Physio - Special Circulation Flashcards
What are the 4 General regulatory principles?
-
Autoregulation
- Mostly myogenic mechanism:
- ↓ perfusion pressure relaxes smooth muscle (vasodilation)
- ↑ perfusion pressure stretches smooth muscle (vasoconstriction)
- Coronary, cerebral, and renal vasculatures = highly autoregulated
- Mostly myogenic mechanism:
-
Pressure Effect
- Tissue edema causes extravascular compression
-
Active Hyperemia
- blood flow to an organ is ↑ _according to metabolic activit_y
-
Exemption = renal vasculature
- blood flow exceeds demand
-
Reactive Hyperemia
- Transient ↑ in organ blood fllow –>occurs after brief period of ischemia
-
Examples:
- transient coronary vasospasm
- application/removal of tourniquet
- arterial clamp during surgery
Note:
- Active & Reactive Hyperemia = due to vasoactive metabolites, hormones, & other humoral agents
Vasodilators vs. Vasoconstrictors
Organ Blood Flow Distribution
At Rest:
- Kidney = gets MOST blood flow
Heavy Exercise:
-
Skeletal Muscle = gets MOST blood flow
- burn ATP like crazy & open up cap beds
- Heart = ↑ 3-5x
- Skin = first ↓ blood flow, then ↑
- Liver/GI = ↓
Always Constant:
- Brain
- Kidney (over time)
Coronary circulation
Basics:
-
Right coronary artery feeds…
- SA mode
- R.A. & R.V.
- Bottom of L.V.
- occlusion –> R.V. MI & most inferior MIs
-
Left coronary artery feeds…
- Majority of L.V.
- occlusion –> anterial or septal MIs
- Majority of L.V.
Coronary Blood Flow:
- Heart = limited to oxidative metabolism
- Blood flow ~5% of CO at rest
- but high O2 consumption per gram (comparable to = mass of exercising skeletal muscle)
- Heart = HIGHLY efficient to extract oxygen from blood
- ↑ in O2 delivery means coronary blood flow must ↑
- MVO2 related to cardiac work
Regulation:
-
Autoregulated by METABOLITES
- Vasodilation in response to hypoxia
- cardiac cells release: adenosine, H+, & CO2
- endothelial cells release: NO
- Vasodilation in response to hypoxia
-
Sympathetic regulation has MINOR role
- vasoconstriction via alpha-1 receptors locally
- counterbalance vasodilation for equal blood flow thru heart layers
- vasoconstriction via alpha-1 receptors locally
Note:
- Coronary blood flow ~ deltaP/ resistance
- DeltaP = Pd – LVEDP
- Resistance: depends on external compression, local metabolites, endothelial factors & sympathetic NS
- DeltaP = Pd – LVEDP
What is the importance of Collateral Blood Flow?
Basics:
- Network of tiny vessels that are normally NOT open
- Provides alternate routes around a blocked artery
When does this happen…
- Coronary artery disease
- People w/ chronic ischemia (low blood flow)
Note:
- Physiologically NOT common
What are the Cardiac Enzymes Released by a Damaged Heart?
-
Myoglobin
- released by skeletal & cardiac muscle
-
earliest to detect
- peaks ~2 hrs
-
Troponin I (cTnI) or Troponin T (cTnT)
- most sensitive test
- released 2-4 hours after injury
- peaks ~12 hrs (stays for 7-14 days)
-
Creatine Kinase (CK-MB isoforms)
- CK-MB1 (CK-MB2 released but converted)
- detectable 3-4 hrs after MI
- peaks ~10-24 hrs (stays 2-5 days)
Older marker:
-
Lactic Dehydrogenase (LDH)
- low specificity
- peaks ~72 hrs (stays 10-14 days)
- low specificity
New marker:
-
Glycogen phosphorylase BB (GP-BB)
- released 1-3 hrs after
- peaks ~7 hrs
- released 1-3 hrs after
Cerebral circulation
Basics:
-
Highly susceptible to ischemia
- few seconds –> loss of consciousness
- few mins –> possible irreversible injury
Regulation:
- Strong autoregulation via metabolites
-
btw 60 - 160 mmHg MAP
- Demand is proportional to neuronal activity
-
btw 60 - 160 mmHg MAP
-
Vasodilation caused by…
-
CO2 & H+
- extreme values –> vasoconstriction & coma
- K+ & Adenosine
- NO (from neurons)
-
CO2 & H+
Notes:
- Sympathetic nerve activity or vasoactive agents = not super important
What is the difference between Ischemic & Hemorrhagic Stroke?
Ischemic or Occlusive Stroke (Clots)
- Obstruction w/in blood vessel supplying blood to brain
- ~87% of all stokes
Hemorrhagic Stroke (Bleeds)
- Weakened blood vessel ruptures
- Commonly caused by uncontrolled HTN
- Other causes:
- aneurysm
- arteriovenous malformation
Pulmonary vasculature
Bronchial vasculature
- Bronchial arteries = branches of thoracic aorta
-
Function = provide nutrients
- tracheo-bronchial tree –> terminal bronchioles
Pulmonary vasculature
- Pulmonary arteries, capillaries and veins
- Function = gas exchange
-
Low resistance & low pressure system (10-25mmHg)
- Less smooth muscles in vascular walls compared to systemic circulation
- Comprised of “capillary sheets”
- vs. tubular vessels in systemic circulation
- Large total surface: 50-70 m2
Key Concepts:
-
Think opposite:
- ↑ O2 = vasodilation
- ↓ O2 = vasoconstriction
-
Hypoxia causes vasocontriction
- route blood to best ventilated alveoli
- maintain optimal ventilation-perfusion ratio
- Regulated by AUTONOMIC NS
- Parterioles = constrict in response to Angiotensin II
- Pvenules = constrict in response to Serotonin & Histamine
Small Intestine Circulation
-
Autonomic Regulation
- Parasympathetic Activation
- MAJOR effect = ↑ secretion & metabolites –> ↑ vasodilation –> ↑ blood flow
- LESSER effect = ↑ motility –> ↑ mechanical resistance –> ↓ blood flow
- Parasympathetic Activation
-
Circulating and Metabolic Factors
-
Constrictors:
- NE, E, Dopamine, Angiotensin II , Vasopressin (ADH)
- ↓ blood flow
- sacrifice GI blood flow
-
Dilators:
- VIP, Gastrin, Cholecystokinin, Glucagon
- ↑ blood flow
- stimulate GI blood flow
-
Constrictors:
Hepatic circulation
Mesenteric circulation
- vasculature of the intestines
Splanchnic circulation
- provides blood flow to the entire abdominal portion of the digestive system
- (+hepatobiliary system, spleen and pancreas)
Hepatic artery
- ~25% of hepatic blood
- under higher pressure
Portal Vein
-
~75% of hepatic blood
- under low pressure (allow for nutrient exchange)
Cutaneous Circulation
Basics:
- At rest, skin = LOW O2 requirement
- Function = Thermoregulation
Regulation:
-
Sympathetic (NE & E)
- initially –> vasoconstruction to shunt blood to core
- ↑ body core temp –> vasodilation & sweating
- Local metabolites = LITTLE effect
Hands, feet, lips, ears and nose:
-
Arteriovenous anastomoses
- Direct shunt for artery/veins
- causes frostbite
- __Can constrict completely & contribute a lot to
thermoregulation
- Direct shunt for artery/veins
-
High level of:
- adjustability
- regional variability
- individual variability
What is the purpose of Countercurrent Heat Exchange?
Purpose:
- minimize heat loss in extremities during cold
How?
- venous blood is directed towards a deep vein
- heat is directly transferred from a parallel running artery
Note:
- Important in animals
- Not crucial in humans
Skeletal Muscle Circulation
Basics:
- Muscle tissue (per gram) has LOW O2 consumption at REST
- comparted to cardiac muscle & brain
- Has the LARGEST change in blood flow during EXERCISE
- flow & O2 increases 10-30x
Regulation at REST:
-
SYMPATHETIC innervation of arterioles
- Alpha 1 receptors –> vascoconstriction
- Beta 2 receptors –> vasodilation
Regulation during EXERCISE:
- Local METABOLITES:
- Adenosine, lactic acid, K+ –>
- Hypoxia,H+, CO2, NO –> vasodilation
- Muscle pump can be overcome by reactive hyperemia
Renal Circulation
Basics:
- Receive HIGHEST blood flow per gram
- prinicple of active hyperemia does NOT apply
- Blood flow to kidneys = dependent on systemic BP
Regulation:
- Blood flow AUTOREGULATION
- via intra-renal vascular resistance sensors
- btw 75-175 mmHg MAP
- via intra-renal vascular resistance sensors
2 Capillary Beds:
- glomerular capillaries –> glomerular filtration
- peritubular capillaries –> homeostatic substance exchange
Note:
- Highest blood flow = renal cortex
- allows plasma filtration
- Lowest blood flow = renal medulla
- prevent washout of osmotic gradient