Cardiovascular Systems Physiology and Pathophysiology V Flashcards
When the pathologic release of AII and aldosterone occurs, and BP remains abnormally elevated, the high pressure baroreceptors can become
Desensitized
Does not increase in response to chronically elevated bP
Urinary output
Abnormal levels of (or increased sensitivity to) An-II appear to be central in some forms of essential hypertension, what can be used to combat this?
- ) ACE inhibitors
- ) Renin inhibitors
- ) AT1 antagonists (angiotensin receptor blockers, ARB)
What is an example of an ACE inhibitor?
Enalapril
What is an example of a renin inhibitor?
Aliskiren
What is an example of an angiotensin receptor blocker (ARB)?
Losartan
Can be given to reduce the stimulatory actions of
catecholaminergic neurotransmitters within the heart and lower BP
Beta blockers (B1 adrenoreceptor antagonists)
Lower BP by impairing inward Ca2+ currents in vascular smooth muscle and/or cardiac muscle
Ca2+ channel blockers
Can be administered to lower blood volume by blocking the effects of aldosterone and/or alterating renal Na+ absorption
Diuretics
The phenomenon of left ventricular hypertrophy (LVH) is commonly observed in patients with
Long-standing hypertension, valve disease, an MI, or a mutation
In the heart, pathologic increases in systolic wall stress and/or diastolic wall stress will over time induce
LVH
In response to pathologic systolic wall (pressure overload) stress the formation of sarcomeres occurs in parallel, and the LV thus forms thick walls and a relatively small cavity; this is called
Concentric LVH
By comparison, chronic diastolic wall stress (i.e. volume overload) stimulates the formation of new sarcomeres in series; this is called
Eccentric LVH
Results in a relatively dilated LV with thin walls
Eccentric LVH
Not selective for simply myocyte hypertrophy and the formation of new sarcomeres, but includes increased apoptosis, interstitial fibrosis, and endothelial cell dysfunction
Pathologic LVH
The molecular mechanisms for pathologic LVH, which make it markedly different than that resulting from exercise include the induction of cell signalling cascades and changes in
Gene transcription
Over time, patholigic LVH can lead to decompensation, resulting in
LV dilation and heart failure
Isotonic exercise (e.g., running) is correlated with increased venous return, causing a condition of intracardial volume overload, and leading to
Eccentric LVH
Isometric exercise (e.g., strength training) causes cardiac pressure overload and
Concentric LVH
Exercise-induced LVH is phenotypically different from pathologic remodeling in that physiologic LVH does not induce
Cardiac interstitial fibrosis
Which is reversible, physiologic (exercise induced) or pathologic LVH?
Physiologic LVH
Unlike pathologic LVH, is NOT associated with heart failure and increased mortality
Physiologic LVH
In Hyoptension, Epi/norepi instigate an increase in
arteriolar TPR that causes a drop in
Capillary pressure
Reduced capillary pressure establishes a gradient that favors reabsorption of H2O from the
-aids in venous return
ECF
Enables increased cardiac output and will therefore increase arterial BP
Increased venous return
The average blood volume is approximately
5-6 L
The displacement of blood per second determines the
Velocity of the blood (v = m/s)
The volume of blood moved per second
Flow (Q)
- Q = volume/s
- Q = mL/s
What term is interchanged with blood flow?
Conductance
The peripheral vasculature is comprised of vessels of varying diameter (cross-sectional area, A), and diameter affects the rate of flow such that
v = Q/A
Which laws describe hemodynamics?
The conservation of mass laws
Must be constant through a given vessel at a specific point in time
Blood flow (Q)
At a given flow, velocity (v) is inversely proportional to
Area (A)
The resistance (R) offered by a vessel must be accounted for because it will of course alter flow. This is accounted for in
Ohms Law
Q = ΔP/R
The difference between arterial pressure and venous
pressure (Pa – Pv) as it relates to flow through the entire systemic vascular network
Total peripheral resistance (TPR)
The parallel nature of the arteriole tree results in less total resistance to systemic flow than would occur in a
Single vessel
The resistance through a single capillary is much greater than through an arteriole, why then is there a much lower pressure drop across the capillary system as compared to a high pressure drop across the arteriole system?
The number of capillaries vastly exceeds the number of arterioles
Changes in arteriole circulation account for the vast majority of
TPR
The diameter of the arteriole network can change by approximately 4x, thus very dramatically
Increasing (via constriction) or decreasing (via dilation) TPR
In general, blood flows equals
% L/min
What are the two types of blood flow that occur?
- ) Laminar flow
2. ) Turbulent flow
A very streamlined movement of blood, and is predominant in the vasculature under normal circumstances
Laminar Flow
The type of blood flow where a blood cell moving through the center of a vessel would tend to stay in the center stream of flow
Laminar blood flow
What is greater during laminar flow, the velocity of blood in the center or towards the periphery?
The center
More random in nature and is characterized by very
complex flow dynamics consisting of eddies, cross-currents, back-flow, etc
Turbulent flow
Can result from extreme increases in pressure, obstructions, the movement of blood over irregular surfaces such as atherosclerotic plaques, and/or increased blood viscosity
Turbulent flow
Increase friction, turbulence, and therefore cause a higher resistance to blood flow
Elevations in blood viscosity
Determined mainly by the percent volume of blood cells (RBCs and WBCs) in whole blood
Blood viscosity
Blood viscosity can be measured by performin a
Hematocrit analysis
Veins are known as
Compliance vessels
The capacitance “side” and is responsible for blood storage and return to the heart
Venous network
What are the two key properties possessed by veins, which react to alterations in arterial BP?
Compliance and distensibility
Distend in response to increased BP
Veins
Aids in lowering resistance in response to elevated arterial BP
Venous distension
Allows continuous laminar flow though the capillary network to be maintained as arterial BP rises
Venous distension
Another venous phenomenon, which can be thought of as the amount of blood that can be stored (accommodated) when arterial BP increases
Compliance
Not very distensible and have low compliance
Arteries
Accommodate approximately 60% of circulating blood
The great veins
Veins have low BP but a high
Flow velocity
What is used as a guide for measuring the central venous pressure (CAP)?
Right atrial pressure (RAP)
RAP = CVP
Determined by balances between RA emptying and venous return to the heart
RAP
Central venous pressure approximates around
2mmHg
Fights venous return to the heart by increasing venous pressures, especially in the upper and lower limbs
Hydrostatic pressure from gravity
What do veins within skeletal muscle have to help them fight the hydrostatic pressure of gravity?
Valves
Anything that disrupts cardiac output (CO) can lead to elevations in
RAP
When we say “left heart failure” we are talking about
Impaired left ventricular emptying
Since the right atrium is open to the vena cava, a significant rise in RAP can lead to increased venous pressures within the
Jugular and Hepatic Portal Circulations
The rhythmic pattern of systolic and diastolic BP in the arteries is known as the
Pulse Pressure
Determined by SV (EDV – ESV), total compliance of the arterial tree, and the least significant factor being force of blood ejection from the LV
Pulse Pressure
Must increase as SV increases in order to maintain normal pulse pressure
Arterial compliance
If arteries become less compliant, we will see an elevation in
-Causes a greater workload on the LV
Systolic arterial BP
Cardiac output and total peripheral resistance determine
Mean arterial pressure (MAP)
-a dependent variable
The myocardium requires high levels of O2. As local O2 concentration diminish, what processes are impaired?
Oxidative phosphorylation and generation of ATP
The impairment of ATP generation leads to the formation of
ADP, AMP, and ultimately adenosie
Blocks Ca2+ entry into vascular smooth muscle and thus induces vasodilation
Adenosine
The three major determinants of myocardial O2 requirements in order of demand are
- ) Ventricular wall stress
- ) HR
- ) Contractility (inotropic state)
The myocardium is supplied with O2 via the
Coronary arteries
Occlusion of the coronary arteries can lead to ischemia and is a common cause of
Coronary heart disease (CHD)
If severe enough, coronary artery occlusion can lead to
Angina pectoris and MI
Peak blood flow within the coronary arteries occurs during
Diastole
Blood flow is greatly reduced due to the compression of the vessels by the surrounding myocardium during
Systole
Flow (Q) is
- ) Directly proportional to
- ) Inversely proportional to
- ) Pressure
2. ) Resistance
Maintanence of perfusion pressure (MAP) is critical for
O2 delivery and CO2 removal
The majority of myocardial O2 uptake occurs during
Diastole
Approximately 70% of the exchange of O2 for CO2 is accomplished within the myocardium during
Diastole
What are some important vasodilators?
NO, CO2, H+, Lactate, Adenosine, and rostacyclins
- ) Which type of adrenoreceptors does the coronary vascular smooth uscle express?
- ) Which one is more predominant?
- ) a1 and a2 adrenoreceptors
2. ) a2 is more predominant
Mediate vasoconstriction in coronary artery vascular smooth muscle
a1 and a2 adrenoreceptors
Occurs if endothelial function is disrupted such that vasodilator production is compromised
-impedes normal blood flow
a2-mediated vasoconstriction
A localized anemia due to a reduction in blood supply
Ischemia
Results from an imbalance between O2 supple and myocardial demand
-produces a localized hypoxia concomitant with the accumulation of waste metabolites
Ischemic heart disease
If severe enough, ischemia will lead to MI; less drastic reductions in delivery can manifest as one or more forms of
Angina
Two general mechanisms underlie the pathophysiology of cardiac ischemia and these are
- ) Fixed vessel narrowing (atherosclerotic plaques)
2. ) Abnormal vascular tone
Very metabolically active tissues which produce a number of factors that mediate vascular smooth muscle
tone and local antithrombotic processes
Vascular endothelium and Vascular smooth muscle
