Study For Final

Question 1

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

Answer 1

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.

Question 2

Bachman’s Bundle

Answer 2

SA Node tracts to Left Atrium

Question 3

Internodal Tracts

Answer 3

Transmit impulses from SA Node thru Right Atrium

Question 4

Right Vagus depresses

Left Vagus depresses

Answer 4

Sinoatrial Node

AV Node

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

Question 5

Fastest cardiac conduction tract

Answer 5

Purkinji Fibers, then His then SA then AV

Question 6

SA generated impulses

Answer 6

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

Question 7

AV Node generated impulses

Answer 7

Usually 40-60 bpm

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

Waves initiating below the Rt Atrium

Question 8

P-Waves

Answer 8

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

Question 9

P-Waves

Answer 9

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.

Question 10

QRS Complex

Answer 10

Represents Ventricular Contraction.

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

Question 11

Hyper-Kalemia/ Digoxin Toxicity

Answer 11

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

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

Question 12

Hyper K+/ Dig Toxicity

Answer 12

Peaky T
Tiny P
Wide QRS

Question 13

Hyper K+/ Dig Toxicity

Answer 13

Peaky Ts
Tiny Ps
Wide QRS

Question 14

Normal Serum Potassium

Answer 14

3.5 - 5.5 mEq/L

Question 15

HypoKalemia

Answer 15

Below 3.5 mEq/L

Question 16

Hyper-Kalemia/ Digoxin Toxicity

Answer 16

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

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

Question 17

Hyper K+/ Dig Toxicity

Answer 17

Peaky Ts
Tiny Ps
Wide QRS

Question 18

Hyper Kalemia

Answer 18

Above 5.5 mEq/L

Question 19

Hypo-Kalemia

Answer 19

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+

Question 20

Hypo K+ EKG Findings

Answer 20

Inverted T or Flat

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

ST Depression

Taller Wider P Waves

Question 21

Axis Deviation

Answer 21

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

Question 22

JNC-8 HTN for 60 & over

Answer 22

over 150/90

Question 23

JNC-8 HTN for under 60yrs

Answer 23

over 140/90

Question 24

Primary HTN

Answer 24

Cause unknown but not due to comorbitity

The most common kind of HTN

Question 25

Most Common Cause of Secondary HTN

Answer 25

Kidney Disease

Question 26

Coarctation of the Aorta

Answer 26

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.

Question 27

Metabolic Syndrome

Answer 27

``` Truncal Obesity Triglycerides over 150 HDL under 40 (m) under 50 (f) Bp 130/85 and over Fasting Blood Sugar over 100 ```

Question 28

``` BP Cuff Sizes Infant Child Small Adult Adult Lg Adult Thigh ```

Answer 28

``` 7 9 10 11 12 13 ```

Question 29

Copper Wiring, Cotton Wool Spots & | Papillodema

Answer 29

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

Question 30

Dx Studies to order if you Dx HTN

Answer 30

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

Question 31

Dx Studies to order if you Dx HTN

Answer 31

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

Question 32

Dx Studies to order if you Dx HTN

Answer 32

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

Question 33

Plasma Renin Test Results

Answer 33

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

Question 34

Widened Pulse Pressure

Answer 34

Systolic and Diastolic diverge over serial Bp Aortic Regurge/Aortic Dissection

Question 35

Test for Cushings Syndrome

Answer 35

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

Question 36

Target BMI

Answer 36

25 Overweight is 26 Obese in the 30s

Question 37

Diabetes over 60, Bp goal is? DM Triglyceride Goal is? A1C goal is

Answer 37

150/90 Under 100 for Triglycerides in DM Under 7

Question 38

First Line HTN Rx:

Answer 38

ACEs & ARBs exp in DM Thiazide Diuretics Calcium Channel Blockers Second line, increase doses of these

Question 39

Thiazide Diuretics MOA

Answer 39

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)

Question 40

THIAZIDES vs LOOPS

Answer 40

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

Question 41

African Descent HTN Rx

Answer 41

CCB (Ca+ Channel Blocker) + Thiazide DON'T use ACE Inhibitors for African Decscent UNLESS there is comorbid CKD

Question 42

Never Combine ACEs with

Answer 42

ARBs

Question 43

Thiazide Diuretics MOA HCTZ Triamterine Chlorthiazide

Answer 43

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)

Question 44

Post MI Rx

Answer 44

Beta Blocker ALWAYS ALWAYS | ACE Inhibitor

Question 45

Loop Diuretic MOA

Answer 45

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

Question 46

ACEI dangerous side effects: Lisinopril

Answer 46

Lymphadenopathy - swollen face, tongue, neck Cough Both due to blocking of Bradykinin degradation and the bradykinin causes the effects

Question 47

Lisinopril Std Dose

Answer 47

20-40 mg/day Work up from 10mg 5 mg in MI if not already on ACE

Question 48

ACEI benefits

Answer 48

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

Question 49

ARBs Valsartan "Sartans"

Answer 49

Same benefits as ACE No bradykinin Cough

Question 50

Diltiazem Verapamil Amlodipine Nifedipine

Answer 50

Calcium Channel Blockers Nifedipine for Reynauds

Question 51

Diltiazem Verapamil Amlodipine Nifedipine

Answer 51

Calcium Channel Blockers Nifedipine for Reynauds Prolongs AV pause by blocking Ca+ channels and slowing depolarization

Question 52

Beta Blocker MOA Metropolol B1/B2 Selective Carvedilol B1/B2 & A2

Answer 52

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

Question 53

Beta Blocker MOA Metropolol B1/B2 Selective Carvedilol B1/B2 & A2

Answer 53

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.

Question 54

Use Esmolol (BBlock) in

Answer 54

SVT

Question 55

Alpha Receptor Antagonists: The ZOSINS

Answer 55

Prevent vessel constriction and thereby bring down Bp Also good for relaxing Prostate in BPH and relaxes detrusor muscle in urine retention

Question 56

Beta Blocker MOA Metropolol B1/B2 Selective Carvedilol B1/B2 & A1

Answer 56

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.

Question 57

Direct Vasodilators

Answer 57

Nitroglycerine Hydralazine (use in pregnancy for eclampsia)

Question 58

Central Alpha 2 Agonists

Answer 58

Clonadine & Methyl Dopa These lower Bp by preventing sympathetic stimulation of Adrenal Epi/Nor release

Question 59

Hypertensive Urgency: Get Bp down 20mmHg in 24 Hrs vs Hypertensive Emergency: Get Bp down 20% in 1 Hr

Answer 59

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

Question 60

Hypertensive Urgency Rx

Answer 60

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.

Question 61

HTN End Organ Damage:

Answer 61

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

Question 62

HTN End Organ Damage: Very High Bp?? DO A FUNDOSCOPIC EXAM!!

Answer 62

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

Question 63

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.

Answer 63

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

Question 64

Hypertensive Urgency: Get Bp down 20mmHg in 24 Hrs vs Hypertensive Emergency: Get MAP down 20% in 1 Hr

Answer 64

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

Question 65

MAP Normal MAP is 70 - 110

Answer 65

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.

Question 66

HTN Emergency Rx

Answer 66

DO use: Esmolol, Labetolol & Nicardipine (a CCB) DO NOT use: Nitroprusside Nitroglycerine Hydralizine These lower MAP too quickly

Question 67

Stroke, Intracerebral Hemorrhage HTN Emergency Rx

Answer 67

DO use: Labetolol & Nicardipine (a CCB) DO NOT use: Nitroprusside Nitroglycerine Hydralizine These lower MAP too quickly

Question 68

General Hypertensive Emergency Rx (no stroke/bleed)

Answer 68

Nitroprusside

Question 69

Orthostatic Hypotension Definition

Answer 69

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

Question 70

Rx causes of Orthstatic Hypotension

Answer 70

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

Question 71

Rx causes of Orthstatic Hypotension Tilt Table Tests for Orthostatic Hypotension

Answer 71

Alpha Blockers (the Zosins for BPH) Diuretics Nitrates Calcium Channel Blockers prolonged bed rest Autonomic Impairment - evaluated by Rectal tone & urinary continence fluid loss

Question 72

Rx for Orthostatic Hypotension

Answer 72

Fludrocortisone/Florinef, increases Na+ retention and bumps up blood volume Midodrine (+ inotrope) constricts vasculature

Question 73

Most Common Artery Occluded by Peripheral Artery Dz

Answer 73

Superficial Femoral Artery Numbness/tingle burn on lateral superficial thigh

Question 74

Most Common Artery Occluded by Peripheral Artery Dz (PAD) PAD = atherosclerosis in limb arteries (legs)

Answer 74

Superficial Femoral Artery

Question 75

Signs of PAD

Answer 75

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

Question 76

Risks of PAD

Answer 76

Smoking #1 DM Hyperlipidemia

Question 77

Signs of PAD

Answer 77

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

Question 78

PAD foot pain vs DM foot neuropathy

Answer 78

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...)

Question 79

PAD encourages Infection due to Stasis

Answer 79

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

Question 80

PAD Diagnostic Testing

Answer 80

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

Question 81

Arteriogram - CT w/Contrast

Answer 81

Pinpoints stenosis and catheter used to stent the artery

Question 82

PAD Rx

Answer 82

Cilostazol (Pletal) Not in CHF Phosphodiesterase Inhibiter + ACE Inhibitors for all PAD Pts

Question 83

Thrombus vs Embolus

Answer 83

Stationary vs On The Move

Question 84

5 P's of Arterial Occlusion (of limb)

Answer 84

``` 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

Question 85

Polycystic Kidney Disease is weirdly comorbid with

Answer 85

Cerebral Aneurysm

Question 86

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

Answer 86

Ruptured Cerebral Aneurysm

Question 87

``` Abdominal Ripping/Tearing Searing Pain in the lumbar back Hypotension Tachycardia Shock ```

Answer 87

Aortic Aneurysm - most common in Lumbar Intervene surgically @ 5.5cm w/stent or, more invasive, an aortic graft

Question 88

Ripping/Tearing pain between scapula

Answer 88

Thoracic Aneurysm Rupture

Question 89

Gold Std for Aortic Aneurysm Imaging

Answer 89

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

Question 90

Gold Std for Aortic Aneurysm Imaging

Answer 90

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

Question 91

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

Answer 91

A Beta Blocker Lobetalol or Esmolol are IV Beta Blockers

Question 92

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

Answer 92

A Beta Blocker Lobetalol or Esmolol are IV Beta Blockers

Question 93

Temporal Arteritis

Answer 93

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

Question 94

Temporal Arteritis Giant Cell Arteritis

Answer 94

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

Question 95

Temporal Arteritis Giant Cell Arteritis

Answer 95

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

Question 96

Most Common Vein for Varicosities

Answer 96

Great Saphenous aka Long Saphenous

Question 97

Peripheral Arterial Disease Vs Chronic Venous Insufficiency

Answer 97

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

Question 98

Stasis Dermatitis

Answer 98

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

Question 99

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

Answer 99

Doppler Ultra Sound

Question 100

Gold Std Varicose Vein Therapy

Answer 100

Sclerosing with FOAM

Question 101

+ Homan's Sign Pain in calf when foot is flexed

Answer 101

Suggestive of Superficial Thrombophlebitis | little clot in vein causes inflammation

Question 102

Palpable nodular cord and (+) Homan's sign | recent IV catheter or PICC line

Answer 102

super ficial thromboplebitis Rx is: Heat NSAIDS Compression Stocking Serious if extends up near Great Saphenous junction with Femoral Vein

Question 103

Virchow's Triad

Answer 103

``` Stasis Vascular Injury Hypercoagulability Factor V Leiden Mutation Polycythemia Thrombocythemia ```

Question 104

Most Common Sites for DVT

Answer 104

Superficial Femoral Popliteal Posterior Tibial

Question 105

Homan's sign is unreliable for

Answer 105

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

Question 106

Test for DVT

Answer 106

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

Question 107

Test for PE

Answer 107

Spiral CT of the Chest to ID PE

Question 108

Rx DVT/PE

Answer 108

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

Question 109

Rx DVT/PE

Answer 109

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

Question 110

Acute Coronary Syndrome

Answer 110

Unstable Angina Stemi N-Stemi

Question 111

Cardiac Injury Panel

Answer 111

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

Question 112

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

Answer 112

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

Question 113

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

Answer 113

Stemi- Full thickness infarction 911 Stabilize, heparinize and send to cath lab in ambulance

Question 114

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

Answer 114

Non-Stemi MI - only a partial thickness MI 911 Stabilize, heparinize/anticoagulate and send to cath lab in ambulance

Question 115

ST Elevations/Depression in II III & AvF

Answer 115

Inferior MI

Question 116

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

Answer 116

Lateral MI

Question 117

V1 & V2 elevation/depression

Answer 117

Anteroseptal

Question 118

V1, V2 V3 V4

Answer 118

Anterior MI

Question 119

V4 V5 V6

Answer 119

Antero-Lateral MI

Question 120

MI Rx:

Answer 120

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

Question 121

PICA

Answer 121

Percutaneous Intervention Coranary Arteriography aka - Catheterization to locate blockage and place stent

Question 122

MI Rx:

Answer 122

``` 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 ```

Question 123

Angina occurs at rest and in clusters

Answer 123

Prinzmetal Angina Caused by vasospasm

Question 124

Typical MI EKG progression

Answer 124

Peaky T w/in minutes = ischemia ST Elevation & Inverted T w/in hrs = necrosis Q-Wave w/in days when scar is formed

Question 125

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

Answer 125

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

Question 126

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

Answer 126

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

Question 127

MI Dx Studies

Answer 127

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

Question 128

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

Answer 128

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

Question 129

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

Answer 129

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

Question 130

Most serious risk of fibrinolytic therapy like TPA or ReOpro

Answer 130

intracranial hemorrhage

Question 131

TPA aka:

Answer 131

Alteplase

Question 132

Abciximab aka:

Answer 132

Reopro

Question 133

If MI pt also has Heart Failure (10%)

Answer 133

start on ACEI

Question 134

VTach 911 Rx

Answer 134

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

Question 135

VFib 911 Rx

Answer 135

Defibrillate Amiodarone IV

Question 136

Pacemaker req if:

Answer 136

2nd degree Heart block does not resolve spontaneously- might use temporary Third Degree Heart block, permanent & implanted

Question 137

Hypotension SBP less than 90 Rx

Answer 137

IV Fluids - | Vasopressors: Dopamine & Dobutamine IV

Question 138

Stable Angina

Answer 138

Pain on exhertion, goes away with rest Nitroglycerine SL spray, tabs patch paste

Question 139

Levine's Sign

Answer 139

Clenched Fist over Mediastinum | Classic Heart Attack sign

Question 140

(+) Stress Test REsult

Answer 140

1mm ST depression/Slope on exertion Refer for Catheterization

Question 141

Hypotension SBP less than 90 Rx

Answer 141

IV Fluids - Vasopressors: Dopamine & Dobutamine IV Dobutamine increases heart rate & contraction Dopamine can do that too but also constrict vasculature

Question 142

Don't use Dobutamine in

Answer 142

Wolf Parkinson White | LBBB or permanent pacemaker - use Adenosine instead

Question 143

Adenosine

Answer 143

Nucleoside that Dilates Coronary Arteries | Only lasts 6 seconds from IV injection so push hard with saline and place high up on arm

Question 144

Electron Beam CT EBCT

Answer 144

Quantifies Coronary Artery Calcificaton

Question 145

Definitive Diagnostic Imaging and Treatmetn for Coronary Artery Disease

Answer 145

Coronary Angiography CATH

Question 146

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

Answer 146

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) ```

Question 147

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

Answer 147

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) ```

Question 148

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

Answer 148

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

Question 149

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

Answer 149

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

Question 150

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

Answer 150

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

Question 151

10mm decline in SBp during inspiration

Answer 151

Pulsus Paradoxis Due to impaired LV filling - Tamponade

Question 152

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

Answer 152

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

Question 153

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

Answer 153

Neurogenic Shock

Question 154

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

Answer 154

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

Question 155

Imaging of choice for Aortic Dissection

Answer 155

CT Chest & CT Abdomen

Question 156

IV insertion or PICC lines cause this venous disease

Answer 156

Superficial venous thrombophlebitis

Question 157

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

Answer 157

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

Question 158

Diagnostic NonInvasive Image of choice for claudication (PAD)

Answer 158

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

Question 159

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

Answer 159

Aortic Aneurysm intervene at 5.5 Stent it

Question 160

PAD Risk Factors

Answer 160

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

Question 161

Giant Cell Arteritis is 50% comorbid with

Answer 161

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

Question 162

#1 Risk Factor for Dissecting Aortic Aneurysm

Answer 162

Uncontrolled HTN

Question 163

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

Answer 163

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

Question 164

Hydralazine as HTN medication

Answer 164

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?

Question 165

Garment Rx for Orthostatic Hypotension

Answer 165

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..

Question 166

Dressler Syndrome

Answer 166

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.

Question 167

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

Answer 167

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

Question 168

#1 Go To HTN Monotherapy if no Comorbidities

Answer 168

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

Question 169

#1 Go To HTN Monotherapy if no Comorbidities

Answer 169

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

Question 170

HTN & BPH??? Easy, use

Answer 170

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.

Question 171

Drug of Choice for Perioperative HTN prep

Answer 171

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

Question 172

Drug of Choice for Perioperative HTN prep

Answer 172

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.

Question 173

First drug on board in an aortic dissection?

Answer 173

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

Question 174

Heart Murmur Study of Choice?

Answer 174

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

Question 175

Endothelial injury and fatty streak formation occur early in

Answer 175

Atherosclerosis

Question 176

Don't do a stress echo if

Answer 176

Resting Angina Severe Aortic Stenosis Unstable Rhythm Duh...

Question 177

Study to monitor a KNOWN abd aneurysm

Answer 177

Abdominal Ultrasound To Diagnose it - CT

Question 178

#1 Most Common cause of orthostatic hypotension

Answer 178

Dehydration/ hypovolemia

Question 179

Drugs that commonly cause Hypotension

Answer 179

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

Question 180

Fludrocortisone std Rx for

Answer 180

Orthstatic Hypotension, | Mineral corticoid stimulates the RAAS system to retain more salt

Question 181

Midrodine MOA

Answer 181

Alpha 1 agonist | Promotes peripheral vascular constriction

Question 182

When to use Dobutamine?

Answer 182

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

Question 183

Beta Receptor Agonists: Epi, Dobutamine, Isoproteronol, albuterol Antagonists: Beta Blockers

Answer 183

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.

Question 184

Alpha Receptors A1 Agonists: Midrodrine, Phenylepherine A2 Antagonists: Tamulosin (Flomax) Prazosin (MiniPress A2 Agonists: Clonadine, Methyl Dopa A2 Antagonists: Yohimbe not much used

Answer 184

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.

Question 185

grades IV, V & VI will have a thrill:

Answer 185

Heart Murmurs

Question 186

Standing Manuver in Murmur MOA

Answer 186

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

Question 187

Standing/Squatting/Valsalva Manuver in Murmur MOA Double Bp Cuff Inflation manuver:

Answer 187

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.

Question 188

These Murmurs are ALWAYS pathologic

Answer 188

Diastolic only murmurs

Question 189

Most common cause of mitral stenosis

Answer 189

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.

Question 190

Opening Snap in early Diastole best heard over Apex in decubitus

Answer 190

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

Question 191

Opening Snap in early Diastole best heard over Apex in decubitus

Answer 191

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.

Question 192

Holosystolic Murmur

Answer 192

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.

Question 193

Lub Dub...

Answer 193

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.

Question 194

Lub Dub...

Answer 194

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.

Question 195

Holodiastolic Murmur

Answer 195

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.

Question 196

Most common cause of all murmurs except in Tricuspid murmurs

Answer 196

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.

Question 197

Systolic Crescendo-Decrescendo radiates to the neck

Answer 197

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.

Question 198

Systolic Crescendo-Decrescendo radiates to the neck

Answer 198

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.

Question 199

Stenosis sounds _______ while Regurg sounds ________

Answer 199

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.

Question 200

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

Answer 200

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

Question 201

THIS STENOSIS IS USUALLY CONGENITAL

Answer 201

Pulmonic | Associated w/ Tetrology of Fallot

Question 202

end diastolic volume

Answer 202

110 - 120 ml

Question 203

stroke volume

Answer 203

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

Question 204

ejection fraction

Answer 204

%age of end diastolic volume that is actually ejected should be 60% use ECHO to calculate

Question 205

Heart Failure =

Answer 205

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.

Question 206

Heart Failure =

Answer 206

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

Question 207

Systolic Heart Failure vs Diastolic Heart Failure

Answer 207

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.

Question 208

True Cor Pulmonale Originates in the

Answer 208

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

Question 209

True Cor Pulmonale Originates in the

Answer 209

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

Question 210

True Cor Pulmonale Originates in the

Answer 210

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.

Question 211

True Cor Pulmonale Originates in the

Answer 211

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

Question 212

CardioMyopathies

Answer 212

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

Question 213

CardioMyopathies

Answer 213

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.

Question 214

CardioMyopathies

Answer 214

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.

Question 215

Dilated Cardiomyopathy

Answer 215

Globular Stretched Out CHF-y Heart | Presents and is Treated like CHF

Question 216

HYPERTROPHIC CARDIOMYOPATHY

Answer 216

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.

Question 217

Restrictive Cardiomyopathy

Answer 217

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

Question 218

Most common location of Atrial Septal Defect

Answer 218

Osteum Secundum Mid-Septum below FOSSA Ovalis

Question 219

Most common location of Atrial Septal Defect

Answer 219

Osteum Secundum - Mid-Septum below FOSSA Ovalis also Osteum Venosus - Sup. Atrium near SVC Osteum Primum - Inf Atrium near tricuspid

Question 220

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

Answer 220

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

Question 221

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...

Answer 221

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

Question 222

Wide 'Fixed' Split S2

Answer 222

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

Question 223

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

Answer 223

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

Question 224

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

Answer 224

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

Question 225

Rx for Patent Foramen Ovale and small septal defect

Answer 225

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...

Question 226

Eisenmenger Syndrome

Answer 226

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

Question 227

Eisenmenger Syndrome

Answer 227

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

Question 228

MOST Common Septal Defect

Answer 228

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

Question 229

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.

Answer 229

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.

Question 230

Continuous Machinery Like Subclavicular Murmur possibly with a THRILL

Answer 230

Patent Ductus Arteriosus is very noisy Give NSAIDS and Fix It ASAP

Question 231

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.

Answer 231

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.

Question 232

EISENMENGER'S Syndrome

Answer 232

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

Question 233

Tetrology of Fallot Blue perioral/nasal, fingers & toes Tet Spells

Answer 233

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.

Question 234

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.

Answer 234

Pulmonary Valve Atresia #1 Keep Ductus Arteriosis patent w/E1 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.

Question 235

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

Answer 235

Hyperplastic Left Heart Syndrome #1 Keep ductus patent w/E1 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.

Question 236

Transposition of the Great Vessles

Answer 236

Blue Blood goes out the aorta, Red blood goes to the lungs. #1 keep the ductus patent w/E1 #2 Bedside Balloon Atrial Septostomy (we poke a hole through the septum and join the atria. #3 We switch the great vessels back (0:

Question 237

``` This category of drugs blocks: Na+ K+ Ca+ and Beta Adrenergic Receptors ```

Answer 237

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

Question 238

Most Potent Na+ Channel Blocker

Answer 238

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

Question 239

``` This category of drugs blocks: Na+ K+ Ca+ and Beta Adrenergic Receptors ```

Answer 239

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...

Question 240

Digoxin For AFIB (crazy) A Flutter (sawtooth, fast but reg) It prevents many of those ectopic beats from reaching the ventricles

Answer 240

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)

Question 241

Hyperkalemia Signs & Findings

Answer 241

Peaky Ts, Tiny Ps and wide sloppy QRS Dig Toxicity K+ over 5.5

Question 242

PAC Vs PVC

Answer 242

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.