Week 2 Flashcards
1
Q
cardiac index
A
CO normalized to body size. Nl=2.5-3.5
2
Q
what happens to the metabolism when O2 transport is inadequate?
A
it becomes anaerobic, which is unsustainable
3
Q
oxygen delivery
A
the quantity of O2 transported from the lungs to the systemic circulation per unit time
4
Q
extraction fraction
A
only a certain percent of O2 delivery can be transferred to the tissues. usually about 25%
5
Q
consequence of increasing extraction fraction
A
accompanied by compensatory decrease of pO2 in capillaries, which decreases the pressure gradient that ultimately drives the transfer
6
Q
what drives the O2 transfer from blood to tissues in the capillaries?
A
pO2 gradient
7
Q
how would you increase the extraction fraction?
A
decrease the pO2 in the capillaries in order to decrease the %Hb saturation
8
Q
maximum extraction fraction possible
A
85%, drops pO2 in caps to 15mmHg, which is the lowest possible to drive O2 into tissues
9
Q
consequences of inadequate CO at rest
A
decreased O2 delivery to satisfy tissue metabolic requirements=drop in systemic venous O2 content, capillary pO2, & pressure gradient (in attempt to increase extraction fraction)
10
Q
ultimate limitation of decreased CO
A
decreased O2 transfer rate to mitochondria=switch to anaerobic=lactic acidosis
11
Q
fick measurement of CO
A
oxygen acts as the indicator. added in lungs, concentration is measured downstream in systemic circulation
12
Q
thermal dilution measurement of CO
A
heat is measured at PA after cooled saline is injected into RA
13
Q
normal systemic venous O2 sat
A
75%
14
Q
significance of venous O2 sat
A
measures the adequacy of CO to meet metabolic requirements. bad to be low!!
15
Q
role of systemic arterial pressure
A
provides the potential energy that drives systemic blood flow to all systemic tissues
16
Q
how is the SAP principally modulated?
A
via SVR
17
Q
neural control center of SVR
A
medulla- receives and integrates pressure, volume, & chemical info
18
Q
arterial baroreceptors
A
stretch induced Ca receptors located at carotid sinus and aortic arch, fast response.
19
Q
atrial baroreceptors
A
sense atrial distension and stimulate the release of ANP–diuretic action to decrease intravascular volume
20
Q
renal baroreceptors
A
in the JGA. release renin, which leads to production of angiotensin 2=vasoconstriction and h2o/na retention
21
Q
principal determinant of local resistance
A
local metabolic rate
22
Q
ANP
A
released in response to atrial stretch
23
Q
BNP
A
released in response to ventricular stretch
24
Q
autonomic control of venous smooth muscle
A
adrenergic stimulation=constriction
muscarinic stimulation=dilation
25
ECG characteristics of LVH
increased QRS voltages (due to increased mass), inversion of T wave, neg p in V1 indicates LA hypertrophy in response to increased LAP
26
ECG characteristics of RVH
tall p wave
27
marked ST elevation
indicates MI
28
ECG indication of myocardial death after MI
initial Q waves in QRS
29
what happens on ECG when drugs is given that blocks K channels
prolonged QT>1/2RR. puts patient at risk for arrhythmias
30
what is the main effector in regards to vasoregulation?
ARTERIOLES.
31
resistance relationship to radius
R is proportional to r^4 (tiny changes in radius have huge resistance effects)
32
what regulates the arteriolar diameter?
VSMC tone, which is based on Ca concentration
33
three types of intrinsic control of VSMC tone
1. myogenic autoregulation
2. endothelium mediated auto regulation
3. metabolic mediated autoregulation
34
myogenic autoregulation
increased arterial inflow pressure=increased VSMC tone via stretch activated Ca channels
35
endothelium mediated autoregulation
increased endothelial shear stress=NO release=decreased VSMC tone
36
metabolic mediated autoregulation
increased tissue metabolic activity=release of adenosine from ATP breakdown=decreased VSMC tone
37
extrinsic VSMC tone control
via adrenergic (responsiveness varies based on tissues) and RAAS systems
38
Coronary Heart Disease (CHD)
clinical manifestations of alterations in delivery of blood supply to myocardium
39
determinants of myocardial O2 demand
myocardial wall tension, myocardial contractility, HR (anything that increases work)
40
epicardial arteries
large conductance vessels arising from the ascending aorta, primary role is conductance
41
coronary disease
obstruction of epicardial arteries
42
small penetrating coronary arteries
invisible on angiograms, source of collateral blood supply in CAD
43
intramyocardial coronary arteries
responsible for the majority of coronary vascular resistance (vascular tone regulation)
44
where in the heart are capillaries most dense?
endocardium>epicardium
45
what determines the pressure gradient within the heart?
difference between central aortic pressure (origin of coronaries, 120/80) and LVEDP (since flow occurs during diastole, 10)
46
when does coronary blood flow occur?
during diastole
47
why does coronary blood flow only during diastole?
extravascular resistance (systolic compressive forces) increase R on capillaries and limits flow (Q=P/R)
48
what is the problem with increasing HR and the coronary arteries?
with increasing HR, the diastolic time shortens, and therefore the time to deliver blood via the coronaries shortens
49
where are extravascular compressive forces strongest within the heart?
greatest on the sub-endocardial regions
50
why is the endocardium more at risk for ischemia than the epicardium?
greater extravascular compressive forces=lower coronary blood flow=more vulnerable to ischemia (so the endocardium has higher density of capillaries)
51
vascular autoregulation
resistance changes which keep flow constant in face of changing pressure (Q=P/R)
52
vasodilator reserve
the amount by which R can decrease (total amount vessels can dilate to keep flow constant to pass a stenosis or obstruction)
53
how can we test for early endothelial dysfunction?
ACh infusion-healthy endothelium will vasodilate
54
angina pectoris
chest pain due to narrowing of one or more coronary arteries (>70%)
55
how to treat angina pectoris
nitrates, anti-platelet agents, beta blockers, coronary stents, CABG
56
unstable angina
clinical syndrome of progressive chest pain or acute onset of chest pain--due to rupture of atherosclerotic plaque=platelet aggregation, thrombus, vasospasm
57
treatment for unstable angina
nitrates, anti-thrombotic agents, platelet inhibitors, stent, CABG
58
acute MI
plaque rupture and secondary thrombus and platelet accumulation resulting in complete or nearly complete occlusion of coronary vessel
59
treat acute MI
stent or thrombolysis
60
coronary artery spasm
severe, focal, reversible narrowings in epicardial arteries
61
treat coronary artery spasm
nitrates, Ca channel blockers
62
small vessel disease
poorly defined syndrome characterized by angina, no obvious narrowings in epicardial arteries, decreased vasodilator reserve
63
what is the dicrotic notch and what causes it?
notch in atrial pressure waveform at beginning of diastole. due to closure of semilunar valve and arrest of reverse flow back towards the ventricles
64
consequence of lowering aortic pressure?
inadequate perfusion to head=syncope
65
consequence of raising aortic pressure?
increases LV work (after load) and the stress of the arterial vessels
66
consequence of decreasing atrial diastolic pressure?
would decrease diastolic distention (preload) of the ventricles-- would initiate systole from a shorter myocardial length=decreased contraction=decrease SV=decreased CO
67
consequence of increasing RAP
would increase RV preload to increase SV & CO. but would also expose the venous system to excessive pressure=peripheral edema, ascites, hepatic distention & nutmeg liver
68
consequence of increasing LAP
would increase pressure in pulmonary capillaries causing pulmonary edema and impaired gas exchange
69
EDP is greater in which ventricle and why
LVEDP>RVEDP because RV is thinner walled and requires less distending pressure than the LV to achieve a given diastolic myocardial fiber length
70
respiratory effect on cardiac cycle
inspiration: systemic venous inflow is increased (higher LVEDP) & pulmonary venous inflow is decreased
expiration: reverse from inspiration=higher RVEDP
therefore preload varies beat to beat
71
how do you measure the PCWP?
block the capillary inflow and measure the pressure against the wedge (the reverse pressure from the LA)
72
what does the PCWP represent?
LAP
73
which atrial wave is higher normally?
the V wave (venous inflow filling)
74
when would the A wave>the V wave?
in times of decreased ventricular compliance (i.e. the atrial kick needs to be stronger to achieve EDV)
75
how to tell which atrial wave is which?
the A wave should start to rise in concert with the p wave on the ECG
76
hypertrophy
morphological clinical diagnosis defined by increased myocardial mass (ECG, echo, post-mortem weight)
77
RWT (relative wall thickness)
N=0.34, describes the wall thickness relative to the cavity diameter
78
acute volume overload consequences
increased volume=increased preload=increased SV=increased CO to meet increased volume demand. also increase the HR
79
max increase in SV
180%
80
max increase in HR
220-age
81
acute pressure overload consequences
increased systolic ejection pressure=increased afterload=decreased SV=limited diastolic filling=must contract from increased EDV for greater forces & increases inotropy
82
failure of acute adaptation to volume or pressure overload
increased myocyte metabolism can't be sustained--> hypertrophy occurs to minimize the metabolism by normalizing wall strain
83
how does LVH decrease O2 consumption and metabolism?
will consume more o2 overall but decreases individual myocyte O2 consumption by more efficient distribution
84
what type of chronic overload leads to concentric hypertrophy?
pressure overload
85
morphological change associated with concentric hypertrophy
increase in wall thickness to dissipate increased work imposed by higher pressures. increase in RWT>0.45 (cavity stays the same)
86
what type of chronic overload leads to eccentric hypertrophy?
volume overload
87
morphological change associated with eccentric hypertrophy
increased diastolic chamber size to accommodate increased SV. RWT is normal at 0.34
88
myocyte hyperplasia
occurs during intrauterine and early life. formation of myocytes
89
genes involved in hypertrophy
hypertrophy reactivates the intrauterine genes used in myocyte hyperplasia--DONT make new ones though. just ABNORMALLY change the size of the ones we already have and augment current intracellular components
90
change in sarcomeres-Concentric hypertrophy
parallel
91
change in sarcomeres-Eccentric hypertrophy
series
92
interstitial changes in hypertrophy
capillary proliferation can't keep up with increasing myocyte mass=promotes ischemia and fibrosis=less compliant heart
93
3 stages of hypertrophy
1. acute load-circulation changes & activation of genes
2. chronic phase- subclinical dysfunction-myocytes become increasingly abnormal
3. end stage-heart failure due to decreased CO, and cardiomyopathic dilation
94
how do cells die in hypertrophy?
apoptosis, autophagy, necrosis
95
two categories of bradyarrhythmias
impulse formation (SAN disease) and impulse conduction (AVN or HisPurkinje disease)
96
SA node disease
SA node isn't fast enough or doesn't transmit impulse normally
97
manifestations of SA node dysfunction
sinus bradycardia, sinus arrhythmia, chronotropic incompetence, tachy-bradycardia syndrome
98
sinus bradycardia
resting HR<60, not always abnormal
99
sinus arrhythmia
HR<60 and there is irregularity in the intervals
100
chronotropic incompetence
resting HR is normal, but fails to augment for increased metabolic demands.
101
how does chronotropic incompetence manifest?
fatigue or lightheadedness upon exertion
102
tachycardia-bradycardia syndrome
atrial fibrillation and sinus node dysfunction. treat with pacemaker for bradycardia and meds for arrhythmia
103
how do you diagnose sinus node dysfunction in electrophysiology lab?
pace the atrium and then measure how long it takes to make its first impulse upon discontinuation of the pacing. N=1s
104
sinoatrial exit block
sinus node is generating normal impulses but one or more fail to leave the node and activate the atrium
105
sinoatrial exit block on ECG
p followed by QRS, large gap, next p. this abnormal p to p interval will = p-p-p interval (basically one beat is skipped)
106
types of impulse conduction disorders
1st degree AV delay, 2nd degree block, 3rd degree complete block
107
first degree AV delay
every p wave conducts to the ventricle (has a QRS) but PR interval is >200--represents a delay at the level of the AV node
108
Mobitz type 1, 2nd degree heart block
WENCKEBACH. benign, block at level of AV node, narrow QRS, grouped beating, PR interval gets progressively longer after the drop (decremental slowing of AV conduction)
109
Mobitz type 2, 2nd degree heart block
block at HisPurkinje system, wide QRS, PR interval stays constant (all or none), can progress to complete block
110
complete heart block
no p waves conduct to the ventricle. junctional rhythm takes over=AV dissociation.
111
define heart failure
the heart is unable to pump blood at a rate commensurate with the bodes requirements OR can only do so from an elevated filling pressure
112
syndrome of heart failure
dyspnea, fatigue, exercise intolerance, swelling (legs or abdomen)
113
stages of heart failure
A-high risk patients
B-structural heart disease w/o symptoms
C-prior or current symptoms
D-refractory
114
classes of heart failure
1-asymptomatic
2-symptomatic w/ exertion
3-symptomatic w/ mild exertion
4-symptomatic at rest
115
women vs men in regards to heart failure
bc women have smaller hearts, for a given LVEDP, they eject smaller volumes=less compliant/stiffer hearts=more frequently elderly women have HFpEF
116
systolic HF
HFrEF=LVEF <40%.
117
diastolic HF
HFpEF=LVEF>50%
118
goal of ventricular remodeling in heart failure
maintain MAP/restore CO at all costs
119
eccentric hypertrophy & HF
basketball analogy: heart becomes spherical and muscle fibers (including papillary) are splayed apart=reduced LVEF=HFrEF
120
concentric hypertrophy & HF
heart becomes a bigger, thicker football=HFpEF
121
which type of HF is associated with MV regurgitation?
eccentric/HFrEF
122
LBBB & HF
patients with HF more susceptible to LBBB, which alters the dynamics of the electromechanical synchrony, which= further reduction in LVEF, CO, and MAP, which= further remodeling and progression
123
what do all the neurohormonal pathways that contribute to HF have in common?
they all ultimately lead to vasoconstriction
124
sympathetic activation and HF
SNS activated by baroreceptor reflex (indicating low bp) and becomes overactive chronically=further disease progression
125
symptoms of overactive SNS in HF
diaphoresis, anxiety, palpitations, tachycardia, arrhythmias, remodeling, cool/clammy extremities, increased SVR
126
why is overactive SNS in HF bad?
oversignalling to cardiac=myocyte hypertrophy
| oversignalling to vasculature=peripheral vasoconstriction, oversignalling to kidneys=activation of RAAS
127
what is the main effector in the RAAS system?
angiotensin 2
128
effects of angiotensin 2
positive inotrope/chronotrope, aldosterone production, potentiates SNS, interstitial fibrosis
129
clinical symptoms of overactive RAAS system in HF
thist, salt craving (all in despite of volume overload), increased SVR, LVH
130
arginine vasopressin
stimulated by AG2 & baroreceptors in times of low CO (HF)--increases SVR, reduces water clearance==hypervolemic hyponatremia==crazy thirst
131
main hormonal mediators of HF progression
NE & AG2
132
what are the heart's counteregulatory mechanisms against HF?
downregulates beta receptors, releases natriuretic hormones
133
CRT (cardiac resynchronization therapy)
insertion of a biventricular pacemaker to treat LBBB
134
shock
acute inadequate delivery of oxygen and other metabolic substrates to the tissues
135
chronic shock
HF
136
clinical indication of vasoconstriction
cool & clammy skin
137
types of shock
cardiogenic, hypovolemic, distributive, obstructive
138
hypovolemic shock
volume depletion=decreased preload=decreased SV=decreased CO=reflex SNS activation=increased HR, SVR
139
treatment for hypovolemic shock
volume infusion
140
cause of distributive shock
usually sepsis
141
distributive shock
endotoxins=decreased SVR (systemic vasodilation)=decreased afterload=increase HR/SV as compensation=ramped up CO (but wasteful since doesn't go where needed)
142
clinical presentation of septic shock
warm and flushed
143
cardiogenic shock
MI=loss of myocardium=decreased LVEF=decreased CO=compensatory increase in SVR via SNS activation=increased afterload=decreased SV=decreased CO (vicious cycle)
144
obstructive shock
pulmonary embolism obstructs PA=increased PVR=increased R heart pressures=RHF=decreased preload in LA=decreased CO
145
pericardial tamponade
fluid filled pericardium creates pressure that opposes distending pressures in the heart=decreased CO
146
pulsus paradoxus
inspiratory drop in systolic blood pressure due to an exaggeration of normal inspiratory filling of LV-used to diagnose tamponade
147
treatment of shock
TREAT UNDERLYING CAUSE
148
O2 carrying capacity
HB x 1.34
149
O2 content
O2 capacity x %sat
150
arterial % sat
98
151
venous % sat
75
152
what is the importance of the top shoulder of the Hgb dissociation curve?
provides reserve capacity: if pO2 in lungs decreases down from 100 to 60ish, the O2 content doesn't decrease
153
what is the importance of the steep slope of the Hgb dissociation curve?
permits the blood to unload a large amount of O2 over a narrow range of pO2
154
effect of anemia on ficks calculations
decreased Hgb=decreased plum sat=increased extraction fraction--> pulling more O2 off the Hgb that you have
155
effect of CHF on ficks calculations
bc CO is decreased, must extract a greater fraction of transported O2 in order to deliver requisite supply for demand (will have decreased venous o2 content)
156
effect of sepsis on ficks calculations
increased CO with decreased extraction fraction/increased venous o2 content
157
Sympathetic organization
short preganglionic fibers that synapse with postganglionic via ACh nicotinic receptors. postganglionic synapse at end organ to release NE/E at beta/alpha adrenergic receptors
158
Parasympathetic organization
long preganglionic fibers that synapse with post via ACh nicotinic receptors. release ACh at end organ via muscarinic receptors
159
pre-post ganglionic receptors (SNS & PNS)
nicotinic (ACh)
160
end terminal receptors (SNS)
beta/alpha adrenergic (NE/E)
161
end terminal receptors (PNS)
muscarinic (ACh)
162
vasovagal reaction
vagal activation=decrease in MAP (drop in SVR), bradycardia (decreased SAN automaticity, AVN conduction)
163
alpha adrenergic receptors
vascular smooth muscle vasoconstriction
164
beta 1 adrenergic receptors
heart: myocardium inotropy & chronotropy (increase SA impulse formation, decrease AVN refractoriness)
kidney: JGA renin secretion
165
beta 2 adrenergic receptors
vaso & bronchodilation
166
beta and baroreceptor reflex
beta1 activity overcomes baroreceptor mediated slowing of the HR (diminished when B1 mixed with alpha without B2)
167
beta2/alpha
cancel each other out
168
which adrenergic agonists increase SVR & decrease CO and therefore could be used to treat sepsis?
NE, phenlyephrine
169
which adrenergic agonists increase CO & decrease SVR and therefore could be used to treat cardiogenic shock?
isopreteronol, dobutamine
170
contractility
intrinsic property of cardiac muscle that determines the strength of the contraction regardless of other factors
171
how do inotropes all work?
***they all increase intracellular Ca (and cAMP)*****
172
how to treat digoxin toxicity
specific antibody reverses inhibition of ATPase pump
173
phosphodiesterase type 3
associated with the SR. inhibitors can increase contractility without affecting HR and act independently of beta receptors--also potent vasodilators==POSITIVE INOTROPES & DECREASE AFTERLOAD
174
pros of beta adrenergic inotropy in HF
increased contractility
175
cons of beta adrenergic inotropy in HF
weak vasodilators, worsens diastolic function, tachcardia, proarrthymic potential
176
pros of PDEi inotropy in HF
increased contractility, improved diastolic function, vasodilation
177
cons of PDEi inotropy in HF
proarrythmic potential, tachycardia, HYPOTENSION, thrombocytopenia
