Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physio Review > Cardio > Flashcards

Cardio Flashcards

1
Q

CNS/NMJ vs ANS major differences

A

in the ANS:

  • synapses are not as tight (en passant)
  • metabotropic receptors, slower transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

comparison between sympathetic and parasympathetic divisions of the ANS

A

Symp: thoracolumbar; more exist points; short pres (Ach- nicotinic), long posts (Ne/e- adrenergic)

PS: craniosacral; long pres (Ach- nicotinic), short post (Ach- muscarinic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

EC coupling in skeletal muscle

A
  • electrically activated -
    1. AP (Ach gated channels at NMJ) to t-tubule
    2. depolarization activates DHPR
    3. DHPR changes conformation and activates Ryr
    4. Ca2+ released from SR
    5. Ca2+ binds troponin
    6. troponin moves tropomyosin to actin groove
    7. myosin (thick) binds actin (thin)
    8. crossbridge/power stroke
    9. Ca2+ is sequestered by SRCA/relaxatio
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

EC coupling smooth muscle (vascular system) - NO t-tubules

A
  • no electrical event -
    1. increased in Ca2+ (hormones- IP3, pacemakers- voltage, NTs- ligand)
    2. 4 Ca2+ binds calmodulin
    3. activates myosin light chain kinase
    4. phosphorylates light chain
    5. P-myosin can bind actin (form cross bridge) with hydrolysis of ATP
    6. inactivated by myosin light chain phosphatase

alpha- vasoconstriction
beta- vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does calcium modulate sodium channel activity? what happens with hypercalcemia? hypokalemia?

A
  • Ca binds to proteins surrounding Na channel, makes environment more positive, h-gate closes, less APs
  • Na+ channels become inactive (less available), conduction slows
    signs: weak reflexes
  • low K+ = prolonged QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

sequence of electical activity

A 
SA
atrial muscle
AV
His 
Bundle 
Purkinje
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

P-R interval

A

conduction time from atrial muscle-AV node-his-purkinje- 200 ms (most is AV nodal conduction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

QRS interval

A

conduction time from endocardial to epicardial surface in ventricular muscle- 100 ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

1st, 2nd, 3rd degree heart block

A

1st- abnormal prolongation in P-R interval
2nd- some atrial impulses fail to activate ventricles; not all P waves followed by QRS (e.g. 2:1 conduction)
3rd- complete AV block; no consistent P-R interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does digitalis inhibit and what can it cause

A
  • inhibits Na/K ATPase (sodium out, potassium in), reverses Na/Ca2+ pump (sodium in, Ca out)
  • DADs by abnormally increasing intracellular Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

conduction of ventricular tachycardia

A

does not go through his-purkinje, goes through muscle in longitudinal way, conduction is slower, see slurred QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does the QT interval represent? what does the ST wave of the EKG correspond to?

A

QT- AP duration/systole (not conduction parameter)

the plateau- normally records nothing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

slow vs fast cardiac action potentials

A

slow- AV and SA node, long refractory (Ca2+)

fast- atrial & ventricular muscle, His-Purkinje, fast refractory (Na+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation? heart rate is slower during expiration/inspiration?

A

AV node refractory characteristics; expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

electrical mechanisms responsible for dysrhythmias

A

altered automaticity, re-entry of excitation, triggered activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mechanism of EC coupling in the heart

A
  • Ca2+ induced Ca2+ release*
    1) AP goes down into T-tubules
    2) Depolarization activates L-type Ca2+ currents on sarcolemma & t-tubule membrane (small Ca2+ influx)
    3) Influx of Ca2+ binds to SR and opens Ryr channels
    4) Released Ca2+ binds to troponin C
    5) Relaxation occurs when Ca2+ is removed via Ca2+ ATPase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does PKA phosphorylate in the catecholamine cascade? (Ne/E binds, activates cAMP, cAMP phosphorylates 3 things)

A

1- Ca2+ channels of sarcolemma- increases calcium influx
2- phospholamban- increases SRCA rate (relaxation- plb normally inhibits Ca2+ re-uptake)
3- troponin I- activate TI- reduces troponin C’s affinity for calcium

1&2 increase strength of contraction
2&3 decrease time course of relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

4 factors that determine cardiac output

A

heart rate, myocardial contractility, preload, after-load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is after-load and what are 3 things that cause it

A
  • any force that resists muscle shortening
    1. higher arterial blood pressure
    2. dilated heart
    3. aortic stenosis
20
Q

what is contractility

A

inherent ability of actin and myosin to form cross-bridges and generate tension based on Ca2+ ; give digitalis

  • raises peak isometric tension
  • enhances the rate of relaxation (sympathetics)
  • increases the amount of muscle shortening
  • increases the velocity of shortening
21
Q

if you give someone a transfusion, how does it increase cardiac output?

A

increase end diastolic volume, increases max amount of force you can achieve by stretching the sarcomere, increases systolic pressure

22
Q

3 requirements for re-entry of excitation ; 3 causes

A

1- geometry for conduction loop
2- slow or delayed conduction
3- unidirectional conduction block

causes:
ischemia
infarction
congenital bypass tracts (WPW)

23
Q

systolic vs diastolic heart failure

A

systolic- decrease in contractility curve shifts out

diastolic- decrease in compliance curve shifts up (but same contractility)

24
Q

difference between end systolic and end diastolic on PV curve

A

stroke volume

25
Q

A-C-V wave (atrial pressures)

A

a- atrial contraction
c- increase in pressure during systole (bulging of tricuspid/mitral)
v- filling and emptying of atrium

26
Q

wiggers diagram phases

A

atrial systole- isovol contract (both valves closed)- rapid ejection-reduced ejection- isov relaxation (both valves closed)- rapid ventricular filling- reduced ventricular filling

T wave occurs b4 aortic valve closes
isovolumetric relaxation b4 3rd heart sound

27
Q

relationship between cardiac output and CVP

A

as cardiac output increases, central venous pressure decreases

28
Q

what changes cardiac fxn curve? vascular function curve?

A

cardiac fxn- sympathetics, heart failure (drugs, afterload)
vascular fxn- transfusion, hemorrhage

29
Q

systolic pressure primarily determined by ____; diastolic pressure primarily determined by _____

A
  • stroke volume

- peripheral resistance (hypertension)

30
Q

left axis deviation; right axis deviation

A

left: -30 and -90

right : 105 and 150

31
Q

Pouiseuille’s law and what is arterial pressure related to

A
  • Blood flow= change in pressure/resistance *
  • pressure is directly related to cardiac output and inversely related to radius ^4 regulated by smooth muscle contraction (small radius change, huge pressure change)
32
Q

main determinants of arterial blood pressure

A

1) cardiac output (heart rate x stroke volume)

2) total peripheral resistance (vessel radius, blood viscosity (direct relationship with hct))

33
Q

what is wall tension and is it high or low in capillaries

A

tension = (pressure x radius)/thickness

- low in capillaries, allows them to withstand high amounts of pressure

34
Q

mechanisms which govern vascular resistance

A

central: neuronal (adrenergics) and hormonal (at/aldosterone)
local: myogenic, metabolic, endothelial (NO), mechanical (compression)

35
Q

actions of angiotensin II

A
  • vasoconstriction (renal and systemic)
  • aldosterone release from adrenal gland
  • ADH release from hypothalamus
36
Q

primary determinant of coronary blood flow; primary regulator of coronary blood flow; left ventricular coronary blood flow primarily occurs during

A

determinant: aortic pressure
regulator: metabolism
diastole

37
Q

which region of the heart is more at risk for ischemia?

A

endocardium pressure is high

38
Q

factors affecting myocardial oxygen supply

A

diastolic perfusion pressure

coronary vascular resistance

39
Q

factors affecting myocardial oxygen demand

A

afterload
heart rate
contractility

40
Q

ischemia is not enough supply/too much demand

A

too much demand

41
Q

factors that precipitate edema

A

1 reduction in plasma protein
2 increase in capillary hydrostatic pressure
3 increase in permeability of capillary membrane
4 lymphatic obstruction

42
Q

velocity of blood is faster/slower in a stenotic region

A

faster (transmural pressure decrease)

43
Q

which vessels have the lowest total resistance

A

capillaries- have largest total cross sectional area

44
Q

what are your capacitance vessels and what are the resistance vessels?

A

capacitance- veins

resistance- arteries

45
Q

CV response to exercise

A
  1. sympathetics increase CO- increase heart rate, contractility
  2. sympathetics vasoconstrict- increases resistance, shunts to brain/lungs/heart
  3. Metabolic vasodilation- overcomes sympathetics, lowers resistance
  4. Muscle capillaries open
  5. Right shift in O2 curve - O2 bound less tightly to Hb
  6. Venous return increases (sympathetics)
  7. Systolic pressure increases, diastolic pressure pretty much stays the same
46
Q

continuous vs fenestrated vs discontinuous capillaries

A

continous- muscle, connective tissue
fenestrated- kidney, intestine
discontinuous- bone marrow, liver, spleen

47
Q

what is the mean arterial pressure?

A

diastolic pressure + 1/3 pulse pressure (difference between systolic and diastolic)

Physio Review (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions