Cardiovascular Systems Physiology and Pathophysiology V Flashcards by Joel Glotfelty

When the pathologic release of AII and aldosterone occurs, and BP remains abnormally elevated, the high pressure baroreceptors can become

Desensitized

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Does not increase in response to chronically elevated bP

Urinary output

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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)

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What is an example of an ACE inhibitor?

Enalapril

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What is an example of a renin inhibitor?

Aliskiren

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What is an example of an angiotensin receptor blocker (ARB)?

Losartan

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Can be given to reduce the stimulatory actions of

catecholaminergic neurotransmitters within the heart and lower BP

Beta blockers (B1 adrenoreceptor antagonists)

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Lower BP by impairing inward Ca2+ currents in vascular smooth muscle and/or cardiac muscle

Ca2+ channel blockers

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Can be administered to lower blood volume by blocking the effects of aldosterone and/or alterating renal Na+ absorption

Diuretics

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The phenomenon of left ventricular hypertrophy (LVH) is commonly observed in patients with

Long-standing hypertension, valve disease, an MI, or a mutation

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In the heart, pathologic increases in systolic wall stress and/or diastolic wall stress will over time induce

LVH

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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

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By comparison, chronic diastolic wall stress (i.e. volume overload) stimulates the formation of new sarcomeres in series; this is called

Eccentric LVH

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Results in a relatively dilated LV with thin walls

Eccentric LVH

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Not selective for simply myocyte hypertrophy and the formation of new sarcomeres, but includes increased apoptosis, interstitial fibrosis, and endothelial cell dysfunction

Pathologic LVH

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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

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Over time, patholigic LVH can lead to decompensation, resulting in

LV dilation and heart failure

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Isotonic exercise (e.g., running) is correlated with increased venous return, causing a condition of intracardial volume overload, and leading to

Eccentric LVH

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Isometric exercise (e.g., strength training) causes cardiac pressure overload and

Concentric LVH

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Exercise-induced LVH is phenotypically different from pathologic remodeling in that physiologic LVH does not induce

Cardiac interstitial fibrosis

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Which is reversible, physiologic (exercise induced) or pathologic LVH?

Physiologic LVH

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Unlike pathologic LVH, is NOT associated with heart failure and increased mortality

Physiologic LVH

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In Hyoptension, Epi/norepi instigate an increase in

arteriolar TPR that causes a drop in

Capillary pressure

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Reduced capillary pressure establishes a gradient that favors reabsorption of H2O from the

-aids in venous return

ECF

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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?

1. ) 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

1. ) Ventricular wall stress 2. ) HR 3. ) 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 1. ) Directly proportional to 2. ) Inversely proportional to

1. ) 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

1. ) Which type of adrenoreceptors does the coronary vascular smooth uscle express? 2. ) Which one is more predominant?

1. ) 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

1. ) 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