Pathophysio Review Flashcards
1
Q
sinus pause
A
- if > 3 sec, place pacemaker
- no medical therapy options
2
Q
1˚ AV block
A
- PR > 200ms
- test for lyme disease
- no therapy if asymptomatic
- watch AV blocker meds
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
4
Q
2˚ Mobitz II AV block
A
- fixed PR interval then non-conducted
- never physiologic
- stop AV blocking drugs
- pacemaker
5
Q
3˚ AV block w/ narrow QRS
A
- high AV node escape rhythm
- stop AV blocker meds
- pacemaker
6
Q
3˚ AV block w/ wide QRS
A
- escape rhythm below AV node, possible ventricular escape
- stop AV blocker meds
- pacemaker
7
Q
RBBB
A
- RsR pattern in V1-2 (rabbit ear)
8
Q
LBBB
A
- negative QS wave in V1
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
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
11
Q
SVT or PSVT
A
- no p waves
- ventricular rate ~160-220
- break with adenosine
- narrow QRS: avnrt
- WPW pattern: avrt
- ablation therapy
12
Q
monomorphic VT
A
- AV dissociation
- comes from one part of ventricle (prior scar likely/old MI)
- risk factor for sudden death
- ICD
13
Q
polymorphic VT
A
- check QT length
- stop any QT prolonging medication, treat ischemia, consider ICD
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
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
16
Q
Purpose of antiarrhythmics
A
- maintain sinus rhythm and prevent atrial fibrillation recurrence
- reduce frequency of ICD discharge by preventing v tach/fib
17
Q
mech of arrhythmogenesis
A
- abnormal impulse conduction (90% reentry)
- abnormal impulse generation (abnormal automaticity, triggered activity)
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
19
Q
Class I a-a
A
- Na channel blockers
- use dependent effects: greater effect with faster hr
20
Q
Class IA
A
- Na and K channel blockade
- intermediate binding and dissociation properties
- WPW
21
Q
Class IB
A
- rapid binding and dissociation properties
- V tach
22
Q
Class IC
A
- slow binding and dissociation
- A fib with structurally normal heart
23
Q
Class I effects
A
- QRS widens
- phase 0 slope decreases
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
25
Q
Class III effects
A
- QT lengthens
- phase 3 duration increases
26
Q
Class II
A
- beta blockers
27
Q
Class IV
A
- Ca channel blockers
- non-dihydropyridine (type 1): block AV node, SVT
- dihydropyridine (type 2): htn, chronic stable angina
28
Q
proarrhythmia: precipitation of life threatening ventricular arrhythmias
A
- Class III (prolonged QT -> early afterdepolarization (EAD)
29
Q
proarrhythmia: exacerbation of bradycardia
A
- AV node blockers: Class II and Class IV non-dihydropyridine
30
Q
proarrhythmia: worsening of BBB
A
- Class I
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
32
Q
Natural compensation for reduced blood flow
A
- collateral artery formation
- dilation of distal arterioles
- reduced tissue metabolism
- increased O2 extraction
33
Q
low perfusion pressure results from:
A
- hypotension
- congestion
34
Q
high resistance results from:
A
- decreased lumen radius (blockage or vasospasm)
- longer blockades
- increased viscosity
35
Q
ASCVD risk factors
A
- dyslipidemia
- DM
- htn
- smoking
- family hx
- obesity/sedentary
- male
- age
- lipoprotein a
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
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»_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
