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CRAAB 5 > Nordgren- Cardiovascular Function in Pathological Situations > Flashcards

Nordgren- Cardiovascular Function in Pathological Situations Flashcards

1
Q

What is circulatory shock?

A

Severe reduction in blood supply to the body tissues (metabolic needs of tissues aren’t met)

-arterial pressures are LOW (even w/ compensatory mechanisms)

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2
Q

A pt suddenly loses consciousness after losing a lot of blood. What’s wrong with them?

A

Severe shock

Inadequate blood flow to the brain leads to LOC (syncope)

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3
Q

A loss of blood pressure results in a decrease in what two variables?

A

CO or TPR

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4
Q

Primary disturbances that cause circulatory shock are generally accelerated by what kinds of cardiovascular crises?

A
  1. Severely depressed myocardial function
  2. Gross inadequate filling due to low MFP
  3. Extreme vasodilation (d/t powerful vasodilators or loss of normal tone)
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5
Q

Severe arrythmias, abrupt valve malfunction, MI, coronary occlusions can cause what types of shock?

A

Cardiogenic shock

Cardiac pumping insufficient>
decreased CO

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6
Q

Significant hemorrhage, fluid loss from severe burns, chronic diarrhea, prolonged vomiting can cause what type of shock?

A

Hypovolemic shock

Depletion of body fluids >
decreased blood volume>
reduced cardiac filling>
reduced SV>
decreases CO
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7
Q

How does anaphylactic shock affect TPR and CO?

A 
Allergic rxn to ag sensitivity>
release of histamine, PGs, LKs, bradykinin>
decreased arteriolar vasodilation>
increased microvascular permeability>
loss of VENOUS TONE>
decreased TPR and CO
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8
Q

What is septic shock?

A

Severe vasodilation due to release of substances into blood stream by infective agents

(ENDOTOXIN released from bacteria induces formation of nitric oxide synthase in endothelial cells)

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9
Q

What is neurogenic shock?

A

Loss of vascular tone d/t inhibition of normal tonic activity of sympathetic vasoconstrictor nerves.

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10
Q

What can cause neurogenic shock?

A
  1. Deep general anesthesia
  2. Reflex response to deep pain associated with traumatic injury

**Can also be accompanied by increased vagal activity> decreased HR> vasovagal syncope

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11
Q

What causes pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction?

A

Drop in PRESSURE>
Compensatory mechanism to INCREASE BP>
Increased SNS acdtivity

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12
Q

What happens when a compensatory response is weak?

A

Abnormally low arterial pressure>
reduced cerebral perfusion>
dizziness, confusion, LOC

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13
Q

What are additional compensatory processes that happen in response to circulatory shock?

A
  1. Rapid, shallow breathing> promotes VENOUS RETURN via action of respiratory pump
  2. Increased RENIN release
  3. Increased circulating levels of VASOPRESSIN
  4. Increased circulating levels of EPINEPHRINE
  5. Reduced capillary hydrostatic pressure resulting from intense arteriolar constriction
  6. Increased glycogenolysis in the liver (induced by epi and norepinephrine)
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14
Q

What is autotransfusion?

A

Reduced HP and increased glucose>
keeps fluid in the CVS and out of the tissues

The body can move as much as 1 L of fluid into VASCULAR SPACE in first hour after onset of shock.

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15
Q

DEcompensatory responses to circulatory shock can lead to an overwhelming amount of vasoconstriction. How does this affect the body?

A

Severely reduced perfusion of tissues>
permanent damage of organs

(Body homeostasis deteriorates with prolonged reduction in organ blood flow> adversely affect the CV system> further reduces flow)

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16
Q

What is progressive shock?

A

CV situation progressively degenerates

17
Q

What is irreversible shock?

A

No intervention can stop collapse of CV system>

death

18
Q

What is CAD?

A

Atherosclerosis of large coronary arteries>
increase vascular resistance>
reduce coronary flow>
ischemia

**If not too severe, local metabolic vasodilator mechanisms compensate to reduce arteriolar resistance to improve coronary flow

19
Q

What is SYSTOLIC dysfunction (CHF)?

A

Left ventricular EF

reduced CO at any given filling pressure

20
Q

What pathological processes can lead to reduced myocyte function?

A

Sustained cardiac challenges> chronic state of failure

  1. Progressive CAD
  2. Sustained elevation in cardiac afterload
  3. Reduced functional muscle mass following MI
21
Q

What alterations occur in systolic dysfunction?

A

Decrease in intracellular Ca concentrations> decreased contractility

  1. Reduced Ca sequestration by SR> upregulation of NCX> Low intracellular Ca concentration
  2. Low affinity of troponin for Ca

Alteration in O2 consumption in ischemic tissue

  1. Shift from fatty acid to glucose oxidation
  2. Impaired respiratory chain activity> impaired energy production (glucose oxidation isn’t as efficient)
22
Q

How does systolic dysfunction affect CO?

A

Decreased CO>
decreased arterial pressure>
increased sympathetic activity>
less dramatic compensatory response

23
Q

How does the body compensate for systolic dysfunction long term?

A

Higher than normal SNS activity>
RENIN release>
RISE in BLOOD VOLUME>
increased MAP

*CO gets closer to normal and allows for REDUCTION in SNS activity

24
Q

What is a “compensated state of heart failure”?

A

Enough fluid retained>

normal CO achieved w/ normal symp nerve activity

25
Q

What are the negative aspects of long term compensation in systolic dysfunction?

A

FLUID RETENTION>
Elevated peripheral and central venous pressures higher than normal>
chronically high EDV>
excessive cardiac dilation>
increased total wall tension/stress req to generate adequate P in enlarged chamber>
INCREASE myocardial O2 demand

26
Q

How does fluid retention adversely affect organs?

A

High venous pressure>
increased transcapillary fluid filtration>
edema and congestion

27
Q

What are sxs associated with L sided failure?

A
  1. Pulmonary edema
  2. Dyspnea
  3. respiratory crisis
28
Q

What are sxs associated with R sided failure?

A
  1. Distended neck veins
  2. Ankle edema
  3. Fluid accumulation in abdomen with lever congestion and dysfunction
29
Q

The most common sxs associated with systolic dysfunction are related to what two causes?

A
  1. Inability to increase CO> low exercise tolerance, fatigue

2. Fluid accumulation> tissue congestion, SOB, peripheral swelling

30
Q

What causes diastolic dysfunction?

A

Stiffened heart during diastole>
increase in cardiac filling P>
doesn’t produce increase in EDV

31
Q

What is heart failure with preserved systolic function?

A

Diastolic dysfunction

32
Q

What are potential cause of diastolic dysfunction?

A

NORMAL systolic function is present but there’s an INCREASE in P during diastole without an increase in EDV

  1. Decreased cardiac tissue passive compliance
  2. Increased myofibrillar passive stiffness
  3. Delayed myocyte relaxation in early diastole
  4. Inadequate ATP levles
  5. Residual, low-grade cross-bridge cycling during diastole
33
Q

Left ventricular chamber enlargement with CHF increases the wall tension required to generate a given systolic pressure?

T or F

A

True

La Place- tension is directly related to pressure and radius

34
Q

What are the two types of hypertension?

A
  1. Pulmonary

2. Systemic

35
Q

Systemic edema, chest pain and fatigue are associated with what type of hypertension?

A

Pulmonic (PA pressure > 20 mmHG)

Linked to chronic hypoxia (COPD, cystic fibrosis)

36
Q

Increased risk of CAD, MI, heart failure and stroke is associated with what type of hypertension?

A

Systemic- elevation of MAP > 140/90 mmHG

> 20% of adult western world population

37
Q

What percent of hypertension cases have an unknown cause? What does this mean for treatment?

A

90%

You can’t treat the primary disturbance so you treat the CAUSE.

38
Q

How does hypertension affect urinary output rate in an individual with hypertension?

A

Need HIGH pressure to get normal urine output in an individual with hypertension.

39
Q

How do you treat hypertension?

A
  1. Restrict salt intake (lowers bp> reduced req for water retention to osmotically balance salt load)
  2. Diuretic therapy (inhibit renal tubular salt and fluid resorption)
  3. Beta blockers (inhibit SNS influences on heart and renin release)
  4. ACE inhibitors and ARBS (block renin-angio system)

CRAAB 5 (9 decks)

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