1
Q
Blood pressure formula
A
Cardiac output X systemic vascular resistance
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.
3
Q
Where is the highest % of blood contained?
A
Venule
4
Q
What are the 3 tunica layers of an artery wall?
A
Tunica externa - tunica media - tunica intima
5
Q
Where is the smooth muscle found in an artery wall?
A
In the tunica media
6
Q
Where is the tunica intima found in an artery wall?
A
Between the endothelium and internal elastic membrane.
7
Q
What is found between the internal and external elastic membranes in an artery wall?
A
Tunica media and the smooth muscle.
8
Q
What do JNC-8 recommendations for BP look at?
A
High importance on age: > 60 < 60 > 18 with CKD > 18 with diabetes
9
Q
What are the six summaries of JNC-8?
A
- Target goal <140/90
- Relaxation of BP “in the elderly” (>60 yrs)
- No pre-HTN group
- Beta – blockers degraded as fourth line
- Diuretic retained as first line
- Special consideration given to African-Americans, CKD, and DM
10
Q
Define atherosclerosis
A
Slow progressive disease of the large elastic and large and medium sized muscular arteries
AKA: arteriosclerosis
11
Q
Atherosclerosis is characterized by…
A
the formation of atherosclerotic plaques/atheroma
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
13
Q
Atherosclerosis involves…
A
the deposition of fatty (cholesterol) plaque (atheroma)
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
15
Q
What do atherosclerosis symptoms rely on?
A
- the degree of blockage (size)
2. the distribution of the artery (location, location, location)
16
Q
Atherosclerosis rupture
A
can lead to thrombus formation and further blockage/symptoms
17
Q
Atherosclerosis risk factors
A
- Hyperlipidemia – and specifically hypercholesterolemia
- HTN
- Cigarette smoking
- Diabetes mellitus type I/II
18
Q
Minor risk factors
A
- Physical inactivity
- Stress and behavior patterns
- Obesity
- Long term oral contraceptive use
- Tooth decay
19
Q
Non-alterable risk factors
A
- Age (older worse than younger)
- Gender (male > female)
- Genetic predisposition (folks had it – you’ll have it)
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
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
22
Q
What are the 4 soluble lipoproteins?
A
- Chylomicrons
- Pre-beta lipoproteins (“very low density lipoprotein”, VLDL)
- Beta lipoproteins (“low density lipoprotein”, LDL)
- Alpha lipoproteins (“high density lipoproteins”, HDL)
23
Q
Chylomicrons
A
primarily transport dietary triglycerides and, to a lesser extent, dietary cholesterol
24
Q
Pre-beta lipoproteins (VLDL)
A
primarily transport endogenously produced hepatic triglycerides to adipose and muscle tissue
25
Beta lipoproteins (LDL)
primarily transport endogenous cholesterol and are the major plasma cholesterol carriers
26
Alpha lipoproteins (HDL)
primarily transport endogenous cholesterol acquired from extra-hepatic tissues and returns it to the liver.
27
Atheroma development
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
28
Atheroma development cont.
- 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
29
Presence of foam cells
signifies that you have a maturing atheroma
30
What signifies immature atheroma?
Fatty streaks
31
Further atheroma evolution creates...
- a fibro-fatty atheroma
32
How is the fibrous cap formed? What if it ruptures?
- 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
Consequences of fibrous cap rupture
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
What symptoms do atherosclerotic plaques produce?
- stable angina
- TIA
- PAD
35
Why do TIA S&S usually go away within 24 hrs?
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
What organ produces renin?
The kidneys
37
What organ produces angiotensinogen?
The liver
38
What is renin's function?
Converting angiotensinogen to angiotensin I (A1)
39
How is A1 converted to angiotensin II (A2)?
By ACE - angiotensin converting enzyme
40
Where is ACE produced?
In the lungs
41
What are the functions of angiotensin II (A2)?
- 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
What is pulse pressure?
Systolic – diastolic = pulse pressure (120 – 80 = 40)
| NOTE: elasticity of the aorta dampens the systolic pulse
43
Narrowed pulse pressure
- drop in LV stroke volume
- blood loss/shock (insufficient preload leading to decrease CO)
- CHF
- aortic valve stenosis
- cardiac tamponade is #1 cause
44
Widened pulse pressure
- 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
What is a normal LVEF?
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
EF diagnoses
- 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
Causes of decreased LVEF
- MI
- CHF – defined by decreased LVEF
- CAD
- Tamponade
- Cardiomyopathy
- Valve disease
48
Note: see table of ventricular volumes, slide 29
Note: see table of ventricular volumes, slide 29
49
Define shock
- 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
Shock symptoms
- extremely low blood pressure.
- anxiety or agitation/restlessness
- circumoral cyanosis
- mottling of skin
- delayed capillary refill
- chest pain
- confusion
- dizziness, lightheadedness, or faintness
- pale, cool, clammy skin
- low or no urine output
- diaphoresis, moist or dry skin
- rapid but weak (thready) pulse
- shallow breathing
- unconsciousness
51
Initial approach to treatment
- Oxygen – mask at 10-15 liters/min, intubation
- Pulse oximetry
- Telemetry – cardiac monitor
- IV/IO/central line access
- BLS as indicated
- FSBS
52
What are the 4 categories of shock?
1. Hypovolemic shock
2. Distributive shock
3. Cardiogenic shock
4. Obstructive shock
53
What are the 2 kinds of hypovolemic shock?
Non-hemorrhagic and hemorrhagic
54
What are the 3 kinds of distributive shock?
1. Shock
2. Anaphylactic
3. Neurogenic
55
What are the 2 kinds of cardiogenic shock?
1. Bradydysrhythmia
| 2. Tachydysrhythmia
56
What are the 4 kinds of obstructive shock?
1. Tension pneumothorax
2. Cardiac tamponade
3. PE (pulmonary embolism)
4. Ductal-dependent outflow obstruction
57
Non-hemorrhagic hypovolemic shock
```
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
Hemorrhagic hypovolemic shock
- Control external bleeding
- Fluid resuscitation
- Transfuse PRBCs as indicated
- O blood, Rh (+) versus (-)
59
What is distributive shock?
results from excessive vasodilation and the impaired distribution of blood flow.
60
What is the most common form of distributive shock?
Septic shock --> leading cause of non-cardiac death in ICUs
61
Septic shock tx (distributive)
Pressure
Cultures
Antibiotics – ceftriaxone (Rocephin) 50 mg/kg q 24h
62
Define anaphylactic shock (distributive)
massive decrease in systemic vascular resistance d/t massive release of histamine
63
Anaphylactic shock tx (distributive)
- IM epi (or EpiPen)
- Antihistamines H1 and H2
- IV corticosteroids
- Albuterol via nebulizer
64
Neurogenic shock (distributive)
- Definition: loss of vascular tone normally supported by sympathetics
- Pressure
- Head trauma or child abuse
65
Cardiogenic shock types
1. Bradydysrhythmia
2. Tachydysrhythmia
There is a specific algorithm to fix the dysrhythmia.
66
What else can cause cardiogenic shock?
- Myocarditis
- Cardiomyopathy
- Poisoning (Ca++ channel blocker, β-blocker)
- Tx with vasopressors
67
Tension pneumothorax (obstructive)
-Decreased breath sounds, mediastinal shift, PEA, flat hemidiaphragm, falling BP with rising pulse
Treatment:
- Needle decompression
- Tube thoracostomy
68
Cardiac tamponade (obstructive)
-Distant heart sounds, low voltage QRS, widened heart shadow on CXR, narrow pulse pressure, fluid on FAST
Treatment:
-Pericardiocentesis
69
PE (pulmonary embolism) [obstructive]
Consider thrombolytics
70
Ductal-dependent outflow obstruction
- 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
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