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Cardiology > HTN Physiology > Flashcards

HTN Physiology Flashcards

1
Q

Describe primary and secondary HTN

A

Primary: idiopathic, there is no recognizable cause for their HTN.

Secondary: d/t some underlying dz.

  • renal dz
  • endocrine disorder
  • obstructive sleep apnea
  • pheochromocytoma
  • thyroid problem
  • aortic coarctation
  • Birth control pills
  • Cold medicines
  • OTC pain relievers
  • Rx drugs
  • illegal drugs (cocaine, amphetamines)
  • alcohol abuse/chronic use
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2
Q

Physiological mechanisms involvement in primary HTN

A
  • autonomic nervous system
  • cardiac output
  • Peripheral resistance
  • Renin-angiotensin-aldoserone system
  • Other factors:
  • -ANP, Bradykini, Endothelin, Endothelial derived relaxing factor)
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3
Q

Blood pressure is dependent upon what two factors?

A

-CO * Peripheral resistance

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4
Q

Systolic Blood Pressure definition

A

-systolic pressure is the force that blood exerts on the artery walls as the heart contracts to pump out the blood.

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5
Q

High systolic pressure is a greater risk factor than diastolic pressure for heart, kidney, and circulatory problems and for death in middle-aged adults, true or false?

A

True.

Aside: the wider the spread between the systolic and diastolic measurements, the greater the danger.

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6
Q

Diastolic Blood Pressure definition

A

the measurement of force as the heart relaxes to allow the blood to flow into the heart.

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7
Q

What is a high predictor of heart attack and stroke in young adults?

A

high diastolic pressure

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8
Q

What is Mean Arterial Pressure (MAP) ? How do you calculate it?

A
  • the average arterial blood pressure during a single cardiac cycle

Calculation:
-MAP = (COxSVR) - CVP

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9
Q

Arterial Pulse Pressure

  • what is this?
  • what does it indicate?
A

What is this: the difference between the systolic and diastolic readings during ejection.

Indications:

  • indicator of stiffness and inflammation in the blood-vessel walls.
  • the greater the difference between systolic and diastolic numbers, the stiffer and more injured the vessels are thought to be.
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10
Q

What is peripheral vascular resistance?

A

-the resistance to flow that must be overcome to push blood through the circulatory system?

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11
Q

What is systemic vascular resistance?

A

the resistance offered by the peripheral circulation.

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12
Q

Neural Mechanism on BP

  • Autonomic Nervous system mechanisms
  • Central Nervous System mechanisms
A

ANS:

  • Intrinsic: baroreceptors and chemoreceptors
  • extrinsic: pain, cold, isometric exercises
  • Higher neural control: sympathetic & parasympathetic

CNS:
-change in mood or emotion

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13
Q

Where is the most important baroreceptor for regulating arterial pressure located?

A

-carotid sinus

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14
Q

Where are the most important chemoreceptors located? They communicate with the vasomotor center and induce widespread _____.

A

carotid bodies and aorta

-they communicate with the vasomotor center and can induce widespread vasoconstriction

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15
Q

What role does the sympathetic and parasympathetic system play in vascular function?

A
  • sympathetic can stimulate both arteriolar constriction and dilation, maintains normal blood pressure
  • parasympathetic contributes to the regulation of heart function, but has little control over the blood vessels.
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16
Q

In vascular smooth muscle, stimulation of alpha receptors produces _______ and stimulation of beta receptors causes _______.

A

alpha receptors produce vasoconstriction

-beta receptors causes vasodilation

17
Q

What are some CNS and ANS responses that elevate blood pressure?

A

CNS:

  • CNS Ischemic Response
  • Cushings Reflex (increased intracranial pressure, leading to increase systolic and pulse pressure)

ANS:

  • Postural Stress
  • Valsalva Maneuver
  • Face Immersion: increased vessel resistance in cold water, leading to increases in pressure. used in past to break SVT.
18
Q

BP = ____ x ____

A

CO x PVR

Peripheral Vascular Resistance

19
Q

Peripheral Vascular resistance is determined by which vesseles?

A

-the small arterioles, the walls contain smooth muscle cells. Contraction of smooth muscle cells raises intracellular calcium concentration leading to structural changes and thickening of the arteriolar vessel walls leading to irreversible rise in PVR.

20
Q

What causes the release of renin? Where is renin released from?

A
  • underperfusion (low volume)
  • reduced salt intake
  • stimulation from sympathetic nervous system (beta 1 receptors on JG cells in response to catecholamines)

-released from the JG cells located in the wall of the afferent arteriole.

21
Q

The renin-angiotensin system is not always directly responsible for the rise in BP in essential HTN, many HTN pts have low levels of ____ and ____ especially in ____ and _____.

A
  • low levels of renin and angiotensin II

- especially in elderly and african americans)

22
Q

African and elderly population HTN is better managed with?

A

-diuretic, calcium channel blocker, or beta blocker.

23
Q

How do Natriuretic peptides help control BP? What are the two pathways? Give an example of a Natriuretic Peptide.

A

-involved in long-term regulation of sodium and water balance, blood volume and arterial pressure.

Pathways:

  1. Vasodilator effects:
  2. Renal effects leading to natruresis and diuresis

Example:
Atrial Natriuretic Peptide (ANP)
Brain-type Natriuretic Peptide (BNP)

24
Q

What does an elevated ANP lab value indicate?

What does BNP tell you?

A

tells you if there is volume overload, atrial distension.

-synthesized in the brain and ventricles, tells you if there is volume over load in the ventricles.

25
Q

Endothelin and NO functions

A

NO: produced by arterial and venous endothelium, induces smooth muscle vasodilation.

Endothelin: vasoconstriction

26
Q

Bradykinin function?

A
  • a potent vasodilator that is inactivated by ACE.

* increase in bradykinin causes cough with ACE inhibitor.

Cardiology (12 decks)

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