Cardiac Physiology Flashcards

(145 cards)

1
Q

Vitamin deficiency that can cause heart failure

A

Vitamin B1 or Thiamine

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2
Q

Which is not targeted in drug therapy for heart failure?
a. Preload
b. Afterload
c. Relaxation
d. contractility

A

Relaxation

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3
Q

In the ECG, what correlates with the plateau phase (phase 2) of ventricular contraction?

A

ST segment

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4
Q

What part of the electrical conductance of the heart does the PR interval correlate with?

A

Conduction velocity through AV node

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5
Q

Formula of MAP and normal value

A

2/3 Diastole + 1/3 Systole
Diastole + 1/3 PP
Normal value = 100 mmHg

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6
Q

ARTERIES VS. ARTERIOLES
Greatest resistance

A

Arterioles

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7
Q

ARTERIES VS. ARTERIOLES
Highest pressure

A

Arteries

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8
Q

How much of the blood volume is contained in the veins?

A

64%

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9
Q

Fastest blood flow velocity is in?
Slowest?

A

Aorta
Capillaries

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10
Q

Formula for blood flow velocity

A

V = Q/A

V = velocity (cm/sec)
Q = blood flow (ml/min)
A = cross-sectional area (cm2)

Velocity is directly proportional to blood flow but inversely proportional to cross-sectional area

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11
Q

Formula for blood flow is derived from?

A

OHM’S LAW

CO = mean arterial pressure - right atrial pressure/TPR

CO = BP/TPR

BP = CO x TPR

BP = (HR x SV) x TPR

Inc. HR, SV and TPR will all lead to increased BP

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12
Q

3 principal factors affecting venous return

A

Right atrial pressure
* Inc RAP = dec. VR
* dec RAP = inc. VR

Mean systemic filling pressure
* Inc MSFP = inc. VR
* dec MSFP = dec. VR

Resistance to venous return
*Inc RVR = dec VR
*dec RVR = inc VR

FORMULA
VR = MSFP - RAP/RVR

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13
Q

What is the formula that serves as the basis for resistance to blood flow?

A

Poiseuille law
R = 8ήl/Πr^4

R = resistance
ή = viscosity of blood
l = length of blood vessel
r = radius of blood vessel raised to the 4th

Resistance is directly proportional to viscosity and blood vessel length, but indirectly proportional to radius

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14
Q

Formula for Reynold’s number (to determine turbulent blood flow)

A

N = pdv/ή

N = reynolds number (higher number, >2,000 is associated with turbulent blood flow and bruits)
p = density of blood
d = diameter of blood vessel
v = velocity of blood flow
ή = viscosity

Reynolds number is directly proportional with density of blood, diameter of blood vessel, and velocity of blood flow, but inversely proportional with viscosity

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15
Q

Will an atheromatous vessel have an increased/decreased blood flow velocity? How about the turbulence, will it increase/decrease?

A

Firstly, based on the formula of Blood flow velocity, which is V = Q/A, blood flow velocity (V) is inversely proportional to cross-sectional area (A). An atheromatous vessel will have a decreased cross sectional area than a normal blood vessel.

Next, to determine turbulence of blood flow, we utilize the Reynolds number (>2000 will be turbulent BF). This formula is N = pdv/ή. Reynolds number (N) is directly proportional to velocity of blood flow (V). Thus, a greater velocity = greater turbulence.

Finally, atheromatous vessel —> inc blood flow velocity —> inc turbulence of blood flow

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16
Q

POLYCYTHEMIA VS. ANEMIA
Turbulent blood flow

A

Anemia

Formula for determining probability of turbulent blood flow
N = pdv/ή

N = reynolds number (higher number, >2,000 is associated with turbulent blood flow and bruits)
p = density of blood
d = diameter of blood vessel
v = velocity of blood flow
ή = viscosity

Reynolds number is inversely proportional to viscosity, this means that with a lesser viscosity (e.g. anemia), the Reynolds number would be higher.

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17
Q

POLYCYTHEMIA VS. ANEMIA
Increased resistance to blood flow (reduced)

A

Polycythemia

Formula for resistance to blood flow

Poiseuille law
R = 8ήl/Πr^4

R = resistance
ή = viscosity of blood
l = length of blood vessel
r = radius of blood vessel raised to the 4th

Resistance is directly proportional to viscosity (correlated with hct). The greater the viscosity (e.g. polycythemia), the greater the resistance would be

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18
Q

Formula for capacitance of blood vessel

A

C = V/P

C = capacitance/compliance
V = volume
P = pressure

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19
Q

When does blood flow of coronary arteries occur?

A

Diastole

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20
Q

Right atrial pressure synonym: _______________________________
Left atrial pressure estimated by:
_______________________________, measured using ______________

A

Central venous pressure
Pulmonary capillary wedge pressure
Swan-Ganz catheter

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21
Q

Formulas for pulse pressure and normal pulse pressure value

A

SBP - DBP
SV/AC (Arterial compliance)

40 mmHg

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22
Q

What happens to my pulse pressure when I’m old and have arteriosclerosis? HAHA

A

Widened. Because decreased arterial compliance. PP = SV/AC

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23
Q

Conditions that increase/widen pulse pressure

A

Well-conditioned endurance runner
Old age
Aortic regurgitation
Aortic sclerosis
Severe iron deficiency anemia
Arteriosclerosis
Hyperthyroidism

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24
Q

Conditions that decrease/narrow pulse pressure

A

Heart failure
Blood loss
Aortic stenosis
Cardiac tamponade

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25
AV BLOCKS All atrial impulses reach ventricles, but PR interval is prolonged (>0.20 secs)
1st degree AV block
26
AV BLOCKS Not all impulses conducted to ventricles, ventricular rate < atrial rate, p wave not always followed by QRS Sporadically occurring with constant PR intervals before block
2nd degree AV block Mobitz Type II
27
AV BLOCKS Not all impulses conducted to ventricles, ventricular rate < atrial rate, p wave not always followed by QRS ECG shows gradual increase of PR interval before block
2nd degree AV block Mobitz Type I: (+) Wenkebach phenomenon
28
AV BLOCKS Atrioventricular dissociation May cause fainting, syncope, worsening exercise tolerance from cerebral ischemia Can be caused by amyloidosis, sarcoidosis, SLE
3rd degree (Complete) AV block
29
ECG PATTERNS: Saw tooth appearance
Atrial flutter
30
ECG PATTERNS: Flat/inverted T waves
Hypokalemia
31
ECG PATTERNS: Prominent u waves (inc susceptibility to Torsades de Pointes)
Hypokalemia
32
ECG PATTERNS: Inc amplitude and width of P waves
Hypokalemia
33
ECG PATTERNS: ST depression, QT prolongation
Hypokalemia
34
ECG PATTERNS: Low P waves, tall-peaked T waves
Hyperkalemia
35
ECG PATTERNS: Prolonged QT interval Associated with long QT syndrome (sudden fainting and death), Torsades de Pointes (ventricullar arrythmias and fibrillation)
Hypocalcemia
36
ECG PATTERNS: Shortened QT interval
Hypercalcemia
37
ECG PATTERNS: ST Segment elevation
Q-wave infarct/Transmural infarct
38
ECG PATTERNS: ST Segment depression
Non-Q-wave infarct/Subendocardial infarct
39
When can the fetal heartbeat be heard using UTZ? How bout using Doppler?
UTZ - 6 weeks Doppler - 10 weeks
40
When does Troponin I levels rise in an MI episode? What about when it peaks? And how long does it remain elevated?
Rise: 6 hours Peak: 12 hours Remain elevated: 1-2 weeks
41
Which of the following is NOT an inferior MI component? a. Ventricular tachycardia b. Cardiogenic shock c. Hypotension d. Heart block
A. Ventricular tachycardia (myatay na gane ang myocytes, magpapakabilis pa ba siya for the life?)
42
How long should one do lifestyle modifications only (no meds) for newly diagnoses Stage 1 hypertensives?
3-6 months
43
Possible cause of sudden onset heart failure
Coronary artery disease
44
Erratic electrical activity, Vfib, Vtach?
Vfib
45
Meaning of e wave and a wave in 2D-echo
e wave - early diastolic filling from left atrium to left ventricle a wave - atrial kick
46
Isoelectric portion of the ECG that corresponds to complete ventricular depolarization
ST segment
47
Where is the pacemaker placed when ECG has no P wave but has normal QRS complex and T wave
Atrioventricular (AV) node
48
Two P waves preceding each QRS in ECG means?
Decreased conductance through AV node
49
Stable RMP of Cardiac
-90 MV
50
Inotropes affect
Ventricular contraction (SV)
51
Dromotropes affect
Cardiac contractility (AV node)
52
Chronotropes affect
Heart rate (SA node)
53
INCREASE OR DECREASE SV: During PVC
Decrease
54
INCREASE OR DECREASE SV: Normal beat after PVC
Increased (Greater Ca influx due to increased ventricular filling time)
55
FRANK-STARLING MECHANISM
Inc VR —> Inc SV —> Inc CO (Increased venous return —> increased right atrial pressure —> increased end-diastolic volume —> increased stretch of sarcomeres (inc ventricular fiber length) —> Greater force of contraction —> Increased stroke volume —> Increased cardiac output)
56
BAINBRIDGE REFLEX
Inc VR —> Inc HR —> Inc CO (Increased venous return —> increased right atrial pressure —> Stimulation of cardiopulmonary baroreceptors (low pressure receptors) —> Increased heart rate —> Increased cardiac output)
57
Cardiac preload is equivalent to _______________, which in turn is influenced by _________________. An increased preload will ________________ cardiac output.
End-diastolic volume; Right atrial pressure; Increase
58
Cardiac preload is equivalent to _______________ in the left ventricle and to _______________ in the right ventricle. An increased afterload will ________________ cardiac output.
Aortic pressure; Pulmonary artery pressure; Decrease
59
Which is not affected by stroke volume? A. Pulse pressure B. Preload C. Afterload D. Contractility
C. Afterload
60
Definition of SV Formula for SV Normal value for SV
Blood ejected by ventricles per heartbeat SV = EDV - ESV Normal value = 70 ml
61
Definition of EF Formula for EF Normal value for EF
Percentage of EDV that is actually ejected by ventricle EF = SV/EDV Normal value = 55%
62
Definition of CO Formula for CO Normal value for CO
Total blood volume ejected per unit time CO = HR x SV Fick equation —> CO = VO^2/a-VO^2 (VO^2 - steady state oxygen consumption; AVO^2 - difference in arterial O2 content and mixed venous O2 content) Normal value = 5L/min (resting) *Max CO for non-athletes = 20L/min *Max CO for athletes = 30L/min
63
What happens to EF in Hypertrophic Cardiomyopathy?
Preserved Ejection Fraction
64
Main energy used for stroke work (work of heart in each beat)
Fatty acids
65
7 Phases of Cardiac Cycle
1. Atrial contraction 2. Isovolumic contraction 3. Rapid ventricular ejection 4. Reduced/slow ventricular ejection 5. Isovolumic relaxation 6. Rapid ventricular filling 7. Reduced/slow ventricular filling
66
Important events in ATRIAL CONTRACTION ECG: Atrial pressure: Ventricular pressure: Ventricular volume: Atrial pressure curve: Heart sound:
1. ATRIAL CONTRACTION ECG: preceded by P wave Atrial pressure: Increases slightly Ventricular pressure: Increases slightly Ventricular volume: Increases sligtly Atrial pressure curve: a-wave Heart sound: 4th heart sound
67
Important events in ISOVOLUMIC CONTRACTION ECG: Atrial pressure: Ventricular pressure: Ventricular volume: Atrial pressure curve: Heart sound:
2. ISOVOLUMIC CONTRACTION ECG: preceded by QRS complex Atrial pressure: Ventricular pressure > atrial pressure --> closure of AV valves Ventricular pressure: Increased (Ventricular pressure < Aortic pressure --> no movement of blood from ventricle to aorta/semilunar valves closed) Ventricular volume: Remains the same Atrial pressure curve: c-wave Heart sound: 1st heart sound (closure of AV valves
68
Important events in RAPID VENTRICULAR EJECTION Ventricular pressure: Ventricular volume:
3. RAPID VENTRICULAR EJECTION Ventricular pressure: Ventricular Pressure > Aortic pressure --> opening of semilunar valves --> blood goes from left ventricle to aorta Ventricular volume: Rapidly decreases
69
Important events in Reduced/Slow Ventricular Ejection ECG: Ventricular pressure: Ventricular volume: Aortic pressure:
4. REDUCED-SLOW VENTRICULAR EJECTION ECG: T-wave occurs Ventricular pressure: Decreases Ventricular volume: Decreases Aortic pressure: Decreases (runoff of blood from large arteries to smaller arteries)
70
Important events in ISOVOLUMIC RELAXATION ECG: Atrial pressure: Ventricular pressure: Ventricular volume: Atrial pressure curve: Heart sound:
5. ISOVOLUMIC RELAXATION ECG: preceded by T-wave Atrial pressure: Lower than ventricular pressure Ventricular pressure: Ventricular pressure > atrial pressure --> AV valves still closed --> no blood goes from atria to ventricles; Ventricular pressure < aortic pressure --> semilunar valves close Ventricular volume: Remains the same Atrial pressure curve: v-wave Heart sound: 2nd heart sound INCISURA/DICROTIC NOTCH - closure of aortic valve causes vibrations in the aorta near the aortic valve --> slight increase in aortic pressure
71
Important events in RAPID VENTRICULAR FILLING Atrial pressure: Ventricular pressure: Ventricular volume: Heart sound:
6. RAPID VENTRICULAR FILLING Atrial pressure: Higher than ventricular pressure Ventricular pressure: Lower than atrial pressure --> AV valves open --> blood flows from atria to ventricles Ventricular volume: Rapidly increases Heart sound: 3rd heart sound
72
Important events in REDUCED/SLOW VENTRICULAR FILLING Ventricular volume:
7. REDUCED/SLOW VENTRICULAR FILLING Ventricular volume: Reduced increase
73
Longest phase of cardiac cycle
Phase 7: Reduced/Slow Ventricular Filling (Diastasis)
74
Meaning of the peak waves in atrial pressure curve
a-wave: atrial contraction c-wave: ventricular contraction (causes the valves to bulge into the atria --> increased pressure; also carotid pulse) v-wave: venous return of blood to atria
75
What phase in the cardiac cycle is the v-wave seen in an atrial pressure curve?
Isovolumic relaxation
76
What phase in the cardiac cycle is the a-wave seen in an atrial pressure curve?
Atrial contraction
77
What phase in the cardiac cycle is the c-wave seen in an atrial pressure curve?
Isovolumic contraction
78
What phase in the cardiac cycle is the dicrotic notch/incisura seen?
Isovolumic relaxation
79
Heart sounds and their meanings 1st: 2nd: 3rd: 4th:
1st heart sound: S1, closure of AV valves 2nd heart sound: S2, closure of semilunar valves 3rd heart sound: S3, rapid ventricular filling 4th heart sound: S4, atria contracting against stiff ventricles
80
What phase in the cardiac cycle may the 3rd heart sound be heard?
Phase 6: Rapid ventricular filling
81
What phase in the cardiac cycle can the 1st heart sound be heard?
Phase 2: Isovolumic contraction
82
What phase in the cardiac cycle can the 2nd heart sound be heard?
Phase 5: Isovolumic relaxation
83
What phase in the cardiac cycle may the 4th heart sound be heard?
Phase 1: Atrial contraction
84
CARDIAC CYCLE PHASES: Ventricular pressure is high but still lower than aortic pressure, semilunar valves remain closed thus there is no blood flow from left ventricle to aorta. Also, AV valves are closed in this phase
Phase 2: Isovolumic contraction
85
CARDIAC CYCLE PHASES: Ventricular pressure is now higher than the aortic pressure, semilunar valves open and there is rapid blood flow to aorta, decreasing the ventricular pressure rapidly
Phase 3: Rapid Ventricular Ejection
86
CARDIAC CYCLE PHASES: Atrial pressure is higher than ventricular pressure, leading to opening of AV valves and rapid blood flow from atria to ventricles
Phase 6: Rapid Ventricular Filling
87
CARDIAC CYCLE PHASES: Ventricular pressure is now decreasing but still higher than atrial pressure, AV valves remain closed, and there is no blood flow from atria to ventricles. Since the aortic pressure now is higher than ventricular pressure, semilunar valves close
Phase 5: Isovolumic relaxation
88
CARDIAC CYCLE PHASES: What phase of the cardiac cycle corresponds to the phase with the highest ventricular volume?
Phase 2: Isovolumic contraction
89
CARDIAC CYCLE PHASES: What phase of the cardiac cycle corresponds to the phase with the highest ventricular and aortic pressure?
Between Phase 3 and Phase 4: Between Rapid Ventricular Ejection and Reduced/Slow Ventricular Ejection
90
CARDIAC CYCLE PHASES: What phase of the cardiac cycle corresponds to the phase with the lowest ventricular volume?
Phase 5: Isovolumic relaxation
91
Most common cardiac rhythm disorder with ECG findings of narrow complex "irregularly irregular" pattern with no distinguishable p waves
Atrial fibrillation
92
Atrial contraction during atrial systole
Atrial kick
93
Wide QRS complex typically seen in atrial fibrillation
Ashman syndrome
94
Auscultatory hallmark of Atrial Septal Defect (ASD)
Fixed splitting
95
Conditions with Wide Split S2/Exaggeration of normal splitting
RBBB Pulmonic Stenosis Mitral valve regurgitation VSD
96
Paradoxical splitting of the 2nd heart sound has a common ECG finding of
LBBB
97
Explain mo ba sab sa sarili mo bakit may Physiologic S2 Splitting
Inhale --> decreased thoracic pressure --> HIGOP more of the right, less of the left --> VR is increased in right and VR is decreased in left --> more blood to the right and less blood to the left (going from atria to ventricles) --> Later closure of pulmonic valve and lesser closure of aortic valve --> Physiologic S2 split
98
THIS MURMUR SOUNDS FAMILIAR Murmur with wide pulse pressure Early diastolic murmur Accentuated when leaning forward in full expiration
Aortic regurgitation
99
THIS MURMUR SOUNDS FAMILIAR De Musset Sign (head bobbing in synchrony with heartbeat) is seen in?
Aortic regurgitation/insufficiency
100
THIS MURMUR SOUNDS FAMILIAR Early systolic murmur with JVP distention
Tricuspid regurgitation
101
THIS MURMUR SOUNDS FAMILIAR Usually associated with RHD Holosystolic murmur in 5th ICS MCL Loudest at apex Radiates to axilla Enhanced by expiring and making a fist
Mitral regurgitation
102
THIS MURMUR SOUNDS FAMILIAR Decreased Pulse pressure Prominent systolic ejection click Crescendo-decrescendo murmur over right sternal border Radiates to carotid arteries
Aortic stenosis
103
THIS MURMUR SOUNDS FAMILIAR Opening snap (OS) Low-pitched diastolic rumble Loud S1 Presystolic accentuation
Mitral stenosis
104
THIS MURMUR SOUNDS FAMILIAR Midsystolic ejection click Late diastolic accentuation
Mitral valve prolapse
105
MURMURS AND MANEUVERS Hand grip
↑ Afterload ↑ AR, MR, VSD ↓ Hypertrophic Obstructive Cardiomyopathy (HOCM) and Mitral valve prolapse
106
MURMURS AND MANEUVERS Squatting
↑ preload ↑ AS, MS, AR, MR ↓ HOCM, MVP
107
MURMURS AND MANEUVERS Valsalva
↓ preload ↑ HOCM, MVP ↓ AS, MS, AR, MR, VSD
108
MURMURS AND MANEUVERS Standing abruptly
↓ preload ↑ HOCM, MVP ↓ AS, MS, AR, MR, VSD
109
MURMURS AND MANEUVERS Amyl nitrite
↓ afterload ↑ AS, HOCM, MVP ↓ AR, MR, VSD
110
Vasomotor area of medulla that serves as the "Excitatory area" (↑HR and ↑BP)
Lateral portion *Outer - Extrovert
111
Vasomotor area of medulla that serves as the "Inhibitory area" (dec. HR and BP)
Medial portion *Inner - Introvert
112
Last ditch stand before death
CNS Ischemic response Starts at less than 60 mmHg and optimal at 15-20 mmHg All systemic arterioles vasoconstrict severely, except CORONARY AND CEREBRAL VESSELS
113
Cushing reflex triad
Hypertension, bradycardia, irregular respirations
114
Branch of CN IX that carries signals from the carotid sinus to Nucleus Tractus Solitarius
Hering nerve
115
To what signals (increased or decreased BP) do carotid baroreceptors respond to?
Increased and decreased BP (nonselective) BP within 50-180 mmHg
116
To what signals (increased or decreased BP) do aortic baroreceptors respond to?
Increased BP only (selective) BP >80 mmHg
117
Na sensor in DCT
macula densa
118
↑ Capillary Hydrostatic Pressure - EDEMA
- Arteriolar dilatation - Venous constriction - ↑ venous pressure - Heart failure - ECF volume expansion - Standing
119
↓ Capillary Oncotic pressure - EDEMA
- ↓ Plasma protein - Severe liver disease - Protein malnutrition - Nephrotic syndrome
120
↑ Filtration coefficient (capillary permeability x surface area)
- Burns - Inflammation (due to release of histamine, cytokines)
121
Organs capable of autoregulation
1. Brain 2. Heart 3. Kidneys
122
What will happen to the brain if there is increased CO2?
Cerebral vessels will vasodilate --> permit wash out of CO2
122
Angiogenesis occurs in response to?
Hypoxia
123
Most potent vasoconstrictor
Vasopressin
124
VASOCONSTRICTOR VS. VASODILATOR Prostacyclin
Vasodilator
125
VASOCONSTRICTOR VS. VASODILATOR Serotonin
Vasoconstrictor
126
VASOCONSTRICTOR VS. VASODILATOR Endothelin
Vasoconstrictor
127
VASOCONSTRICTOR VS. VASODILATOR PGF
Vasoconstrictor
128
VASOCONSTRICTOR VS. VASODILATOR Thromboxane A2
Vasoconstrictor
129
VASOCONSTRICTOR VS. VASODILATOR Lactate
Vasodilator
130
VASOCONSTRICTOR VS. VASODILATOR Adenosine
Vasodilator
131
VASOCONSTRICTOR VS. VASODILATOR Nitric oxide
Vasodilator
132
VASOCONSTRICTOR VS. VASODILATOR Acetylcholine
*Generally vasodilator by increasing production of NO in vascular smooth muscle *Vasoconstrictor during endothelial damage due to decreased NO
133
VASOCONSTRICTOR VS. VASODILATOR PGE
Vasodilator
134
VASOCONSTRICTOR VS. VASODILATOR Histamine
Vasodilator
135
VASOCONSTRICTOR VS. VASODILATOR Bradykinin
Vasodilator
136
Vasoactive metabolites of coronary vessels
Hypoxia Adenosine
137
Vasoactive metabolites of cerebral vessels
CO2 H+
138
Vasoactive metabolites of muscles
Lactate K+ Adenosine
139
Vasoactive metabolites of pulmonary vessels
Hypoxia (vasoconstriction)
140
At what PO2 level will neuronal activity begin to decline?
Cerebral PO2 <20 mmHg
141
Cerebral blood is kept constant at a MAP of
60-140 mmHg
142
RAAS pathway
↓ Na delivery to macula densa in DCT --> stimulation of Juxtoglomerular (JG) cells --> renin release --> liver angiotensinogen is converted to Angiotensin 1 by renin --> Angiotensin I is converted to Angiotensin 2 by lung ACE --> Release of aldosterone --> effect on principal cells and intercalated cells of kidney --> Principal cells: ↑ Na reabsorption, ↑ K secretion; Intercalated cells: ↑ K reabsorption, ↑ H secretion (Net effect is still ↓↓↓ K) --> Na causes water reabsorption --> Increased IVC --> ↑ VR and ↑ CO --> ↑ BP :)
144
Cardiac AP
Phase 1: Na influx Phase 2: K efflux = Ca influx Phase 3: K efflux Phase 4: Stable RMP
145
SA node AP
Phase 4: slow Na influx Phase 0: Ca influx (depolarization) Phase 3: K efflux (repolarization)