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Pathophysiology > Week 3 Hypertenstion & Heart Failure > Flashcards

Week 3 Hypertenstion & Heart Failure Flashcards

1
Q
  1. What is the tern used to describe the pressure exerted by circulating blood on the walls of the blood vessels?
    HINT: COxSVR
  2. What effect does pregnancy, meds and bradycardia have on blood pressure?
A
  1. Blood Pressure (BP)

2. Low BP

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2
Q
  1. Describe what is meant by mean arterial pressure.
  2. What is the reference value of MAP?
  3. How do we increase MAP and decrease MAP?
A
  1. MAP is the average arterial pressure during a single cardiac cycle (SBP+ 2 x DBP)/3
  2. 70-100mmHg
  3. Increase MAP: primary HTN
    Decrease MAP: cardiac failure and sepsis
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3
Q
  1. What is the term for the volume of blood pumped by the heart per minute (mL/blood/min)?
  2. How can we increase this term? How do we decrease the volume of this term?
A
  1. Cardiac output
  2. Increase - increase MAP, increase circulating volume
    Decrease - decrease MAP, decrease circulating blood volume or decrease strength of ventricular contraction, heart failure
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4
Q
  1. What is the volume of blood in the ventricles immediately before contraction known as?
  2. What is this term directly related to?
  3. Stroke volume is?
  4. How do we increase and decrease stroke volume?
A
  1. End Diastolic Volume (EDV)
  2. Directly related to the preload; the greater the preload the greater the EDV
  3. SV is the amount of blood pumped by the heart per cardiac cycle
  4. Increase SV by increasing circulating volume + inotropes (ex. Digoxin)
    Decrease SV when contractility is impaired and valve is dysfunctional
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5
Q
  1. What is the measurement of resistance or impediment of the systemic vascular bed to blood flow?
  2. How do hypovolemic shock and vasoconstrictors affect the SVR?
  3. How do vasodilators, morphine, anaphylactic shock and late septic shock affect the SVR?
A
  1. Systemic Vascular Resistance
  2. Increase SVR
  3. Decrease SVR
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6
Q
  1. Explain the Frank-Starling Mechanim.
  2. How does increase blood volume affect the stretch of the heart and force of contraction?
  3. How does increased SV affect EDV and force of the next contraction?
  4. When does increased SV become ineffective?
A
  1. The greater the stretch, the greater the force.
  2. Increase blood volume increases the stretch of the heart and thus increases the force of contraction
  3. Increased SV will increase EDV and increase the force of the next contraction
  4. Becomes ineffective once the heart becomes overfilled and the muscle becomes over-stretched
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7
Q
  1. What does LAPLACE’s law state?
  2. What is the equation for LAPLACE’s law?
  3. As wall thickness increases, how does it affect wall tension?
  4. What type of relationship do radius and tension have?
  5. How does dilation affect the work of the heart?
A
  1. As the radius increases, so does the tension
  2. Wall tension = intraventricular presure x internal radius/wall thickness
  3. As wall thickness increases wall tension decreases (inverse relationship)
  4. Radius and tension have an direct relationship.
  5. Requires the heart to work harder to pump blood.
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8
Q
  1. Define the term used for pressure generated at the end of diastole.
  2. What 2 primary factors determine the preload?
  3. What affect does increased preload have on cardiac output? How does this affect stretch?
A
  1. Preload
  2. A) The amount of venous return to the ventricle
    B) Blood left in the ventricle after systole of end-systolic volume
  3. Increased preload increases cardiac output (volume of blood pumped per min); Increases stretch and the force of the next contraction
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9
Q
  1. How is preload increased?
  2. How is preload decreased?
  3. When preload is too high this may have a _____ relationship with stroke volume.
A
  1. Preload is increased when venous return is increased via fluid overload or structural heart defects
  2. Preload is decreased when venous return is decreased via hemorrhage, 3rd spacing (edema) or limited ventricular filling via constrictive pericardititis and cardia tamponade (layers of heart becoming filled with blood)
  3. Inverse relationship
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10
Q
  1. Define afterload
  2. What does afterload depend on mainly? (2)
  3. What relationship do afterload and cardiac output share?
A
  1. The force that the contracting heart must generate to eject blood from the filled heart
  2. Depend mainly on a) ventricular wall tension and b) peripheral vascular resistance
  3. Inverse relationship; the greater the afterload the less the cardiac output
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11
Q
  1. How is afterload increased ?
  2. How can increased afterload effect ventricular ejection?
  3. How is afterload decreased?
  4. What is aortic valve stenosis?
A
  1. Caused by increased aortic pressure (ex. Aortic stenosis) and increased SVR (ex. Severe HTN, vasoconstriction)
  2. May impair ventricular ejection if ventricles cannot generate sufficient pressure
  3. Afterload is decreased when SVR is decreased and vasodilation occurs (Ex. Sepsis, hyperthermia); decreased BP, nitrates
  4. Valve does not fully close and valve does not fully open
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12
Q
  1. How do beta-blockers, Ca channel blockers and digoxin affect HR?
  2. How does increased HR affect CO?
  3. How does decreased HR affect CO?
A
  1. Decrease HR
  2. Increased HR shortens diastole and ventricular filling time, so this will decrease CO
  3. Decreased HR also decrease CO; even though SV is similar we are not circulating enough blood per min
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13
Q
  1. Increasing contractility results in increased/decreased SV. This increases/decreases myocardial oxygen consumption.
  2. What 3 factors affect contractility?
  3. What factors could compromise intrinsic contractility?
  4. Which medication increase contractility? Which decrease contractility?
A
  1. Increased SV; Increased myocardial oxygen consumption
  2. Preload; Innervation to ventricles; O2 supply
  3. Poor myocardial perfusion (blockage), degenerative changes that occur with aging, necrosis that occurs from myocardial infarction, medication
  4. Increase: Inotropes (ex. DA, digoxin, dobutamine); Decrease: beta blockers, Ca channel blockers, anesthetic, chemotherapeutic agents
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14
Q

BARORECEPTORS

  1. What are they?
  2. Where are they located?
  3. What is their function?
  4. Provide a clinical example.
A
  1. Pressure-sensitive (or stretch) receptors
  2. Primarily in the carotid sinus and aorta
  3. Respond to changes in the stretch of vessel wall by sending impulses to cardio-centers in the brain stem -> appropriate changes in HR and vascular smooth muscle tone
  4. Blood loss due to trauma -> decreased BP -> increased HR+vasoconstriction and increased contractility
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15
Q

CHEMORECEPTORS

  1. What are they?
  2. Where are they located?
  3. What is their function?
  4. Provide a clinical example
A
  1. Sensory receptors
  2. Located in the medulla oblongata, carotid and aortic bodies
  3. Detect changes in the concentration of O2, CO2 & pH in arterial blood -> send messages to cardioregulatory/vasomotor centres (medullary oblongata) -> SNS and PNS responses in the vessels and heart
  4. Respiratory illnesses (ex. Pulmonary edema) -> decreased arterial O2 concentration/increase in PaCO2 -> increased HR, increased SV and Increased BP
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16
Q
  1. How do kidneys control arterial pressure?
  2. Where is renin released from? What type of molecule is renin? When is it released? What does it act on?
  3. What affect does angiotensin 1 have on the body?
  4. How is angiotensin II formed? Where is it formed? What does angiotensin II do? How is it deactivated?
A
  1. Through changes in ECF volume and the renin angiotensin system
  2. Renin is released from the kidneys; it is protein enzyme; it is released when the arterial pressure falls too low; it acts on angiotensinogen to release angiotensin 1.
  3. Has mild vasoconstrictor properties but not enough to cause significant changes in circulatory function
  4. Formed by ACE enzyme; formed in the lungs; extremely powerful vasoconstrictor; deactivated by angiotensinases;
17
Q
  1. What are the two principle effects that can elevate arterial pressure?
  2. What does increased SVR do to arterial pressure?
  3. How does aldosterone secretion manifest?
  4. How does aldosterone work in the body?
A
  1. Vasoconstriction in many area of the body (arterioles and veins)
    And decrease excretion of both salt and water by the kidneys
  2. Increased SVR increases arterial pressure
  3. Aldosterone is secreted by the kidneys and is initiated by angiotensin II
  4. Increase Na reabsorption; increase H2O reabsorption; increased blood volume; increase CO
18
Q
  1. What effect does increased sodium and water levels have on BP?
  2. Over production of aldosterone has been implicated in _______.
  3. What is vascular auto regulation?
  4. Increased metabolism causes a build up of ___________. This results in ________ of smooth muscle encircling the vessel.
A
  1. Increased BP
  2. HTN
  3. Intrinsic ability of arteries to adjust blood flow according to tissue needs.
  4. Vasodilatory chemicals in the vessels; relaxation
19
Q
  1. What occurs when MAP gets too high or too low?

2. Which organs require the most effective ability to auto-regulate blood flow?

A
  1. Body loses its ability to auto-regulate

2. BRAIN, HEART and KIDNEYS

20
Q
  1. What is HTN?
  2. What are the values for prehypertension?
  3. What are the values for Stage 1 hypertension? What are the values for Stage 2 hypertension?
A
  1. A persistent elevation of systemic arterial blood pressure
  2. Systolic: 120-139 or Diastolic: 80-89
  3. Stage 1: Systolic: 140 to 159 or Diastolic 90 to 99
    Stage 2: Systolic: 160 or higher Diastolic: 100 or higher
21
Q
  1. What are some of the risks of primary HTN?
  2. What is the equation for BP?
  3. Anything that effects ___,____ or ____ will effect BP.
  4. Primary HTN is the result of a complicated interaction between _______ and the _________ leading to ______ vascular tone and blood volume.
A
  1. Advancing age, cigarette smoke and heavy alcohol consumption, diabetes melllitus, obesity, ethnicity, family history, psychosocial stress, socioeconomic status, excessive dietary sodium
  2. BP = COxSVR
  3. SVR, heart rate and stroke volume
  4. Genetics and the environment leading to increased vascular tone and BV
22
Q

SNS

  1. Where is the sympathetic vasomotor centre located?
  2. Which NT is released from the sympathetic nerve endings?
  3. Which receptor does this NT activate?
  4. What do alpha-adrenergic receptors control? Beta-adrenergic receptors?
  5. When SNS is activated how does this affect a) the heart b) SVR c) kidneys d)arterial pressure?
A
  1. Located in the medulla
  2. NE
  3. Receptors in the SA node, myocardium and vascular smooth muscle
  4. Alpha - peripheral vasoconstriction, pupil dilation; beta - HR and contractility
  5. A) Increased HR and contractility b)increased SVR c) release of renin by kidneys d)increased arterial pressure
23
Q
  1. Increased SNS activity causes _______ insulin release.
  2. Increased SNS causes vascular ________ which _________ blood vessels.
  3. Angiotensin II stimulates which hormone? Where is this hormone released from?
  4. Increased renin secretion has been investigated as a cause of _______ peripheral vascular resistance in primary HTN.
A
  1. Increased insulin release
  2. Vascular remodeling; narrows the BV
  3. Stimulates aldosterone; released from the adrenal cortex
  4. Increased peripheral vascular resistance
24
Q
  1. What do natriuretic peptides modulate?
  2. How does tissue ischemia affect glomeruli & tubules?
  3. Which ions can affect the function of natriuretic peptides?
A
  1. Modulate renal sodium excretion
  2. Tissue ischemia causes dysfunction in the glomeruli and tubules which promotes additional sodium retention
  3. Excessive Na intake, inadequate dietary intake of K, Mg and Ca
25
Q
  1. How does inflammation affect the endothelial tissue and HTN?
  2. How does endothelial dysfunction affect HTN?
  3. How does obesity influence HTN?
  4. How does insulin resistance affect endothelial tissue and HTN?
A
  1. Causes endothelial injury and tissue ischemia which damages the kidneys causing increasedNa retention and sustained HTN
  2. Endothelial dysfunction causes decreased production of vasodilators and increased production of vasoconstrictors
  3. Obesity contributes to endothelial dysfunction and renal Na retention
  4. Insulin resistance is associated with endothelial dysfunction

Pathophysiology (1 decks)

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