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SUMPHYS2 > CARDIO-Flow > Flashcards

CARDIO-Flow Flashcards

1
Q

What are the main components of blood pressure?

A
  1. Cardiac output 2. Blood volume 3. Total peripheral resistance
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2
Q

What are local control mechanism for flow and pressure?

A

Local tissue focus on its own survival. Organs focus on how much flow/pressure it needs. Systemic control- focuses on peripheral resistance

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3
Q

This theory is acute rapid local blood flow control occurs when 1. stressed tissue 2. Nutrients are depleted 3. Metabolize Inc, the vessels do what?

A

Vasodilator Theory= INC vasodilator substance into tissue cells. Responds to stress or strain. Lead to vasodialtion which decreases resisitance, and finallly INC blood flow. Fluid travels high to low.

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4
Q

This theory responds to metabolic activity and the tissue cant sustain contraction any longer so tissue will naturally dialte bc runs out of O2.

A

Oxygen demand theory

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5
Q

As total diameter of vessels inc., then pressure will dec. Volume = inverse of pressure, if container gets smaller pressure should inc. Yet, how does our body adjust? What are systemic control mechanism for flow and pressure?

A

The vessles account for that total cross sectional area. Systemic control is total peripheral resistance. Heart regulates change in Pressure, Resistance - is controlled systemic peripheal. 1. Long term 2. Humoral vasoconstrictor, dilators 3. CNS-reflexes, SNS 4. Kidney- RAAS

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6
Q

What is long term mechanism of local control?

A

Slow aniogiogensis. Age dec. body abilty to make new vessels. Vessels form around obstruction.

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7
Q

During exercises, what happen to maintain blood pressure so there is no syncope?

A

Vessels dialate to dec resistance. Heart is always working against TPR

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8
Q

What occurs during acute increase pressure and flow?

A

Autoregulation- starts in 1 min

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9
Q

What causes occurs with acute INC pressure and flow ➝sudden stretch on smooth msk vessels so they contriction. 2. Low pressure➝ smooth msk relax DEC resistance and returning BP to normal?

A

Myogenic theory-autoregulation to suppress the increase- EXCESS O2, contricts

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10
Q

What causes occurs with acute INC pressure and flow ➝sudden excess of nutrients O2 which lead to contrictions?

A

Metabolic theory- autoregulation

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11
Q

What special acute mech. controls blood volume in tubulglomerular feedback? Acute auto Systemic control.

A

INC GFR from acute INC pressure and flow⇾ INC tubule fluid flow rate⇾ Macula densa cells/JGA monitor filtrate detect HIGH IONs still in capillary bc flow to fast didn’t filter out⇾ Macula densa INC resistanc in afferant aa⇾ slower GFR ⇾slower BF⇾ DEC glomerular pressure⇾ 2. OPPOSITE For DILUTE/less filtrate due to LOW Blood flow⇾ dilute/low filtrate⇾mac densa cell DILATE AFFERENT, they think not enough⇾RAAS⇾INC BV and P

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12
Q

What brain mech autoregulate when INC product builds up in brain?

A

Reflexive Washout. INC. in CO2, H+, Vessels vasodilate. Excitable membranse senistive to ions. Vessels (GVE-no pain) BUT stretches on GSA,GSE,GVA tissue⇾ HA

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13
Q

What are the acute hormone vasodilators?

A
  1. NO from endothelia cells- potent, lipophilic. Release during stress from INC pressure and blood flow. Last sec, but purpose for local. 2. Bradykinin, histamine- vasodialate, rhinorhrea, red w/ allergy 3. Atrial Natriuretic peptide- diuresis CHF 4. ETOH- flush Asian, vessel damage 5. Serotonin- chill 6. oxytocin-open cervix 6. K and Mg-
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14
Q

Which substances vasoconstrict vessles?

A
  1. catechol- NE, EPI , Adrenaline 2. Ag II 3. Vasopressin/ADH 4. Caffeine 5. Cortisol 6. Ca2+- MSK contract
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15
Q

What are effects for long term control of BP?

A
  1. Angiogenesis A- Oxygen mediator and trigger of new vessels d/t metabolic demand from new vessels. If O2 demand high, inc vessels, but vessels also require O2.
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16
Q

What is role of ANS SNS on arterial BP?

A
  1. Local Systemic peripheral control 2. Maintains vasocontriction tonal resistants small aa.3. INC HR and contractility 4. Baseline BP 5. Baseline contractility DEC large vessels veins, push blood to heart 5. Affect RAAS- reduces GFR via vasoconstriction d/t release of stress hormones⇾ overall fluid rentetnion⇾oliguria 6. Catecholamines
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17
Q

What occurs during sit to stand, when standing the BP drops?

A

Nuerological reflex- goal is to perfusion brain when standing. 1. Venous vasocontrction 2. maintains CO 3. Rise SV. If no respone syncope with rise

18
Q

What do the stretch receptors in the arch of the aorta detect?

A

Baroreceptors detect BP as blood leaves aorta⇾Vagus nerve⇾ carotids detect stretch⇾Hernigs send to-CNXI

19
Q

What is pathway of baroreceptors?

A

INC pressure⇾stretch vessels quickly⇾barorecptors (carotid+aortic)activated⇾CN XI/X signals PNS⇾vasodialtion vv, aa⇾DEC TPR⇾DEC CO⇾normal BP

20
Q

How do you effect rapid rise in arterial pressure?

A

Via SNS 3 ways-1.. Vasoconstriction aa large vessels 2. INC HR 3. Alter HR and Contractiliy

21
Q

IF trying to affect BP up or down, what is goal?

A

Maintain pressure via CO and TPR

22
Q

What is BP range/zone for carotid barorecptor response?

A

Zones are certain pressure that cause a response from receptros. Some receptors respond to high or low. Carotid-Respond quickly >60mmg. MAX 180. Aortic- respond >30mmg.

23
Q

Diastole. Finishing cardiac cycle, get ready for beg. 1. Heart sounds quiet, 2. no electrical activity. NO Pwave or QRS 3. Vol. Ventricles slowly filling 4. Pressure- Atria and Ventricle low pressure 5. Blood is filling into Atrium via pulmonary veings

A

Total Peripheral Resistance

24
Q

Which receptor is powerful moment-moment, but poor for habituation dt exposure to long term exposure to high BP?

A

Arterial baroreceptors. Age= slower to respond to change in BP

25
Q

What do chemoreceptors respond to?

A

Low O2, CO2, excess H+. NOT powerful until arterial BP falls below 80. Important to prevent further DEC

26
Q

What reflex is related to Banbridge effect?

A

Arterial stretch INC HR. Arterial pulmonary have “low pressure receptors”. Responds to stretch d/t blood volume⇾INC venous pressure/vol = backflow somewhere⇾INC cardiac input/INC vol⇾arterial stretch⇾CNS medulla⇾INC HR⇾INC CO

27
Q

How does arterial pressure affect RAAS?

A

FIX-Arterial pressure triggers RAAS⇾dialtes afferent artery in kidney⇾inc. GFR⇾inc.fluid in tubules⇾filtrate + secretion of H2O= INC URINE output

28
Q

What signals brain to DEC ADH? How does this DEC blood volume?

A

FIX-Arterial pressure INC⇾CNS Brain detects INC volume⇾DEC ADH⇾no water channels in tubule for H2O resorb⇾filtrate + secretion of H2O= INC URINE output

29
Q

Describe long term effect w/ Kidney function?

A

Slow but power. DEC Kidney function overtime , will INC blood pressure. Drop in GFR related to INC Blood pressure after 40. INC arterial pressure+INC Blood vol. w/o vessel alter⇾INC renal output H20 and NA =diuresis and natriuresis

30
Q

Why IV fluids when pt. is AKI?

A

Na/H20 Inc pressure to improve R-shift of Renal fx curve. Kidney requries higher pressure. IN HTN, low CO, due to systemic constriction cause Kidey dysfx

31
Q

How is the renal fx curve shifted?

A
  1. pressure rise= INC urine output 2. Long term determinants A. salt/water intake, B. DEC renal fx shift to RIGHT, need higher pressure to inc urine output
32
Q

How is RAAS affecting high BP from lack of CO, thus low kidney perfusion?

A

LOW blood volume from systemic constriction and LOW CO⇾triggers renin/angiotensogen release by kidney⇾Angiotensongen converted to AGI liver⇾AGI convert to AGII lungs (get to system)⇾1. vasoconstriction INC TPR, INC vv return 2. DEC Na/H2O excretion via kidneys via ALDO and ADH.⇾floor inc BP an volume, slow

33
Q

Does Kidney respone help the heart?

A

No, last thing a dysfx pump needs is excess volume

34
Q

What if MAP is over 110?

A

Hypertension.

35
Q

How is MAP calculated

A

DBP+ (1/3xPP) N PP= 40=120-80. MAP= 93. closer to DBP. MEAN arterial pressure-emphasizes DBP, we spend more time diastole than quick systole.

36
Q

What does HTN do long term? What does HTN L/T?

A
  1. INC workload-lvh, chf, mi, cad 2. MAP INC less relaxation in arteries, vessels stretched, Inflamm, damage- strokes 3. HIGH BP damage Kidney, they don’t have internal pump
37
Q

When prescribing meds for HTN, what is important to keep in mind?

A

BP related to volume and resistance. 1. Most require two meds 2. First Volume, Tone, Volume, Tone 3. Don’t do drug with same affect at same time

38
Q

What is HTN caused by renal artery stenosis?

A

HTN 2/2 Goldblatt HTN, narrow renal artery⇾INC RAAS⇾inc vol. and constriction

39
Q

What occurs in young pt when the Arm BP is HIGHER than ankle BP?

A

Coarctated of Aorta

40
Q

What is sum of all changes in flow that CNS is trying to control?

A

Preclampsia -BP 140/90 at 20 week, proteinuria, swelling

41
Q

What is idiopathic, >90% of HTN cases, MAP INC, Renal flow+output DEC, GFR DEC, overtime?

A

Essential HTN. KIDNEY activated bc needs high pressure

SUMPHYS2 (27 decks)

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