema.

Since the blood flows slowly from the atrium into the LV, its a good idea to anticoaguate w/warfarin or xaralto to prevent clot formation as a clot forming in the pulmonary veins or LA might go right out to the carotids and cause an embolic stroke. Here though we have a bit more leeway than AFIB and are seeking an INR of 2.5 - 3.5 instead of a 2-3.

Replace the valve or get BALLOON VALVULOPLASTY (non invasive option is preferred) if the orafice is less than 1.5cm2 or if if ADLs and/or exercise are impaired by the blockage.

192
Q

Holosystolic Murmur

A

Heard throughout Systole

This would be Regurg of blood back through Mitral/Tricuspid.

It there was also prolapse, you’d hear a snap as the prolapsed leaflet hit its full backward extension and snapped back.

193
Q

Lub Dub…

A

Lub - S1 - Closing of Mitral/Tricuspid Valves
the ventricle is FULL
Diastole/filling precedes S1
Lub is usually softer than Dub

Dub - S2 - Closing of the Aortic/Pulmonic
The Ventricle is EMPTY
Systole/Emptying/Contraction
Precedes S2

If there is a stenosis of the Mitral or Tricuspid, it will be heard between between S2 and S1 during Diastole (before the Mitral/Tri closes at S1) as the Atria struggle to push blood through the gunky valve. There will be an opening Snap usually early to mid diastole

If there is stenosis of the Aortic/Pulmonic Valves, it will be heard between S2 and S1 during systole
as the ventricles are attempting to push blood through the gunky aortic/pulmonic valves during systole

If there is regurg/prolapse of the Mitral/Tricuspid, as happens when MI causes necrosis of the papillary muscles or rupture of the chord that anchor the valve leaflets during systole, both regurge and prolapse will be heard mid systole as blood rushes backwards (regurg) from the contracting ventricle into the atrium or when the partially untethered valve leaflet prolapses backwards into the atrium with the backward regurge of blood and “snaps” it’s remaining tethers tight during late systole.

If there is regurg or prolapse of the aortic/pulmonic semilunar valves, this will be heard during diastole, after the ventricles have contracted (in systole). The seminars are supposed to keep blood from flowing backwards from the aorta/pulmonary arteries into the ventricles while the ventricles are filling during diastole. Damaged leaflets allow blood to back flow throughout diastole and if they are so damaged as to prolapse - you may even hear the leaflet “pop” backwards or “snap” once it has fully extended back into the ventricle - that noise will happen in mid to late diastole, before the mitral/tricuspid close and the ventricles contract forcing blood through the aortic/pulmonic again in the intended direction.

194
Q

Lub Dub…

A

Lub - S1 - Closing of Mitral/Tricuspid Valves
the ventricle is FULL
Diastole/filling precedes S1
Lub is usually softer than Dub

Dub - S2 - Closing of the Aortic/Pulmonic
The Ventricle is EMPTY
Systole/Emptying/Contraction
Precedes S2

If there is a stenosis of the Mitral or Tricuspid, it will be heard between between S2 and S1 during Diastole (before the Mitral/Tri closes at S1) as the Atria struggle to push blood through the gunky valve. There will be an opening Snap usually early to mid diastole

If there is stenosis of the Aortic/Pulmonic Valves, it will be heard between S2 and S1 during systole
as the ventricles are attempting to push blood through the gunky aortic/pulmonic valves during systole

If there is regurg/prolapse of the Mitral/Tricuspid, as happens when MI causes necrosis of the papillary muscles or rupture of the chord that anchor the valve leaflets during systole, both regurge and prolapse will be heard mid systole as blood rushes backwards (regurg) from the contracting ventricle into the atrium or when the partially untethered valve leaflet prolapses backwards into the atrium with the backward regurge of blood and “clicks” it’s remaining tethers tight during late systole.

If there is regurg or prolapse of the aortic/pulmonic semilunar valves, this will be heard during diastole, after the ventricles have contracted (in systole). The seminars are supposed to keep blood from flowing backwards from the aorta/pulmonary arteries into the ventricles while the ventricles are filling during diastole. Damaged leaflets allow blood to back flow throughout diastole and if they are so damaged as to prolapse - you may even hear the leaflet “pop” backwards or “click” once it has fully extended back into the ventricle - that noise will happen in mid to late diastole, before the mitral/tricuspid close and the ventricles contract forcing blood through the aortic/pulmonic again in the intended direction.

195
Q

Holodiastolic Murmur

A

This would be aortic/pulmonic regurge. If there were a click during diastole, it would be the aortic/pulmonic leaflets reaching max backward extension into the ventricles.

196
Q

Most common cause of all murmurs except in Tricuspid murmurs

A

Rhumatic Fever

Now likely only in older adults in US due to antibiotic treatment

Tricuspids are usually attached by Staph usually IV drug users or people who use needles a lot and don’t clean the skin 1st.

Abnormal valve or impaired papillary muscles or short thick chordae tendinae can also cause it.

197
Q

Systolic Crescendo-Decrescendo radiates to the neck

A

Aortic Stenosis. Unlike with Mitral/Tricuspid stenosis, there won’t be an “opening snap” because the seminars are smaller and have 3 leaflets and just don’t snap even if they’re burdened with gunk.

The blood moving through the narrowed space does make a lot more noise though and it’s louder in early systole (when the force of contraction is greater) and falls off during late systole (decrescendo) as the ventricle’s force wanes.

198
Q

Systolic Crescendo-Decrescendo radiates to the neck

A

Aortic Stenosis. Unlike with Mitral/Tricuspid stenosis, there won’t be an “opening snap” because the seminars are smaller and have 3 leaflets and just don’t snap even if they’re burdened with gunk.

The blood moving through the narrowed space does make a lot more noise though and it’s louder in early systole (when the force of contraction is greater) and falls off during late systole (decrescendo) as the ventricle’s force wanes.

Possessors of this stenotic murmur may get dizzy during exercise as brain oxygenation may not keep pace with use of oxygen and it takes longer to push blood through the stenotic valve out to the brain.

199
Q

Stenosis sounds _______ while Regurg sounds ________

A

Stenosis is high pitched and there’s a crescendo/decrescendo

Regurg is low and rumbly and the same throughout unless there’s a ‘click’ when a prolapsing leaflet snaps backward at full extension in a mitral/tri regurg.

200
Q

Blowing diastolic murmur heard along the left sternal border (LSB)

A

Aortic Regurg - no click as with Mitral/Tri as the semilunar leaflets are tiny and have no chord tendinae to snap them.

When there is aortic stenosis or regurge, the left ventricle has to work extra hard and may hypertrophy therefor. This may cause a third heart sound to be heard (S3).

In a regurg situation, you want to decrease the after load so the pressure in the aorta is lower, decreasing the extent of the regurgitation of the blood and the pro laps of the valve leaflet. Use an ACE

201
Q

THIS STENOSIS IS USUALLY CONGENITAL

A

Pulmonic

Associated w/ Tetrology of Fallot

202
Q

end diastolic volume

A

110 - 120 ml

203
Q

stroke volume

A

should be at least 70 ml, leaving 40-50 ml remaining in the ventricle after contraction. That’s the end diastolic volume.

204
Q

ejection fraction

A

%age of end diastolic volume that is actually ejected

should be 60%

use ECHO to calculate

205
Q

Heart Failure =

A

Decrease of ejection fraction/ stroke volume due to decreased strength in the left ventricle. Ventricle can be damaged from MI or from chronic HTN causing hypertrophy.

Visible sxs & signs of heart failure are Dyspnea on Exertion as the heart can’t supply the body with enough O2 during exertion.

Also, if left sided ventricular failure has backed up the pulmonary blood delivery, that pressure can continue backwards through the lung and increase pressure in the lung, making it more difficult for the right ventricle to force blood into the lung and causing Right Ventricular hypertrophy and poor performance. If this occurs, blood will back up into the vena cava and throughout the venous system resulting in edema in the legs and feet, possibly the Right Arm/hand.

Diagnose Heart Failure with Echo

Rx it with CBB (diltiazem) to keep the heart from struggling to compensate for its damaged state. This will lead to greater dyspnea on exertion but will “conserve” heart effort. Heart failure patients just have to move slower and work less.

You should also decrease after load for the tired heart so it doesn’t have to push so hard to get blood out of the ventricles - use a diuretic to decrease blood volume and bring down after load: Thiazide if GFR is over 30, LOOP if GFR is under 30 or if K+ loss isn’t a big concern.

And you might also add a Beta Blocker, though with the CBB, this might really disable the PT on exertion and you do want them to be able to walk. If there has been an MI though, a BB is required and you can tinker with the CBB to maximize the pts ability to exercise.

206
Q

Heart Failure =

A

Decrease of ejection fraction/ stroke volume due to decreased strength in the left ventricle. Ventricle can be damaged from MI or from chronic HTN causing hypertrophy.

Visible sxs & signs of heart failure are Dyspnea on Exertion as the heart can’t supply the body with enough O2 during exertion.

Also, if left sided ventricular failure has backed up the pulmonary blood delivery, that pressure can continue backwards through the lung and increase pressure in the lung, making it more difficult for the right ventricle to force blood into the lung and causing Right Ventricular hypertrophy and poor performance. If this occurs, blood will back up into the vena cava and throughout the venous system resulting in edema in the legs and feet, possibly the Right Arm/hand.

Diagnose Heart Failure with Echo

Rx it with CBB (diltiazem) to keep the heart from struggling to compensate for its damaged state. This will lead to greater dyspnea on exertion but will “conserve” heart effort. Heart failure patients just have to move slower and work less.

You should also decrease after load for the tired heart so it doesn’t have to push so hard to get blood out of the ventricles - use a diuretic to decrease blood volume and bring down after load: Thiazide if GFR is over 30, LOOP if GFR is under 30 or if K+ loss isn’t a big concern.

And you might also add a Beta Blocker, though with the CBB, this might really disable the PT on exertion and you do want them to be able to walk. If there has been an MI though, a BB is required and you can tinker with the CBB to maximize the pts ability to exercise.

If the failure occurred second to Afib, you will still need an antiarrythmic on board to regulate the sinoatrial node and for Afib with Heartfailure, Amiodarone is recommended. Watch out for pulmonary fibrosis and your pt turning blue.

See http://emedicine.medscape.com/article/151066-medication for a chart on a fib Rx

207
Q

Systolic Heart Failure

vs

Diastolic Heart Failure

A

Systolic HF - Ventricles can’t pump due to damage or poor blood supply. This could be caused by MI or CAD

Diastolic HF- Ventricles can’t fill enough. This is usually caused by hypertrophy. The classic sign is (S3), the ventricular creak of the stiff tissue trying to expand and the atrial KICK (S4) as the atria work over time to force blood into the stiff ventricle.

208
Q

True Cor Pulmonale Originates in the

A

LUNGS - Lung tissue damage increases pulmonary pressure, a pressure problem that makes it harder for the Left Ventricle to push Blood Through the lungs.

This causes back up to the LV and LV Hypertrophy and blood backs up even further to the Left Atrium and even up into the Vena Cava. At this point, edema begins in the feet/legs and maybe the Right arm/hand

209
Q

True Cor Pulmonale Originates in the

A

LUNGS - Lung tissue damage increases pulmonary pressure, a pressure problem that makes it harder for the Left Ventricle to push Blood Through the lungs.

This causes back up to the LV and LV Hypertrophy and blood backs up even further to the Left Atrium and even up into the Vena Cava. At this point, edema begins in the feet/legs and maybe the Right arm/hand.

Studies:
EKG may show Right axis deviation if there dis right ventricular hypertrophy

CXR should show pulmonary edema “Bat Wing” perhaps even a bilateral fluid line and Kerly B lines at the lateral pulmonary edges

BNP levels should rise as the right atrium will get stretched out by blood the Right Ventricle can’t take in.

BUN/Cr will likely show renal impairment

Rx:
Get the volume down with thiazide diuretics, loops if GFR is under 30

Get a CCB on board (diltiazem) to spare the heart extra effort

Get an ACE on board to protect those kidneys

210
Q

True Cor Pulmonale Originates in the

A

LUNGS - Lung tissue damage increases pulmonary pressure, a pressure problem that makes it harder for the Left Ventricle to push Blood Through the lungs.

This causes back up to the LV and LV Hypertrophy and blood backs up even further to the Left Atrium and even up into the Vena Cava. At this point, edema begins in the feet/legs and maybe the Right arm/hand.

Studies:
EKG may show Right axis deviation if there dis right ventricular hypertrophy

CXR should show pulmonary edema “Bat Wing” perhaps even a bilateral fluid line and Kerly B lines at the lateral pulmonary edges

BNP levels should rise as the right atrium will get stretched out by blood the Right Ventricle can’t take in.

BUN/Cr will likely show renal impairment

Rx:
Get the volume down with thiazide diuretics, loops if GFR is under 30

Get a CCB on board (diltiazem) to spare the heart extra effort

Get an ACE on board to protect those kidneys

If a fib has been caused by stretching of the right atrium and the SA node, control arrythmias with amiodarone or, if that doesn’t work, consider an implacable pacemaker.

211
Q

True Cor Pulmonale Originates in the

A

LUNGS - Lung tissue damage increases pulmonary pressure, a pressure problem that makes it harder for the Left Ventricle to push Blood Through the lungs.

This causes back up to the LV and LV Hypertrophy and blood backs up even further to the Left Atrium and even up into the Vena Cava. At this point, edema begins in the feet/legs and maybe the Right arm/hand.

Studies:
EKG may show Right axis deviation if there dis right ventricular hypertrophy

CXR should show pulmonary edema “Bat Wing” perhaps even a bilateral fluid line and Kerly B lines at the lateral pulmonary edges

BNP levels should rise as the right atrium will get stretched out by blood the Right Ventricle can’t take in.

BUN/Cr will likely show renal impairment

Rx:
Get the volume down with thiazide diuretics, loops if GFR is under 30

Get a CCB on board (diltiazem) to spare the heart extra effort

Get an ACE on board to protect those kidneys

If a fib has been caused by stretching of the right atrium and the SA node, control arrythmias with amiodarone or, if that doesn’t work, consider an implacable pacemaker.

Low Sodium Diet & contact Dr if gain of lbs in a day

212
Q

CardioMyopathies

A

Damage to the cardiac muscle:

Dilated (DCM)- Grossly dilates all 4 heart chambers. Globular shaped heart
-Alcohol, Post Partum from so much
extra blood & chemotherapy
-Dyspnea, S3 & JVD on presentation
Rales possible & CHF sxs likely
Rx: ACE, Diuretic, BBl, & Dig
maybe even Spironolactone
Low Sodium Diet as in CHF
- Really, this IS CHF

Hypertrophic (HCM) Massive Hypertropy of Septum and Left Ventricle
- THIS IS a GENETIC DEFECT,
Under 30
Sudden MI death, even athletes
-Dyspnea, Exertional Angina
- Left Axis Dev on EKG
- Tiny left ventricular space on ECHO

Restricted (RCM) Ventricles unable to stretch due to fibrosis and/or thickening of muscle and this also makes the valves function poorly. Ecstasy, the drug, a 5HT2 receptor agonist causes this as did several other drugs mainly pulled now for this side effect.
-Amyloidosis, Light Chain
-2nd to Multiple Myeloma
Lupus, RA, TB
-LV is small & thick, low output on ECHO
Rx: Reduce Preload w/Diuretic
to ease stretch of the little ventricle
Beta Block to slow rate, O2 use
CCB to increase filling time
DON’T give ACE/ARBS to amyloidosis

213
Q

CardioMyopathies

A

Damage to the cardiac muscle:

Dilated (DCM)- Grossly dilates all 4 heart chambers. Globular shaped heart
-Alcohol, Post Partum from so much
extra blood & chemotherapy
-Dyspnea, S3 & JVD on presentation
Rales possible & CHF sxs likely
Rx: ACE, Diuretic, BBl, & Dig
maybe even Spironolactone
Low Sodium Diet as in CHF
- Really, this IS CHF

Hypertrophic (HCM) Massive Hypertropy of Septum and Left Ventricle
- THIS IS a GENETIC DEFECT,
Under 30
Sudden MI death, even athletes
-Dyspnea, Exertional Angina
- Left Axis Dev on EKG
- Tiny left ventricular space on ECHO

Restricted (RCM) Ventricles unable to stretch due to fibrosis and/or thickening of muscle and this also makes the valves function poorly. Ecstasy, the drug, a 5HT2 receptor agonist causes this as did several other drugs mainly pulled now for this side effect.

214
Q

CardioMyopathies

A

Damage to the cardiac muscle:

Dilated (DCM)- Grossly dilates all 4 heart chambers. Globular shaped heart
-Alcohol, Post Partum from so much
extra blood & chemotherapy
-Dyspnea, S3 & JVD on presentation
Rales possible & CHF sxs likely
Rx: ACE, Diuretic, BBl, & Dig
maybe even Spironolactone
Low Sodium Diet as in CHF
- Really, this IS CHF

Hypertrophic (HCM) Thickened septum and Left Ventricle
-

Restricted (RCM) Ventricles unable to stretch due to fibrosis and/or thickening of muscle and this also makes the valves function poorly. Ecstasy, the drug, a 5HT2 receptor agonist causes this as did several other drugs mainly pulled now for this side effect.

215
Q

Dilated Cardiomyopathy

A

Globular Stretched Out CHF-y Heart

Presents and is Treated like CHF

216
Q

HYPERTROPHIC CARDIOMYOPATHY

A

This is the Genetic Defect - Massive Septum & Left Ventricle, Tiny LV Volume on ECHO

Implant Defibrillator. Check entire family if someone dies of MI under 30.

217
Q

Restrictive Cardiomyopathy

A

Amyloidosis A, light chains

Fibrosis of the left ventricle, thick but tiny

2nd to chronic inflammatory comorbidity

Reduce preload, rate, use CCB to increase filing time

218
Q

Most common location of Atrial Septal Defect

A

Osteum Secundum

Mid-Septum below FOSSA Ovalis

219
Q

Most common location of Atrial Septal Defect

A

Osteum Secundum - Mid-Septum below FOSSA Ovalis

also Osteum Venosus - Sup. Atrium near SVC

Osteum Primum - Inf Atrium near tricuspid

220
Q

Oxygenated Blood shunts from High pressure LEFT Atrium into Low Pressure RIGHT Atrium

A

Atrial Septal Defect (ASD ) OR
Patent Foramen Ovale

ASD usually discovered via ultrasound in utero
ECHO Dx study of choice once born

     -can get to adulthood, Systolic Ejection 
      Murmur @ 2nd Left inercostal space with
      a WIDE SPLIT S2

If it’s over 6mm in diameter they close it with a patch via catheter

221
Q

Patent Foramen Ovale is COMMON!!

Stroke Risk if pressure in Rt atrium somehow overcomes that of left and a clot moves thru from the leg…

A

25-30% in the General Population!!!
Ranging from 1mm to 10 mm in diameter

Systolic Ejection Murmur along 2nd or 3rd ICS at the Left Sternal Border. Could be taken for Tricuspid Regurg but sounds different

Wide Fixed Split S2

222
Q

Wide ‘Fixed’ Split S2

A

This signifies a hole somewhere, likely in the atrium.

The extra blood flowing from L to Rt Atrium & then to Rt Ventricle causes the Pulmonic Valve to close a titch after the Aortic Valve, resulting in 2 S2 valve closures.

“Fixed” as in doesn’t vary with inspiration
Splitting that goes away with inspiration is common in young people

223
Q

Patent Foramen Ovale is COMMON!!

Stroke Risk if pressure in Rt atrium somehow overcomes that of left and a clot moves thru from the leg…

Suspect PFO in strokes under 50

A

25-30% in the General Population!!!
Ranging from 1mm to 10 mm in diameter

Systolic Ejection Murmur along 2nd or 3rd ICS at the Left Sternal Border. Could be taken for Tricuspid Regurg but sounds different

Wide Fixed Split S2

224
Q

Patent Foramen Ovale is COMMON!!

Stroke Risk if pressure in Rt atrium somehow overcomes that of left and a clot moves thru from the leg…

Suspect PFO in strokes under 50

A

25-30% in the General Population!!!
Ranging from 1mm to 10 mm in diameter

Systolic Ejection Murmur along 2nd or 3rd ICS at the Left Sternal Border. Could be taken for Tricuspid Regurg but sounds different

Wide Fixed Split S2

TEE Bubble study is image of choice
Noninvasive & Diagnostic

225
Q

Rx for Patent Foramen Ovale and small septal defect

A

Aspirin for both if you’re not fixing it, unless there’s been a stroke already, in which case Warfarin is in order

Can’t risk a clot slipping thru should lung pressure somehow increase raising RA pressure over LA pressure and reversing the shunt.

Well.. I say we “can’t” risk the clot but it seems we really do risk it. Fixing the hole even after a stroke is still controversial. Deb says send your patient to a neonatal cardiologist and he’ll fix it up nice, insurance may not pay though…

226
Q

Eisenmenger Syndrome

A

This is when the dreaded increase in Pulmonary pressure does occur in the setting of Patent Foramen Ovale or Atrial Septal Defect and the Rt Atrial Pressure exceeds the left

Also occurs with ventricular septal defect but it there we don’t need any input from the lungs to create havoc, it’s inherent.

DeOxygenated blood from the Rt mixes with the Oxygenated blood from the left and the body is suddenly less oxygenated

Dyspnea, Hypoxia, Cap Refill not so good

227
Q

Eisenmenger Syndrome

A

This is when the dreaded increase in Pulmonary pressure does occur in the setting of Patent Foramen Ovale or Atrial Septal Defect and the Rt Atrial Pressure exceeds the left

Also occurs with ventricular septal defect but it there we don’t need any input from the lungs to create havoc. If the ventricular defect is big enough it’s inherent.

DeOxygenated blood from the Rt mixes with the Oxygenated blood from the left and the body is suddenly less oxygenated

Dyspnea, Hypoxia, Cap Refill not so good

228
Q

MOST Common Septal Defect

A

Ventricular Septal Defect

Visible on Ultra Sound Prenatally
75% close on their own before 2 yrs and remain asymptomatic

Presents with a THRILL over 3-4th LICS if big enough to be troublesome

ECHO is diagnostic but you’ll likely have done inconclusive CXR, EKG and CT first….

Patch big ones early & prevent pulmonary HTN

229
Q

Patent Ductus Arteriosis

Continuous
Machinery-Like
Subclavicular
Murmur with a Thrill
In 
The 
Neonate/Infant

These babies will either get this fixed or have CHF very early, fail to thrive and die.

A

The fetal passageway for Oxygenated Blood from the Umbillicus to get into the systemic circulation.

It closes at birth in response to neonatal lung production of Bradykinin, secreted when the lungs expand with normal breathing. Bradykinin opposes Prostaglandin E2 a placental prostaglandin that is still circulating in the neonate after birth.

In Premies before 37 weeks, the lungs may not produce enough bradykinin to shut down Prostaglandin E2’s action at the ductus arteriousis and the duct remains patent, leading to hypoxia from the mixing.

BUT … there’s a simple fix: NSAIDS, specifically regular old Ibuprofin can block the action of Prostaglandin E2 and premies all get it UNLESS

Unless it’s better for the babe to keep it open, as in the congenital defect Transposition of the Great Arteries. In this case, the patent duct is the ONLY way oxygenated blood gets from the lungs to the body in the neonate. In this case, E2 will be administered to KEEP the duct open until the defect is repaired.

230
Q

Continuous Machinery Like Subclavicular Murmur possibly with a THRILL

A

Patent Ductus Arteriosus is very noisy

Give NSAIDS and Fix It ASAP

231
Q

Patent Ductus Arteriosis

Continuous
Machinery-Like
Subclavicular
Murmur with a Thrill
In 
The 
Neonate/Infant

These babies will either get this fixed or suffer Pulmonary Edema & CHF very early, fail to thrive and die.

A

The fetal passageway for Oxygenated Blood from the Umbillicus to get into the systemic circulation.

It closes at birth in response to neonatal lung production of Bradykinin, secreted when the lungs expand with normal breathing. Bradykinin opposes Prostaglandin E2 a placental prostaglandin that is still circulating in the neonate after birth.

In Premies before 37 weeks, the lungs may not produce enough bradykinin to shut down Prostaglandin E2’s action at the ductus arteriousis and the duct remains patent, leading to hypoxia from the mixing.

BUT … there’s a simple fix: NSAIDS, specifically regular old Ibuprofin can block the action of Prostaglandin E2 and premies all get it UNLESS

Unless it’s better for the babe to keep it open, as in the congenital defect Transposition of the Great Arteries. In this case, the patent duct is the ONLY way oxygenated blood gets from the lungs to the body in the neonate. In this case, E2 (well actually it is E1 for some reason) will be administered to KEEP the duct open until the defect is repaired.

232
Q

EISENMENGER’S Syndrome

A

This is when the Left to Right shunt through the atrial septal

233
Q

Tetrology of Fallot

Blue perioral/nasal, fingers & toes

Tet Spells

A

Collection of 4 Congenital Defects

Ventricular septal opening
Stenosed Pulmonic Valve
Overriding (dilated) Aorta
Right Ventricular Hypertrophy

Rx #1 Keep Ductus Arteriosus Patent w/E1

 Surgery to widen the pulmonic valve and fix the septal defect with a patch

Still, there may be hypoxia, fix the Tet Spell by bringing knees to chest to increase intrathoracic pressure.

234
Q

The great vessels are Not transposed and there are no HOLES in the septum BUT, the pulmonary valve is not there and the pulmonary artery is completely blocked

These babies are hypoxic on 100% O2 within minutes of birth - need to move very fast with that E1.

A

1 Keep Ductus Arteriosis patent w/E1

Pulmonary Valve Atresia

Then poke a hole in the septum with a balloon catheter. I have no idea why we don’t poke a hole into the pulmonary artery and install a synthetic valve there but we don’t.

235
Q

The mitral valve is not open and the aorta narrows in the arch and may even have a coarctation. The left ventricle is tiny

But

The right side is perfectly fine

A

1 Keep ductus patent w/E1

Hyperplastic Left Heart Syndrome

Why we can’t just OPEN the mitral valve, I don’t know. But we don’t. We make a ventricular septal defect and cut out the coarctation then stent and re-anastomose the aorta.

You’ll need an echo to ID this though the babe will go blue right off so the E1 needs to be given asap before you have time to sort Hyperplastic from PV Atresia

Even after surgery, 5 year survival isn’t good. 65% We do transplants for this.

236
Q

Transposition of the Great Vessles

A

1 keep the ductus patent w/E1

Blue Blood goes out the aorta, Red blood goes to the lungs.

237
Q 
This category of drugs blocks:
Na+
K+
Ca+
and
Beta Adrenergic Receptors
A

Antiarrythmics: 4 Classes

Class I Blocks Na+ & K+
Ia) Qunidine for SVT/VTach
Replaced by Amiodarone
Ib) Lidocaine for VTACH w/Ischemia
Ic) Flecanide - dangerous only for life threat
VTACH and SVT refractory to
amiodarone.

Class II: Blocks

238
Q

Most Potent Na+ Channel Blocker

A

Flecanide - careful though, only for refractory SVT and life Threat VTAC refractory to Lidocaine

239
Q 
This category of drugs blocks:
Na+
K+
Ca+
and
Beta Adrenergic Receptors
A

Antiarrythmics: 4 Classes

Class I Blocks Na+ & K+
Ia) Qunidine for SVT/VTach
Replaced by Amiodarone
Ib) Lidocaine for VTACH w/Ischemia
Ic) Flecanide - dangerous only for life threat
VTACH and SVT refractory to
amiodarone.

Class II: Beta Blockers

Class III: Blocks Na+, K+, Ca+ & Beta Receptors

   - Amiodarone Does It ALL....
   - Sotalol  only blocks K+ & Beta Receptors

Class IV: Calcium Channel Blockers
-Diltiazem
-Verapamil (SO CAREful “Verapakill” easy
to give too much…

240
Q

Digoxin

For

AFIB (crazy) A Flutter (sawtooth, fast but reg)

It prevents many of those ectopic beats from reaching the ventricles

A

Blocks Na/K ATPase as Dig competes with K+ for the same site on the pump - hence K+ stays high extracellularly and HYPER-KALEMIA develops

Slows conduction thru AV Node so extra atrial impulses don’t get through to the ventricles
BUT
It can build up to toxic levels if the kidneys aren’t clearing it properly in which case Pt may:

See Yellow Halos
Have Dangerous Bradycardia
Very high K+ (peaky T, tiny T, wide sloppy QRS)

241
Q

Hyperkalemia Signs & Findings

A

Peaky Ts, Tiny Ps and wide sloppy QRS

Dig Toxicity
K+ over 5.5

242
Q

PAC

Vs

PVC

A

PAC: Premature ATRIAL Contraction.
This is an extra P tossed off by an ectopic
pacemaker..

The ectopic P wave will have a different shape than those coming from the SA node.

PVC: Premature VENTRICULAR Contraction

Purkinje Fibers ‘Toss Off An Impulse” that causes an odd ventricular contraction which shows on the EKG as a HUGE mess coming out of nowhere
Bigeminy: Purkinje’s toss off 2 contractions
Trigeminy: They toss off 3 before returning
to normal.

GEN MED II Final EXAM (2 decks)

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