Module 6: Cardiovascular Flashcards Preview

Physiology Module > Module 6: Cardiovascular > Flashcards

Flashcards in Module 6: Cardiovascular Deck (237)
Loading flashcards...
151

Caliber of veins adjusted by:

1. the circulating Vasoactive subs
2. Vasomotor Nerves

152

- Capacity of tissues to regulate their own blood flow
*Due to the intrinsic contractile response of smooth muscle to stretch (Myogenic Theory of Autoregulation)
*Due to vasodilator metabolites that accumulate in active tissues (Metabolic Theory of Autoregulation)

- Well developed in the Kidneys

AUTOREGULATION

153

VASOCONSTRICTORS (local)

1. Serotonin
2. drop in temperature – localized vasoconstriction
3. increased calcium conc.
4. Sl. decrease H† conc.

154

SUBSTANCES SECRETED BY ENDOTHELIUM

a. PROSTACYCLIN – inhibits platelet aggregation and promotes vasodilation

b. THROMBOXANE A2 - produced by platelets; promotes platelet aggregation and vasoconstriction

c. EDRF (Endothelium Derived Relaxing Factors) now called NITRIC OXIDE (NO) - Vasodilator

d. ENDOTHELIN 1 – potent vasoconstrictor

155

Vasoconstrictor Hormones:

- Norepinephrine (NE) – powerful vasoconstrictor
- Epinephrine – less powerful than NE; may cause vasodilation in coronary arteries during increased heart activity
- Angiotensin II
- Vasopressin – more powerful than Angiotensin II as a Vasoconstrictor
- KININS - bradykinin
- VIP

156

Antagonizes the action of vasoconstrictor agents and lowers BP

Atrial Natriuretic Peptide

157

NEURAL FACTOR (Rapid Control of ABP)

• All blood vessels except capillaries and venules contain smooth muscle and receive innervation from sympathetic nervous system
- The fibers to the arterioles regulate tissue blood flow and arterial pressure
- The fibers to the capacitance vessels vary the volume of blood stored in the veins
Ex. Venoconstriction
♣ decreased venous capacity
♣ increased venous return

158

NORADRENERGIC FIBERS TO BLOOD VESSEL

• vasoconstriction
• contain NEUROPEPTIDE Y – which is a vasoconstrictor
• vasoconstrictor fiber exhibit tonic activity
(S tone to blood vessel)
Cut S to b.v. → b.v. dilates
• S vasoconstrictor effects esp. powerful in the kidneys, spleen, skin; less in brain and skeletal muscles

159

SYMPA CHOLINERGIC TO BLOOD VESSEL SKELETAL MUSCLES

• Vasodilator – called Sympathetic Vasodilator System
• Contain VIP which produced Vasodilation
*NO tonic activity

160

ARTERIAL PRESSURE CONTROL

1. begins with life saving measures of the nervous control mechanism
2. continues with the sustaining characteristics of the intermediate mechanisms
3. finally, is stabilized at the long term mechanism by the renal – body fluid mechanism

161

Arterial pressure is regulated by several inter-related systems each of which performs a specific function

CONTROL MECHANISM

162

(CONTROL MECHANISM)

- begins to act within seconds or minutes but cannot maintain ABP because they adapt to prolonged change in pressure
- attempts to restore BP rapidly toward normal
- Involves participation baroreceptors and chemoreceptors located in the peripheral circulation
- begin to act within seconds or minutes
- Powerful control mechanism
- most nervous control of BP is achieved by reflexes that originate in the baroreceptors and chemoreceptors located in the peripheral circulation outside the brain

Rapidly Acting Pressure Control Mechanism

163

(Rapidly Acting Pressure Control Mechanism)

- Activated instantly by any BP change
- Attempts to restore BP rapidly toward normal
- Cannot maintain BP because they adapt to prolonged change in pressure. Thus, Short – term Regulator of ABP
- Involves participation of baroreceptors in arch of aorta and carotid sinus

Baroreceptor Feedback Mechanism

164

Rapidly Acting Pressure Control Mechanism

A. Baroreceptor Feedback Mechanism

B. CNS ISCHEMIC MECHANISM - Ex. Cushing Reaction

C. ATRIAL STRETCH REFLEXES
1. BAINBRIDGE REFLEX (Atrial Reflex control of HR)
2. VASOPRESSIN / ADH

D. CHEMORECEPTOR MECHANISM
- Chemoreceptors in the Carotid and Aortic bodies

165

Intermediate Time Period Control Mechanism

A. RAAS
B. Capillary Fluid Shift Mechanism
C. Stress – Relaxation of the Vasculature

166

- It takes a few hours to show significant response
- This mechanism can eventually return the arterial pressure all the way back to normal pressure that will provide normal output of salt and water by the kidneys
- Has multiple interactions with the RAAS and the Nervous System

The Renal Body Fluid Pressure Control Mechanism or Renal-Blood Volume Pressure Control Mechanism

167

- Reflex Arc Components
- Vasomotor Area or VMC (groups of neurons in the Medulla Oblongata responsible for the main control of ABP)
- Afferent fibers end in the Nucleus of Tractus Solitarius (NTS)
- After the baroreceptor signals have entered the NTS of Medulla, secondary signals inhibit the VMC (Gaba) and excite the CIC (Glutamate)
- VMC transmits sympathetic impulses to blood vessels
- Lateral portion of VMC transmit excitatory impulses through S to heart
- Medial portion of VMC transmits PS signals to dorsal motor nucleus of CN X to heart

Baroreceptor Reflex/ Sino-aortic Reflex/ Marey’s Law of the Heart

168

Practical application of baroreceptor reflex

- Changes in body posture
- Direct pressure on the carotid sinus – ↓ HR
*This maneuver is used to treat paroxysmal tachycardia

169

Increases baroreceptors discharge decreases ABP. How?

1. inhibits the tonic discharge of the vasoconstrictor nerves→vasodilation→ decreases PR
2. excites the vagal innervation of the heart→decreases HR and CO
3. Venodilation - decreases ABP due to pooling of blood

170

- Not stimulated by pressure between 0mmHg and 50 to 60 mmHg
- Responds rapidly above this level and reach a maximum of 180 mmHg

Carotid Sinus Baroreceptors

171

Factors that affect the Vasomotor Area or VMC: Excitatory inputs from

1. Excitatory inputs from the higher centers like hypothalamus and cortex
Ex. Emotions like anger and sexual excitement
→ Increased HR and vasoconstriction
→ Increased ABP

2. Excitatory inputs pain pathways and muscles
Ex. Acute pain → increased BP via afferent impulses in the reticular formation converging on the VMA

Exception: Prolonged severe pain→ Vasodilation → decreased BP → fainting

172

Factors that affect the Vasomotor Area or VMC: Inhibitory Inputs from

1. Cortex via hypothalamus
Ex. Fear and grief → bradycardia and vasodilation → decreased BP→ Syncope

2. Lungs
Inflation of lungs → inhibit vasomotor discharge through CN X→ Vasodilation and decreased BP

173

- ABP also controlled by the VMC in the brain in response to diminished blood flow to the brain

Cerebral Ischemia → increased ABP → decreased HR

CNS ISCHEMIC MECHANISM

174

- is an example of the response to cerebral ischemia
- is a special type of the CNS ischemic response that results from an increased pressure in the cranial vault
- happens when CSF pressure rises to equal ABP
*compresses arteries in the brain
*cuts off blood supply to brain
*cerebral ischemia
*increases ABP to a level higher than CSF pressure
*blood flows once again to brain vessels
8relieve the cerebral ischemia

- SIG: helps protect the vital centers of the brain from loss of nutrition when the CSF pressure rises at a level high enough to compress the Cerebral arteries

CUSHING REACTION

175

- operates primarily as an emergency arterial control system that acts rapidly and powerfully to prevent further decrease in ABP when blood flow to brain decreases. Called the “LAST DITCH STAND” pressure control mechanism
- is one of the most powerful of all the activators of the Sympathetic vasoconstrictor system because can elevate MAP to as high as 250 mmHg, to a point that some peripheral vessels become almost totally occluded.
*Ex. Kidneys almost entirely stop production of urine because of arteriolar constriction
- Powerful so that ABP rise high enough to correct brain ischemia before it causes nutritional depression and death of neuronal cells

CNS INSCHEMIC RESPONSE

176

- elicits reflexes parallel to baroreceptor reflex
- BAINBRIDGE REFLEX
- this reflex help prevent damming of blood in veins, in atria, and in pulmonary circulation

ATRIAL STRETCH REFLEXES

177

- Rise in CVP as in increased blood volume
→ distend right atrium
→ (+) atrial stretch receptors
→ afferent signals to medulla through CN X
→ efferent signals to heart through S
→ increased HR and contractility

BAINBRIDGE REFLEX

178

ATRIAL STRETCH REFLEXES

- under conditions of HYPERVOLEMIA, Bainbridge reflex predominates over sino – aortic reflex
- under conditions of HYPOVOLEMIA, sino – atrial reflex predominates over Bainbridge reflex

179

- involved in the regulation of BP in response to hemorrhage, but not in minute to minute regulation of normal BP
- synthesized mainly by the supra-optic nuclei of hypothalamus and to a lesser extent by the paraventricular nuclei
- stored and released by posterior pituitary gland

VASOPRESSION (ADH)

180

adequate stimulus for ADH release:

decreased blood volume ADH is released when atrial receptors detect a decrease in blood volume