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Cardiovascular > Cardiovascular Exam 3 Cards > Flashcards

Cardiovascular Exam 3 Cards Flashcards

1
Q

Action potential of a pacemaker call

A

4 - Na+ influx through funny channels
0 - Ca++ influx
3 - K+ efflux

Needs to repolarize before it can fire again

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2
Q

Phases of cardiac cell action potential

A

0 - Influx of sodium through non-funny chanels
1 - K+ and Cl- out for initial descent (I 1&2)
2 - Ca++ in K+ out for plateau (Ca-L & Slow K)
3 - K out of ALL channels
4 - K in through inward rectifier

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3
Q

Lineup of muscle cell potential with EKG

A

Peaks where the Q wave peaks

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4
Q

4 classes of heart drugs

A

I -Fast sodium channels (not funny)
II - Beta blockers
III - Potassium channels
IV - Calcium channel blockers

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5
Q

Types of class I antiarrhythmics

A

A - Slow the rate of the rise of the action potential - action potential is LONGER repolarizing and depolarizing
B - Shorten action potential duration - used on ischemic tissue
C - Dissociates from the channels with slow kinetics - no change in repolarization (widens QRS but no long QT

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6
Q

Quinidine

A

Class IA Antiarrhythmic
Prolonged QT - Torsades
Anticholinergic and Bradycardia

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7
Q

Procainamide

A

IA
Only used for wide complex tachycardia - WPW
Prolongs QT

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8
Q

Disopyramide

A

IA
Anticholinergic
QT prolongation
CI in HFrEF
Used in hypertrophic cardio myopathy

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9
Q

Lidocaine

A

IB - only injectable
Selective to ischemic tissue
Used for MI with Ventricular arrhythmia
Cleared hepatically - neuro effects if toxic

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10
Q

Mexiletine

A

IB
Oral form of lidocaine
Scar mediated refractory ventricular arrhythmias - maybe a patient who is getting shocked a lot by defibrillator

Neurologic effects are big

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11
Q

Flecainide

A

IC
Slows conduction velocity of purkinje fibers
A fib or A flutter
May cause rapid VT
Avoid in ANY structural disease

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12
Q

Propafenone

A

IC
Metallic taste in mouth
Afib/flutter
No use in structural heart issues

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13
Q

Beta Blockers

A

Class II
-olol
Metoprolol is most common
Esmolol IV for rapid afib/flutter
Suppress dysrythmias usually used in conjunction
Bradycardia, exercise intolerance, sexual dysfuntion (low tolerance in the young)

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14
Q

Amiodarone

A

Class III
All 4 classes
QT prolongation, no inotropic function
High number of systemic effects
Slows heart
28 day half life
SEs are cumulative over time - must monitor

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15
Q

Potential areas of amiodarone buildup

A

Lungs, thyroid eyes, heart, liver, skin, GI, nerves
Pulmonary toxicity - annual CXR or PFT to test for pulmonary fibrosis

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16
Q

Amiodarone and thyroid
Lungs

A

Breaks down to iodine - causes hypothyroidism - can treat if mild and not stop
Stop if severe hypo or hyperthyroidism

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17
Q

Amiodarone and eyes

A

Need a yearly eye exam

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18
Q

Skin and amiodarone

A

Blue gray discoloration - avoidance of sun will help avoid reaction
Papa Smirf

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19
Q

Sotolol

A

Class III
Nonselective beta blocker “more than a beta blocker ;)”
Prolongs atrial and ventricular refractoriness
Prolonged QT
Can’t start stop on a dime for low HR
CI in HFrEF

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20
Q

QT at which to stop sotolol

A

550+

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21
Q

Dofetilide

A

Class III
Prolonged QT
Safe in LV dysfunction
Start in hospital and monitor for 3 days
Works on atria more

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22
Q

Drugs not to combine with dofetilide- 6

A

Cimetidine
Ketoconazole
Megestrol
Prochlorperazine
Bactrim
Verapamil

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23
Q

Dronedarone

A

Class III
Similar to amiodarone; “watered down”
CI in HF and Liver issues
Brady and QT prolongation
No thyroid or Pulm toxicity

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24
Q

Ibutilide (Corvert)

A

Class III
IV for afib/flutter cardioversion ONLY
Can cause torsades
Monitor while giving
Avoid in LV dysfunction

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25
Q

Calcium channels blockers for arrhythmias

A

Class IV
Verapamil and Diltiazem
Decrease automaticity and AV conduction
Neg ionotropic effects - Not for LV dysfunction

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26
Q

Digoxin
Action
EKG
Dosing
SE
Arrhythmiasit can cause

A

Other drug
Blocks AV node for high atrial rates - slows conduction and prolongs refractory period
EKG - Long PR with ST depression
Dose in mcg/mL!!!
Causes a yellow tint
Toxicity can cause ANY arrhythmia w/o preference

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27
Q

Dosing of digoxin

A

36 hour half life - daily
MICROGRAMS

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28
Q

Adenosine

A

Used for cardiac stress test
Inhibits AV and SA nodes
Used for SVT
Very short half life - causes “death”
Allows the SA note to pick back up
6,6,12

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29
Q

Atropine

A

Other
Parasympatholytic drug for symptomatic bradycardia
Blocks acetylcholine
Tachy and poor outcomes in MI [atients
Slows HR in Mobitz II or third degree heart block
ACLS drug!!

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30
Q

Typical site for PAD blockage

A

At a vessel bifurcation

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31
Q

Risk factors for PAD- 8 with 2 STRONGEST

A

Smoking - Strongest
HLD
HTN
Alcohol
Fam Hx
Prior MI
Renal insufficiency
DM - Strongest

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32
Q

Categories to be screened for PAD

A

70+ y/o
50-69 w/ hx of smoking
40-49 w/ DM and 1+ risk factor for atherosclerosis
Known athersclerosis at other sites

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33
Q

Locations of PAD

A

Popliteal/Femoral - MC - frequent in black patients
Aorta in white, male smokers 50-60
Tibial in diabetics

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34
Q

Presentation of PAD

A

20-50% w/ no symptoms
Atypical leg pain - no sense
Classic claudication 10-35% = More work =more pain
Critical limb ischemia
Limb ulcer - pressure points
Hanging limb off the bed improves symptoms

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35
Q

Classic claudication

A

Hurts with exercise
Should be reproducible
Goes away 10 minutes after exercise

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36
Q

Way to differentiate nervous or MSK problem from an actual arterial blockage

A

Test pulses

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37
Q

Pseudoclaudication

A

Numbness, tingling, burning
Takes longer to go away than actual claudication

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38
Q

Critical limb ischemia presentation

A

Gangrenous, black extremities - lower
Wet or dry gangrene

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39
Q

TASC II

A

MC used classification system for PAD

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40
Q

PE for PAD patients

A

Listen to heart
Peripheral pulses
Listen for bruits
BP in BOTH arms
Aorta size

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41
Q

Pulse grading

A

3+ Bounding
2+ Brisk-normal
1+ Diminished
0 Absent pulses

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42
Q

Tissue w/o blood flow findings

A

Cold, tight, blue or white, Loss of hair distally, Thick dead nails, Calf atrophy is SEVERE

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43
Q

Bergers Test

A

Lift foot up and it turns white, hang it down in turns red (dependant rubor)

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44
Q

Classic arterial ulcer

A

Thick black eschar - may NOT be on a pressure point

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45
Q

Charcot foot

A

Sign of PAD - Convex foot dorsum

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46
Q

First line diagnostic for PAD

A

Ankle brachial index - take BP of lower extremities

Workup further if results are inconclusive - False negative

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47
Q

ABI Interpretation

A

1.5+ - Non-compressible vessel - further testing
1.4-1 - Normal
.99-.91 - Borderline
.90-.70 - PAD Mild (diagnostic)
.69-.40 - MOderate
Less than .40 - Severe PAD

Can be insensitive when there is collateral circulation

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48
Q

ABI calculation

A

Get elimination pressure with US and BP cuff
Highest lower extremity reading over Highest brachial reading

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49
Q

Toe brachial index

A

2nd to ABI
.7 or lower is diagnostic
Needs a toe BP

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50
Q

Treadmill exercise test

A

Defines how much their disease effects them
Can use with non-diagnostic ABI if they can tolerate it

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51
Q

Segmental limb pressure

A

Uses multiple BP cuffs to determine level of blockage
Drop of 30+mmHg between limbs if a red flag

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52
Q

Arterial duplex for PAD

A

NOT A SCREENING TEST
Used to determine severity of disease and for surgery prep
Increased pressure across the blockage!!

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53
Q

CTA or MRA for PAD

A

Surgical planning
Carful in die sensitive - CKD, DM
Used for surgical planning NOT first line or screening!!

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54
Q

Gold standard for PAD

A

Digital subtraction angiography
Catheter based performed by interventional radiology to guide therapy

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55
Q

Tx for PAD

A

Lifestyle - DM, HTN, HLD, Smoking
Rehab with progressive exercise

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56
Q

Pharm for PAD

A

Statin, Antiplatelet therapy - ASA or clopidegrel alone if asymptomatic with ABI under .90; dual once a stent is placed etc., SGLT-2 inhibitor, ACEI for HTN

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57
Q

Cilostazol - Pledal

A

Vasodilator for PAD
Not first line
CI in HF
HA, Dizziness, Take w/o food

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58
Q

Exercise therapy for PAD

A

3-5 sessions per week
35-50 minutes per session
Walking to near maximal claudication
6 months of rehab

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59
Q

Surgical bypass and endovascular indications for PAD

A

Indicated if not resolution with other treatments or severe w/ critical limb ischemia

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60
Q

Acute arterial occlusion of a limb presentation

A

No time to for collateral flow
Cool to touch, painful limb w/o pulses and abnormal neuro function - loss of light touch(TIME IS TISSUE)
Severe ABI
Pain at rest, Pulselessness, Palor, Paresthesia, Paralysis, Polar/Poikilothermia (Patchiness)

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61
Q

Window for acute limb occlusion revascularization

A

3 hours from presentation

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62
Q

MCC of embolus causing acute limb blockage

A

A fib
Figure out what caused it after the fact

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63
Q

Diagnosis for acute limb occlusion

A

Often clinical
Doppler to confirm if wanted
No CTA or MRA

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64
Q

Diagnostics for acute limb occlusion acute

A

EKG - Afib
CBC, PT/INR for pre-op
Echo - LATER

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65
Q

Management for acute limb occlusion
Pharm and Surgery

A

Revascularization
Start heparin until we can get them to surgery - bolus and then continuous
Endovascular or open surgical approach

Determine source if stable

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66
Q

Warfarin therapy goal post acute limb occlusion

A

INR 2-3

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67
Q

Thrombus vs. embolus prognosis for amputation

A

Greater w/ embolus

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68
Q

Abdominal Aortic Aneurism

A

Usually asymptomic but palpable
5.5 cm is threshold for intervention
Back pain preceding rupture

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69
Q

AAA criteria

A

Dilation of 3+ cm
Rare to rupture under 5cm
Usually below renal arteries

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70
Q

Fusiform and sacular aneurism

A

Sacular is more of an outpouching, fusiform is more symmetrical

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71
Q

Rupture risk threshold for AAA

A

5.5cm

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72
Q

Diagnostics for AAA

A

Ultrasound is study of choice - CT scan is more reliable but NOT 1st line - used for surgical planning

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73
Q

Monitoring of AAA

A

CTA with contrast once it reaches 5cm
Watch serially to see dilation

3-3.4 every 2 years
3.5-4.4 - Every 12 months
4.5-5.4 - Every 6 months

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74
Q

AAA screening

A

Male smokers 65-75 have ever smoked or those with considerable risk factors
Medicare will only pay for one screening

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75
Q

Indications for AAA repair

A

Elective with over 5.5
Rupture - Emergent
Inflammation

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76
Q

Repair for AAA

A

Open - Higher mortality and comnlications, can cause an MI
Endovascular - Less mortality, more likelihood of problems caused by surgery

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77
Q

Thoracic aortic aneurism- 2 risk factors

A

Tank in BP w/ rupture
Risk in Ehlers-Danlos and Marfan
Bicuspid aortic valve

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78
Q

Presentation of TAA

A

Asymptomatic sometimes
Hoarseness, Back pain - restrosternal, dysphagia, dyspnea, aortic regurg

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79
Q

Imaging for TAA

A

May pick of up CXR
CT is better for diagnosis
MRA can also be useful if uncertain

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80
Q

Indications for TAA surgical repair

A

Location, Rate of growth, 5.5+ cm
Endovascular only possible with descending aorta

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81
Q

Screening for TAA

A

No current guidelines
Control BP for management

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82
Q

Aortic dissection

A

Pooling of blood between intima and other aortic layers - high risk of rupture

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83
Q

Aortic dissection presentation

A

Sudden searing chest pain radiating to the back with hypotension
Wide mediastinum on CXR
Pulse discrepancy in extremities - upper vs. lower
Acute aortic regurg may develop - diastolic murmur

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84
Q

Types of aortic dissection

A

Type A - Before subclavian artery
Type B - After

I - Just before
II - Both
III - Just after

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85
Q

5 Risk factors for aortic dissection

A

MC in men over 50
Aging
HTN
Pregnancy
Aortic coarctation

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86
Q

Diagnostics for aortic dissection

A

LVH on EKG
Widened mediastum on CXR
CT is essential for surgery w/ contrast is diagnostic of choice
TEE can be used but may take too long

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87
Q

BP management for Aortic dissection

A

Get SBP 100-120 - Labetolol or Esmolol
2nd line - CCB - Nifedipine or Nitroprusside

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88
Q

Pain management for Aortic dissection

A

Morphine is 1st line

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89
Q

Thromboangiitis obliterans

A

Bergers disease
Male smokers
Smoking cessation is essential

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90
Q

Presentation of Buergers disease

A

Male under 40
Less pain/claudication with ulceration, rest pain
Superficial thrombophlebitis
Warm to touch
May be in feet and hands

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91
Q

Diagnostics for buergers

A

Corkscrew vessels on a CTA/MRA - Diagnostic

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92
Q

Management of Buerger’s disease

A

Tobacco Cessation is a must
Hard to revascularize - Amputation
NSAIDs or Opiods for pain control

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93
Q

Most common source of cardiac tumors

A

Usually metastatic - do head and chest CT/MRI

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94
Q

Types of cardiac tumors

A

Endocardial - stroke with no risk factors
Valvular - CHF symptoms, Sudden death or syncope
Pericardial - Arrhythmias, tamponade, cardiac effusion
Myocardial - EKG changes, dysfunction, coronary involvement

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95
Q

Diagnostic for cardiac masses

A

Echo
Best is cardiac MRI or gated CT scan

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96
Q

Management of cardiac tumors

A

Best to do resection
May do chemo radiation to reduce
Cardiac transplant if candidate

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97
Q

Benign primary cardiac tumors

A

Cardiac myxoma - MC
Papillary fibroelastoma - increasingly detected
Rhabdomyoma - MC in kids

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98
Q

Cardiac Myxoma

A

Mushroom inside the heart
50% of tumors
Mean age = 50 can be genetic
Friable leading to embolus
MC in left atria

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99
Q

Presentation of cardiac myxoma

A

Tumor plop - early diastolic extra heart sound
Stroke w/o risk factors

100
Q

Diagnostics for mysxoma

A

Made via echo - continue to follow
Pathology of embolus
TX - Remove

101
Q

Papillary fibroelastoma

A

Sea anenome of the heart
May cause thrombi
Older is more common but can happen from 3-86
MC in left sided valves, aortic MC

102
Q

Diagnostic for papillary fibroelastoma

A

Echo
Stroke with no risk factors

103
Q

Lipoma of the heart

A

Easy to resect - may only need removed if they are causing problems
Echo or MRI to diagnose

104
Q

Cardiac fibroma

A

Get larger
MC in pediatric population
MC in left ventricle
Difficult to resect
Death due to mass effect

105
Q

Rhabdomyomas

A

R for remain = Don’t usually need to resect
Young infant - can be seen prenatally
Usually resolve

106
Q

End root for malignant cardiac tumors

A

-Sarcoma!!

107
Q

Malignant primary cardiac tumors - sarcomas

A

Sarcomas most common
20-49 year old patients
Tumors are very aggressive - poor prognosis

108
Q

Cardiac lymphomas

A

Less common, more aggressive, usually found post mortem

109
Q

Cardiac mesothelioma

A

Dual identity tumors - not due to asbestos if cardiac
MC pericardial tumor
Pericardial effusion, retrosternal pain/pericarditis
May result in a heart block

110
Q

MC sources of metastic cardiac tumors

A

Melanoma or Renal cell carcinoma

111
Q

Presentation of metastic cardiac tumors

A

May seed in various places
Symptoms depend on tumor location

112
Q

Intracardiac thrombus

A

MCC = A fib leading to blood stuck in LA
Outpouching of atrium - Left atrial appendage causing a thrombus
Also may see in Left ventricle with dilated cardiomyopathy or mitral stenosis - blood stuch in left atria
Results in embolic events

113
Q

Intracardiac thrombus stability

A

LV thrombus is MORE stable

114
Q

Management for Intracardiac thrombus

A

Warfarin is the only approved oral anticoagulat
Can bridge from heparin or lovenox
INR 2-3
Needs to be done until clot is resorbed - at least 3 months

115
Q

Warfarin treatment length for intracardiac thrombus

A

At least 3 months

116
Q

Indications for thrombectomy for intracardiac thrombus

A

Planned open heart surgery for another reason
Failure of anticoagulation
Anticoagulation os contraindicated

117
Q

Varicose veins

A

Dilated tortuous suoerficial veins
Aching pain or asymptomatic
Due to high pressure in the vein and distension of valves
Long standing or heavy lifting

118
Q

2 Main things that contribute to venous reflux and hypertension

A

Venous reflux
Venous hypertension

119
Q

MC area for varicose veins

A

Typically the great saphenous vein

120
Q

Presentation of varicose veins

A

Legs feel achy when standing for long periods
Relieved by leg elevation
Skin discoloration - hemociridan deposits
Fibrosis
Pruritis
Severity is NOT correlated to number of varicosities

121
Q

Diagnostics for Varicose veins

A

Via observation
Get venous duplex if there is a clot and surgery is indicated

122
Q

Management for varicose veins

A

Compression hose - 20-30mmHg at all waking hours
Leg elevation - above the heart

123
Q

Surgical management for varicose veins

A

Sclerotherapy - Closes off the veins
Endovenous laser/Radiofrequency ablation therapy - Laser destroys vein
Vein stripping - Last resort!!

124
Q

Chronic venous insufficiency

A

Complication of varicose veins or DVT
Edema and skin hyperpigmentation
Too much pressure in the venous system
Obesity is a major risk factor

125
Q

Presentation of chronic venous insufficiency

A

Lower extremity edema - check BNP for CHF
Darkening skin color - staining
Inflammation of skin - stasis dermatitis
Worse with standing
Taut, shiny skin

126
Q

Difference between stasis dermatitis and cellulitis

A

Cellulitis will be PAINFUL, SD will NOT BE
Cellulitis will usually NOT be BILATERAL, SD will be

127
Q

Lipodermatosclerosis

A

Inflammation of fatty tissue around distal lower extremity - inverse bowling pin

128
Q

Atrophy blanch

A

Ivory white atrophic plaques - star shaped with surrounding hyperpigmentation - CVI

129
Q

Corona phlebectactica

A

Dialted veins around the ankle

130
Q

Venous versus arterial disease process

A

Arterial - Dry, pulseless, cool, clear borders on lesion
Venous - Wet, Pulses, Warm, Poor borders on lesions

131
Q

Diagnostics for CVI

A

Doppler US
MDCT - not routine

132
Q

Management for CVI

A

Compression hose
Patient education - raise legs
Pneumatic compressions

133
Q

Unna boot

A

Management for CVI ulceration - wrap with medication - DON’T take off

134
Q

Vein treatment for CVI

A

Sclerotherapy to prevent resurgence of ulcers

135
Q

Venous thrombophlebitis

A

Raised re painful induration along the source of an IV
Staph is MC
May result in a clot, may not need abx if caught early
d/t trauma, pregnancy, varicose veins
Localized to veins

136
Q

Presentation of superior venous thrombophlebitis

A

Palpable chord along affected vein
Localized disease process - MC
r/o DVT
May get hemociridan deposits along length of vessel

137
Q

Evaluation of thrombophlebitis

A

Clinical
Doppler US if we are concerned about presentation

138
Q

Management of thrombophlebitis

A

Pain management - NSAID/ASA
Compression hose to prevent additional blood pooling
Immediate IV removal

139
Q

Anticoagulation for venous thrombophlebitis

A

Anticoagulant for LARGE vessels - Arixtra, LMWH, Xarelto for 5cm+ length

140
Q

ABX for thrombophlebitis

A

ONLY if the patient is septic

141
Q

Presentaiton of lymphangitis

A

Inflammation of lymph vessels - follows lymph cessel with proximal affected lymph node
Abrasion distal to the site of infection

142
Q

MC bacteria of lymphangitis

A

Hemolytic strep or staph
Consider others depending on environment of acquisition (ie. Aeromonas w/ fresh water)
Tenderness and tachycardia are possible

143
Q

Nodular lymphangitis

A

Formation of painful OR painless nodular swellings along the course of lymphatic channels

144
Q

Diagnostics and treatment for lymphangitis

A

I&D of abcess for C&S
Lymphangiography
Treat with ABX - cover GABHS - Keflex
Surgery for nodular lymphangitis

145
Q

Lymphedema presentation

A

PAINLESS with lower extremity edema - pitting
MC in young females
Fam hx or malignancy or surgery
No ulceration, varicosities, stasis, pigmentation
Limits ADLs

146
Q

Management of lymphedema

A

Leg elevation
Compression hose
Ulcer prevention
Refer to wound care is needed

147
Q

Things to r/o in lymphedema

A

Cancer - involved lymph node or mass

148
Q

Risk factors for a serious cause of palpitations

A

Serious dysrythmia hx at a young age
History of syncope in self or family
Structural heart disease
Chest pain
Prolonged QT!! - Palpitations are torsades until proven otherwise
Heart block
NEW Onset

149
Q

SVT palpitations presentation

A

Starts and stops on a dime

150
Q

Exercise induced arrhythmias

A

RED FLAG - sinus rate can’t suppress the abnormal rhythm

151
Q

PMH for arrhythmias

A

Alcohol use
Stimulants
Sudden deaths in the family

152
Q

Holter monitor

A

24-48 hours ONLY
Not good for more infrequent palpitations
Monitor beat to beat
Have the patient record symptoms to compare with how the patient is feeling

153
Q

Real-time vs. Event monitors

A

Real time monitors everything
Event monitor requires the patient to record using a device

154
Q

Loop recorder

A

Implanted under the skin can be done in office
If we can’t detect anything on 30 month test, or if they have a cryptogenic stroke

155
Q

Electrophysiology study

A

Invasive approach to arrhythmia management

156
Q

Cardioversion

A

Shock via electrodes to cause a prolonged repolarization and reset the heart
Indicated for - SVT, AF, VT, VF
Need informed consent if the patient is able to provided

157
Q

Complications of cardioversion

A

Myocardial necrosis
Thomboembolus
Hypotension - transient
Skin burns

158
Q

Catheter ablation

A

Map PVC cells that are misfiring and ablate them
Highly invasive, and expensive
Most often for PVCs - can cause esophageal issues, CI in atrial septal defects

159
Q

Pacemaker

A

Can only speed your heart rate up

160
Q

Defibrilator (ICD)

A

Always includes a pacemaker
Can also shock the patient back into a normal rhythm

161
Q

Pacemaker indications

A

Symptomatic bradycardia
High grade AV block
Afib with symptoms
No reversible causes

162
Q

ICD indications

A

EF 35% or less or long QT, brugada, Hypertrophic cardiomyopathy
Secondary prevention after sudden cardiac arrest
Put on the side of the non-dominant hand

163
Q

ICD/Pacemaker leads

A

One to three
RV - Single chamber
RA and RV - Dual chamber
RV, LV +/- RA - Biventricular

164
Q

How to distinguish a defibrillator on a CXR

A

Shock coil present!!

165
Q

Danger of pacing inside of the T wave

A

Can cause torsades

166
Q

Affect of magnet of pacemaker

A

Causes it to pace at a set rate rather than pacing the heart

167
Q

Cause of nocturnal pauses on monitoring of EKG

A

Sleep apnea

168
Q

Sinus dysrythmia

A

Faster breathing in, Slower breathing out

169
Q

Sinus brady cardia

A

HR under 60, Severe under 45
Usually not symptomatic until in the 30s
Sick sinus syndrome
Can be due to heightened vagal tone

170
Q

Chronotropic incompetence

A

Heart rate does not increase with exercise

171
Q

Potential causes of bradycardia

A

Medication - ie. Clonidine, Dig, Amiodarone
Increased intercranial BP
Sleep Apnea (nocturnal bradycardia and pauses)
Hypothyroidism
Inferior Wall MI (RCA) - Acute

172
Q

Sick Sinus Syndrome

A

Supraventricular arrhythmias and sinus arrest
Can’t reach 50% maximal HR during exercise
Pacemaker is appropriate, check for medications and stop if possible first

173
Q

Indication for Pacer pads in bradycardia

A

If the patient is symptomatic/dying

174
Q

Drug to speed up the heart

A

Atropine

175
Q

Sinus tachycardia

A

HR over 100
Exercise, anger, stress, fever, volume depletion
Treat underlying cause usually

176
Q

How to check if it is sinus tachycardia

A

Carotid sinus massage
Vagal manuevers
Deep Breathing

Should make S Tach go down

177
Q

When to treat S tach

A

If there is structural heart disease present esp. Mitral stenosis

178
Q

Inappropriate sinus tachycardia

A

HR jumps up randomly making the pt light headed - may be fear, etc. Similar to POTS

Will usually grow out of POTS

179
Q

Tx for S Tach

A

Can try a BB - Young people may not tolerate
NDHP-CCB - Verapamil and Diltaezem
Ivabradine (Corlanor) - Off Label

180
Q

Causes of 1st degree and Mobitz I AV block

A

Can be normal
Medication related
Electrolyte
Lyme, Fibrosis, Infection, Ischemia (RCA)

181
Q

Six Mobitz II AV block causes

A

ALMOST ALWAYS due to organic disease
Degenerative
IHD
Medications
Trauma
Myocarditis
Amyloidosis

182
Q

Signs and Symptoms of first degree AV block

A

Should be Asymptomatic

183
Q

S/S of Mobitz I and II AV block

A

Palpitations, Dyspnea on exertion (DOE), dizziness, Irregular rhythm on auscultation

184
Q

Third degree heart block symptoms

A

Worse with exertion, Bradycardia, DOE, near syncope or syncope, bradycardia, HF - look for lower extremity edema, Regular rhythm

185
Q

Diagnostics for heart blocks

A

Review medications
12 lead EKG
Echo for structural abnormalities
Cath for ischemia -NO STRESS TEST
CBC CMP TSH

186
Q

Management of first degree AV block

A

Avoid AV node blocking agents

187
Q

Management of Mobits I AV block

A

Treat identifiable cause, Avoid conduction sloing drugs
Rarely need a permanent pacemaker

188
Q

Management of Mobitz II and Third degree AV blocks

A

Unstable rhythms - require permanent pacemaker in majority, some are transient (ie. STEMI that is resolved)

189
Q

Premature Atrial Contraction

A

P wave comes in early
No compensatory pause - nonregularity differentiates it from Heart block
May be a precursor for A fib or A flutter
May be normal

190
Q

s/s and management of PACs

A

Should not cause SOB or syncope
May feel skipped beats
Beta Blockers for significant symptoms
IC antiarrhythmic second line

191
Q

PVCs

A

May be normal if limited
May be triggered by lack of sleep, lack of exercise, Caffeine, Thyroid - Keep a journal
Should diminish with exercise!! (if not, red flag)

192
Q

When PVCs are most normal

A

When lying down for a nap/at night

193
Q

Treatment for PVCs

A

Manage underlying cause
Beta Blocker - Lopressor or Metoprolol - first line
Class IC or III AAD - second line
Catheter ablation is an option (send to electrophysiology)

194
Q

Labs for PVCs

A

Echo
BMP
Magnesium
Thyroid

195
Q

Cardiomyopathy that can occur with frequent PVCs

A

Dilated cardiomyopathy with over 30% PVCs

196
Q

Sinus rhythm pathways through AV node

A

Fast path blocks off slow path

197
Q

PAC pathways through AV node

A

PAC comes down slow pathway and goes back up the fast pathway and into the atria

198
Q

Clinical features of SVT

A

Awareness of rapid breath, chest pain
Rapid onset
Narrow QRS

199
Q

Management for SVT

A

Valsalva - Bear down, Resist pressure on abdomen
Cold
Holding breath/ Coughing
Carotid Sinus Massage - PROVIDER ONLY

200
Q

Pharm for SVT

A

Adenosine - FIRST LINE
CCB - Verapmil, Diltaezem
Beta blocker - Esmolol, Lopressor

Amiodarone if Refractory
Procainamide if WIDE complex
Cardioversion is UNSTABLE

201
Q

Long term management for SVT

A

Catheter Ablation - First Line
Medications - BB,CCB
Send WPW patients to an EP

202
Q

Ectopic atrial rhythms

A

Onset and termination occur abruptly
Rate 50 to 180 bpm
Unifocal or Multifocal
Absence of normal P waves delineates from sinus rhythm

203
Q

Causes of ectopic atrial arrhythmias

A

May be seen in normal hearts
In the elderly
Can be due to structural issues
Not as common with IHD
Get an ECHO

204
Q

Management of ectopic atrial tachycardia

A

BB or CCB - Unifocal
CCB - Multifocal
Ablation, Class Ic

205
Q

Stages of A fib

A

Paroxysmal - Short episodes, respond to medication
Persistent - Bursts don’t fix themselves - have to shock or give Corvert
Long Standing - Persitent for 1+ years
Permanent - All the time, can’t reverse

206
Q

Treatment goals for A fib

A

Paroxysmal - work to keep in sinus rhythm
Permanent - Keep HR normal

207
Q

Risk factors for A fib

A

Age
CHF
HTN
CAD
Valvular Heart disease
Alcohol use - holiday heart
Thyroid disease
Sleep apnea

208
Q

Lone A fib

A

Young patients with NO obvious cause/family history - may have a risk of recurrence

209
Q

Presentation of A fib

A

Depends of phase - more prominent, less accustomed in paroxysmal
Palpitations, Hypotension, SOB, chest pain, syncope
Irregular rhythm on exam, CHF signs, difficult to obtain peripheral pulses

210
Q

2 things to watch for in a fib

A

Persistent tachycardia with CHF
Stroke from clots

211
Q

Trust the monitor or the pulse ox?

A

Trust the EKG monitor

212
Q

Evaluation for A fib

A

ECHO
Stress test ONLY if IHD suspected
BMP, TSH, MAG

213
Q

Management of A fib management - Elements

A

Rate control
Rhythm control
Clot control

214
Q

Keep in a fib or not

A

If they feel fine in a fib keep them there

215
Q

Rate control drugs for A fib
Three options each with a CI

A

CCBs - CI in HFrEF
BB - CI in asthma
Digoxin - CI in CKD

216
Q

Ablation for A fib

A

AVN Ablation - If you cannot do ANY of those; will need a permanent pacemaker

217
Q

Rhythm control drugs for A fib w/ no heart disease OR hypertension w/o LVH

A

FL - - Class IC - Dronedarone, Flecanide, Propafenone, Sotolol
SL - - Amiodarone, Dofetalide OR catheter ablation

218
Q

Rhythm control drugs for A fib w/ HTN and LVH

A

Amiodarione - - FL
OR Catheter ablation

219
Q

Rhythm control drugs for A fib with CAD

A

FL - - Dofetalide, Dronedarone, Sotalol

SL - - Amiodarone OR catheter ablation

220
Q

Rhythm control drugs for A fib with HF

A

FL - - Amiodarone or Dofetalide

SL - - Catheter ablation

221
Q

Ablation success with Afib

A

Less good with consistent A fib

222
Q

Guidelines for cardioversion in unstable a fib

A

Cardiovert immediately if unstable regardless of duration

223
Q

Guidelines for elective cardioversion in stable a fib

A

MUST BE:
Less than 48 hour duration
Confirmed no thrombus with Trans esophageal echo
3 weeks of therapeutic anticoagulation

224
Q

Anticoagulation requirement after A fib cardioversion

A

Continue for 4 weeks

225
Q

CHADS2-VASc Criteria

A

Congestive Heart Failure
Hypertension
Age >75 +2
Diabetes Mellitus
Prior TIA or Stroke +2
Vascular disease - Actual MI intervention
Age 65-75
Sc - Sex category, Female (+0 if ONLY criteria met, Else +1)

226
Q

2 point categories in CHADS VASc

A

Age over 75
Prior TIA for stroke

227
Q

Stroke prevention with CHADVASc

A

Start treating at 2, stroke risk increases
0 - No antithrombic therapy
1 - ASA OR Oral anticoagulation - borderline
2 - Oral anticoagulation

228
Q

HAS-BLED score

A

Estimates risk of bleeding 0-9 points
5 = 9% risk of bleeding

229
Q

Anticoagulation for A fib

A

Heparin inpation
Warfarin - Only for valvular A fib
Apixaban (Eliquis), Xarelto (Rivaroxaban) - once a day, Dabigatran (Pradaxa)

230
Q

Long term management of A fib

A

Educate patient on potential evolution
Avoid alcohol
Ambulatory monitoring
Control risk factors
No cure for A fib

231
Q

Atrial flutter

A

Organized A fib - Saw tooth EKG pattern
Same as A fib EXCEPT that an ablation can be CURATIVE

232
Q

Symptoms and Management for Junctional Rhythms

A

May be asymptomatic, may have palpitations, dizziness, syncope
Treat underlying cause no need for pacemaker, etc.

233
Q

Idioventricular Rhythm

A

60-120 = Accelerated
Drug slowing down V Tach or Escape Rhythm
May be after acute MI - BB, will go away

234
Q

Sustained V tach

A

Greater than 30 seconds, does not terminate spontaneously
160-240 BPM
MI, Cardiomyopathy, Catecholaminergic Polymorphic

235
Q

Polymorphic PVCs

A

SOMETHING is WRONG - May be catecholaminergic

236
Q

Long QT syndromes

A

Rare in US
Consider meds or electrolytes first for prolonged QT
Torsades triggered bby long QT
3 types of congenital:
1 and 2 - MC, Exercise and sudden auditory stimuli are triggers
3 - Most lethal, occurs during sleep at slower rates

237
Q

Brugada

A

ST segment in anterior precordial leads elevation with RBBB
No chest pain of STEMI
3 types - MC in Asian,
Presentation of syncope = syndrome

238
Q

Management of long QT or Brugada

A

Beta Blocker - Propranolol and Nadolol
ICD - Esp. for Brugada
Avoid QT prolonging medications

239
Q

Presentation of V Tach

A

Palpitations, Syncope, Sudden Death

240
Q

Management of V Tach

A

ACLS - CPR, etc. if UNSTABLE
STABLE - Sedate and shock or start on IV Amiodarone (won’t have to sedate)

241
Q

Long term therapy for V Tach

A

ICD if recurring/Not due to reversible cause
BB
Amiodarone/Sotalol
Catheter ablation

242
Q

Long term therapy for non-sustained V Tach

A

Beta blocker indicated IF:
Symptomatic
OR
Structural Heart Disease and Low EF

243
Q

V fib

A

Leading cause of sudden death
SHOCK - Unsynchronized
ICD

244
Q

Causes of Intraventricular conduction delays

A

Ischemia, Inflammation, Infiltrative, Invasive surgery

245
Q

LBBB Treatment

A

Rule out underlying ischemic heart disease
LAD - Most commonly involved
If new LBBB w/ symptoms- Treat as a STEMI
Look for heart disease risk factors
Echo
Treat underlying Cause

246
Q

RBBB treatment

A

Blood flow also from LAD
Related to Lung Strain
VSD
Generally asymptomatic and do not require tx - symptomatic management

247
Q

Bifascicular block treatment

A

Usually asymptomatic
Echo for structure
ECG monitoring if the present with syncope - involve EP!!

Cardiovascular (5 decks)

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