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Cardio > Pathophysio Review > Flashcards

Pathophysio Review Flashcards

1
Q

sinus pause

A
  • if > 3 sec, place pacemaker

- no medical therapy options

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2
Q

1˚ AV block

A
  • PR > 200ms
  • test for lyme disease
  • no therapy if asymptomatic
  • watch AV blocker meds
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3
Q

2˚ Mobitz I AV block

A
  • progressive increase in PR then non-conducted
  • often physiologic form
  • no therapy if asymptomatic
  • consider stopping AV blocker meds
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4
Q

2˚ Mobitz II AV block

A
  • fixed PR interval then non-conducted
  • never physiologic
  • stop AV blocking drugs
  • pacemaker
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5
Q

3˚ AV block w/ narrow QRS

A
  • high AV node escape rhythm
  • stop AV blocker meds
  • pacemaker
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6
Q

3˚ AV block w/ wide QRS

A
  • escape rhythm below AV node, possible ventricular escape
  • stop AV blocker meds
  • pacemaker
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7
Q

RBBB

A
  • RsR pattern in V1-2 (rabbit ear)
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8
Q

LBBB

A
  • negative QS wave in V1
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9
Q

atrial fib

A
  • irregularly irregular
  • lumpybumpy baseline
  • no p waves
  • anti-coagulation to prevent stroke
  • AV node blockers to prevent rapid ventricular beating
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10
Q

atrial flutter

A
  • sawtooth baseline
  • ventricular rate is multiple of arterial rate
  • anti-coagulation to prevent stroke
  • AV node blockers to prevent rapid ventricular beating
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11
Q

SVT or PSVT

A
  • no p waves
  • ventricular rate ~160-220
  • break with adenosine
  • narrow QRS: avnrt
  • WPW pattern: avrt
  • ablation therapy
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12
Q

monomorphic VT

A
  • AV dissociation
  • comes from one part of ventricle (prior scar likely/old MI)
  • risk factor for sudden death
  • ICD
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13
Q

polymorphic VT

A
  • check QT length

- stop any QT prolonging medication, treat ischemia, consider ICD

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14
Q

goals of A fib/A flutter therapy

A
  • prevent stroke when CHADS2 elevated: systemic anticoagulation
  • rate control: AV node blockers (beta blockers or Ca channel blockers)
  • rhythm control: electrical cardioversion, type IA or IC with normal heart structure, type III with abnormal heart structure
  • ablation to prevent recurrence
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15
Q

V tach therapy

A
  • look for underlying structural heart disease, electrolyte abnormality, QT prolongation
  • acute therapy: class III or IB (if stable); defibrillation/cardioversion
  • chronic therapy: ICD
  • anti-arrhythmia meds only used to reduce ICD firing frequency
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16
Q

Purpose of antiarrhythmics

A
  • maintain sinus rhythm and prevent atrial fibrillation recurrence
  • reduce frequency of ICD discharge by preventing v tach/fib
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17
Q

mech of arrhythmogenesis

A
  • abnormal impulse conduction (90% reentry)

- abnormal impulse generation (abnormal automaticity, triggered activity)

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18
Q

arrhythmias that use reentry and therapy

A
  • AVNRT (AV node): ablate slow path
  • AVRT (bypass tract and AV node): ablate bypass tract
  • A flutter (around tricuspid annulus): ablate cavo-tricuspid isthmus
  • monomorphic VT (around a ventricular scar): ablate region around scar
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19
Q

Class I a-a

A
  • Na channel blockers

- use dependent effects: greater effect with faster hr

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20
Q

Class IA

A
  • Na and K channel blockade
  • intermediate binding and dissociation properties
  • WPW
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21
Q

Class IB

A
  • rapid binding and dissociation properties

- V tach

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22
Q

Class IC

A
  • slow binding and dissociation

- A fib with structurally normal heart

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23
Q

Class I effects

A
  • QRS widens

- phase 0 slope decreases

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24
Q

Class III

A
  • K channel blockers
  • reverse use dependent effects: greater effect at slower hr
  • A fib/flutter when heart is structurally abnormal
  • V fib/tach to reduce ICD discharge frequency
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25
Q

Class III effects

A
  • QT lengthens

- phase 3 duration increases

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26
Q

Class II

A
  • beta blockers
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27
Q

Class IV

A
  • Ca channel blockers
  • non-dihydropyridine (type 1): block AV node, SVT
  • dihydropyridine (type 2): htn, chronic stable angina
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28
Q

proarrhythmia: precipitation of life threatening ventricular arrhythmias

A
  • Class III (prolonged QT -> early afterdepolarization (EAD)
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29
Q

proarrhythmia: exacerbation of bradycardia

A
  • AV node blockers: Class II and Class IV non-dihydropyridine
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30
Q

proarrhythmia: worsening of BBB

A
  • Class I
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31
Q

types of vascular disease

A
  • arterial obstructive: atherosclerosis/thrombosis, vasospasm, fibro-muscular-dysplasia, inflammation, embolism
  • arterial wall dilation and aneurysms formation
  • arterial wall dissection
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32
Q

Natural compensation for reduced blood flow

A
  • collateral artery formation
  • dilation of distal arterioles
  • reduced tissue metabolism
  • increased O2 extraction
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33
Q

low perfusion pressure results from:

A
  • hypotension

- congestion

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34
Q

high resistance results from:

A
  • decreased lumen radius (blockage or vasospasm)
  • longer blockades
  • increased viscosity
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35
Q

ASCVD risk factors

A
  • dyslipidemia
  • DM
  • htn
  • smoking
  • family hx
  • obesity/sedentary
  • male
  • age
  • lipoprotein a
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36
Q

statin function

A
  • HMG-CoA reductase inhibitors (block key step in cholesterol synthesis)
  • effectively lower LDL-C
  • consistent morbidity/mortality improvement
  • low cost formulations
  • secondary and primary prevention
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37
Q

other cholesterol drugs

A
  • PCSK9 inhibitors and ezetemibe: lower LDL-C

- fish oil, fibrates, niacin: lower tryglycerides and raise HDL-C

38
Q

platelet inhibition

A
  • aspirin blocks COX to reduce prostaglandin met (reduce thromboxane-mediated platelet aggregation)
  • P2Y12 receptor blockers prevent ADP-mediated platelet aggregation
  • dual antiplatelet therapy for stent thrombosis
39
Q

ASCVD clinical manifestations

A
  • CAD: angina (stable vs. acute), dyspnea
  • carotid: TIA or stroke
  • aortoiliac: butt/leg claudication, impotence
  • superficial femoral: calf claudication
  • tibial: calf claudication, ischemic foot ulceration/gangrene
40
Q

causes of decreased O2 delivery

A
  • decreased perfusion pressure
  • increased coronary artery resistance (blockage)
  • increased microvascular resistance (wall hypertrophy)
  • decreased blood O2
41
Q

causes of increased O2 demand

A
  • tachycardia
  • increased contractility
  • increased LV wall stress
  • ventricular hypertrophy
42
Q

nitrates

A
  • main: venodilation to lower preload
  • arterial dilation for short-lived increase in coronary blood flow
  • tolerance can develop
  • interaction w/ PDE5 inhibitors: extreme vasodilation/hypotension
43
Q

nitrates: effect on demand

A
  • good: decrease preload, decrease after load
  • bad: reflex tachycardia, increased inotropy
  • net: reduced myocardial O2 demand
44
Q

beta blockers

A
  • reduce resting and exercise hr, contractility, co, and bp
  • improve exercise tolerance and reduce anginal attack frequency
  • useful when SNS heightened
45
Q

beta blockers: effect on demand

A
  • good: reduce hr, bp (afterload), contractility
  • bad: increase wall tension acutely when lv dysfunction present
  • net: reduce myocardial O2 demand
46
Q

non-dihydropyridine Ca channel blockers

A
  • negative inotrope and chronotrope properties
  • moderately potent vasodilators, effective in mild to moderate htn
  • block AV node
47
Q

dihydropyridine Ca channel blockers

A
  • greater effect on vascular smooth muscle
  • devoid of electrophysiological myocardial effects (no AV node effect)
  • great for htn
48
Q

Ca channel blockers: effect on demand

A
  • good: reduce hr, bp (afterload), contractility
  • bad: reduce contractility, AV node block
  • net: reduce myocardial O2 demand
49
Q

Type I MI

A
  • acute thrombotic occlusion of coronary artery
50
Q

Type II MI

A
  • O2 supply inadequate due to increased demand in setting of fixed blockage, vasospasm, supply-demand imbalance
51
Q

coronary syndromes show

A
  • troponin rise and fall
52
Q

STEMI

A
  • acute thrombotic coronary artery occlusion
53
Q

NSTEMI/UAP

A
  • subacute coronary artery occlusion

- demand ischemia or sub-occlusive coronary thrombus

54
Q

acute MI treatment

A
  • restore blood flow!
  • PCI: stent
  • thrombolytic therapy: TPA
  • surgical: CABG
55
Q

in-hospital MI complications

A
  • cardiac arrest (VT/VF)
  • CHF
  • cardiogenic shock
  • ruptured papillary muscle
  • ruptured iv septum
  • ventricular free wall rupture
  • pseudoaneurysm
  • aneurysm
56
Q

long term post MI complications

A
  • progressive CAD leading to another MI (statin, aspirin, revascularization)
  • systolic dysfunction leading to CHF (ACEi, beta blocker, mineralocorticoid receptor blocker)
  • scar leading to VT/VF (defibrillator)
57
Q

limb threatened ischemia

A
  • pulselessness
  • pallor
  • pain
  • paralysis
  • paresthesia
  • immediate attention
58
Q

therapy for chronic claudication

A
  • behavior modification
  • pletal: vascular smooth muscle dilation
  • statin
  • surger: angioplasty/stent, bypass
59
Q

acute ischemia: aortoiliac occlusion

A
  • rare
  • limb ischemia, acute abdominal pain
  • treatment: revascularization
  • poor prognosis
60
Q

acute ischemia: infrainguinal occlusion

A
  • more common
  • often embolic
  • treatment: remove emboli, bypass
  • good prognosis if treated early
61
Q

AAA triad

A
  • abdominal/back pain
  • hypotension
  • pulsatile abdominal mass
62
Q

arterial dissection

A
  • spontaneous disruption of intima
  • false channel created in wall of aorta
  • can occlude branch vessels or lead to rupture
  • aorta, carotid arteries, coronary arteries
63
Q

aortic dissection: type A

A
  • involve ascending aorta
  • may cause aortic valve insufficiency and pericardial effusion
  • urgent surgical repair
64
Q

aortic dissection: Type B

A
  • involves descending aorta only
  • usually just beyond left subclavian
  • medical therapy
  • surgery only for critical tissue loss
65
Q

TIA treatment

A
  • symptomatic: carotid endarterectomy

- asymptomatic: repair when stenosis >75%

66
Q

aortic valve stenosis

A
  • pressure overload
  • systolic murmur
  • concentric LV hypertrophy
  • etiology by age: early - bicuspid, mid - rheumatic, late senile
67
Q

aortic valve regurgitation

A
  • volume overload
  • diastolic murmur
  • eccentric LV hypertrophy
  • valve etiology: congenital, rheumatic, endocarditis, trauma
  • aortic root dilation etiology: Marfan, cystic medial necrosis, htn
68
Q

mitral stenosis

A
  • rheumatic fever
  • diastolic murmur
  • increased LA pressure to maintain LV filling
  • pathology: inflammation and fibrosis, calfication
  • valve replacement or balloon dilation
69
Q

mitral regurgitation

A
  • rheumatic fever, prolapse, endocarditis, LV dilation
  • systolic murmur
  • LV dilation from volume overload
  • afterload reduction and diuretics
  • valve replacement or repair
70
Q

systolic HF

A
  • reduced ejection fraction

- reduced contractility due to loss of functional myocardium, dilated LV

71
Q

diastolic HF

A
  • preserved ejection fraction
  • LV hypertrophy with abnormal diastolic relaxation
  • increased myocardial stiffness requiring increased pressure
72
Q

restrictive cardiomyopathy

A
  • myocardial infiltration with foreign protein/process
73
Q

amyloid cardiomyopathy

A
  • abnormal proteins infiltrate myocardium -> stiff and decreased compliance
  • LV wall thickened, normal LV volume
  • slightly reduced EF
  • R HF
74
Q

correctable causes of HF

A
  • MI from CAD
  • pressure overload
  • volume overload
  • prolonged tachycardia
  • hypo or hyperthyroid disease
75
Q

chronic treatment for HF

A
  • ACEi, angiotensisn receptor blockers, beta blockers, mineralocorticoid receptor blockers
  • ICD
76
Q

acute treatment of HF

A
  • diuretics
  • vasodilators
  • inotropic agents
  • O2
  • ventricular assist devices
  • transplantation
77
Q

types of shock

A
  • hypovolemic: low preload
  • cardiogenic: decreased contractility
  • septic: vasodilation/dehydration
  • obstructive: physical blockage
78
Q

shock definition

A
  • life threatening oxygen and nutrient deficit that impairs tissue function
79
Q

ASD VSD differentiation

A
  • check oxygen levels in RA vs RV
80
Q

patent foramen ovale is a type of ____ and can cause ____.

A
  • ASD

- paradoxical embolus

81
Q

indication for ASD closure

A
  • symptoms
  • size, direction
  • Qp:Qs (>2:1)
  • RV enlargement
  • pulmonary htn
  • arrrhythmias
82
Q

ASD

A
  • fixed split S2, flow murmur and RV heave

- women

83
Q

VSD

A
  • systolic murmur and palpable thrill

- most membranous

84
Q

PDA

A
  • continuous murmur during systole and diastole
  • women
  • maternal rubella and lithium
85
Q

Eisenmenger’s syndrome

A
  • increased pvr (from arterial remodeling) causes shunt reversal
  • Qp < Qs
  • cyanosis, death, polycythemia, hyperviscosity, paradoxical embolus, arrhythmia, hemoptysis, clubbing
86
Q

blue babies

A
  • Qp < Qs
  • tetralogy of fallot
  • tricuspid atresia
  • single ventricle
  • D-transposition of great arteries
  • generally need surgery
87
Q

pink babies

A
  • Qp > Qs
  • ASD
  • VSD
  • PDA
  • generally no surgery until Qp:Qs > 2:1, pulmonary htn, symptoms
88
Q

coarctation of aorta

A
  • males
  • LV pressure overload
  • distal to subclavian: arm bp&raquo_space; leg bp
  • assoc: bicuspid aortic valve, PDA
  • may cause aortic dissection
  • intervention: gradient > 20-30 mmHg, htn and lvh, leg fatigue, collateral arteries
89
Q

pericardial disease

A
  • pericarditis
  • pericardial hemorrhage (aortic dissection, trauma)
  • neoplasm (malignant pericardial effusion)
90
Q

pericarditis

A
  • sharp chest pain worse with inspiration, better with leaning forward
  • ECG: ST elevation w/o occlusion
  • friction rub
  • treatment: nsaids
91
Q

tamponande

A
  • pericardial fluid pressure compresses RA and RV during diastole
  • absent Y descent
  • equal diastolic filling pressures
  • idiopathic, viral, malignancy
  • hypotension and shock
  • treatment: drainage
92
Q

pericardial constriction

A
  • rapid early diastolic filling from scar tissue/calcification
  • pronounced Y descent, Kussmaul
  • chronic infection, radiation
  • severe fluid overload
  • treatment: surgical stripping

Cardio (4 decks)

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