Physiology Cardiovascular Ch. 11-15

Front 1

What is the Bulk Flow relationship in terms of CO & TPR?

Back 1

Bulk Flow = Pressure Gradient/Resistance

↓

CO = MAP/TPR

Thus...
MAP = CO x TPR

Front 2

Briefly explain what the Baroreceptor relfex is?

When speaking of the Baroreceptor reflex, what would be the sensor, integrator/comparator & effector?

Back 2

The Baroreceptor reflex is the neurally-mediated rapid response system for BP that operates as a negative feedback loop.

Sensor: Baroreceptors
Afferent pathway: Aortic depressor nerve & Carotid sinus nerves
Integrator/Comparator: Cardiovascular control centers of medulla
Efferent pathways: SNS & PNS
Effectors: Heart, arteries, arterioles & veins

Front 3

What are the (3) main Cardiovascular Coordinating Centers? (1 for parasympathetics & 2 for sympathetics)

Back 3

Cardioacceleratory center & vasomotor (vasoconstrictor) center project via the bulbospinal pathways to sympathetic preganglionic neurons in the lateral horn of T1-L3.

The Cardioinhibitory center is the dorsal motor nucleus of the vagus which inhibits HR.

All these centers are tonically active and their level of activity is regulated by the projection from the nucleus tractus solitarius

Front 4

What is the 'short term control' and 'long term control' systems of blood pressure?

Back 4

Short term control of BP: Baroreceptor reflex

Long term control of BP: Renin-Angiotensin system

Front 5

Understand why the Baroreceptor reflex affects each of the components on the otherside of this card...

Back 5

Front 6

An ↑Baroreceptor firing rate would cause ↑ or ↓ in BP?

A ↓Baroreceptor firing rate would cause ↑ or ↓ in BP?

Back 6

↑Baroreceptor firing rate = ↓BP

↓Baroreceptor firing rate = ↑BP

Front 7

Again...simply know and understand the card on the other side!!

Back 7

Front 8

Why is the Baroreceptor reflex limited in long term control of BP?

Back 8

The Baroreceptor set point resets every 1-2 days to whatever pressure level they are exposed to.

Front 9

How can a strong emotional and stressful response affect BP?

Back 9

Emotions and stress can increase the vasomotor center and cardioacceleratory center via the hypothalamus.

This increase in BP was most likely designed to increase blood flow to particular organs such as muscles during a fight or flight response.

Front 10

How do chemoreceptors maintain BP?

Back 10

Adjacent to the aorta and carotid are bodies which are sensitive to changes in PaO2, PaCO2 & pH. When BP falls below a critical level, the chemoreceptors become stimulated b/c of a ↓PaO2, ↑PaCO2 & ↑H+ ions. The afferent fibers excite the vasomotor center resulting in a sympathetic outflow and ↑BP.

Front 11

What is the Ischemic response and Cushing reaction?

Back 11

When BP falls, PaCO2 & H+ raised causes cerebral ischemia and a massive sympathetic outflow which is termed the "CNS Ischemic response". Response maybe so sever to reach ~250 mmHg BP and totally exclude blood flow to some organs.

When CSF pressure rises higher than BP, the blood supply is compromised, the cerebral ischemic response is initiated which increases BP and thus CSF pressure. This cushing reaction protects vital centers of the brain from loss of nutrients if the CSF pressures rise high enough to compress cerebral arteries.

Front 12

How is long term BP controlled?

Back 12

Angiotensin II and the angiotensin-renin system!

Front 13

What is the role of volume receptors in controlling BP?

Back 13

Volume/low pressure receptors are found in the veins, pulmonary artery & atria which respond to high blood volume and mostly located on the venous side of the circulation. If blood volume increases, these receptors initiate responses such as:
1) Atrial natruietic peptide (ANF) - vasodilation of renal afferent arterioles of kidneys which ↑GFR thus ↑salt & H2O excretion and ↓ECF volume
2) ↓ADH secretion resulting in ↑H2O excretion
3) ↑HR through Baindridge reflex

Front 14

What is CO?

What is VR?

Back 14

CO is volume of blood pumped into aorta each minute OR volume of blood that flows around the circulation/min

VR is the volume of blood flowing from the veins into the right atrium each min.

Front 15

What factors will affect CO? (SNS, PNS, Drugs)

Back 15

SNS:
NE acting on β1 receptors: ↑HR
Epinephrine β1: ↑HR

PNS:
ACh acting on M2 receptors: ↓HR

Drugs:
β1 agonists: ↑HR
M2 antagonists: ↑HR

β1 antagonists: ↓HR
M2 agonists: ↓HR

These can change CO b/c: CO = HR x SV

Front 16

How would changing TPR affect CO?

Back 16

↓TPR = ↑VR = ↑CO

↑TPR = ↓VR = ↓CO

Front 17

Describe a CO curve?

Back 17

By changing contractility or RAP the CO will be changed

Front 18

What factors alter the CO curve?

Back 18

Contractility & RAP

Front 19

Describe a vascular function curve?

Back 19

Front 20

Would exercise increase/decrease CO?

Back 20

Increase

Front 21

What is the Mean Systemic Filling Pressure (MSFP)?

Back 21

The mean systemic filling pressure is when the pressure gradient between the RA and veins is zero...There is no gradient for blood to travel down its pressure gradient

Front 22

What (3) factors affect MSFP and how do they affect MSFP?

Back 22

MSFP affected by:
1) Blood volume - ↑blood volume = ↑VR
2) Venomotor tone - ↑tone = ↑VR
3) Arteriolar resistance - ↑TPR = ↓VR (blood held in arterial side)

Front 23

Describe a Guyton Cross Plot?

Back 23

Front 24

How does an increase in contractility affect the Guyton Cross Plot?

Back 24

Front 25

How does blood volume affect the Guyton Cross Plot?

Back 25

Front 26

How does an increase in TPR affect the Guyton Cross Plot?

Back 26

Front 27

How does a +ve and -ve Inotrope agent affect CO?

Back 27

+ve Inotrope agents (Digoxin) will ↑CO and ↓RAP

-ve Inotrope agents will ↓CO and ↑RAP

Front 28

How does a decrease in TPR affect the Guyton Cross Plot?

Back 28

Front 29

How would cardiac failure affect the Guyton Cross Plot?

Back 29

Heart failure = ↓CO, ↓VR & ↑RAP

Front 30

How does standing from a supine position initially affect CVP, EDV, SV, MAP & Sympathetic response?

Back 30

Front 31

During a sympathetic response, such as a posture change from supine to standing, arterial vasoconstriction through α1 receptors causes ↑TPR to maintain blood pressure. Are we also decreasing blood flow to the brain in order to maintain blood flow? Explain?

Back 31

Cerebral arteries have very few α1 receptors which ensures our brain will not be deprived of blood during sympathetic responses such as supine to standing.

Front 32

What are the vascular changes that occur during Valsalva maneouvre? (Phase I, II, III, IV)

Back 32

Front 33

How is HR and BP affected during the Valsalva Maneuver in the following phases:

(out of order to make us think)
Phase 4?
Phase 2?
Phase 1?
Phase 3?

Back 33

Phase 4: ↑BP & ↓HR

Phase 2: ↓BP & ↑HR

Phase 1: ↑BP & ↓HR

Phase 3:↓BP & ↑HR

Front 34

What is a disease associated w/ an attenuated HR slope during the Valsalva Maneuver?

Back 34

Diabetic Neuropathy: ↓HR in Phase 4 is < normal

Front 35

How does exercise effect HR, BP, CO, SV and VR?

Back 35

Exercise causes an ↑ in HR, BP, CO, SV & VR

Front 36

What type of exercise (static or dynamic) raises diastolic pressures and which one raises systolic pressures?

Back 36

Front 37

In a healthy individual, does diastolic BP increase/decrease during exercise?

In a healthy individual, does systolic BP increase/decrease during exercise?

Does PP in the same individual increase/decrease?

Does MAP increase/decrease in the same individual?

Back 37

Slight ↓ in diastolic

↑ Systolic

↑ PP

MAP is more or less MAINTAINED

MAP = DP + 1/3 PP

Front 38

How does age affect the CVS? (elastin, BP, workload, PP)

Back 38

Front 39

What is "Systolic Hypertension of the Elderly"?

Back 39

A greater increase in systolic BP as we age, directly related to loss of elastin & dilation of the aorta.

Front 40

What does immersing someones face in cold water do to HR?

What can this be used for?

Back 40

Immersing someones face in cold water causes bradycardia which can be used as a home treatment for supraventricular tachycardias.

Front 41

What is hypertension?

Back 41

A chronic, progressive raised arterial pressure

Front 42

What are the classifications of hypertension?

Back 42

Front 43

What ultimately causes hypertension?

Back 43

Vascular smooth muscle hypertrophy

Front 44

What are the characteristic features of shock? (skin, pulse, PP, breathing, urine output, consciousness, O2 & glucose delivery to brain, baroreceptor reflex)

Back 44

Shock: ACUTE failure of CVS to adequately perfuse tissues

1) Cold, sweaty, clammy skin (due to ↑SNS)
2) Rapid & weak pulse: tachycardia & small SV
3) ↓PP (MAP may be normal)
4) Rapid & shallow breathing
5) ↓Urine output
6) Often altered consciousness, weakness and collapse
7) ↓O2 & glucose to brain
8) ↑Baroreceptor reflex

Front 45

What are the (4) categories of shock?

What are they due to and what do they physiologically cause?

Back 45

Front 46

What are the physiological consequences of Hypovolemic shock?

Back 46

Hypovolemic shock: Hemorrhage
Normal blood volume ~5L (65% in veins)

Consequences of blood loss:
5-10% Modest ↓MAP: reflexes = full recovery
15-20% MAP 60-80 mmHg: rarely fatal
30-40% MAP 50-70 mmHg: serious shock responses which may become irreversible
>50% Fatal

Front 47

What are the short and long term compensatory responses to hemorrhage?

Back 47

Front 48

How does the Renin Angiotensin System help correct blood volume?

Back 48

Front 49

What is syncope?

Back 49

A sudden, transient loss of consciousness due to a fall in BP resulting in reduced cerebral perfusion. Can be triggered by hypovolemia, standing up suddenly (particularly w/ patient taking α1 antagonists) or psychological stress (psychogenic fainting)

Front 50

What is chronic congestive heart failure?

Back 50

Pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate w/ requirements of the metabolising tissue

Front 51

What are the consequences of cardiac failure?

Back 51

↓SV = ↓Ejection fraction = ↑EDV

↑EDV = ↑Venous Pressure = ↑Capillary Hydrostatic Pressure = Edema formation

↑EDV = Dilation of the heart

Front 52

What are the compensatory mechanisms of mild cardiac failure?

Back 52

Frank-Starling mechanism - increase volume

Baroreceptor reflex - increase sympathetics

Front 53

What are the consequences of moderate to severe cardiac failure?

Back 53

1) SV & CO continue to fall
2) increased EDV dilates the heart, making its contractions weaker and weaker
3) A-V orifices dilated causing A-V valve leakage
4) sympathetic drive increases HR which increases workload
5) Down regulation of beta 1 receptors means the heart responds less to sympathetic drive
6) Renin-angiotensin system increase volume causing increased filling pressure and edema
7) Overproduction of Ang. II has a deleterious affect on heart
8) increased cytokine production causing cardiac hypertrophy