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Cardiology Flashcards

1
Q

when is using troponin not helpful and what should you use instead

A

during re-infarctions - use CK-MB instead

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2
Q

Acute Coronary Syndrome Tx =

A 
MONA BASH C 
m- morphine
o- oxygen 
n - nitrates - HOME (if continuous angina) 
a- aspirin - HOME 
b - beta blockers - HOME 
a- ace inhibitor - HOME
s- statins- HOME 
h- heparin - LMWH 
c- clopridogrel
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3
Q

For ACS tx what are protocols for clopridogrel

A
  • give if stent placed
  • if drug eluting stent - tx = 1 year
  • if metal stent - tx = 1 month
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4
Q

why are beta blockers important for ACS tx

A

prevent mortality in first 24 hrs due to ventricular arrythmias

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5
Q

when should TPA be given for ACS

A

when stents cannot be placed for >60 min

rural settings basically

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6
Q

what type of MI are nitrates contraindicated for

A

right sided - leads II, III, aVF with ST segment elevation - this is due the RV being pre load dependent and nitrates decrease preload

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7
Q

stable angina basics

A

due to fixed atherosclerotic lesions that narrow the major coronary arteries

occurs when O2 demand exceeds available blood supply

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8
Q

coronary ischemia due to

A

imbalance between blood supply and oxygen demand leading to inadequate perfusion

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9
Q

major risk factors for ischemic heart disease

A 
DM
HLD
HTN 
Smoking 
Age: men >45, women<55
FMHX of CAD men <55, women< 65
low levels of HDL
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10
Q

prognostic indicators of CAD

A

LV function - Ejection Fraction

<50% = increased mortality

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11
Q

vessels involved with severe ischemia

A

left main coronary artery - poor prognosis - due to covering 2/3 of heart

2 or 3 vessel CAD - worse prognosis

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12
Q

what is the LDL goal in a pt with CAD

A

<100mg/dL

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13
Q

typical anginal chest pain

A

substernal
worse with exertion
better with rest or NTG

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14
Q

metabolic syndrome X

A

combo of: HTN, hypercholesteremia, hypertrigyceridemia, imparied glucose tolerance, diabetes and hyperuricemia

key factor = insulin resistance (due to obesity)

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15
Q

syndrome X

A

exertional angina with normal coronary arteruigra

pts present with CP after exertion but have no coronary stenosis at catheritization

exercise test and nuclear imagin show evidence of MI
prognosis = excellent

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16
Q

Q Waves are consistent with

A

prior MI

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17
Q

if ST segment of T wave abnormalities are present during an episode of Chest pain –> tx =

A

treat as Unstable angina (USA)

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18
Q

how do you calculate a persons max HR

A

220 - age

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19
Q

what is the best initial test for all forms of CP

A

ECG

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20
Q

stress testing is used in what situations

A
  • to confirm dx of angina
  • to eval response of therapy in patients with documented CAD
  • to ID pts with CAD who may have high risk acute coronary events
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21
Q

what makes for a (+) stress test

A

if any of these occur during exercise

  • ST segment depression
  • CP
  • hypotension
  • significant arrhythmias
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22
Q

exercise induced ischemia results in

A

subendocardial ischemia, producing ST segment depression

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23
Q

pts with a (+) stress test –>

A

go to get cath

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24
Q

exercise induced ischemia is evidenced by

A

wall motion abnormalities

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25
Q

stress echocardiography can detect

A
  • can assess LV size and function
  • can dx valvular dz
  • can be used to ID CAD in the presence of pre-existing ECG abnormalities
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26
Q

pts with (+) stress echo –>

A

go to cardiac cath

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27
Q

types of stress test

A

exercise ECG –> ST segment depression

exercise or dobutamine echocardiogram –> wall motion abnormalities

exercise or dipyridamole perfusion study (thallium/technetium) –> decreased uptake of the nuclear isotope exercise)

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28
Q

areas of reversible ischemia may be rescued with

A

percutaneous coronary intervention or CABG

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29
Q

pharm stress test

A

IV adenosine, dipyridamole, or dobutamine

  • adenosine and dipyridamole - cause generalized coronary vasodilation - further worsening dz arteries
  • dobutamine - increased myocardial o2 demand by increasing HR, bp, and cardiac contractility
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30
Q

holter monitor uses

A

detecting silent ischemia (ECG changes not accompanied by symptoms)

evaluating arrhythmiasm heart rate variability and assess pacemaker and implantable cardioverter-defribillator function

evaluating unexplained syncope and dizziness

  • continuous monitoring 24-72hr
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31
Q

definitive test for CAD

A

coronary angiography

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32
Q

indications for cardiac catheterization

A

after + stress test
acute MI with intent of performing angiogram and PCI

pt with angina + noninvasive test are non dx
angina that occurs despite medical therapy
angina that occurs soon after MI
any angina that is a dx dilemma

for eval of valuvar dz and to determine need for sx intervention

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33
Q

most accurate method for identifying the presence and severity of CAD

A

coronary arteriography (angiography)

standard test for delineating coronary anatomy

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34
Q

most accurate method of determining a specific cardiac dx

A

cardiac catheterization

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35
Q

main purpose of coronary arteriography

A

ID pts with sever coronary dz and to determine whether revascularization is needed

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36
Q

coronary stenosis > 70%

A

may be significant

can produce angina

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37
Q

on a arteriography what qualifies as severe and in need of revascularization

A

left main or three vessel dz

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38
Q

standard of care for stable angina

A

aspirin
beta blocker
(only ones that lower mortality)

nitrates for CP

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39
Q

diet modifications for ischemic heart disease

A

reduce intake of saturated fats <7%

reduce cholesterol <200mg per day

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40
Q

side effects of nitrates

A

HA
orthostatic Hypotension
tolerance
syncope

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41
Q

aspirin basics in CAD

A

indicated in all pts with CAD
decrease morbidity
reduces risk of MI

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42
Q

beta blockers basics in CAD

A

block sympathetic stimulation of heart
reduce HR, BP, and contractility , Cardiac work
reduce myocardial oxygen consumption

reduce the frequency of coronary events

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43
Q

first line choices for beta blockers in CAD

A

atenolol and metoprolol

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44
Q

nitrates in CAD

A

cause generalized vasodilation

relieved angina - reduce preload myocardial oxygen demand - reduce LVEDV

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45
Q

calcium channel blockers in CAD

A

cause coronary vasodilation and afterload reduction
reduces contractility

secondary tx when beta blockers and nitrates not fully effective

DO NOT DECREASE mortality

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46
Q

if CHF also present along with CAD tx with

A

ACE- I and/or diuretics

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47
Q

revascularization basics in CAD

A

DOES NOT reduce incidence of MI

does result in significant improvement of symptoms

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48
Q

mild CAD disease

A

normal EF
mild angina
single vessel dz

tx - aspirin, beta blockers and nitrates (+Ca channel blockers if symptoms dont improve)

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49
Q

moderate CAD disease

A

normal EF
moderate angina
two vessel dz

tx - if nml regiment does work consider arteriography + PCI or CABG

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50
Q

severe CAD disease

A

decreased EF
severe angina
3 vessel/ left main or left anterior descending dz

tx - coronary angiography and possibly CABG

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51
Q

Percutaneous coronary intervention (PCI)

A

coronary angioplasty with ballon and stenting

best used for proximal lesions

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52
Q

risk in PCI

A

higher frequency of revascularization procedures

restenosis is a significant problem - however if it does not occur at 6 months your golden

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53
Q

CABG

A

standard of care for high risk dz

main indicators:
- 3 vessel dz with >70% stenosis in each vessel
left main coronary dz with >50% dz
- left ventricular dysfunction

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54
Q

unstable angina (USA) pathophysiology

A

oxygen demand is unchanged - supply is decreased secondary to reduced resting coronary flow

indicates stenosis that has enlarged via thrombosis, hemorrhage, or plaque rupture –> may lead to total occlusion of a coronary vessel

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55
Q

example of pts with USA

A
  • pt with chronic angina with increasing frequency, duration, or intensity of CP
  • pts with new onset angina that is severe and worsening
  • ts with angina at rest
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56
Q

what is the difference between USA and NSTEMI

A

NSTEMI - has elevated cardiac enzymes while USA does NOT

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57
Q

stress testing only detects flow limiting high grade lesions so even with a (+) stress test what can be missed

A

an MI can be missed due to an MI being an acute plaque rupture onto a moderate lesion

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58
Q

pts with USA have a higher risk of adverse events during a

A

stress test - they should be stabilized with medical management prior to performing one or undergo cardiac cath

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59
Q

tx of USA

A

admit
MONA BASH C
Clopidogrel for 2 days

glycoprotein IIb/IIIa ihibitors (abciximab, tirofiban) - if pt undergoing stenting

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60
Q

DOC for the H in MONA BASH C

A

Low molecular weight heparin - specifically enoxaprin

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61
Q

variant angina

prinzmetal

A

transient coronary vasospasm that is usually accompanied by a fixed atherosclerotic lesion (but can occur in nml coronary ateries as well)

  • angina at rest and associated with ventricular dysrhythmias that can be life threating
  • angina classically occurs at night
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62
Q

hall mark of prinzmetal

A

transient ST segment elevation on ECG during CP which represents transmural ischemia

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63
Q

definitive test for prinzmetal

A

coronary angiography - displaying coronary vasospasm when pt given IV ergonovine or acetylcholine to provoke vasocosntriction

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64
Q

tx of prinzmetal

A

calcium channel blockers and nitrates and risk modification

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65
Q

MI is due to

A

necrosis of myocardium as a result of interruption of blood supply –> after thrombotic occlusion of coronary artery previously narrowed by atherosclerosis

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66
Q

most cases of MI are due to

A

acute coronary thrombosis - atheromatous plaque ruptures into vessel lumen and thrombus forms on top of this lesion –> vessel occlusion

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67
Q

Mortality rate of MI

A

30% and half of deaths are prehospital

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68
Q

clinical features of MI

A

intense substernal pressure (crushing elephant on chest)
radiation to neck, jaw, arms, or back (left side)

pain does not respond to NTG
epigastric discomfort
diaphoresis, dyspnea, weakness, fatigue,
N/V, syncope

can be asymptomatic in 1/3 - women, post op pts, elderly, diabetics

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69
Q

ECG markers of ischemia/infarction

A

Peaked T waves - occur very early

ST segment elevation - transmural injury and can be dx of acute infarct

Q waves - evidence of necrosis - late sign - old infarct

T wave inversion

ST segment depression - subendocardial injury

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70
Q

what comb of symptoms strongly indicates acute MI

A

substernal CP persisting longer than 30 min

diaphoresis

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71
Q

presentation of a RV infarct

A 
inferior ECG changes 
hypotension 
elevated jugular venous pressure 
hepatomegaly 
clear lungs
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72
Q

what is contraindcated in RV infarct

A

nitrates or diuretics as will cause cardiovascular collapse due to RV being preload dependent

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73
Q

anterior infarct ECG changes

A

ST segment elevation in V1-V4 (acute/active)

Q waves in leads V1-V4 (late changes)

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74
Q

posterior infarct ECG changes

A

large R waves in V1 and V2
ST segment depression in V1 and V2
upright and prominent T waves in V1 and V2

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75
Q

lateral infarct ECG changes

A

Q waves in leads I and aVL (late change)

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76
Q

inferior infarct ECG changes

A

Q waves in leads II, III and aVF (late change)

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77
Q

ST segment elevation infarct indicates

A

transmural - involves entire thickness of wall tends to be larger

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78
Q

Non ST segment elevation infarct indicates

A

subendocardial - involves inner 1/3 to 1/2 of the wall - tends to be smaller

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79
Q

CHF pt with EF <35% and not Class IV tx = ?

A

AICD to prevent sudden cardiac death

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80
Q

tx of CHF exacerbation

A 
LMNOP 
L - lasix 
M - morphine 
N - nitrates 
O - oxygen 
P- position
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81
Q

gold standard for myocardial injury test

A

cardiac enzymes

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82
Q

troponin (trop I and T)

A

increases within 3-5hrs
peaks at 24hrs

returns to normal 5-14 days

must do serial troponins every 8hrs for 24hrs

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83
Q

how can Troponin I be falsely elevated

A

in renal failures pts

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84
Q

CK-MB

A

increases within 4 to 8hrs
reaches peak at 24hrs
returns to normal 48-72hrs - thus making it more helpful in detecting recurrent infarction

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85
Q

the higher the peak and the longer the enzyme levels

A

the more severe the myocardial injury and the worse the prognosis

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86
Q

In MI what drugs are shown to reduce mortality

A

aspirin
beta blocker
ace inhibitors

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87
Q

a high frequency of PVCs may predict

A

VFIB

VT

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88
Q

HTN affects on afterload

A

increases afterload and thus oxygen demand

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89
Q

tx of an MI patient

A 
admit 
aspirin 
beta blockers 
ace i 
statins 
oxygen 
nitrates 
morphine sulfate
heparin 
revascularization
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90
Q

aspirin basics for MI

A
  • antiplatelet agent reduces coronary reocclusion by inhibiting platelet aggregation on top of the thrombus

has been shown to reduce mortality

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91
Q

beta blocker basics for MI

A

block stimulation of HR and contractility to reduce oxygen demand and decrease the incidence of arrhythmias

reduce remodeling of the myocardium post MI

reduce mortality

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92
Q

ace inhibitor basics for MI

A

initiate within hours of hospitlization

reduce mortality

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93
Q

statins basics for MI

A

reduce the risk of further coronary events

stabilize plaques and lower cholesterol

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94
Q

statin of choice for MI patients

A

atorvastatin 80mg

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95
Q

revascularization benefit is highest when

A

performed <90min of pts arrival

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96
Q

urgent CABGs are performed when

A

mechanical complications of acute MI
cardiogenic shock
life threatening ventricular arrhythmias
failure of PCI

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97
Q

thrombolytic therapy for MI

A

outcome is best if given within 6hrs

indications: ST segment elevation in 2 contiguous ECG leads - in pts with pain onset <6hrs who have been refractory to NTG

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98
Q

thrombolytic of choice for MI

A

alteplase

alternatives - streptokinase, tenecteplase, reteplase, lanotelplase and urokinase

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99
Q

absolute contraindications to thrombolytic therapy

A 
trauma 
previous stroke 
recent invasive procedure or surgery 
dissecting aortic aneurysm
active bleeding or bleeding diathesis
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100
Q

papillary muscle infarction/ ischemia leads to

A

mitral regurgitation - pt presents with new murmur

tx - emergent surgery - with valve replacement + afterload reduction with sodium nitroprusside or intra-aortic ballon pump

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101
Q

pts who suffer an acute MI have a high risk of what developing

A

stroke for the next 5 years

the lower the EF and the older the pt the higher the risk of stroke

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102
Q

complications of acute MI

A

pump failure = CHF - mc cause of in hospital mortality - tx if mild ace-i and diuretic

arrhythmias

  • PVCs - tx - obs
  • Afib
  • VT - tx - if stable - IV amiodarone - if unstable = electrical cardioversion
  • V fib - immeidate unsynchronized defib and CPR
  • sinus tach - worsens ischemia
  • av block - if 1st degree or 2nd degree type I = no tx
    - but if 2nd deg type II or 3rd degree pacemaker is indicated and IV atropine initially
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103
Q

what arrhythmia is a common occurance in the early stages of an acute MI

A

sinus bradycardia - especially right sided/ inferior MIs

may be protective - reduces myocardial oxygen demand

  • tx - if symptomatic = atropine
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104
Q

if asystole is clearly the cause of an arrest s/p acute MI tx =

A

transcutaneous pacing - however mortality is very high

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105
Q

if there is repeat ST segment elevation on ECG within the first 24 hrs after infarction suspect

A

suspect recurrent infarction

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106
Q

mechanical complications of an acute MI

A

free wall rupture - occurs during 1st 2 weeks post MI - mc 1-4 days s/p MI –> leads to hemopericardium and cardiac tamponade

rupture of interventricular septum - within 10 days of MI

papillary muscle rupture

ventricular pseudoaneurysm - seen by bedside echo

ventricular aneursym

acute pericarditis

dressler syndrome

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107
Q

tx of free wall rupture s/p acute MI

A

usually fatal

hemodynamic stabilization
immediate pericardiocentesis
surgical repair

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108
Q

MC cause of death in first few days after MI

A

is ventricular arrhythmia (VTach or VFib)

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109
Q

acute pericarditis s/p MI - tx

A

aspirin

NSAIDs, corticosteroids are contraindicated (may hinder myocardial scar formation)

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110
Q

dressler syndrome s/p MI

A

immuno based syndrome - fever, malaise, pericarditis, leukocytosis, and pleuritis occurring weeks to months after MI

tx = aspirin (1st line) and IBU 2nd line

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111
Q

the most common cause of noncardiac chest pain in the ED

A

GI disorders

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112
Q

if NTG relieves the pain then

A

a cardiac cause is more likely (although esophageal spasm) is still a possibility

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113
Q

cardiac cause of the pain is highly unlikely if what symptoms appear

A

if CP changes with respiration (pleuritic) or if there is tenderness of chest wall

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114
Q

CHF overview definition

A

results from the hearts inability to meet the body’s circulatory demands under nml physiologic conditions

often both systolic and diastolic dysfunction

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115
Q

pathophys of CHF - frank sterling relationship

A

in nml heart incresing preload -> increase contractility

when preload is low (rest) - there is little difference between nml and failing heart

but –> with exertion a failing heart produces relatively less contractility and symptoms occur

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116
Q

systolic dysfunction

A

impaired contractility - decreased EF

heart is too flabby to squeeze blood out

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117
Q

causes of systolic dysfunction

A 
ischemic heart dz 
recent MI 
HTN - cardiomyopathy 
valvular dz
myocarditis (post viral)
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118
Q

diastolic dysfunction

A

impaired ventricular filling during diastole
impaired relaxation or increased stiffness of ventricle or both

heart is too thick = no space for blood to fill

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119
Q

echo of a heart with diastolic dysfunction will show

A

impaired relaxation of LV

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120
Q

in high output HF an increase in cardiac output is needed for

A

the requirements of peripheral tissues for oxygen

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121
Q

causes of high output HF

A 
chronic anemia
pregnancy 
hyperthyroidism 
AV fistulas 
Wet beriberi 
paget dz of bone 
Mitral regurg
aortic insufficiency
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122
Q

causes of diastolic dysfunction

A

MCC = HTN leading to myocardial hypertrophy

valvular dz - aortic stenosis, mitral stenosis, and aortic regurg

restrictive cardiomyopathy - amyloidosis, sarcoidosis, hemochromatosis

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123
Q

symptoms of left sided heart failure

A

dyspnea - secondary to pulm congestion/edema
orthopnea - stack pillows for relief
paroxysmal nocturnal dyspnea - awake 1-2hrs after sleep due to SOB

nocturnal cough
confusion and memory impairment - inadequate brain perfusion

diaphoresis and cool extremities at rest

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124
Q

signs of left sided HF on exam

A

displaced PMI - due to cardiomegaly

pathologic S3(ventricular gallop) - rapid filling 
S4 gallop - stiff LV

crackles/rales
dullness to percussion
decreased tactile fremitus

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125
Q

NYHA classification of heart failure

A

I - symptoms only with vigorous activity
II - symptoms with prolonged or mod exercise - slightly limiting
III - symptoms with usual daily activities extremely limiting
IV - symptoms occur at rest

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126
Q

symptoms /signs of Right sided HF

A 
peripheral pitting edema 
nocturia - due to increased venous return 
JVD
hepatomegaly/heptojuglar reflex 
ascites 
right ventricular heave
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127
Q

Pathologic S3

A

rapid filling phase into noncompliant LV chamber (LV failure)
nml in kids - pathologic in adults
heard best at apex with bell of stethoscope

S3 follow S2 (kentucky noise)
low freq diastolic sound

tx - diuretics for symptomatic relief

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128
Q

S4 gallop

A

atrial systole as blood is ejected into a noncompliant or stiff LV chamber

heard best at left sternal border withbell of stethoscope
S4 precedes S1 (tennesse sound)

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129
Q

pathophys behind crackles/rales seen in CHF

A

caused by fluid spilling into alveoli indicating pulmonary edema
rales heard over lung bases suggest at least moderate severity of LV HF

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130
Q

what is the cause of the dullness to percussion and decreased tactile fremitus seen in pts with HF

A

pleural effusion

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131
Q

what tests do you want in a new pt with CHF

A

CXR - pulm edema, cardiomegaly, r/o COPD

ECG + cardiac enzymes - r/o MI

CBC - anemia

Echo- estimate EF, r/o pericardial effusion

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132
Q

normal pulse pressure

pulse pressure change seen in CHF

A

nml = 30-50 (systolic - diastolic)

CHF < 30

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133
Q

Murmur chart

A 
S                  D 
------------------------------
A - S      / A - R
P - S .    / P - R
T - R .    / T - S
M - R     / M - S
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134
Q

grades of murmurs

what needs a workup

A 
I - S1S2 > Murmur 
II - S1S1 = murmur 
--------------------------
III - S1S2 < Murmur 
IV - palpable thrill 
V - almost 6 - stethoscope half off chest 
VI - hear without stethoscope

below line need workup = echo and any diastolic murmur

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135
Q

mitral stenosis basics

A

blood backs up in LA -> LA dilation -> blood in lungs
path - Rheumatic heart disease - young pt 20-30s

atrial stretch –> possible A FIb

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136
Q

mitral stenosis auscultation =

A

diastolic murmur - best heard at cardiac apex - 5th ICS MCL

opening snap followed by low pitched diastolic rumble

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137
Q

aortic insufficiency (regurgitation) basics

A

weak floppy valve -> blood backs up into LV –> dilated floppy heart

path - infection or infarction, aortic dissection
head bobbing, uvula bobs

widened pulse pressure

tx - medical emergency - replace valve

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138
Q

acute and chronic presentation of aortic insufficiency (regurgitation)

A

acute - cardiogenic shock, flash pulmonary edema, tearing chest pain (if aortic dissection) radiating to back

chronic - CHF and CP

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139
Q

auscultation of aortic insufficiency (regurgitation)

A

diastolic murmur - best heard at base of heart - 2nd ICS right sternal border

pistol shots heard over the femoral arteries

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140
Q

aortic stenosis basics

A

stiff valve –> little blood gets through –> LV dilates -> big loose floppy heart –> HF symptoms

path - atherosclerosis, calcium deposits

bicuspid valve - speeds up stenosis

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141
Q

presentation of aortic stenosis patient

A

old man with atherosclerosis

CP, HF symptoms, syncope

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142
Q

auscultation of aortic stenosis

A

systolic murmur - best heard at the base of the heart right sternal border a crescendo decresendo murmur that radiates to carotid arteries aorit

S4
diminished and delayed carotid upstrokes

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143
Q

mitral insufficiency basics

A

leaflets dont come together -> increased pressure in LA –> blood backs up into lungs -> left atrial sketch -> afib + CHF symptoms

endocarditis - staph, papillary rupture s/p MI, Rheumatifc fever

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144
Q

mitral insufficiency presentation acute vs chronic

A

acute - cardiogenic shock, flash pulmonary edema,

Chronic - CHF, afib

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145
Q

mitral insufficiency auscultation

A

holostyolic murmur - high pitched blowing murmur

best heard at apex 5th ICS MCL

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146
Q

MS, MR , AS, AR

what worsens these murmurs

what improves these murmurs

A

increasing venous return - squatting, leg lifting - worsens murmur

decreasing venous return - valsalva maneuver - improves murmur

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147
Q

hypertrophic cardiomyopathy murmur (HCOM) basics

A

unilateral septum hypetrophy -> covers the aortic opening -> left ventricular outflow obstruction

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148
Q

pt with HCOM

A

ppl with sarcomere mutations
young athlete with sudden death or SOB or Syncope with exertion

FMHX is signficant

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149
Q

auscultation of HCOM

A

sounds like AS (systolic murmur)

but more blood improves the murmur opposite of AS

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150
Q

tx of HCOM

A

avoid dehydration
beta blockade
maintain preload
no exercise

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151
Q

mitral valve prolapse basics

A

leaflets too big donnt touch well due to excessive or. redundant mitral leaflet tissue due to myxomatous degeneration of leaflets and/or chordae tedineae

congenital young women, pregnant women

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152
Q

auscultation of mitral valve prolapse

A

murmur gets better with more blood - mitral regurg but better with more blood

midsystolic or late systolic click
mid to late systolic murmur

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153
Q

tx of mitral valve prolapse

A

avoid dehydration

beta blockade

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154
Q

tx of NYHA classifications

A 
I = ace-I + beta blocker 
II = ^^ + diuretics (furosemide, bumetanide)
III = ^^ + spironolactone or hydralazine and  isosorbide dinitrate (BiDil) 
IV = ^^ + LVAD, transplant
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155
Q

initial test of choice for CHF

A 
echocardiogram 
- determines whether systolic or diastolic 
- determines the cause 
- estimates EF 
shows chamber dilation/hypertrophy
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156
Q

BNP

A

released from the ventricles in response to ventricular volume expansion and pressure overload

useful for differentiating between dyspnea caused by CHF and COPD

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157
Q

BNP levels >150

a NT pro-BNP <300

A

correlate strongly with the presence of decompensated CHF

virtually excludes a dx of HF

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158
Q

what is a common cause of CHF that can be treated by reducing preload and afterload

A

HTN

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159
Q

systolic dysfunction HF - tx =

A

sodium restriction <4g/ fluid restriction 1.5 to 2.0 L
weight loss/smoking cess/exercise

diuretics 
spironolactone 
ace -i 
beta blockers 
digitalis 
hydralazine
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160
Q

role of diuretics in HF tx

A

most effective means of providing symptomatic relief

DONT REDUCE MORTALITY

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161
Q

diuretic of choice for HF

A

loop diuretics - furosemide - most potent

thiazides - hydrochlorothiazide - modest potency

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162
Q

role of spironolactone in HF tx

A

(aldosterone antagonist)
PROLONG SURVIVAL
effective only in advanced stages of HF - III and IV

monitor K+ and renal function

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163
Q

what is an alternative to spironolactone that does not cause gynecomastia

A

eplerenone

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164
Q

role of ACE-I in HF tx

A

cause venous and arterial dilation —> decreased preload and decreased afterload

REDUCE MORTALITY
prolong survival and alleviate symptoms in all grades of CHF

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165
Q

what is a contraindication for spironolactone in the tx of patients with HF

A

renal failure

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166
Q

what combo is the initial tx for HF patients who are symptomatic

A

diuretics (loop) and ACE- I (prils)

standard also includes beta blocker

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167
Q

what is an indication for the use of ACE-I in HF

A

LV systolic dysfunction with EF <40%

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168
Q

why do you always start pts with a low dose on ACE-I

A

to prevent hypotension

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169
Q

if patients have a persistent cough while on ACE-I what med do you switch to

A

ARBS - angiotensin II receptor blockers (artans)

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170
Q

what signs are you monitoring in a pt with CHF

A

weight - unexplained weight gain can be an early sign of worsening CHF

peripheral edema

electrolytes, K, BUN, dig levels

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171
Q

MCC of death from CHF =

A

sudden death from ventricular arrhythmias

ischemia -> provokes ventricular arrhythmias

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172
Q

role of beta blockers in tx of CHF

A

DECREASE MORTALITY in pts with post MI HF

slow the progression by slowing down tissue remodeling

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173
Q

beta blocker of choice for HF

A

carvedilol

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174
Q

digatlis

A

+ inotropic agent
useful in pts with EF <40%, severe CHF, AFib

short term relief - no change to mortality

serum digoxin levels should be checked periodically

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175
Q

role hydralazine and isosorbide dinitrates play in CHF tx

A

used in pts who dont tolerate ACE-I

COMBO IMPROVES MORTALITY in African americans with CHF

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176
Q

what meds are contraindicated in CHF

A

metformin - potentially lethal lactic acidosis

thiazolidinediones - fluid retention

NSAIDs - increase risk of CHF exacerbation

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177
Q

role of an ICD in CHF tx

A

LOWERS MORTALITY - prevents sudden death cardiac death

indicated for pts - >40 days post MI with EF <35% and class II or III CHF not controlled

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178
Q

cardiac resynchronization therapy role in CHF tx

A

biventricular pacemaker

indications > 40 days post MI with EF <35% class II or III CHF not controlled + prolonged QRS >120msec

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179
Q

diastolic dysfunction HF tx

A

NO MEDS DECREASE MORTALITY

beta blockers
diuretics

DIGOXIN AND SPRIONOLACTONE SHOULD NOT BE USED

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180
Q

signs of digoxin toxicity

A

GI - N/V and anorexia

Cardiac - ectopic (ventricular) beats, AV block, A Fib

CNS - visual disturbances, disorientation

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181
Q

Calcium channel blockers (CCB) role in CHF tx

A

no role -may increase mortality

BUT amlodipine and felodipine are safe to use in CHF (if another indication like HTN exists that needs controlling)

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182
Q

what is the overall 5 year mortality rate of CHF

A

50%

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183
Q

tx of class I and II HF (mild)

A

mild restriction of sodium intake and physical activity

start loop diuretic if volume overload or pulmonary congestion is present

use an ACE-I as first line agent

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184
Q

tx of class II and III HF (moderate)

A

start a diuretic (loop) and ACE-I (pril)

add a beta blocker if mod dz is present and the response of nml tx is suboptimal

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185
Q

tx of class III and IV HF (mod -severe)

A

add digoxin (to loop and ACE-I)

in pts with class IV symptoms who are still symptomatic despite above tx - add Spironolactone

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186
Q

ventricular assist device (VAD) role in CHF tx

A

used to support LV and RV or both

pump is implanted in the abdominal cavity with cannulation to the hart

system controller and battery worn externally

lifelong anticoagulation with heparin or warfarin is required without exceptions due to the devices being so thrombogenic

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187
Q

acute decompensated HF signs and causes

A

acute dyspnea - elevated left sided filing pressure with or without pulmonary edema

MC - due to lV systolic or diastolic dysfunction

flash pulmonary edema - severe form of HF with rapid accumulation of fluid in the lungs

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188
Q

tx of acute compensated HF

A

oxygenation and ventilatory assistance with nonrebreather face mask, NPPV, or intubation

diuretics to tx volume overload and congestive symptoms (MOST IMPORTANT) ^^^

nitrates

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189
Q

pts in acute compensated HF with pulmonary edema despite use of oxygen and diuretics and nitrates may benefit from what tx

A

dobutamine (inotropic agent) -works much quicker then digoxin which takes weeks

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190
Q

premature atrial complexes

A

early beat arises within atria firing on its own

early P waves that differ morphology
nml QRS

may be a precursor of ischemia in a diseased heart

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191
Q

causes and tx of symptomatic premature atrial complexes

A

causes: adernergic excess, drugs, alcohol, tobacco, electrolyte imbalances, ischemia and infection

tx if symptomatic = beta blockers

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192
Q

premature ventricular complexes

A

early beat fires on its own from ventricle then spreads to other ventricle

since conduction is not going thru nml pathways but thru ventricular muscle = slower than nml –> WIDE QRS complex that is bizarre with compensatory pause

buried P wave

presence in nml hearts - associated with increased mortality

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193
Q

PVCs causes and tx

A

can occur in pts with and without structural heart disease

causes: hypoxia, electrolyte abnormalities, stimulants, caffeine, meds, structural heart dz

tx - beta blockers if symptomatic - dizziness, palpitations

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194
Q

pts with frequent, repetitive PVCs and underlying heart disease are at increased risk for

A

sudden death due to VFib

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195
Q

the use of antiarrhythmic drugs to suppress PVCs after MIs increases

A

the risk of death

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196
Q

PVCs
couplet
bigeminy
trigeminy

A

couplet - 2 successive PVCs

bigeminy - sinus beat followed by a PVC

trigeminy - 2 sinus beats followed by a PVC

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197
Q

atrial fibrillation pathophys

A

multiple foci in the atria fire continously in a chaotic pattern - totally irregular, rapid ventricular rate

atrial rate >400 bpm but most of these impulses are blocked at the AV node so ventricular rate = 75-175

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198
Q

pts with AFib and underlying heart disease are at increased risk for

A

thromboembolism

hemodynamic compromise

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199
Q

causes of AFib

A 
heart dz - CAD, MI, HTN, surgery 
pericarditis and pericardial trauma 
pulm dz - PE 
hyperthyroidism or hypothyroidism 
systemic illness
stress
excessive alcohol intake 
sick sinus syndrome 
pheochromocytoma
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200
Q

clinical features of afib

A

fatigue and exertional dyspnea
palpitations, dizziness, angina syncope
irregularly irregular pulse
blood stasis

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201
Q

blood stasis mechanism in afib

A
  • secondary to ineffective contraction - leads to formation of intramural thrombi which can embolize to the brain
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202
Q

dilated cardiomyopathy

A

chambers are dilated - thin walled - floppy

little actin and myosin overlap - decreased contractiliy

problem pumping so systolic HF

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203
Q

some causes of dilated cardiomyopathy

A

viruses
wet beriberi
alcohol
ischemia

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204
Q

hypertrophic cardiomyopathy (HCM)

A

asymmetric septal wall thickening -> left ventricle outlet obstruction -> covers aortic opening

genetic mutation in sarcomeres

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205
Q

presentation of HCM

A

young athlete syncope, SOB, sudden death

murmur sounds like AS but gets better with increased venous return

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206
Q

tx of HCM

A

etoh ablation - for poor surgical candidates

myectomy - remove obstruction in muscle

ACID for pts with increased risk of death (prior ventricular arrhythmias)

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207
Q

concentric hypertrophy cardiomyopathy

A

diastolic HF

filling problem

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208
Q

causes of restrictive cardiomyopathy

A

sarcoidosis
amyloid
hemachromatosis

cancer and fibrosis

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209
Q

sarcoidosis in cardiomyopathy

A
  • echo = patchy all over
  • pt with pulmonary disease
  • african american

Dx - cardiac MRI –> endomyocardial biopsy

tx - glucocorticoids

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210
Q

amyloidosis in cardiomyopathy

A

echo - bright and speckled pattern
peripheral neuropathy

fat pad biopsy (gingival biopsy)

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211
Q

hemachromatosis in cardiomyopathy

A

cirrhosis and bronze diabetes

screen with ferritin which will be elevated –> genetic testing

tx - phlebotomy or deferoxamine

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212
Q

definitive tx for cardiomyopathy

A

transplant

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213
Q

causes of pericardial dz

A

infections - virus (coxsackie) bacteria (staph/strep), fungal, TB

autoimmune - RA, lupus, dressler, Uremia

penetrating trauma > blunt trauma
aortic dissection

cancer - breast, lung, esophageal, lymphoma

214
Q

pericarditis

A

viral, urimia

CP, pleuritic, positional (leaning forward better, leaning back worse)

215
Q

dx of pericarditis

A

ECG - diffuse ST segment elevation everywhere

and depressed PR segment is key

216
Q

tx of pericarditis

A

NSAIDs and Colchicine - best
no NSAIDs if - CKD, thrombocytopenia, peptic ulcer dz
no colchicine if - dose limiting due to diarrhea

steroids - worst due to increasing the recurrence of pericarditis (especially viral)

217
Q

tx of pericarditis if the cause is uremia

A

dialize - diaylsis is curative

218
Q

dx test of choice for pericardial effusion

A

echo - see the fluid

219
Q

tx of pericardial effusion if refractory

A

pericardial window - allowing fluid to drain into a body cavity to be absorbed

220
Q

presentation of pericardial tamponade

A

CHF symptoms - specifically Right sided HF –>

becks triad - hypotension, JVD, decreased heart sounds

pulsus paradoxus >10mmHg

clear lungs

221
Q

tx of pericardial tamponade

A

pericardiocentesis - if cant be done right away then IVF to increase BP temporarily

222
Q

constrictive pericarditis

A

recurrent pericarditis –> scaring forming a rigid box

as the heart expands in diastole –> pericardial knock is heard

diastolic CHF presentation

223
Q

dx test of choice for constrictive pericarditis and tx

A

dx - echo

tx - pericardiectomy - remove rigid portion

224
Q

dx of afib

A

ECG - irregularly irregular rhythm - irregular RR intervals

NO P WAVES

225
Q

tx of afib

A

if hemodynamically unstable –> immediate electrical cardioversion

if stable –> rate control (60-100) beta blockers or CCBs –>
- if <48hrs –> cardioversion

  • if >48 hours –> either TEE or anticoagulate for 3wks –> cardioversion
226
Q

cardioversion basics

A

delivery of shock that is in synchrony with QRS complex

terminates certain dysrhythmias - PSVT or VT

227
Q

an electric shock during a T wave can cause

A

V fib

228
Q

indications for cardioversion

A

afib
atrial flutter
VT with plse
SVT

229
Q

defibrillation basics

A

delivery of shock that is not in synchrony with QRS complex

purpose is to convert a dysrhythmia to a normal sinus rhythm

230
Q

indications for defribillation

A

vfib

VT without a pulse

231
Q

indications for automatic implantable defribillator

A

vfib

VT that is not controlled by medical therapy

232
Q

in afib if LV systolic dysfunction is present what should you consider adding to the tx regiment

A

digoxin or amiodarone

233
Q

candidates for cardioversion in afib

A

hemodynamically unstable
those with worsening symptoms
those having first ever case of afib

234
Q

if pharmacologic cardioversion is going to happen for afib what drugs do you use

A 
parenteral ibutilide 
procainamide
flecainide
sotalol 
amiodarone
235
Q

anticoagulation in afib pts

A

prevents embolic CVA
if >48hrs risk for embolization = 2-5%

anticoagulate pts 3wks before and 4wks after

INR of 2-3 is goal

236
Q

how to avoid anticoagulating 3wks before cardioversion

A

TEE - transesophageal echocardiogram - images LA if no thrombus –> start IV heparin and perform cardioversion within 24hrs then 4wks of anticoagulation

237
Q

chronic afib anticoagulation

A

> 60 tx with warfarin

risk is increased in pts with heart dz as well

238
Q

in afib what is superior rate or rhythm control

A

rate control

239
Q

aflutter pathophys

A

one irritable automaticity focus in atria fires 250-350bpm –> the longer refractory period in the AV node allows only 1/2 1/3 flutter waves to conduct to the ventricles

240
Q

causes of atrial flutter

A

heart failure (MC association)
RHD
CAD
COPD

241
Q

atrial flutter ECG

A

saw tooth baseline with a QRS after every 2nd or 3rd tooh

best seen in inferior leads - II, III, and aVF

242
Q

multifocal atrial tachycardia

A

occurs in COPD pts

ecg - variable p wave morphology at least 3 different types of P waves

243
Q

tx of multifocal atrial tachcardia

A

if LV function is not preserved use digoxin diltiazem or amiodarone

if LV function is preserved - CCB, beta blockers, digoxin amiodarone, IV flecainide and IV propafenone

244
Q

paroxysmal supraventricular tachycardia pathophys

A

most often due to reentry
two pathways within AV node one fast one slow so the reentrant circuit is within the AV node

initiated or terminated by PACs

245
Q

most common cause of SVT

A

PSVT

246
Q

ECG of PSVT

A

narrow QRS complexes with no discernible P waves since they are buried in QRS complexes

247
Q

causes of PSVT

A

ischemic heart disease

digoxin toxicity - most common arrhythmia associated with digoxin toxicity

248
Q

narrow QRS complexes suggest that the arrhythmia originates

A

at or above the level of the AV node

249
Q

wide QRS complexes suggest that the arrhythmia originates

A

outside of the normal conducting system or there is a supraventricular arrhythmia with coexisting abnormality in the HIS-purkinje system

250
Q

side effects of adenosine

A 
HA 
flushing
SOB 
chest pressure 
nausea
251
Q

tx of PSVT (nonpharm)

A

maneuvers that stimulate the vagus delay AV conduction and thus block the reentry mechanism
- valsalva manuever, carotid massage, breath holding, head immersion in cold water (ice bag to face)

252
Q

acute tx of PSVT (pharm)

A

IV adenosine - DOC - short duration of action and effectivess in terminating SVTs

IV verapamil (CCB) and IV esmolol (BB) or digoxin are alternatives for pts with preserved LV function

253
Q

prevention of PVST

A

verapamil or beta blockers

radiofrequency catheter ablation of either AV node or accessory tract

254
Q

wolf parkinson white syndrome pathophys

A

accessory conduction pathway from atria to ventricle through the bundle of kent –> causes premature ventricular excitation because it lacks the delay seen in the AV node

255
Q

wolf parkinson white syndrome may lead to

A

paroxysmal tachycardia

256
Q

dx of wolf parkinson white

A

ecg - delta wave (upward deflection seen before QRS complex)
narrow complex tachycardia
short PR interval

257
Q

tx of wolf parkinson white syndrome

A

radiofrequency catheter ablation of one arm of the reentrant loop

procainamide or quinidine

258
Q

what drugs should you avoid in wolf parkinson white syndrome

A

drugs that are active on AV node (digoxin, verapamil, beta blockers) –> they accelerate conduction through the accessory pathway

259
Q

ventricular tachycardia

A

rapid and repetitive firing of 3 or more PVCs in a row at a rate of 100-250bpm

originate below bundle of HIS

260
Q

causes of VTach

A 
CAD with prior MI = MCC 
active ischemia, hypotension 
cardiomyopathies
congenital defects
prolonged QT
261
Q

sustained Vtach

A

> 30seconds
always symptomatic
associated with hemodynamic compromise

life threatening
can progress to vfib

262
Q

nonsustained vtach

A

brief self limited runs of vtach
asymptomatic

when CAD and LV dysfunction are present - risk factor for sudden death

263
Q

VTach after an MI

A

poor prognosis especially if it is sustained

264
Q

what cause 75% of cardiac arrests

A

vfib

Vtach

265
Q

torsades de pointes

A

rapid polymorphic Vtach
can lead to afib

associated with factors that prolong QT interval

tx - IV magnesium

266
Q

clinical features of Vtach

A

palpitations, lightheadedness, dyspnea
sudden cardiac death
cardiogenic shock

cannon A waves in neck

267
Q

dx of vtach

A

wide and bizarre QRS complexes
monomorphic or polymorphic

does NOT respond to vagal maneuvers or adenosine

268
Q

the presence of VT or PVCs in pts with underlying heart dz and LV dysfunction are at high risk for

A

risk for sudden death

269
Q

pt with wide (>0.12) QRS tachycardia suspect

A

VTach

270
Q

tx of sustained vtach

A

hemodynamically stable pts - IV amiodarone, IV procainamide or IV sotalol

unstable pts - immediate synchronous DC cardioversion followed bby IV amiodarone

ICD (unless EF = nml)

271
Q

tx of unstained vtach

A

no underlying heart dz - dont tx

if underlying heart dz - ICD placement
pharm therapy = 2nd line - amiodarone

272
Q

wide complex tachycardia in adults with hx of structural heart dz is much more likely to be due to

A

Vtach than SVT

273
Q

cardiac arrest definition

A

sudden loss of output

potentially reversible if circulation and oxygen delivery are promptly restored

274
Q

sudden cardiac death definition

A

unexpected death within 1hr of symptom onset secondary to cardiac cause

275
Q

narrow complex tachycardias originate

A

above ventricles

276
Q

wide complex tachycardias originate

A

within ventricles and are more ominous because they are more likely to progress to vfib

277
Q

vfib basics

A

multiple foci in ventricles fire rapidly leading to chaotic quivering of the ventricles and no cardiac output

most episodes begin with vtach except acute ischemia

278
Q

if vfib develops ,48hrs of an acute MI

A

long term prognosis is favorable and recurrence rate is low

279
Q

causes of vfib

A

ischemic heart dz = mcc
antiarrhythmic drugs - especially those that cause torsades de pointes
afib with very rapid ventricular rates in pts with wolf parkinson white syndrome

280
Q

clinical features of afib

A

cannon measure bp

absent heart sounds and pulse

281
Q

dx of vfib

A

ecg - no atrial p waves, no QRS complexes

282
Q

tx of vfib

A

medical emergency - immediate defribillation and CPR
give up to 3 sequential shocks

if persists –> CPR - intubate - epi 1mg every 3-5 min (decreases defribillation threshold by increasing myocardial and cerebral blood flow

IV amiodarone followed by shocks

if cardioversion is successful maintain IV infusion of effective agent - typically amiodarone

283
Q

sinus bradycardia

A

Clinically significant <45

caused: ischemia, increased vagal tone

284
Q

tx of sinus bradycardia

A

atropine - elevates sinus rate by blocking vagal stimulation to the Sinoatrial node

285
Q

sick sinus syndrome

A

sinus node dysfunction characterized by persistent spontaneous sinus bradycardia
elerly, dizzy, confused, syncope, fatigue, CHF

286
Q

defribrillation and asystole

A

doesnt really work

epi and CPR

287
Q

pulseless electrical activity (PEA)

A

electrical activity on the monitor but no pulses even with doppler

grim prognosis

288
Q

first degree AV block

A

PR interval is prolonged (>0.20sec)
a QRS follows each P wave
no tx

289
Q

second degree AV block type I (wenckebach)

A

progressive prolongation of PR interval until a P wave fails to conduct (qrs dropped)
no tx

290
Q

second degree AV block type II

A

P wave fails to conduct suddenly without preceding PR interval prolongation
QRS just drops suddenly
often progresses to complete heart block

site block is in His-purkinje system
tx - pacemaker

291
Q

third degree complete AV block

A

absence of conduction of atrial impulses to the ventricles - no communication between the 2

characterized by AV dissociation

tx - pacemaker

292
Q

chemo drugs that cause dilated cardiomyopathy

A

doxorubicin

adriamycin

293
Q

infectious causes of dilated cardiomyopathy

A

viral
chagas dz
lyme dz
HIV

294
Q

vasovagal syncope

A

vagus nerve stimulation –> dumps Ach –> bradycardia and vasodilation

decrease in systolic BP of 50mmhg

typically there is a prodrome (they know its coming)

295
Q

causes of vasovagal syncope

A

visceral organ stimulation - (cough, defecation, micturition)

carotid bodies - (turning head, shaving, tie too tight)

psychogenic - (site of blood)

296
Q

dx and tx of vasovagal syncope

A

dx - tilt table test (not really necessary)

tx - beta blockers

297
Q

orthostatic syncope

A

systolic drop >20
diastolic >10
HR >10

298
Q

causes of orthostatic hypotension

A

volume down causes:

  • diarrhea
  • dehydration
  • diuresis
  • hemorrhage

ANS issues:

  • diabetes
  • parkinson’s
  • advanced age
299
Q

tx of orthostatic hypotension

A

volume down - IVF

ANS - doesnt respond to fluids - get up slowly

300
Q

cardiogenic syncope

A

mechanical:
- valve problem - rest no issue - issue with exertion
young athlete - HCOM
old person random exertion - Aortic Stenosis

Arrhythmia:

  • sudden no prodrome
  • dx halter monitor or event recorder
301
Q

neurogenic syncope

A

posterior circulation issue - vertebrobasilar insufficiency

dx CT angiogram

302
Q

LDL

A

brings cholesterol to the periphery – if too much accumulates there it leads to plaque formation

303
Q

HDL

A

bring cholesterol back to liver for processing

304
Q

who needs statin

A

1 - vascular dz- MI, CVA, PVD, CS
2- LDL >190
3 - LDL 70-189 + age (40-75) + DM
4 - LDL 70-189 + age (40-75) + calculated

305
Q

ppl who dont need statins

A

LDL <70

306
Q

high intensity statins

A

atorvastatin 40-80

rosuvastatin 20, 40

307
Q

those who should be on moderate intensity statins

A

age >75
liver dz
renal dz

308
Q

moderate intensity statins

A 
atorvastatin 10, 20
rosuvastatin 5,10
simvastatin 20,40
pravastatin 40,80
lovastatin 40
309
Q

how often should lipids be assessed

A

annually

310
Q

if signs of statin toxicity

A

stop statins and when symptoms get better start them again

311
Q

basline studies needed before statins

A

lipid panel
A1c
CK
LFTs

312
Q

ADR of statins

A

myositis and hepatitis –> if pt develop these stop statins and then restart on lower doses

313
Q

if you cant use a statin next best drug

A

fibrates - same ADR profile (myositis and increased LFTs)

314
Q

fibrates

A

decrease TGLs and increase HDL

lipoprotein lipase inhibitor

315
Q

ezetimibe

A

decrease LDL
prevent cholesterol absorption
ADR - fatty stool osmotic diarrhea

316
Q

niacin

A

increase HDL and decrease LDL

decrease FA release
Decrease LDL synthesis

ADR - flushing tx with prophylactic aspsirin

317
Q

bile acid resins

A

decrease LDL

decrease bile acid resorption

adr - diarrhea

318
Q

ST segment elevation in inferior leads II, III, aVF

A

inferior wall MI - most commonly RCA 4:1 (LCX)

319
Q

ST elevation in V1-v6

A

anterior MI - LAD

320
Q

posterior wall MI

A

ST depression in v1-v3

ST elevation I and aVL (LCX)

ST depression in I and aVL (RCA)

321
Q

ST elevation I, aVL, V5, V6

ST depression II, III, aVF

A

lateral wall MI LCX

322
Q

right ventricle MI signs

A

RCA

ST elevation in V4-V6r

323
Q

decreased CO in CHF –>

A

increase in RAAS –> increased ADH –> increase angiotensin II

324
Q

increase in angiotensin II leads to

A

vasoconstriction of afferent and efferent glomerular arterioles (more so in efferent)

increased intraglomerular pressure to maintain GFR

decreased Na delivery to distal tubules

325
Q

ST depression in V1-v3
ST elevation I and aVL = ?
ST depression I and aVL = ?

A

elevation in I and aVL = LCX

depression in I and aVl = RCA

326
Q

ST depression in V1-v3
ST elevation I and aVL = ?
ST depression I and aVL = ?

A

elevation in I and aVL = LCX

depression in I and aVl = RCA

327
Q

S4 indicates

A

a stiff LV which occurs in the setting of:
-restrictive cardiomyopathy
or
- hypertrophy from prolonged HTN

328
Q

ascending aortic aneurysm leads to –>

A

aortic regurgitation (diastolic murmur)

329
Q

severe Aortic stenosis signs

A
  • delayed (slow rising) and diminished (weak) carotid pulses
  • single and soft S2
  • mid to late peaking systolic murmur with max intensity at 2nd R ICS radiating to the carotids
330
Q

pulsus parvus and tardus

A
  • delayed (slow rising) and diminished (weak) carotid pulses
331
Q

prominent capillary pulsations in the fingers or nail beds is seen in

A

aortic regurgitation - due to the widened pulse pressure

332
Q

Most common side effect of amiodarone

A

pulmonary toxicity - longer term use months to years

333
Q

acute limb ischemia causes

A
  • cardiac/ arterial embolus (severe and sudden)
  • arterial thrombus
  • iatrogenic/ blunt trauma
334
Q

clinical signs of acute limb ischemia

A 
pain 
pallor 
parethesias 
pulselessness
poikilothermia (cool extremity) 
paralysis (late sign)
335
Q

management of acute limb ischemia

A

anticoagulation - heparin

thrombolysis vs sx

336
Q

DVT presentation

A

dull aching pain
swelling
tenderness of LE
pulse is present

337
Q

cause of ascending aortic aneurysms

A

cystic medial necrosis

connective tissue disorders

338
Q

cause of descending aortic aneurysms

A

atherosclerosis

339
Q

CXR of thoracic aortic aneursyms

A

widened mediastinal silhoutte
increased aortic knob
tracheal deviation

340
Q

decreased left ventricular preload can be seen in

A

cardiac tamponade

341
Q

septic shock cardiac findings

A

hypotensive, tachy

reduced cardiac afterload – decreased systemic vascular resistance –> due to overall peripheral vasodilation

decreased pulmonary capillary wedge pressure
increased mixed venous O2 saturation

342
Q

what is the initial tx of choice for a hyperthyroidism pt with afib

A

beta blockers

343
Q

meds for stable afib pt

A

beta blockers
diltiazem
digoxin

344
Q

CHA2DS2-VASc score = thromboembolic risk

A 
C- CHF
H- HTN 
A2 - age >75 (2pts) 
D- Diabetes mellitus 
S- stroke/TIA/thromboembolism (2pts) 
V-vascular dz (prior MI, periph artery dz, plaques) 
A- age 65-74 (1pt)
S- sex category female

max score = 9

345
Q

major side effects for amiodarone

A

cardiac - sinus brady, heart block QT prolongtion
pulm - chronic interstitial pneumonitis
endocrine - hypo/hyperthyroidism

GI/hepatic - elevated transaminases, hepatitis
occular - corneal microdeposits, optic neuropathy

derm = blue gray skin discoloration
neuro - peripheral neuropathy

346
Q

MCC of mitral regurgitation in a developed country

A

mitral valve prolapse

347
Q

lifte style modifications recommended for HTN

A

diet: <2.4g salt per day, K supplements, DASH, no etoh
exercise: 30min/day or 2hrs per week

Weight: lost weight if obese, or BMI>25

348
Q

stage 1 HTN

A

systolic < 140
diastolic <90

LSM or if 10% risk LSM + 1 drug

349
Q

stage 2 HTN

A

systolic >140
diastolic >90

LSM + 2 drugs

350
Q

hypertensive urgency vs emergency

A

> 220 systolic + >120 diastolic
only difference is that emergency has end organ damage

papilledema, HA, AMS

351
Q

tx for HF or CAD + HTN

A

beta blocker (carvedilol, metoprolol) - ACE-I

352
Q

tx for stroke + HTN

A

thiazide + ACE-I

353
Q

tx for CKD + HTN

A

ACE-I or ARB (except in stage IV)

354
Q

tx for diabetes + HTN

A

ACE-I

355
Q

tx for new onset HTN alone

A

thiazides, ACE-I (except if your black), CCB

356
Q

dihydroperidine CCB (dipines) basics

A

ADR - peripheal edema

anti anginal

357
Q

ACE- ARBS basics

A

ADR- increased creatinine and K

other ADR for ACE-I = dry cough + angioedema

358
Q

tx of HTN during angioedema caused by ACE-I

A

ARBs

359
Q

thiazides basics

A

HCTZ - works on the collecting duct - ADR - decreased k+

will also decreased urinary Ca which helps prevent kidney stones

360
Q

beta blockers basics for HNT

A

useful for HF with decreased EF

ADR - decreased HR, Obstructive lung disease

361
Q

Spironolactone

epleronone

A

ADR - increased K and sprinolacotne (gynecomastia) so use epleronone instead

CHF class III

362
Q

Hydrazaline

A

arteriolar dilator - useful for CKD V - ADR - reflex tachycardia and drug induced SLE

363
Q

isosorbide nitrate

A

venous dilator

dont use with other nitrates or PDE I

364
Q

alpha antagonist

A

useful if also treating BPH but can cause orthostatic hypotension

365
Q

ADR of clonidine

A

rebound hypertension

366
Q

tx of hypertensive emergency

A

IV nitrates or CCB to get MAP down 25% in first 2-6hrs

367
Q

hyperaldosteronism (primary aldosteronism)

A

refractory HTN or HTN and hypokalemia

renin > 20
CT pelvis

368
Q

hypercalcemia and HTN

A

polyuria, AMS, “moans, bones, groans”
kidney stones

check free Ca

369
Q

aortic coarctation

A

children = warm arms, cold legs, claudications

adults = rib notching, BP differential in legs and arms

CXR, angiogram, CT angio

370
Q

renovascular HTN

A

DM or glomerulonephritis

young woman = FMD
old guy RAS
renal bruit, hypo K

371
Q

pheochromocytoma HTN

A 
pallor 
palpitations
pain 
perspiration 
pressure

24hr urinary metanephrines
CT

372
Q

cushings

A

diabets, HTN, central obesity, Moon facies

low dose Dexa, ACTH level
high dose DEXA

373
Q

fast arrhythmia with narrow QRS

A

either SVT or AFib

374
Q

SVT basics

A

no P waves
HR > 150 and regulr

tx - adenosine 6mg –> 12mg –> 12mg

375
Q

afib basics

A

no p waves irregularly irregular
heart rate <150

CCBs = beta blockers for rate control except in CHF use digoxin or amiodarone

376
Q

saw tooth pattern =

A

atrial flutter

377
Q

fast arrhythmia with wide QRS

A

torsades or V tach

378
Q

torsades basics

A

changing amplitude (ribbon like)

tx magnesium (amiodarone too)

379
Q

v tach basics tx

A

stable - amiodarone

unstable - shock

380
Q

in valvular afib DOC for anticoagulation =

A

warfarin

381
Q

Slow rhythm and wide QRS

A

3rd degree AV block or idioventricular rhythm

no atropine for either rhythm but pace them

382
Q

slow rhythm and narrow QRS

A

sinus brady - atropine and pace
1st degree block - atropine and pace
2nd degree type I block - atropine and pace
2nd degree type II block - pace

383
Q

differences between AV blocks

A

1st - just PR prolongation - no dropped beats

2nd type I - PR prolongation with drop after

2nd type II - nml PR length with random dropped beats

384
Q

fast and narrow rhythm tx =

A

adenosine

385
Q

fast and wide rhythm tx =

A

amiodarone

386
Q

squatting increases the intensity of all murmurs except

A

MVP and HCM

387
Q

clinical manifestations of acute pericarditis

A

chest pain
pericardial friction rub
diffuse ST elevation and PR depression

pericardial effusion without tamponade

388
Q

diastole dysfunction in constrictive pericarditis

A

early diastole - rapid filling

late diastole - halted filling

389
Q

constrictive pericarditis - when intracardiac volume reaches the limit set by the noncompliant pericardium

A

ventricular filling is halted abruptly

390
Q

in cardiac tamponade ventricular filling

A

is impeded throughout diastole

391
Q

if pat has clinical signs of cirrhosis (ascites, hepatospleomegaly) and distended neck veins perform tests to r/o out

A

constrictive pericarditis

392
Q

imaging test of choice for dx of pericardial effusion and cardiac tamponade

A

echo

393
Q

CXR findings of pericardial effusion

A

cardiac silhoutte - water bottle appearance

enlarged heart without pulmonary vascular congestion

394
Q

cardiac tamponade causes

A

rapid accumulation of. 200ml or slow accumulation of 2L

mechanically impairs diastolic filling
pressures in RV, LV, RA, LA equalize
decreased stroke volume
decreased cardiac output

395
Q

becks triad

A

hypotension

muffled heart sounds JVD

396
Q

pulsus paradoxus

A

systolic bP drop >10mmHg on inspiration

397
Q

complications of mitral stenosis

A

hemoptysis - due to elevated LA pressure ruptures anastomoses of small bronchial veins

thromboembolism - afib

398
Q

tricuspid regurg

A

IV Drug users, LV failure - mcc

blowing holosystolic murmur at LLSB

399
Q

pt with new murmur and unexplained fever or bacteremia suspect

A

endocarditis

400
Q

acute endocarditis

A

MCC - staph aureus

nml heart valves

401
Q

subacute endocarditis

A

strep viridans and enterococcus

damaged heart valves

402
Q

prosthetic valve endocarditis

A

staph epidermidis > staph aureus

403
Q

endocarditis in IV drug users

A

staph aureus is MCC other causes include streptoccoci, enteroccocci, candida and pseudomonas

404
Q

dx of endocarditis

A 
DUKE criteria (2 maj, 1 maj + 2min, 5 min) 
TEE
405
Q

situations that require prophylactic tx for endocarditis

A

proesthetic heart valves
hx of infective endocarditis
congenital heart dz
dental procedures

406
Q

nonbacterial thrombotic endocarditis (1)

nonbacterial verrucous endocarditis (2)

A

1 - metastic cancer - deposits of fibrin and platelets along closure line of cardiac valve leaflets

2- aortic valves in SLE pts - small warty vegetations on both side sof valve leaflets

407
Q

first step if pt has severe HA and markedly elevated BP

A

lower Bp(hydraazine) then CT –> if CT neg –> LP

408
Q

managment of hypertensive crisis

A

reduce mean arterial pressure by 25% in 1-2 hrs

if severe - IV hydralazine, esmolol, nitroprusside, labetalol, NTG

409
Q

types of aortic dissections and dx

A

type a = ascending - anterior chest pain - tx surgical + IV beta blockers, IV sodium nitroprusside

type b = descending - interscapular back pain - tx medical

dx - cxr - widened mediastinum >8mm on AP view + TEE

410
Q

presentation of. aortic dissection

A

severe tearing/ripping/stabbing pain
abrupt onset
anterior chest or back of the chest

pulse or bP asymmetry between limbs

411
Q

predisposing factors for aortic dissections

A

long standing HTN
cocaine, trauma
Connective tissue diseases (marfans, ehlers danlos)

3rd trimester of pregnancy

412
Q

AAA

A

located between renal arteries and iliac bifurcation
more common in. men 65-70 (women more likely to tear)

multifactorial - atherosclerotic weakening of aortic wall, HTN, trauama, vasculitis, smoking

syphillis, and CT diseases marfasn - thoracic more tho

413
Q

clinical features of AAA

A

sense of fullness
pulsatile mas on abd exam
ecchymoses on back and flanks, around umbilicus

414
Q

presentation of ruptured AAA

A

abd pain
hypotension
palpable pulsatile abdominal mass

emergency laparotomy indicated

415
Q

test of choice for AAA

A

US of abdomen

416
Q

meds that improves long term survival in pts with LV systolic dysfunction

A

beta blockers
ACE-I
ARBs
mineralcorticoid receptor antagonists

hydralazine + isosoribide nitrates in black

417
Q

symmetric duskiness and coolness of all fingertips can be caused by

A

pressers such as NE - lead to ischemia of distal fingers and toes secondary to vasospasm not painful

418
Q

raynauds phenomenom

A

finger ischemia that is typically painful and due to cold exposures or stress

419
Q

Formation of AV fistulas can occur from

A

trauma –> leading to high output cardiac failure by shunting blood from arterial side to venous side –> increasing cardiac preload –>HF

420
Q

CHA2DS2-VSAc score interpretation

A

0 - no tx
1- aspirin or more
2 - blood thinner (wafarin, -bans)

421
Q

drugs that inhibit cyp450 –> increasing warfarin effect

A 
acetominophen, NSAIDs 
ABX, antifungals 
amiodarone 
thyroid hormones 
cimetidines 
cranberry juice + vit E 
omeprazole 
SSRIs
422
Q

drugs that induce cyp450 –> decreasing warfarin effect

A 
st johns wort, ginseg 
carbameapine, phenytin
rifampin 
OCPs 
phenobarbital
423
Q

dx test of choice for cardiac tamponade

A

echo

424
Q

some causes of. low pulmonary capillary wedge pressure

A

acute PE due to impaired blood flow
sepsis

hypovolemic shock

425
Q

complication of mitral stenosis

A

afib –> thromboembolic stroke –> hemiparesis

426
Q

beta blocker overdose

A

bradycardia
AV block
hypotension
diffuse wheezing

antidote = glucagon

427
Q

in cardiogenic shock what happens to the pulmonary capillary wedge pressure

A

pulmonary capillary wedge pressure will be elevated

428
Q

SVR in sepsis, hypovolemia, cardiogenic shock

A

sepsis - decrease SVR
hypovolemia - increase SVR
cardiogenic shock - increase SVR

429
Q

non selective beta blockers can trigger

A

bronchoconstriction in patients with underyling asthma

430
Q

late complication of radiation therapy

A

constrictive pericarditis

431
Q

pts with endocarditis with abnormal conduction on ECG –> think

A

perivalvular abscess

432
Q

fibromuscular dysplasia

A

women, internal carotid artery stenosis -> recurrent headaches, pulsatile tinnitus, TIA, stroke

renal artery stenosis -> secondary HTN

subaruicular systolic bruit, abd bruit

tx - antiarrhythmias (ACE-I or ARBs)

433
Q

pheochromocytoma presentation

A

secondary HTN - due to secretion of catecholamines

episodes of HA sweating, diaphoresis

434
Q

primary hyperaldosternism

A

secondary HTN
decreased K+
metabolic alkalosis

435
Q

conditions associated with AFIB

A

HTN, CAD, CHF, valvular dz, hypertrophic cardiomyopathy

obstructive sleep apnea, PE, COPD, acute hypoxia

obesity, hyperthyroidism, DM, Alcohol

436
Q

cushing syndrome

A 
central obesity 
glucose intolerance 
hirsutism 
abdominal striae
elevated BP
437
Q

digoxin toxicity

A

GI - anorexia, N/V, abd pain

cardiac - life threatening arrhythmias

neuro - fatigue, confusion, weakness, color vision alterations

438
Q

viral myocarditis

A

young pt
viral prodrom

causes - parvovirus B19, coxsackie, HSV -6, adenovirus, HIV, influenza

eho - 4 chamber dilation, impaired contractile function

439
Q

renovascular dz clues

A

HTN resistant to tx
malignant HTN (end organ damage)
onset of severe HTN > 55y/o

asymmetric renal size
abdomial bruit

unexplained increase in serum creatinine >30% after starting on ACE-I or ARBs

440
Q

renin pathway

A

low bp or low volume -> JGC -> converts angiotensinogen –> angiotensin I –> ace converts it into –> angiotensin II –> vasoconstriction + increased aldosterone

441
Q

management of symptomatic bradycardia and/or complete heart block

A

transcutaneous pacing

442
Q

supravalvular aortic stenosis

A

aortic outflow obstruction - develop LV hypertrophy and can have exertional anginal due to subendocardial ischemia -> increased myocardial oxygen demand during exercise

443
Q

primary hyperparathyroidism

A 
muscle weakness
recurrent kidney stones 
neuropysch problems 
hypercalcemia
secondary HTN
444
Q

MEN type I

A

hyperparathyroidism
pancreatic tumors
pituitary tumors

445
Q

MEN type II a

A

medullary thyroid carcinoma
pheochromocytoma
parathyroid hyperplasia

446
Q

MEN type IIb

A

medullary thyroid carcinoma
pheochromocytoma
mucosal neuromas
marfanoid habitus

447
Q

ADR of dihydropyridine Ca channel antagonist

A

peripheral edema

448
Q

peristent AFIB in WPW syndrome patient should be treated with

A

if unstable - electrical cardioversion

if stable - rhythm control with ibutilide or procainamide

449
Q

pain relief from NTG is due to

A

decreased LV wall stress

450
Q

inf wall MI with delayed presentation followed by sudden onset hypotension, dyspnea, tachypnea, pulm edema and a soft systoli cmurmur is indicative of

A

acute MR due to posteromedial papillary muscle rupture

451
Q

clinical presentation of amyloidosis in cardiomyopathy

A

unexplained CHF
proteinuria
left ventricular hypertrophy in the absence of HTN hx

452
Q

ADR of class IC anti arrhythmics (fleicande)

A

increase in QRS duration

453
Q

statins MOA

A

inhibit HMG CoA reductase -. intracellular synthesis pathway

decrease coenzyme q10 synthesis

454
Q

ACE-I moa

A

extracellular enzyme blocker and increase levels of bradykinin

455
Q

the strongest predictor of AAA expansion and ruputre =

A

smoking

diameter of AAA and speed of expansion of AAA

456
Q

younger pt has exertional dyspnea
pounding heart sensation when lying on left side
widened pulse pressure

dx=

A

AR - increase in LV size bring the ventricular apex close to the chest wall

457
Q

the most common cause of AR in developed countries =

A

aortic root dilation or congenital bicuspid valve

458
Q

complication of aortic dissection

A

AR and cardiac tamponade

459
Q

most common ectopic foci in afib

A

pulmonary veins

460
Q

underlying pathophys of atrial flutter

A

involves reentreant circuit around the tricuspid annulus

461
Q

murmurs that require workup

A

diastolic and continous murmurs

ECG –> echo

462
Q

murmur that does nOT require workup

A

midsystolic murmur in otherwise young asymptomatic adult

463
Q

decreased tracer uptake in technetium 99 scan at rest and with exercise indicates

A

fixed defect - likely scar issue with decreased perfusion and CAD

464
Q

decreased tracer uptake in technetium 99 scan only with exercise indicates

A

ischemia and CAD (reversible)

465
Q

dx test of choice for aortic dissection causing hemopericardium and rapidly progessing cardiac tamponade

A

CT angiography

466
Q

increased incidence of orthostatic hypotension in the elderly is due to

A

progressively decreasing baroreceptor sensitivity and defects in the myocardial response to this reflex

467
Q

GFR changes in the elderly

A

decreases -> promotes sodium retention

468
Q

common causes of pulm HTN

A

LV systolic or diastolic dysfunction

tx - loop diuretics and (ACE-I or ARBs)

469
Q

ventricular aneursym

A

late complication of MI (wks to months)

ECG - persistent localized ST seg elevation and eep Q waves in the leads correspondingto previous MI

470
Q

modification with greatest benefit on decreasing high BP

A

1) weight loss
2 DASH diet
3 exercise
4 sodium

471
Q

tx of hypertrophic cardiomyopathy

A

neg inotropic agents:

beta . bockers, verapamil, disopyramide (not first line due to ADR)

472
Q

situational syncope

A

neurally mediated syncope associated with micturition, cough, defecation

473
Q

what is the tx for acute thormbotic occlusions

A

heparin

474
Q

MOA of dihydropyridiine CCBs

A

decreases afterload by systemic vasodilation

475
Q

exertional heat stroke

A

strenous activity in hot humid weather
dehydration, obesity

core temp >104, AMS, organ/tissue damage

476
Q

management of exertional heat stroke

A

rapid cooling
fluid resuscitation
electrolyte correction
management of end organ complications

477
Q

cardiac sarcoidosis

A

dz of noncasseating granuloma infiltration of the myocardium and can result in

serios arrhythmias
cardiomyopathy HF
sudden cardiac death

478
Q

lyme carditis

A

1-2 months after borrelia burgdorferi inf

AV block is the MC abnormality seen

479
Q

common cardiac issues in marfans syndrome

A

mitral valve prolapse

aortic dilation -> aortic dissection -> aoritc regurgitation = early diastolic murmur

480
Q

hypovolemic shock cardiac values

A

decreased CO
decreased BP
decreased PCWP

increased SVR

481
Q

abrupt onset of regular tachycardia that resolves with cold water immersion =

A

PSVT - can be treated with vagal maneuvers

482
Q

MOA of vagal maneuvers to terminate AV nodal reentrant tachycardia

A

increase parasympathetic tone -> temporary slowing of conduction in the AV node –> increase in the AV node refractory period –> termination

483
Q

MCC of sudden cardiac arrest in the immediate post infraction period in pts with acute MI

A

reentrant ventricular arrhythmias (vfib)

484
Q

tricuspid regurgitation affect during inspiratioin

A

murmur increases

485
Q

dobutamine moa

A

strong affinity for beta 1-r, weak affinity for beta-2-r + alpha 1-r

stimulate increased myocardial contractility -> increased EF -> reduced LV end systolic volume

improvement of symptoms of decompensated HF

486
Q

clinical signs of acute decompensated HF

A

acute dyspnea, orthopnea
HTN, Hypotension(if severe)
accessory muscle suse, tachycardia, tachypneic

diffuse crackles with possible wheezes
JVD, peripheral edema

487
Q

tx of acute decompensated HF

A

O2 and furosemide +

NTG - HTN
NE or dobutamine - hypotension

488
Q

cardiac signs of cor pulmonale

A

tricuspid regurgitation murmur
ECG - RBBB, RAD, RVH, RA enargment

echo - pulm HTN, dilated RV,

right heart cath (gold standard) - RV dysfunction, elevated pulmonary artery systolic pressure >25mmHg

489
Q

abnormal causes of S3

A

HF
restrictive cardiomyopathy
high output states

490
Q

abnormal causes of S4

A

acute MI
young adults, kids
ventricular hypertrophy

491
Q

MCC of aortic stenosis > 70 y/o and <70 y/o

A

> 70 - senile calcific aortic stenosi

< 70 - bicupsid aortic valves

492
Q

pulsus paradoxus can be seen in

A

cardiac tamponade

severe asthma

severe COPD

493
Q

chagas disease

A

preceded by megacolon

dilated carditis

protozoal infection

494
Q

diptheria myocarditis

A

preceded by URI
underdeveloped country

no vaccine hx

495
Q

MC site of occlusion in peripheral vascular dz

A

superficial femoral artery (hunter cannal)

smoking = biggest risk factor

496
Q

calf claudication

buttock and hip claudication + cave claudication

A

femoral or popliteal

aortoilliac occlusive

497
Q

Normal ABI is between

A

0.9 - 1.3

>1.3 - is due to noncompressible vessels and indicates severe disease

498
Q

cholesterol embolization syndrome

A

due to showers of cholesterol crystals

triggered by surgical or radiographic intervention

blue/black toes

499
Q

superficial thrombophlebitis

A

local tenderness, erythema, along course of superficial vein

UE - site of IV infusion

LE - varicose vein association

tx - analgesics - monitor for spread or cellulitis

500
Q

cardogenic shock

A

decreased CO
increased SVR
increased PCWP

501
Q

hypovolemic shock

A

decreased CO
increased SVR
decreased PCWP

502
Q

neurogenic shock

A

decreased CO
decreased SVR
decreased PCWP

503
Q

Septic shock

A

increased CO
decreased SVR
decreased PCWP

504
Q

afterload reducing agents

A

NTG

nitroprusside

505
Q

what is the best indicator that tht etx of shock is effective

A

monitoring urine output as well as a pulmonary artery catheter and/or central venous line

506
Q

septic shock is asociated with

A

severe peripheral vasodilation (flushing, warm skin)

507
Q

hypovolemic shock is associated with

A

peripheal vasoconstriction (cool skin)

508
Q

most common cause of. death in ICU

A

septic shock

509
Q

SIRS

A 
2 or more: 
Fever > 38 or hypothermia <36
hyperventilation or PaCO2 <32
tachy 
increased WBCs
510
Q

ADR of nitroprusside

A

cyanide toxicity especially in those with continouse infusions

lactic acidosis, AMS, Seizure Coma

511
Q

tx of vasospastic angina

A

CCB for prevention and NTG for abortive tx

512
Q

long standing systemic HTN ECG signs

A

high voltage QrS complexes
lateral ST segment depression
lateral T wave inversion

513
Q

when is metoprolol C/I in the tx of an acute MI

A

when pulmonary edema is present along with acute decompensated HF

514
Q

MCC of constrictive pericarditis in developing countries

A

tuberuculosis

515
Q

presentation of interventricular septum

A

3-5 days after MI
suddent onset cardiogenic shock with hypotension
biventricular failure

new harsh holosystolic murmur with palpable thrill at the. left sternal border

516
Q

what lifestyle modification can greatly decrease TGLs

A

reducing or no longer consuming alcohol

517
Q

ventricular aneursyms

A

5days to 3 months post PI
thin and scarred fibrotic myocardium
ecg - presents with persistent ST segment elvation after recent MI

can eventually lead to –> MR

518
Q

ECG findings that suggest an arrhytmia that can cause syncope

A 
inappropiate sinus brady
sinoatrial block 
sinus pauses 
AV block 
nonsustained ventricular arrhthyias 
short or prolonged QTc interval
519
Q

symptomatic management of carotid stenosis is. required whwen

A

TIA CVA, stenosis 70-99%

520
Q

digoxin and furosemides role in CHF

A

provide symptomatic relief but will not decrease mortality

521
Q

MCC of isolated AR in a young adult in developed countries

A

congenital bicupsid aortic valves

522
Q

uremic pericarditis

A

BUN levels >60
no classical pericarditis ECG findings

tx- hemodyialysis

523
Q

pathphys behind the ADR of niacin

A

high dose niacin -> flushing - due to prostaglandin induced periheral vasodilation and can be reduced by low dose aspsirin

524
Q

primary mitral valve abnormality in pts with hypertrophic cardiomyopathy is the presence of

A

systolic anterior mitral valve - > anterior motion of the mitral valve leaflets towards the interventricular septum and when connected to thickened septum during systole to LV outflow tract obstruction

525
Q

what is the most common finding associated with HF and an elevated BNP

A

S3 - sign of increased cardiac filling pressures

526
Q

hemodynamics in HF

A

decreased contractility
decreased CO
increased afterload
increased SVR

527
Q

the goals of the initial therapy of aortic dissection

A

pain control

reduction of systolic bp to 100-120
decreased CV contractility to reduce aortic wall stress
(tx of these 2 beta blockers)

528
Q

most important predisposing factor associated with the development of aortic dissection

A

systemic HTN

if <40 y/o 50% are due to marfans syndrome

529
Q

electrical alternans + sinus tachy

A

large pericardial effusion

530
Q

poor prognostic factors for CHF

A 
hyponatremia
resting tachycardia
s3 
mod to severe MR 
LBBB 
severe LV dsyfunction 
pulm HTN

Step 2 Rotation Cards (14 decks)

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