CV 4 Flashcards
— is the driving force for blood flow to all organs.
MAP
MAP = (3)
CO x TPR
MAP = (HR x SV) x TPR MAP = (HR x (EDV-ESV)) x TPR
Factors that influence MAP (3)
- Flow In (CO) and Out (TPR) of Systemic Arteries
- MAP α Total Blood Volume
- Distribution of blood between arteries and veins
Flow of blood through the blood vessels
can be thought of as the flow of a
fluid
through a tube.
Flow in > Flow out;
Hydrostatic pressure in tube will increase due to
fluid accumulation.
Flow in < Flow out;
Hydrostatic pressure in tube will decrease due to
fluid depletion.
Systemic Circulation function can be thought of as the function
of — different tubes connected in series
three
Venous System
Function: (2)
Regulation: (1)
PVP
VR
Systemic
Arterial System
Function: (1)
Regulation: (1)
MAP =
Keep MAP constant
Systemic
CO x TPR
Capillary System Function: (2) Control: (1) Ftissue = Due to myogenic autoregulation, changes in the Rtissue used to regulate (2)
Deliver O2 and nutrients, Pick up CO2 and other metabolic waste
Local (Active Hyperemia)
MAP/Rtissue arteriole
Pc and flow
Baroreceptor Reflex (4)
Short term response (minutes to hours) NS mediated homeostatic process Alters CO and TPR to restore MAP to homeostatic levels Override Local Control of blood flow
Baroreceptor Reflex Stimulus = Reflex Receptor = Afferent Pathway = Integrating Center = Efferent Pathway = Effectors = Effector Response = Feedback Regulation =
Stimulus = ΔMAP
Reflex Receptor = Baroreceptors (Aortic Arch and Carotid Arteries)
Afferent Pathway = Visceral Sensory Neurons
Integrating Center = Medullary CV control centers in Medulla Oblongata (Brainstem)
Efferent Pathway = Autonomic Motor Neurons
Effectors = Cardiac Muscle (AR and Contractile cells), Arteriolar Smooth Muscle, Venous Smooth Muscle
Effector Response = Change rate and force of contraction (CO), Change arteriolar resistance (TPR), Change venous tone (VR>EDV >CO)
Feedback Regulation = Negative
Other Baroreceptors
Large systemic veins, the pulmonary vessels, and the walls of
the heart also contain baroreceptors.
Baroreceptor Function (3)
Immediate changes to restore MAP to homeostatic level
Allows time for other mechanisms to occur to eliminate
disturbance (ex. Total Blood Volume)
Adapt overtime (decrease rate of firing with prolonged increased MAP)
Patients with chronically elevated MAP have baroreceptor
reflexes that function around a
higher than normal setpoint
MAP affected by other stimuli and reflexes aside from baroreceptor reflex.
Changes triggered by signals from
other receptors or higher brain centers that activate Medullary CV control center or autonomic neurons directly
Stimuli that increase MAP (8)
decrease Arterial [O2] increase Arterial [CO2] decrease Brain Blood Flow Pain Originating in skin Stress Anger Eating Sexual Activity
Stimuli that decrease MAP (3)
Pain Originating in Viscera or joints
Sleep
Happy Mood
Hypotension
Low blood pressure
Hypotension causes (4)
- Hemorrhage
- Shock
- Orthostatic
- Other causes
Hemorrhage Compensatory Mechanisms Rapid (12-24 hours) (2) Long Term (days to Weeks) (2)
- Baroreceptor Reflex
- Autotransfusion
- Endocrine System
- Behavior
- Baroreceptor Reflex (2)
Returns MAP toward normal
Increasing CO and TPR
- Autotransfusion (3)
Movement of interstitial fluid into capillaries
Arteriolar constriction > decreases PC
Net absorption of fluid into capillaries
- Endocrine System (2)
ANGII, Aldosterone, ADH - Restore volume and osmolarity
Erythropoietin – Restore Hematocrit
- Behavior (1)
Thirst and consumption of H2O
Shock
This is a condition in which there is inadequate blood flow to meet tissue needs.
Three types of shock
- Hypovolemic shock
- Vascular shock
- Cardiogenic shock
- Hypovolemic shock (2)
results from
followed by (4)
‒ It results from a large loss of blood, so there is a drop in blood volume.
‒ This usually follows hemorrhage, severe vomiting, severe diarrhea, and extensive burns.
- Vascular shock (6)
‒ Blood volume is normal, but circulation is poor due to abnormal expansion of the vascular bed caused by extreme vasodilation.
‒ Huge drop in TPR leads to a drop in MAP
‒ The most common causes:
• loss of vasomotor tone associated with anaphylaxis (allergic reaction; anaphylactic shock)
• a loss of nervous system regulation (neurogenic shock)
• septicemia (septic shock; a bacterial infection).
- Cardiogenic shock (2)
‒ This is pump failure. The heart can not sustain adequate circulation.
‒ This is usually the result of myocardial damage following a severe MI or multiple MIs.
Orthostatic Hypotension
Drop in MAP upon standing
The effects of gravity cause a
decrease VR decrease EDV decrease SV decrease CO decrease MAP
Hypertension
Chronically elevated MAP
why is hypertension a silent killer?
because most people don’t know that they
have it until it has caused significant damage.
Prolonged hypertension is the major cause of (4)
heart failure,
renal failure,
stroke, and
vascular disease.
Two major forms of hypertension
- Primary (Essential) Hypertension
2. Secondary Hypertension
- Primary (Essential) Hypertension (2)
90% of Hypertension Patients
Idiopathic
- Secondary Hypertension (3)
10 % of Hypertensive Patients
Secondary to a disease state
Treat disease state and MAP returns to normal
Factors that are involved in the development of primary hypertension
include: (8)
–Diet: high Na+, high cholesterol etc. –Diabetes mellitus –Obesity –Age (clinical signs appear ~40) –Gender (males get it more than females until menopause) –Genetics (runs in families, black more prevalent [salt sensitive forms] than whites) –Stress –Smoking
can we cure Primary (Essential) Hypertension?
no
We can manage it with diet, exercise, life-style
changes, and medication.
Diseases associated with secondary hypertension (6)
Tumor of the adrenal medulla (excess Epinephrine)
Cushing’s disease (Glucocorticoid excess)
Atherosclerosis of the renal arteries (RAS)
Renal Hypertension (Kidney disease) (RAS)
Arteriosclerosis
Hyperthyroidism (TH excess)
hypertrophic remodeling (5)
Large vessels that do not constrict in response to increased MAP
Size of VSM cells increase
Increase in EC matrix proteins to support wall
increase total cross sectional area of vessel
Makes large vessels stiffer (less compliant)
inward eutrophic remodeling (3)
Small vessels that constrict in response to increased Map
VSM growth around narrowed lumen (decrease r; increase R)
No change in total cross sectional area of vessel
- Laminar Flow
When vessels are: (3)
straight
endothelium is healthy
smaller vessels
With laminar flow, the velocity of flow is always greater in the
center of the vessel compared to the outside.
Laminar Flow
— profile of flow
Parabolic
Shear:
When adjacent layers of blood move at different
velocities—can break up RBC aggregates
Reynold’s Number (Re) is the calculation of the
tendency for turbulent flow
If Re is greater than 2000, flow is most likely turbulent.
Greater than 3000, always turbulent.
Re =
(V d ρ)/ η
Velocity of blood flow (V)
Diameter of vessel (d)
Density of blood (ρ)
Viscosity of blood (η)—hematocrit
Turbulent flow:
increases (3)
Increases friction and the energy required to drive flow
Increases the risk of endothelial injury & plaque development
Increases the possibility of thrombotic events
Turbulent Blood Flow
in large vessels like (2)
Aorta and Pulmonary Artery
Smaller vessels
(Arterioles) rarely have
turbulent flow
Viscosity-
thickness or thinness of a fluid
Density –
measures spaces between 2 particles in a solution
Heart Failure (CHF)
Heart fails to pump adequate CO
Two Types of CHF
- Diastolic Dysfunction
- Systolic Dysfunction
*Many patients have elements of both
- Diastolic Dysfunction (4)
Ventricles have reduced compliance (wall stiffens)
Creates problems with ventricular filling
Reduced EDV
Most common cause = Hypertension (ventricular hypertrophy)
- Systolic Dysfunction (3)
Ventricle has reduced contractility
Decreased SV at any given EDV
Most common cause = myocardial damage as result of
myocardial infarct
