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Cardiology 1 > Pathophys - CVS > Flashcards

Pathophys - CVS Flashcards

1
Q

Blood pressure formula

A

Cardiac output X systemic vascular resistance

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2
Q

What is the significance of the Poiseuille-Hagen formula?

A

“r” is to the fourth power, so a small change in diameter results in a large change in resistance.

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3
Q

Where is the highest % of blood contained?

A

Venule

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4
Q

What are the 3 tunica layers of an artery wall?

A

Tunica externa - tunica media - tunica intima

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5
Q

Where is the smooth muscle found in an artery wall?

A

In the tunica media

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6
Q

Where is the tunica intima found in an artery wall?

A

Between the endothelium and internal elastic membrane.

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7
Q

What is found between the internal and external elastic membranes in an artery wall?

A

Tunica media and the smooth muscle.

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8
Q

What do JNC-8 recommendations for BP look at?

A 
High importance on age:
> 60
< 60
> 18 with CKD
> 18 with diabetes
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9
Q

What are the six summaries of JNC-8?

A
  1. Target goal <140/90
  2. Relaxation of BP “in the elderly” (>60 yrs)
  3. No pre-HTN group
  4. Beta – blockers degraded as fourth line
  5. Diuretic retained as first line
  6. Special consideration given to African-Americans, CKD, and DM
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10
Q

Define atherosclerosis

A

Slow progressive disease of the large elastic and large and medium sized muscular arteries
AKA: arteriosclerosis

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11
Q

Atherosclerosis is characterized by…

A

the formation of atherosclerotic plaques/atheroma

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12
Q

Atherosclerosis in the general population

A
  • 50% of all deaths in the U.S. are related to cardiovascular disease
  • Atheroma can be observed in almost every individual > 40 years of age
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13
Q

Atherosclerosis involves…

A

the deposition of fatty (cholesterol) plaque (atheroma)

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14
Q

Where are atheromas found?

A

in the intimal layer of affected arteries –> these will grow and push into the lumen
*Leads to restricted or even blocked blood flow

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15
Q

What do atherosclerosis symptoms rely on?

A
  1. the degree of blockage (size)

2. the distribution of the artery (location, location, location)

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16
Q

Atherosclerosis rupture

A

can lead to thrombus formation and further blockage/symptoms

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17
Q

Atherosclerosis risk factors

A
  1. Hyperlipidemia – and specifically hypercholesterolemia
  2. HTN
  3. Cigarette smoking
  4. Diabetes mellitus type I/II
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18
Q

Minor risk factors

A
  • Physical inactivity
  • Stress and behavior patterns
  • Obesity
  • Long term oral contraceptive use
  • Tooth decay
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19
Q

Non-alterable risk factors

A
  • Age (older worse than younger)
  • Gender (male > female)
  • Genetic predisposition (folks had it – you’ll have it)
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20
Q

Cholesterol’s role in metabolic functions

A
  • component with other lipids in the synthesis of cellular membranes
  • used to create steroid-based hormones
  • excreted as an important element of bile acids
  • 93% of the body cholesterol is intracellular
  • 7% is circulating as plasma cholesterol bound to a lipoprotein
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21
Q

Good vs. bad cholesterol

A
  • Elevated levels of HDL have a protective effect

- Elevated levels of blood plasma LDL are directly related to the development of clinically significant atherosclerosis

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22
Q

What are the 4 soluble lipoproteins?

A
  1. Chylomicrons
  2. Pre-beta lipoproteins (“very low density lipoprotein”, VLDL)
  3. Beta lipoproteins (“low density lipoprotein”, LDL)
  4. Alpha lipoproteins (“high density lipoproteins”, HDL)
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23
Q

Chylomicrons

A

primarily transport dietary triglycerides and, to a lesser extent, dietary cholesterol

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24
Q

Pre-beta lipoproteins (VLDL)

A

primarily transport endogenously produced hepatic triglycerides to adipose and muscle tissue

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25
Q

Beta lipoproteins (LDL)

A

primarily transport endogenous cholesterol and are the major plasma cholesterol carriers

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26
Q

Alpha lipoproteins (HDL)

A

primarily transport endogenous cholesterol acquired from extra-hepatic tissues and returns it to the liver.

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27
Q

Atheroma development

A
  1. Endothelial injury that leads to endothelial dysfunction (leads to increased permeability and increased adhesion of cells to the endothelium)
  2. Monocyte adhesion followed by migration into the intima
  3. Platelet adhesion – Von Willebrand factor
  4. Inflammatory mediators are released by activated platelets, macrophages and endothelial cells
  5. Accumulation of lipoprotein – mostly LDL cholesterol, at first inside SM and macrophages then in the matrix
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28
Q

Atheroma development cont.

A
  • Smooth muscle cell proliferation and creation of more extracellular matrix
  • Lipid accumulation within monocytes and smooth muscle cells to create foam cells
  • Infiltration of the extracellular matrix with more lipid leads to FATTY STREAK
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29
Q

Presence of foam cells

A

signifies that you have a maturing atheroma

30
Q

What signifies immature atheroma?

A

Fatty streaks

31
Q

Further atheroma evolution creates…

A
  • a fibro-fatty atheroma
32
Q

How is the fibrous cap formed? What if it ruptures?

A
  • Extracellular matrix with dense collagen develops into a fibrous cap that separates the fatty streak from the vascular lumen
  • Rupture of the fibrous cap can expose serum to the fatty streak and this sets up thrombus formation
33
Q

Consequences of fibrous cap rupture

A
  1. It ruptures and you wind up with a thrombus at that site

2. It ruptures and you have a cholesterol embolus headed somewhere else.

34
Q

What symptoms do atherosclerotic plaques produce?

A
  • stable angina
  • TIA
  • PAD
35
Q

Why do TIA S&S usually go away within 24 hrs?

A

Your own clot degradation mechanisms restore the blood flow or the pressure behind it pushes it through the capillary bed so that it’s not causing symptoms anymore.

36
Q

What organ produces renin?

A

The kidneys

37
Q

What organ produces angiotensinogen?

A

The liver

38
Q

What is renin’s function?

A

Converting angiotensinogen to angiotensin I (A1)

39
Q

How is A1 converted to angiotensin II (A2)?

A

By ACE - angiotensin converting enzyme

40
Q

Where is ACE produced?

A

In the lungs

41
Q

What are the functions of angiotensin II (A2)?

A
  • increases sympathetic activity.
  • stimulates tubular Na, Cl reabsorption and K excretion. H2O retention.
  • stimulates the adrenal gland in the cortex of the kidney to secrete aldosterone.
  • stimulates arteriolar vasoconstriction causing increase in blood pressure.
  • stimulates the pituitary gland to secrete ADH (antidiuretic hormone) which acts on the collecting duct causing H2O reabsorption.
42
Q

What is pulse pressure?

A

Systolic – diastolic = pulse pressure (120 – 80 = 40)

NOTE: elasticity of the aorta dampens the systolic pulse

43
Q

Narrowed pulse pressure

A
  • drop in LV stroke volume
  • blood loss/shock (insufficient preload leading to decrease CO)
  • CHF
  • aortic valve stenosis
  • cardiac tamponade is #1 cause
44
Q

Widened pulse pressure

A
  • during exercise d/t increase in stroke volume
  • aortic stiffness (atherosclerosis)
  • AV fistula
  • Chronic aortic regurg
  • aortic root aneurysm, dissection
  • thyrotoxicosis
  • endocarditis
  • occurs normally in pregnancy
  • ICP: with bradycardia and resp irreg
45
Q

What is a normal LVEF?

A

ranges from 55-70%.

A LVEF of 65, for example, means that 65% of the total amount of blood in the left ventricle is pumped out with each heartbeat.

46
Q

EF diagnoses

A
  • An EF of less than 40% may confirm a diagnosis of heart failure.
  • An EF of less than 35% increases the risk of life-threatening dysrhythmia.
  • Systemic manifestations are constant with LVEFs of <25%.
  • < 30% is a qualifying event for disability with Social Security.
47
Q

Causes of decreased LVEF

A
  • MI
  • CHF – defined by decreased LVEF
  • CAD
  • Tamponade
  • Cardiomyopathy
  • Valve disease
48
Q

Note: see table of ventricular volumes, slide 29

A

Note: see table of ventricular volumes, slide 29

49
Q

Define shock

A
  • a life-threatening condition that occurs when the body is not getting enough blood flow.
  • multiple organs can suffer damage as a result of poor perfusion.
50
Q

Shock symptoms

A
  • extremely low blood pressure.
  • anxietyor agitation/restlessness
  • circumoral cyanosis
  • mottling of skin
  • delayed capillary refill
  • chest pain
  • confusion
  • dizziness, lightheadedness, orfaintness
  • pale, cool, clammy skin
  • low or no urine output
  • diaphoresis, moist or dry skin
  • rapid but weak (thready) pulse
  • shallow breathing
  • unconsciousness
51
Q

Initial approach to treatment

A
  • Oxygen – mask at 10-15 liters/min, intubation
  • Pulse oximetry
  • Telemetry – cardiac monitor
  • IV/IO/central line access
  • BLS as indicated
  • FSBS
52
Q

What are the 4 categories of shock?

A
  1. Hypovolemic shock
  2. Distributive shock
  3. Cardiogenic shock
  4. Obstructive shock
53
Q

What are the 2 kinds of hypovolemic shock?

A

Non-hemorrhagic and hemorrhagic

54
Q

What are the 3 kinds of distributive shock?

A
  1. Shock
  2. Anaphylactic
  3. Neurogenic
55
Q

What are the 2 kinds of cardiogenic shock?

A
  1. Bradydysrhythmia

2. Tachydysrhythmia

56
Q

What are the 4 kinds of obstructive shock?

A
  1. Tension pneumothorax
  2. Cardiac tamponade
  3. PE (pulmonary embolism)
  4. Ductal-dependent outflow obstruction
57
Q

Non-hemorrhagic hypovolemic shock

A 
Examples:
--Resuscitation in adults
--In kids - 20 mL/kg normal saline/lactated ringer bolus 5-20 mins (crystalloid)  consider colloid (blood, plasma) after 3rd NS/LR bolus
--Vasopressors:
Dopamine 2-10 mcg/kg/min
Dobutamine 2-10 mcg/kg/min
Epinephrine 0.1-0.5 mcg/kg/min
Norepinephrine 0.1-0.5 mcg/kg/min
58
Q

Hemorrhagic hypovolemic shock

A
  • Control external bleeding
  • Fluid resuscitation
  • Transfuse PRBCs as indicated
  • O blood, Rh (+) versus (-)
59
Q

What is distributive shock?

A

results from excessive vasodilation and the impaired distribution of blood flow.

60
Q

What is the most common form of distributive shock?

A

Septic shock –> leading cause of non-cardiac death in ICUs

61
Q

Septic shock tx (distributive)

A

Pressure
Cultures
Antibiotics – ceftriaxone (Rocephin) 50 mg/kg q 24h

62
Q

Define anaphylactic shock (distributive)

A

massive decrease in systemic vascular resistance d/t massive release of histamine

63
Q

Anaphylactic shock tx (distributive)

A
  • IM epi (or EpiPen)
  • Antihistamines H1 and H2
  • IV corticosteroids
  • Albuterol via nebulizer
64
Q

Neurogenic shock (distributive)

A
  • Definition: loss of vascular tone normally supported by sympathetics
  • Pressure
  • Head trauma or child abuse
65
Q

Cardiogenic shock types

A
  1. Bradydysrhythmia
  2. Tachydysrhythmia
    There is a specific algorithm to fix the dysrhythmia.
66
Q

What else can cause cardiogenic shock?

A
  • Myocarditis
  • Cardiomyopathy
  • Poisoning (Ca++ channel blocker, β-blocker)
  • Tx with vasopressors
67
Q

Tension pneumothorax (obstructive)

A

-Decreased breath sounds, mediastinal shift, PEA, flat hemidiaphragm, falling BP with rising pulse

Treatment:

  • Needle decompression
  • Tube thoracostomy
68
Q

Cardiac tamponade (obstructive)

A

-Distant heart sounds, low voltage QRS, widened heart shadow on CXR, narrow pulse pressure, fluid on FAST

Treatment:
-Pericardiocentesis

69
Q

PE (pulmonary embolism) [obstructive]

A

Consider thrombolytics

70
Q

Ductal-dependent outflow obstruction

A
  • Newborns – when fetal circulation ducts are necessary to maintain circulation in the presence of congenital heart defects.
  • These defects restrict pulmonary blood flow (eg, pulmonary stenosis, pulmonary atresia), poor arterial-venous mixing (e.g., transposition of the great arteries), and conditions that interfere with systemic circulation (e.g., interruption or coarctation of the aorta).

Treatment: Prostaglandin E1

Cardiology 1 (11 decks)

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