9/18b Cardiac Physiology (Biomedical Sciences) Flashcards
• Apply the principles of hemodynamics to describe the relationships among flow, pressure, and resistance throughout the cardiovascular system. • Discuss the mechanisms that control the distribution of blood flow • Describe the mechanisms that regulate arterial pressure in the short and long term • Describe the cardiovascular responses to the stress of exercise
To meet rang of metabolic needs of the heart, we must regulate
- output of the system (CO=HRxSV)
- Distribution of output (vasculature)
Rigid tube with pressure transducers on left and right sides.
When pressure on left and right sides are the same, what is the flow
ZERO FLOW because no pressure gradient
Rigid tube with pump and pressure transducers on left and right sides.
When pressure on left is more than the pressure on the right and there is a pump in between what is the flow?
Fluid flows from left to right
How do you find the Total peripheral resistance (TPR)?
TPR = (delta P)/Q OR MAP/CO
Rigid tube with pump and pinched at the bottom and pressure transducers on left and right sides.
What is happening if the Q is the same?
- Increasing resistance because we are decreasing the diameter
- radius^4, small change in radius yields a huge change in resistance
- Pright increases
- Pleft decreases because there is less flow into the left side
Rigid tube with pump and split into 100 at the bottom and pressure transducers on left and right sides.
What is happening if the Q is the same?
-if there’s a 10-fold increase in resistance, then we have a 10-fold increase in pressure gradient
when we increase resistance and need to maintain flow, what do you have to do?
INCREASE the pressure GRADIENT, but how do you get the new pressure gradient?
-if there’s a 10-fold increase in resistance, then we have a 10-fold increase in change in pressure gradient
Blood pressure across the system
- Pulmonary Circuit blood pressure
1. Large Arteries: 15
2. Arterioles:
3. Capillaries: 10
4. Large Vein: 8
5. Atrium: 2-5 - Systemic Circuit blood pressure
1. Large Arteries: 90-100
2. Arterioles: 50
3. Capillaries: 20
4. Large Vein: 4
5. Atrium:0-2
What is Q an index of?
Q = delta P/R CO = BP/TPR
what is the BP pressure gradient from one side of the system to the other side?
90-100 mm Hg
Large pressure drop in a region of a system, means
there must be a large resistance
Biggest pressure drop is at what level?
at the level of the arterioles because the arterioles are the greatest source of resistance to flow in the CV system and a key determinate of TPR
If we want to affect TPR, what do we act on?
Arterioles!
If the flow in the systemic circuit is 5l/min the pulm flow is the same too? T/F
TRUE
What determines how much blood a particular organ gets?
Arterioles! decrease blood flow to a given organ -constrict arteriole -decrease radius -increase resistance -decrease flow
How does the vasculature regulate flow?
- Local and Distant Mechanisms
- by regulating arteriole smooth muscle contraction
- contraction = vasoconstriction
- relaxation = vasodilation
Local mechanisms for vasculature regulation
- Tissue metabolites - by products of tissue metabolism (exercising a muscle) and the metabolites influence the degree of arteriolar contraction. In general, it increases vasodilation to a specific vascular bed
- Myogenic - vessels have an intrinsic property in their smooth muscle vascular wall have a degree of control over their ability to adjust the diameter of the vessel in order to maintain flow despite changes in blood pressure.
- Endothelial Factors - the lining of the BVs are endothelial cells that are metabolically active and can produce substances that either constrict or dilate the arterioles based on shear of BF along the vessel wall
Distant mechanisms for vasculature regulation
- Neural (sympathetic) - arterioles are richly innervated with receptors that respond to epi and NE. Typically VASOCONSTRICTION
- Humoral - endocrine mechanisms dilation and constriction
Phenomenon: active and reactive hyperemia
LOCAL Mechanisms within tissue metabolites and endothelial factors of vasoregulation
- active hyperemia (exercise), electrically stimulating the muscle and increasing metabolic rate of a tissue, thus increasing blood flow in proportion to the degree of metabolic activity (accumulation of tissue metabolites K+, phosphate, adenosine, prostaglandins, etc have a vasodilatory effect)
- reactive hyperemia (BP cuff on limb), decrease flow to a limb and then release occlusion to then slowly get BF back to baseline – caused by tissues that don’t have metabolites being cleared out so they accumulate and cause reactive hyperemia b/c of the shear force on the fluid
Phenomenon: Autoregulation by myogenic mechanism
LOCAL
BF to the brain needs to be constant…designed to maintain stable flow
- maintains flow to the organ despite a wide range in blood pressure
- -when BP is low > cerebral arterioles DILATE to decrease resistance in order to maintain flow in the decreased pressure gradient
- -when BP is high > vessels CONSTRICT in order to maintain flow despite elevated pressure gradient
SNS control of vasculature
DISTANT
- primary neurotransmitter is NE and acts on alpha 1 receptors on arterioles and venules > vasoconstriction
- DIRECT neural influence. adrenal cortex > releases epi into blood stream > circulating catecholamines
circulating catecholamines
epi and norepi that are circulating in the blood stream
Humoral control of vasculature
DISTANT
kidney releases hormones that regulate vessel contraction and resistance
–important for long term maintenance of blood pressure
Baroreceptor Reflex - Neural mechanism
- Blood pressure and standing up too quickly from lying down
- -sensors detect a gravity induced pressure gradient between our head and our heart. Receptors in the aortic arch and carotid body that sense the degree of stretch as the BP changes
- -sensors feedback to the brain (processor that determines the drop in BP)
- -effector carries out the response
- —if arterial pressure decreases, response is to increase CO
- —-decrease Parasymp (withdrawal) = HR increase
- —-augmented with increased Symp = HR increase and SV
- –Increase TPR via symp mediated constriction
- IN RESPONSE TO A FALL IN BP, INCREASE CO AND TPR IN ORDER TO BRING BP BACK UP
- SHORT TERM MANAGEMENT
Renin-Angiotensin-Aldosterone System – Humoral
- Kidneys produce renin (catalyzes angiotensinogen to angiontensin I)
- decrease in renal profusion pressure (blood pressure at the kidneys - MAP), get an increased production of renin
- Renin catalyzes its reaction and there is another substance called ACE (angiotensin conversion enzyme) that converts angiotensin 1 to angiotensin 2 (powerful vasoconstrictor to increase blood pressure)
- angiotensin 2 increases sympatehtic acivitiy, direct impact on arteriolar tone, triggers other systems that allow us to retain salt and water to maintain fluid in the system in order to maintain blood pressure
- decrease in MAP > decrease in profusion pressure in kidney > increase in renin > increase in Angiotensin 2 that tends to bring BP back up!
- LONG TERM management of blood pressure
Pharm management of hypertension
- Decrease CO
- Cacium channel blockers
- Beta Blockers - Decrease TPR
- angiotensin converting enzyme inhibitors - Decrease Fluid Volume
- diuretics
what do calcium channel blockers do?
block influx of Ca during plateau of cardiac AP, thereby decreasing cardiac contractility and SV
What do beta blockers to
block SNS stimulation of HR and SV, leading to decreased CO
what do ACE inhibitors do?
Angiotensin Converting Enzyme Inhibitors prevent formation of angiotensin 2
what do diuretics do?
increase production of urine by kidneys
determinants of VO2/fick equation
VO2 = CO x a-VO2diff CO = cardiac output a-vO2diff = (CaO2 – CvO2) -- amount of oxygen delivered to tissues -CaO2 = arterial blood oxygen content -CvO2 = venous blood oxygen content VO2 = oxygen consumption
relationship between work rate and oxygen consumption
- linear until a point where the oxygen uptake plateaus (VO2max)
- VO2peak = highest on the particular test
- same for all people except for the plateau
mechanisms that cause CO to increase
- increase in SV due to:
- -+ionotropiy via sympathetic stimulation
- -increase preload due to increased venous return
- increase in HR due to:
- -parasympathetic withdrawal -> decrease activity of vagus nerve (most due to this until around 100bpm)
- -sympathetic stimulation of SA node -> direct stimulation; circulating catecholamines (starts to kick in above 100bpm)
muscle pumps
- peripheral muscle pump: deep venous lower extremity muscle pumps (responsible for bulk of venous return)…muscle contracts and squeezes veins and because of valves, blood doesn’t fall back down
- respiratory muscle pump: breathing in decreases thoracic pressure, affects lungs and BVs in thorax so we get pump augmenting flow into thorax b/c less than pressure in abdomen (opposite for exhalation)
both work together to augment venous return
how is cardiac output re-distributed?
as exercise intensity increases, the biggest increase we see is in BF to skeletal muscle, but there’s actually a decrease in visceral BF.
From less metabolically active tissue to MORE metabolically active tissue
- -decrease in visceral BF caused by SNS (general arteriolar vasoconstriction - increases resistance to vascular beds and decreases flow to vascular beds)
- -increase in muscle BF because LOCALLY mediated vasodilation
as we increase exercise intensity, what happens to arteriole and venous oxygen content?
- arteriole oxygen content remains the same
- massive drop in venous oxygen content because we’re extracting more oxygen from that blood
as we increase exercise intensity, why are we extracting more oxygen from venous blood?
- Bohr affect: decreases affinity of oxygen to Hb (allows for unloading of oxygen)
- increase BF to active skeletal muscle, so increasing ttl surface area for gas to exchange between vasculature and skeletal muscle
- pressure gradient: increase pressure gradient between capillary and mitchondria
exercise blood pressure
- systolic pressure increases linearly with the workload
- diastolic pressure stays about the same
- if there is a dropping BP with maintained or increases workload, there is definitely an issue happening with the patient
what happens to CO with exercise?
what happens to MAP with exercise?
thus what happens to TPR with exercise?
- CO: increases! 5 L/min -> 25 L/min increases 5 fold
- MAP: increases! 100mm Hg > 110 mmHg
only 10-20% increase - TPR: decreases! BP=QxTPR
