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cards 2 Flashcards

1
Q

any tachycardia arising “above” the ventricles

A

supraventricular tachycardia

atrial tachycardias - a flutter and a fib
sinus tachycardia
*usually paroxysmal supraventricular tachycardia (PSVT)

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2
Q

EKG differences between sinus tach and SVT

A

SVT usually own’t have a P wave

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3
Q

different pathophys of SVT

A

Re-entry: re-entry circuit is formed. presents with sudden incrase in HR

automaticity: “ectopic” area of heart generates its own abnormal electrical signal. presents with a gradual increase and decrease in HR

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4
Q

what is the gatekeeper that limits the activity that reaches the ventricles?

A

AV node

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5
Q

what is the most common cause of regular SVT?

A

AVNRT

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6
Q

what are the causes of AVNRT?

A

possible link to caffeine, alc, stress. 75% of cases occur in females

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7
Q

symptoms of AVNRT

A

palpitations, brief hypotension, chest pain

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8
Q

what is AVNRT?

A

Atrioventricular nodal reentrant tachycardia (AVNRT) is an arrhythmia that occurs because an extra pathway lies in or near the AV node, which causes the impulses to move in a circle and reenter areas it already passed through.

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9
Q

AVNRT pathophys

A

a re-entry circuit forms within/around AV node. involves fast and slow pathways
**NOT to be confused with an ACCESSORY PATHWAY - this involves normal conduction pathway thats in the heart

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10
Q

EKG findings in SVT/AVNRT

A

150-250 bpm
regular
p wave absent or after QRS
Narrow QRS- if not narrow, not SVT. If wide, may be arising from the ventricles –> fatal!

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11
Q

how do you manage AVNRT?

A

goal is to interrupt the circuit and return to normal HR

vagal maneuvers - ice, vasovagal, carotid massage
medications - adenosine (causes complete blockade of AV node) and verapamil

cardioversion

definitive management : radiofrequency ablation of accessory pathway, pacemaker

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12
Q

what happens to the EKG when you administer adenosine?

A

may look like asystole!

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13
Q

what is AVRT?

A

accessory pathway within the myocardium allows direct connection between atrium and ventricle -> allows for pre-exitation (bypasses the AV node, conducts impulses faster than AV node) - why there is usually shortened or absent PR interval

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14
Q

what does AVRT require?

A

two pathways - normal AV conduction pathway + accessory pathway

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15
Q

what is AVRT seen in?

A

wolff-parkinson-white syndrome

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16
Q

is more AVRT orhodromic or antidromic?

A

orthodromic- conduction is bidirectional or retrograde form ventricles to atrium

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17
Q

orthodromic AVRT EKG

A

150-250 BPM
NARROW QRS
inverted P

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18
Q

management of symptomatic AVRT

A

1 stable or unstable? if unstable -> cardiovert

with orthodromic conduction: tx similar to SVT

with antridromic (Wide QRS) - procainamide, avoid adenosine, verapmil - can progress into Vtach

definitive tx: RFA, possibly implantable pacemaker

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19
Q

what is the safest, most effective drug to administer for acute tx of a wide QRS complex tachycardia of unknown etiology

A

procainamide

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20
Q

management of asymptomatic WPW

A

refer for electrophysiological studies

stratify risks: younger age, male gender, inducible AVRT during EP study, multiple acessory pathways

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21
Q

where is a pacemaker inserted into?

A

percutaneously through subclavian vein or cephalic vein (left pectoral usually)

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22
Q

differences in pacemakers/chambers

A

single chamber - 1 lead - sends impulses to one atrium or ventricle

dual chamber - 2 leads- sends impulses to one atrium and one ventricle

biventrical- 3 leads - sends impulses to right atrium and both ventricles

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23
Q

what are indications for pacemakers?

A

depends on symptoms associated with an arrhythmia and location of conduction abnormality

just sinus brady alone is not reason enough to give a pacemaker. Unless they are symptomatic (dizziness, lightheadedness, syncope, fatigue, poor exercise tolerance)

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24
Q

if there is disease present below AV node ( in His-Purkinje system), is pacemaker generally recommended?

A

yes - less stable

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25
Q

what is the number one cause/indicator for a pacemaker?

A

symtomatic sinus bradycardia

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26
Q

indicators for implantable defibrillators

A

can monitor and deliver shocks to terminate Afib with RVR, V tach, V fib. individuals at high risk for cardiac arrest. history of MI with EF

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27
Q

what is the definition of SCD?

A

death arising from cardiac etiology that occurs in short period of time (usually within 1 hour of symptom onset) - can be in a person with known or unknown cardiac disease.

usually due to a fatal arrhythmia

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28
Q

is SCD same as MI?

A

NO- SCD is an electrical problem, MI is more circulation

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29
Q

causes of SCD

A

fatal arrhythmias

vfib - ventricles quiver rapidly and irregularly – heart pumps little or no blood to body

vtach

asystole

structural heart disease (CHD)

HF, hypertrophy, myocarditis, MVP

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30
Q

1 cause of SCD in pt

A

hypertrophic cardiomyopathy

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31
Q

risk factors of SCD?

A

prior MI -especially within th elast 6 months

CAD

EF less than 40%

prior episode of cardiac arrest

**anything that affects the electrical system of the heart or how the myocardium responds to it!

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32
Q

management of SCD?

A

ACLS guidelines

***defibrillation
epinephrine or vasopression if ventricular arrhythmia
atropine if bradycardia or PEA

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33
Q

difference between CAD and CHD?

A

CAD - pathological proess involving the coronary arteries (usually caused by atherosclerosis)

CHD: includes the diagnosis of angina, MI, and silent MI

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34
Q

CAD

A

impaired coronary blood flow which can cause oxygen deprivation and angina- usually caused by atherosclerosis

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35
Q

a fixed lesion obstructing what percent or greater of the lumen is generally required to cause symptomatic ischemia precipitated by exercise?

A

75% or greater

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36
Q

obstruction of what % of lumen can lead to inadequate coronary blood flow even at rest?

A

90%

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37
Q

when does MVO2 (myocardial oxygen demand) increase?

A

directly in proportion to HR
with increased contractility
with increased wall tension (increased preload or afterload)

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38
Q

what increases your risk for CAD/angina?

A

dyslipidemia (low HDL, high LDL, high triglycerides)

age/gender

family history

cigarette smoking

HTN

DM

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39
Q

where do patients usually feel angina?

A

retrosternal
radiation to ulnar surface of left arm, right arm, outer surfaces of both arms
epigastric discomfort alone or in associate with chest pressure is not uncommon

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40
Q

this is caused by an imbalance in coronary perfusion (due to chronic stenosing coronary atherosclerosis) relative to myocardial demand. Angina usually occurs with physical activity, emotional excitement, and any other cause of increased cardiac workload. usually relieved by rest or administering nitroglycerin.

A

stable angina

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41
Q

this is characterized by patients having exertional dyspnea rather than exertional chest pain. Caused by exercise induced Left ventricular dysfunction

A

angina equivalent syndrome

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42
Q

this is an uncommon form of episodic myocardial ischemia that is caused by coronary artery spasm. Angina unrelated to physical activity, HR, or BP. this responds promptly to vasodilators and CCB.

A

prinzmental/variant angina

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43
Q

which patients are more likeley to get variant angina?

A

younger, and don’t exhibit classic cardiovascular risk factors (except for cigarette smoking)

associated with other vasospastic disorders, such as Raynaud’s and migraine headache or its treatment

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44
Q

this is very uncommon, are there are more episodes of silent than painful ischemia in the same pt. difficult to diagnoses, except through holter monitor ad exercise testing.

A

silent ischemia

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45
Q

this refers to a pattern of increasingly frequent pain, often of prolonged duration, that is precipitated by progressively lower levels of physical activity or that even occurs at rest. Caused by the disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization or vasospasm (or both)

A

unstable or crescendo angina - also referred to as preinfarction angina

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46
Q

what is classic angina associated with?

A

ST-segment depression during acute event (stress test)

occurs with the usual precipitating factors. classic angina is usually very predictable to patients and they can tell exactly what causes it and what makes it better

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47
Q

what is angina typically described as?

A

pressure or heaviness - if brief or sharply localized or lancinating usually not angina

48
Q

if angina lasts longer than what, you should consider an MI?

A

over 20-30 minutes

49
Q

physical exam findings during anginal episode

A

hyper/hypotension
s4 gallop due to diastolic filling of ischemic non-compliant ventricle
transient mitral regurgitation murmur
arrhythmias

50
Q

EKG during anginal episode

A

horizontal or downsloping ST segment depression that reverses after the ischemia disappears.

51
Q

goal of exercise testing

A

to induce a controlled, temporary ischemic state during clinical and ECG observation

52
Q

criteria for a “positive” EST = positive for ischemia

A

ST segment depression: 1 mm horizontal or down sloping ST segment beyond baseline

+/- wave flattening or inversion

T segment elevation suggests more sever (transmural) ischemia or coronary vasospasm

target HR much be achieved (85% of max HR - 220-age)

53
Q

false-positive ST results are increased in which patient populations?

A

asymptomatic men under 40 or premenopausal women with no risk factors for premature CAD

54
Q

nuclear EST

A

near equivalent sensitivity/specificity to EST

most useful in patients who cannot exercise

major contraindication in severe bronchospastic lung disease (consider dobutamine study)

55
Q

cardiac catheterization indications

A

suspicion of multi-vessel CAD

determine if CABG/PTCA feasible

rule out CAD in patients with persistent/disabling chest pain and equivocal/normal noninvasive testing

56
Q

CCB MOA

A

arterial dilation/after-load reduction

coronary arterial vasodilation

prevention of coronary vasoconstriction

enhancement of coronary collateral flow

antispasmodic and vasodilator

*tachy arrhythmia or ectopy + angina = first line therapy

57
Q

nitrates MOA

A

nitric oxide - endothelium derived relaxing factor

venous vasodilation/pre-load reduction
arterial vasodilation/after-load reduction
coronary arterial vasodilation

58
Q

what are the side effects of nitrates?

A

*flushing
headache
palpitations
tolerance

59
Q

most common cause of NSTEMI

A

thrombus or thromboembolism, usually arising on disrupted or eroded plaque

60
Q

why do you give a beta-blocker when someone is having an NSTEMI?

A

they block catecholamines (stress response) from binding to beta-adrenergic receptors

reduces myocardial demand by reducing HR, BP, contractility

decreases incidence of primary VF (prevents arrhythmias from occurring)

61
Q

what do you give nitroglycerin when someone is having an NSTEMI?

A

dilates coronary arteries

increases venous dilation and therefore decreases venous return

decreases myocardial demand by decreasing preload

62
Q

why are IIB/IIIA inhibitors given as treatment for an NSTEMI?

A

they block platelet receptor so platelets cannot bind fibrinogen and form clots

given in cath lab

caution in renal disease and with thrombocytopenia

63
Q

what should you not give to a patient pre-surgery or if you suspect they will need a CABG?

A

plavix - LD of 300mg takes about 7 days to clear out

64
Q

what score is used to evaluate likliehood of cardiac event by 14 days?

A

TIMI risk score

65
Q

what is the GRACE prediction score used for?

A

to asses all-cause mortality within 6 months of discharge

66
Q

what indicates MI and helps categorize MI and is a useful adjunct to diagnosis

A

cardiac biomarkers

67
Q

what causes a STEMI?

A

disruption of vulnerable plaque

completely occlusive thrombus –> ST elevation

68
Q

what is the most frequent cause of a STEMI?

A

rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation.

coronary artery vasospasm
ventricular hypertrophy
hypoxia
coronary artery emboli

69
Q

these biomarkers are very specific for cardiac injury and are the prefered markers for detecting myocardial cell injury. They rise 2-6 hours after injury, peak at 12 hours and stay elevated for 5-14 days

A

Troponin T and I

70
Q

this is found in heard muscle, skeletal muscle, and brain and is increased in over 90% of MIs. However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions. Begins to rise in 4-6 hours, peaks at 24 hours, and returns to normal in 2 days.

A

Creatinine Kinase (CK-MB)

71
Q

what is the fastest thing to elevate after infarction?

A

myoglobin - but not specific to heart

72
Q

what must be considered before using contrast dye for coronary angiography and percutaneous revascularization?

A

creatinine levels

73
Q

what is the marker for acute inflammation?

A

C-reactive protein (CRP)

74
Q

what will be on the ECG to show a high probability of ACS?

A

ST segment elevation in two contiguous leads or presence of q waves

75
Q

thrombolytics role in STEMI

A

shown to restore coronary blood flow in 50-80% of patients

contraindication active intracranial bleeding, CVA 2 months, CNS neoplasm, HTN, coagulopathy

intracranial bleed risk major drawback

76
Q

what is the standard “door to balloon” time?

A

90 minutes- percutanous coronary intervention

77
Q

what long term medications are MI pts on indefinitely?

A

aspirin, beta blockers, and statin

ACEI indefinitely in patients with CHF, ejection fraction

78
Q

what dysrhythmia is most common in AMI?

A

PVCs (>90% of patients)

79
Q

if atrial kick is eliminated, how much CO do normal hearts lost?

A

10-20%

80
Q

what does first degree and Mobitz I (Wenckebach) conduction disturbance usually occur?

A

with an inferior AMI- intermittent during the first 72 hours after infarction, but rarely progresses to complete block or pathologic rhythm

81
Q

which conduction disturbance is most common with an anterior AMI?

A

Mobitz II - does usually progress to complete heart block

82
Q

when does Complete Heart block usually occur?

A

setting of an inferior MI. mortality increases when RV is affected

83
Q

what does a new LBBB represent?

A

larger area of infarction - associated with high mortality

84
Q

what percentage of AMI patients develop some degree of CHF?

A

15-20%

85
Q

T or F : LV hypertrophy is protective against mechanical complications of AMI

A

true

86
Q

what is commonly detected for pericarditis in post-AMI patients?

A

pericardial friction rub - more often with inferior wall and right ventricular artivacts and angina

87
Q

what is a post AMI syndrome occuring 2-10 weeks after AMI where the pt presents with chest pain, fever and pleuropericarditis?

A

dressler syndrome

88
Q

most mid systolic murmurs of what grade are benign?

A

2/6 or less

89
Q

what does inhalation do to murmurs?

A

with inspiration - inhalation pressure causes an increase in the venous blood return to the right side of the heart so increases intensity of right-sided murmurs and decreases intensity of left-sided murmurs

90
Q

what does expiration do to murmur intensity?

A

increases left-sided murmurs

91
Q

what does having the patient lie supine and raising their legs up to a 45 degree angle facilitate in?

A

increase in venous return to the right side of the heart, producing effects similar to inhalation-increased blood flow

92
Q

when is s1 heard?

A

right after beginning of systole, due to mitral closing.

93
Q

when do clicks occur?

A

only during systole

94
Q

a click heard in early systole (very hear to S1) means what?

A

congenital aortic or pulmonic stenosis - result from abnormal ventricular wall tension

95
Q

a mid to late systolic click indicates what?

A

mitral or tricuspid valve prolapse (result from abnormal tension on redundant and elongated chordae tendinae or valve leaflets)

96
Q

what is S2?

A

beginning of diastole, due to aortic and pulmonic valve closure

97
Q

what is S3?

A

pathogenic in adults and indicates serious ventricular dysfunction

occurs in EARLY diastole when the ventrical is dilated and noncompliant

in children it can be normal

98
Q

when is a RV S3 heard best?

A

with patient supine during inspiration

99
Q

when is LV best heard?

A

best heard during with the patient in the left lateral decubitus position

100
Q

what is S4?

A

produced by augmented ventricular filling caused by atrial contraction. heard near the end of systole

101
Q

what are the diagnostic testing for valvular heart disease?

A

echocardiogram

exercise testing

cardiac cath - not usually for primary eval

102
Q

what is the most common cause of aortic stenosis?

A

calcific degeneration

103
Q

increased risk factors for AS

A 
males
smokers
HTN
DM
older age
hypercholesterolemia
104
Q

what is considered severe AS?

A

aortic jet velocity > 4 m/s
mean transvalvular pressure gradient > 50 mmHg

AVA

105
Q

what is the AS murmur?

A

classic crescendo-decrescendo systolic murmur of AS begins shortly after the first heard sound (S1)

intensity increases toward midsystole, then decreases

ends just before the second heart sound

** radiates to 1 or both carotid arteries

106
Q

where is an AS murmur best heard?

A

second intercostal space in the right upper sternal border

107
Q

is prophylactic AVR in asymptomatic patients routinely performed?

A

no, due to surgical risks

108
Q

what is mitral stenosis usually associated with?

A

rheumatic fever (40% of RHD result in MS)

presentation 20-40 years after initial episode of rheumatic fever

109
Q

what does significant MS lead to?

A

increase left atrium pressure and pulmonary HTN

110
Q

causes of acute aortic regurgitations

A

aortic disection
valve destruction from endocarditis
traumatic rupture

111
Q

what should you do for acute aortic regurgitation?

A

surgical AV repair or replacement emergently

112
Q

is an IABP (intraaortic balloon pump) recommended for acute aortic regurgitation?

A

no, contraindicated

113
Q

what is chronic mitral regurgitation often caused by?

A

myxomatous (floppy valve) disease or MVP

114
Q

what is diagnostic for tricuspid valve disease?

A

echo

115
Q

most common cause of death in pts with infective endocarditis

A

CHF

116
Q

major complications from infectious endocarditis

A

CHF
major embolic event (to brain, organs, skin)
valve perforation
repture of chordae tendinae or papilary muscles

117
Q

what are myxomas?

A

gelatinous structures consisting of myxoma cells imbedded in a stroma rich in glycosaminoglycans

most pedunculated on a fibrovascular stalk

clin med (12 decks)

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