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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
Class III effects
- QT lengthens | - phase 3 duration increases
26
Class II
- beta blockers
27
Class IV
- Ca channel blockers - non-dihydropyridine (type 1): block AV node, SVT - dihydropyridine (type 2): htn, chronic stable angina
28
proarrhythmia: precipitation of life threatening ventricular arrhythmias
- Class III (prolonged QT -> early afterdepolarization (EAD)
29
proarrhythmia: exacerbation of bradycardia
- AV node blockers: Class II and Class IV non-dihydropyridine
30
proarrhythmia: worsening of BBB
- Class I
31
types of vascular disease
- arterial obstructive: atherosclerosis/thrombosis, vasospasm, fibro-muscular-dysplasia, inflammation, embolism - arterial wall dilation and aneurysms formation - arterial wall dissection
32
Natural compensation for reduced blood flow
- collateral artery formation - dilation of distal arterioles - reduced tissue metabolism - increased O2 extraction
33
low perfusion pressure results from:
- hypotension | - congestion
34
high resistance results from:
- decreased lumen radius (blockage or vasospasm) - longer blockades - increased viscosity
35
ASCVD risk factors
- dyslipidemia - DM - htn - smoking - family hx - obesity/sedentary - male - age - lipoprotein a
36
statin function
- 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
37
other cholesterol drugs
- PCSK9 inhibitors and ezetemibe: lower LDL-C | - fish oil, fibrates, niacin: lower tryglycerides and raise HDL-C
38
platelet inhibition
- 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
ASCVD clinical manifestations
- 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
causes of decreased O2 delivery
- decreased perfusion pressure - increased coronary artery resistance (blockage) - increased microvascular resistance (wall hypertrophy) - decreased blood O2
41
causes of increased O2 demand
- tachycardia - increased contractility - increased LV wall stress - ventricular hypertrophy
42
nitrates
- 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
nitrates: effect on demand
- good: decrease preload, decrease after load - bad: reflex tachycardia, increased inotropy - net: reduced myocardial O2 demand
44
beta blockers
- reduce resting and exercise hr, contractility, co, and bp - improve exercise tolerance and reduce anginal attack frequency - useful when SNS heightened
45
beta blockers: effect on demand
- good: reduce hr, bp (afterload), contractility - bad: increase wall tension acutely when lv dysfunction present - net: reduce myocardial O2 demand
46
non-dihydropyridine Ca channel blockers
- negative inotrope and chronotrope properties - moderately potent vasodilators, effective in mild to moderate htn - block AV node
47
dihydropyridine Ca channel blockers
- greater effect on vascular smooth muscle - devoid of electrophysiological myocardial effects (no AV node effect) - great for htn
48
Ca channel blockers: effect on demand
- good: reduce hr, bp (afterload), contractility - bad: reduce contractility, AV node block - net: reduce myocardial O2 demand
49
Type I MI
- acute thrombotic occlusion of coronary artery
50
Type II MI
- O2 supply inadequate due to increased demand in setting of fixed blockage, vasospasm, supply-demand imbalance
51
coronary syndromes show
- troponin rise and fall
52
STEMI
- acute thrombotic coronary artery occlusion
53
NSTEMI/UAP
- subacute coronary artery occlusion | - demand ischemia or sub-occlusive coronary thrombus
54
acute MI treatment
- restore blood flow! - PCI: stent - thrombolytic therapy: TPA - surgical: CABG
55
in-hospital MI complications
- cardiac arrest (VT/VF) - CHF - cardiogenic shock - ruptured papillary muscle - ruptured iv septum - ventricular free wall rupture - pseudoaneurysm - aneurysm
56
long term post MI complications
- 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
limb threatened ischemia
- pulselessness - pallor - pain - paralysis - paresthesia * immediate attention
58
therapy for chronic claudication
- behavior modification - pletal: vascular smooth muscle dilation - statin - surger: angioplasty/stent, bypass
59
acute ischemia: aortoiliac occlusion
- rare - limb ischemia, acute abdominal pain - treatment: revascularization - poor prognosis
60
acute ischemia: infrainguinal occlusion
- more common - often embolic - treatment: remove emboli, bypass - good prognosis if treated early
61
AAA triad
- abdominal/back pain - hypotension - pulsatile abdominal mass
62
arterial dissection
- 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
aortic dissection: type A
- involve ascending aorta - may cause aortic valve insufficiency and pericardial effusion - urgent surgical repair
64
aortic dissection: Type B
- involves descending aorta only - usually just beyond left subclavian - medical therapy - surgery only for critical tissue loss
65
TIA treatment
- symptomatic: carotid endarterectomy | - asymptomatic: repair when stenosis >75%
66
aortic valve stenosis
- pressure overload - systolic murmur - concentric LV hypertrophy - etiology by age: early - bicuspid, mid - rheumatic, late senile
67
aortic valve regurgitation
- volume overload - diastolic murmur - eccentric LV hypertrophy - valve etiology: congenital, rheumatic, endocarditis, trauma - aortic root dilation etiology: Marfan, cystic medial necrosis, htn
68
mitral stenosis
- rheumatic fever - diastolic murmur - increased LA pressure to maintain LV filling - pathology: inflammation and fibrosis, calfication - valve replacement or balloon dilation
69
mitral regurgitation
- rheumatic fever, prolapse, endocarditis, LV dilation - systolic murmur - LV dilation from volume overload - afterload reduction and diuretics - valve replacement or repair
70
systolic HF
- reduced ejection fraction | - reduced contractility due to loss of functional myocardium, dilated LV
71
diastolic HF
- preserved ejection fraction - LV hypertrophy with abnormal diastolic relaxation - increased myocardial stiffness requiring increased pressure
72
restrictive cardiomyopathy
- myocardial infiltration with foreign protein/process
73
amyloid cardiomyopathy
- abnormal proteins infiltrate myocardium -> stiff and decreased compliance - LV wall thickened, normal LV volume - slightly reduced EF - R HF
74
correctable causes of HF
- MI from CAD - pressure overload - volume overload - prolonged tachycardia - hypo or hyperthyroid disease
75
chronic treatment for HF
- ACEi, angiotensisn receptor blockers, beta blockers, mineralocorticoid receptor blockers - ICD
76
acute treatment of HF
- diuretics - vasodilators - inotropic agents - O2 - ventricular assist devices - transplantation
77
types of shock
- hypovolemic: low preload - cardiogenic: decreased contractility - septic: vasodilation/dehydration - obstructive: physical blockage
78
shock definition
- life threatening oxygen and nutrient deficit that impairs tissue function
79
ASD VSD differentiation
- check oxygen levels in RA vs RV
80
patent foramen ovale is a type of ____ and can cause ____.
- ASD | - paradoxical embolus
81
indication for ASD closure
- symptoms - size, direction - Qp:Qs (>2:1) - RV enlargement - pulmonary htn - arrrhythmias
82
ASD
- fixed split S2, flow murmur and RV heave | - women
83
VSD
- systolic murmur and palpable thrill | - most membranous
84
PDA
- continuous murmur during systole and diastole - women - maternal rubella and lithium
85
Eisenmenger's syndrome
- increased pvr (from arterial remodeling) causes shunt reversal - Qp < Qs - cyanosis, death, polycythemia, hyperviscosity, paradoxical embolus, arrhythmia, hemoptysis, clubbing
86
blue babies
- Qp < Qs - tetralogy of fallot - tricuspid atresia - single ventricle - D-transposition of great arteries * generally need surgery
87
pink babies
- Qp > Qs - ASD - VSD - PDA * generally no surgery until Qp:Qs > 2:1, pulmonary htn, symptoms
88
coarctation of aorta
- males - LV pressure overload - distal to subclavian: arm bp >> leg bp - assoc: bicuspid aortic valve, PDA - may cause aortic dissection - intervention: gradient > 20-30 mmHg, htn and lvh, leg fatigue, collateral arteries
89
pericardial disease
- pericarditis - pericardial hemorrhage (aortic dissection, trauma) - neoplasm (malignant pericardial effusion)
90
pericarditis
- sharp chest pain worse with inspiration, better with leaning forward - ECG: ST elevation w/o occlusion - friction rub - treatment: nsaids
91
tamponande
- 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
pericardial constriction
- rapid early diastolic filling from scar tissue/calcification - pronounced Y descent, Kussmaul - chronic infection, radiation - severe fluid overload - treatment: surgical stripping

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