Week 3 Flashcards
(162 cards)
1
Q
three mechanisms of tachycardias
A
- reentry
- automaticity
- triggered activity (early or delayed after depolarizations)
2
Q
AVNRT
A
slow accessory pathway in AV node. initiated by a perfectly times beat when fast pathway hasn’t recovered yet–so slow pathway propagates it to QRS. when fast pathway recovers, it flows backwards to generate an inverted p wave that then goes back down slow pathway= restarts the cycle
3
Q
WPW
A
accessory pathway between atrium/ventricle leads to ventricular pre-excitation=slow cell to cell conduction down this pathway during AVN delay
4
Q
WPW on ECG
A
delta wave due to slow ventricular pre-excitation=wide QRS
5
Q
AVRT
A
Premature atrial complex (PAC) hits when accessory complex hasn’t recovered=goes down AVN, then travels backwards up the accessory pathway=cycle
6
Q
AVRT on ECG
A
QRS with delta wave, followed by PAC, followed by normal QRS, followed by narrow tachycardia with inverted p waves
7
Q
monomorphic ventricular tachycardia
A
scar related, reentrant tachy. cycles around fibrotic myocytes that act as slow conduction pathway.
8
Q
atrial flutter
A
re-entrance circuit spins around tricuspid valve and RA
9
Q
atrial flutter on ECG
A
saw tooth pattern in II, III, avF
10
Q
2:1 atrial flutter
A
HR=150, 2 saw tooth p waves for each QRS
11
Q
types of re-entry tachycardia
A
AVNRT, AVRT, monomorphic ventricular tachycardia, atrial flutter
12
Q
automaticity in regards to tachycardias
A
tissue other than the SAN develops a more rapid phase four upstroke and becomes the dominant pacemaker
13
Q
two types of automaticity induced tachycardia
A
- atrial tachycardia
2. sinus tachycardia
14
Q
atrial tachycardia
A
a focal (single or multiple) tachycardia originating in atrial muscle
15
Q
sinus tachycardia
A
almost always a physiological reaction
16
Q
delayed after depolarizations
A
due to spontaneous Ca release from SR=increases the Vm so it is easier to reach AP threshold. occur during repolarization phase
17
Q
early after depolarizations
A
occur during plateau phase of AP, particularly susceptible with prolonged plateau (long QT) (decreased HR)
18
Q
the arrhythmia associated with EADs
A
torsade de pointes
19
Q
torsade de pointes
A
twisting around baseline. AEDs cause premature QRS without p waves.
20
Q
atrial fibrillation
A
initiated by automaticity tachy near pulmonary veins. maintained by multiple wavelet re-entry
21
Q
a fib on ECG
A
undulation of baseline with irregularly irregular QRSs. no p waves. BAG OF WORMS
22
Q
why does a fib present with irregular irregularities in the QRSs?
A
the AVN protects the heart by not allowing every atrial wave to pass through.
23
Q
ventricular fibrillation
A
multiple wavelet reentry in the ventricle. people drop dead from this :(
24
Q
v fib on ECG
A
QRS complex replaces with disorganized, low amplitude activity
25
definition of tachycardia
HR>100 bpm
26
where do you measure the mixed venous blood o2 saturation?
at the PA
27
how can the body respond to increasing demand for O2?
increase the AVO2 extraction (increase tissue o2 delivery) or increase the CO (increase O2 transport)
28
limitations to increasing AVO2 extraction
basal extraction is 25% and the lowest achievable venous sat is 20% so at most can get around 85% extraction
29
limitations to increasing CO?
peak HR=220-age, peak SV=2x resting SV
30
why does SVR decrease during exercise?
need to get O2 to the skeletal muscles
31
what ultimately limits the maximum exercise capacity?
reaching anaerobic threshold-the ceiling on O2 delivery for aerobic metabolism
32
why does one become dyspneic at higher METs?
in anaerobic metabolism, muscles produce lactate, which leads to the release of CO2, which stimulates the respiratory drive to try to blow off as much as possible
33
effect of high altitude on exercise performance
arterial O2 sat is decreased, leading to less O2 transport
34
how do highly trained athletes increase CO during exercise?
higher basal SV & reserve due to heart remodeling (eccentric LVH)=increased CO
35
beta blockers effect on exercise
attenuate the ability to raise HR=limits the CO
36
effect of HF on exercise
impaired ability to generate SV=CO is substantially reduced=must rely more on AVO2D to respond to increasing demand=very limited
37
class I antiarrhythmic drugs
local anesthetics, Na channel blockers=delay depolarization in fast tissues to decrease excitability and conduction velocity
38
class II antiarrhythmic drugs
beta blockers (Ca, K, Funny channels)--decrease amount of Ca
39
class III anti arrhythmic drugs
K channel blockers=APD is prolonged, ERP prolonged in fast tissues--no effect on excitability
40
class IV antiarrhytmic drugs
Ca channel blockers=decrease excitability and conduction velocity in slow tissues, decrease SAN automaticity, increase AVN ERP
41
prototype class Ia drug
procainamide
42
prototype class Ib drug
lidocaine
43
prototype class Ic drug
flecainamide
44
prototype class II drug
atenolol
45
prototype class III drug
dofetilide
46
prototype class IV drug
verapamile
47
which anti-arrhythmic drugs predominantly affect AV muscle and the His Purkinje system?
Class I and III
48
what has the main effect on ERP in fast tissues?
changes in APD (which is prolonged by K channel blockers, so classes I and III can increase it in fast tissue)
49
what has the main effect on ERP in slow tissues?
the number of Ca channels active (which is reduced in class II, IV, digoxin, adeosine=ability to increase it in slow tissue)
50
potency of class I anti-arrhythmics
Ic>Ib>Ia
51
what factors increase the potency of class I anti-arrhythmics
more potent in cells with depolarized Vm and with increased HR
52
what factors increase the affect of K channel blocking?
enhanced at slow HR and in hypokalemia (beneficial effects are decreased in times of tachycardia)
53
conditions needed for reentry
potential pathway, unidirectional block, slow conduction
54
how can you treat a single fixed circuit reentry tachy?
1. decrease excitability via class I drugs
| 2. increase ERP via class Ia or III drugs
55
how can you treat monomorphic ventricular tachycardia following MI
decrease excitability via Ia/c drugs, prolong ERP via Ia/III, implantable defibrillator
56
drug of choice to stop AVNRT
adenosine
57
how do you treat a multiple shifting waveform reentry tachy?
increase the wavelength by increasing the ERP or the conduction velocity
58
treatment for a. fib
1. decrease ventricular rate by increasing the AVN ERP (atenolol, class IV, digoxin)
2. terminate fibrillation by incrusting atrial ERP (class Ia/III)
59
torsades de pointes on ECG
twisting. long QTs followed by PVCs
60
how to treat torsade de pointes
remove class Ia and III drugs. give isoproterenol to increase HR
61
risk of using antiarrhythmic drugs in case of long QT with hypokalemia
torsade de points with class Ia/III
62
risk of using anti-arrhythmic drugs with a sick sinus node
worsen sinus bradycardia with class II, digoxin, adenosine
63
risk of using anti-arrhythmic drugs with AV block
higher degree block with class II/IV.
64
risk of using anti arrhythmic drugs with poor systolic function
class I, II, IV are negative inotropes
65
parasympathetic muscarinic antagonists
scopolamine and atropine
66
beta 1 antagonist effects
decrease HR, increase refractoriness & conduction, decrease inotropy, inhibit renin release
67
alpha antagonist effects
vasodilation
68
main effects of beta blockers
decrease HR, impulse conduction, negative inotropy
69
would you give someone in cardiogenic shock a beta blocker?
no because he most importantly needs inotropic support & beta blockers are all negative inotropes
70
would you give someone in stable CHF beta blockers?
yes. etiology is increased RAAS and SNS activation so they would be helpful
71
would you treat someone in complete heart block with beta blockers?
nope. they need as much contraction as possible. don't want to cause further block
72
would you give someone with recent MI or coronary artery disease or chronic stable angina beta blockers?
yes. they improve the O2 supply by decreasing HR and increasing diastole. they also decrease the demand by decreasing contractility.
73
what is the fundamental problem in hypertension?
increased SVR
74
what is the most important ion in hypertension
Na
75
what is the principle role of the kidneys in the pathogenesis of hypertension?
inadequate secretion of Na and water=abnormal regulation of SVR
76
risk factors for hypertension
first degree relative with it, obesity, high dietary sodium uptake
77
two groups of hypertension
primary/essential and secondary
78
types of essential hypertension
resistance and compliance
79
physiologic consequence of hypertension on LV
must generate a higher systolic pressure for the increased after load (SVR)=increased systolic stress=diastolic/concentric LVH=fibrosis=decreased diastolic compliance (HFpEF)
80
physiologic consequence of hypertension on arterial system
must contain the greater P from the LV=increased wall stress=aneurysms/atherosclerosis/arteriolar disease=further increase in SVR (vicious cycle)
81
physiologic consequence of hypertension on the kidney
destroyed via arteriolar disease=decreased ability to excrete Na=further compounds the problem
82
symptoms of hypertension
NONE
83
normal BP
SBP <80
84
prehypertension BPs
SBP 120-139, DBP 80-89
85
stage 1 hypertension BP
SBP 140-159, DBP 90-99
86
stage 2 hypertension BPs
SBP >160, DBP>100
87
mechanisms which should prevent the development of hypertension
baroreceptor reflex, pressure-natriuresis, RAAS
88
rice diet
hospitalized severely hypertensive patients fed diet virtually free of Na=dramatic reductions of BP with resolution of many abnormalities
89
what is natriuretic hormone?
NaK ATPase inhibitor (like digitalis). NOT a natriuretic peptide
90
fuel of hypertension?
in genetically predisposed individuals, increased dietary sodium intake is likely the driver
91
benign hypertension
DBP>90, SBP>140. clinically silent until late in the course
92
malignant hypertension
de novo or follows benign hypertension by 8 yrs, DBP>120, SBP>210, symptomatic, lethal
93
vascular changes associated with hypertension
acceleration of other vascular diseases (atherosclerosis, hyalin arteriosclerosis) and unique adaptive and destructive changes
94
which diseases does hypertension accelerate?
atherosclerosis & hyalin arteriosclerosis
95
atherosclerosis and hypertension
usually associated with hyperlipidemia/diabetes, etc. accelerated. large and medium arteries.
96
hyaline arteriosclerosis
accelerated in hypertension. lumenal deposition of plasma proteins due to endothelial leakage and increased synthesis of ECM (collagen)--pronounced in the kidneys
97
adaptive changes due to benign hypertension
reversible: arteriolar vasoconstriction, medial hypertrophy
irreversible: fibroelastic intimal hyperplasia (usually in renal arteries)
98
consequence of irreversible changes in hypertension?
fixed increase in SVR (makes treatment more difficult)
99
destructive changes due to malignant hypertension
fibrinoid necrosis, hyperplastic arteriolitis, microangiopathic hemolytic anemia
100
fibrinoid necrosis
deposition of fibrin in the walls of arterioles, necrosis of endothelial cells and medial smooth muscle
101
hyperplastic intimal arteriolitis
concentric proliferation of smooth muscle cells and interstitial proteoglycan deposition in small arteries (onion skinning). occurs when fibrinoid necrosis heals-driven by PDGF
102
microangiopathic hemolytic anemia
shearing of RBCs (resulting in schistocytes) by passage through fibrin mesh at increased pressures within the lumen of arterioles
103
cardiac effects of benign hypertension
concentric LVH due to increased P=increased energy demand>supply (augmented by acceleration of CAD)=ischemia=atrophy/fibrosis=decreased compliance=angina&CHF
104
renal effects of benign hypertension
nephroarteriosclerosis=bilateral symmetric decrease in size with reduced cortex, granular surface, fibrosis of glomeruli & tubular atrophy=chronic renal failure=further aggravates hypertension (decreased GFR=decreased Na excretion)
105
cerebral effects of benign hypertension
micro aneurysms that might rupture and lead to intracerebral hemorrhage (also in retina), ischemic strokes due to atherosclerotic acceleration, enlargement of congenital berry aneurysms (rupture would=subarachnoid hemorrhage)
106
renal effects of malignant hypertension
nephrosclerosis, cortical hemorrhages, infarction
107
adrenal effects of malignant hypertension
cortical hyperplasia
108
cerebral effects of malignant hypertension
edema, increased ICP, retinal hemorrhage and papilledema
109
causes of death from malignant hypertension
acute renal failure, stroke, acute CHF (+/- MI)
110
renal cause of secondary HTN?
renal artery stenosis can be cause: atherosclerosis in older patients (usually proximal renal artery) or fibromuscular dysplasia in young women (middle to distal renal artery)
111
aneurysm
localized dilation of a blood vessel, usually an artery. saccular or fusiform.
112
what causes aneurysms?
localized structural weakening of a vessel wall
113
berry aneurysms
saccular aneurysms of branch points in circle of willis. usually related to congenital weakenings in the arterial wall
114
atherosclerotic aneurysm
occur because of acquired weakening of the arterial wall by atherosclerosis--most frequent cause of aortic aneurysms
115
how can aneurysms cause symptoms?
mass effect, distal embolization, rupture
116
where do dissecting hematomas (aneurysm) occur?
in the aortic media
117
pathogenesis of dissection
progressive deterioration of elastic fibers and muscle in aortic media (medial degeneration)=dilation of arteries and disruption of vasa vasorum, which hemorrhage into the media and propagate
118
marfans syndrome
defect in fibrillin 1 (a scaffold for elastic fibers)-more at risk for dissections
119
what initiates a dissection?
bc of shear forces from LV contractions, the vasa vasorum rupture within a weakened media and extension of the hematoma in either direction.
120
exit site of dissection
most often an intimal tear in ascending aorta just above valve. not always present.
121
reentry site of dissection
usually distal, where hematoma can enter aorta. creates a double barrel aorta
122
treatment for dissection
replace the involved portion of the aorta. drugs that decrease bp and LV force (beta blockers)
123
symptoms of dissection
pain (tearing, migratory chest to back), loss of pulse (right side, left carotid (stroke), followed by left arm), rupture (cardiac tamponade)
124
what activates renin?
1. hypovolemia
2. hyponatremia
3. hypotension
4. adrenergic activation
125
role of renin
enzyme that converts angiotensinogen to AG1
126
role of ACE
enzyme that converts AG1 to AG2
127
which protein in the RAAS system has the important systemic effects?
AG2
128
AT1
receptors that propagate the bp raising properties of AG2. located throughout body. causes vasoconstriction, aldosterone release, cell proliferation/matrix deposition/hypertrophy
129
AT2
receptors that are located in uterus and fetus. cause vasodilation. usually overpowered by the effect of AT1
130
AG2 effects in the CNS
- central pressor response due to SNS activation
- release of ADH, ACTH
- thirst and Na appetite
131
AG2 effects on the PNS
-amplifies the SNS (increases release and decreases uptake of NE and enhances sensitivity to it in tissues=vasoconstriction)
132
AG2 effects on adrenal medulla
causes release of catecholamines (NE/E) from chromatin cells
133
AG2 effects on adrenal cortex
stimulates synthesis and release of aldosterone
134
AG2 effects on kidney
- antidiuresis, antinatriuresis
- reduces GFR
- inhibits renin release via negative feedback
135
implication of AG2 vasoconstriction
increases SVR=hypertension
136
implication of AG2 mitotic activity
LVH
137
implication of AG2 pro-inflammatory properties
- induces oxidation of LDL=increased capacity to uptake it into cells=plaque growth=atherosclerosis
- overexpression of VCAM, IL6 (also promote atherosclerosis)
138
beta blockers and RAAS
eliminate one of the activating pathways for renin
139
direct renin inhibitors
work at the RLS. don't really improve clinical function
140
limitations of ACE inhibitors
- there are alternate pathways for production (angiotensinogen straight to AG2), which causes ACE escape over time
- ACE is nonspecific-also inhibits bradykinin so when inhibited, get toxicity from bradykinin accumulation (cough, angioedema)
141
ARBs
AT1 selective blockers. lower bp. but don't get any potential possible effects of bradykinin vasodilation. but also don't get ACEi side effects (cough, angioedema)
142
neuroendocrine reflex
compensatory mechanism that works to maintain bp homeostasis (annoying when we administer drugs to decrease bp, since it works to raise it right back up)
143
components of the neuroendocrine reflex
decreased bp is sensed=SNS activations to increase HR/contractility/CO/SVR && RAAS system is activated to increase AG2=increase SVR and aldosterone (fluid retention)
144
function of cardiac valves
ensure unidirectional flow, maintain pressure gradients and cardiac cycle timing
145
what drives cardiac valves?
mechanical forces exerted by blood and heart
146
valve stenosis
results in increased pressure load of upstream chambers, impairs the ability to increase CO, a chronic disorder
147
valve regurgitation
results in increased volume load of up&downstream chambers. acute or chronic, doesn't impair CO bc SV can be repartitioned
148
what type of wall stress causes mitral regurgitation?
increased diastolic wall stress
149
what type of wall stress causes aortic regurgitation?
increased systolic and diastolic wall stress
150
effects of decreasing valve orifice size
requires increased velocity (continuity equation) to achieve same flow rate, which increases the pressure gradient (bernouilli equation)= the upstream chamber has a pressure load
151
bernouille equation
pressure proportional to velocity^2 (think of it as a conservation of energy equation)
152
continuity equation
flow rate will remain contestant throughout the pipe since it is determined by CO. velocity inversely proportional to CSA
153
why doesn't the LVH work well as a cardiac adaptation in aortic stenosis?
- coronary circulation can't meet the demands of an increased mass
- decreased function leads to fibrosis=decreased diastolic compliance=greater filling pressures required
154
cardiac adaptation to aortic stenosis?
LVH
155
decompensation in aortic stenosis?
- angina pectoris (disparity of supply/demand), effort related syncope (inadequate CO elevation), CHF
- appearance of symptoms means that LVH is failing as an adaptation and patient is in big trouble
156
three layers of each valve
1. fibrosa-distal surface (continuous with annulus fibrosa and chordae tendonae)-provides structural integrity
2. spongiosa- loose connective tissue-provides cushioning
3. ventricularis/atrialis- inflow surface-rich in elastic fibers-provides recoil
157
vascularization of valves?
NOT vascularized
158
what is required for reentrant tachycardia to develop?
more than one electrical pathway, differential conduction, unidirectional block, and a perfectly timed premature beat (NOT AN AED)
159
in AVNRT where is the p wave on the ECG?
buried within or closely associated after the QRS complex (near simultaneous depolarization of QRS and p waves)
160
where is the p wave in AVRT?
after the QRS within the ST segment
161
what decreases the risk of developing torsades de pointes?
atrial pacing to increase HR
162
what increases the risk of developing torsades de pointes?
severe hypokalemia, class Ia antiarrhythmic drugs, SAN dysfunction
