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112 Cards in this Set

  • Front
  • Back
mitral stenosis => buildup of blood in LA => (2)
1. pulmonary hypertension

2. decreased LV filling
when pulmonary hypertension reaches more than 25 mm Hg, _________________________ results
pulmonary edema/congestion
normal pulmonary pressure =
16 mmHg
what does the stethoscope hear when listening to pulmonary edema?
crackles, as water moves around with breathing
**the LA hypertrophies to accommodate ___________________________________________________**
the greater amount of blood that it holds as a result of mitral stenosis
consequences of mitral stenosis:

1. inc. LA pressure

2. dec. EDV => low SV => low aortic BP

3. greater afterload for RV, due to backup from LA
**the most common cause of right HF = **
problem with LA
annulus =
mitral valve ring
mitral insufficiency (doesn't close properly) =>
causes of mitral insufficiency:

1. ruptured chorda tendinae/papillary muscles

2. damaged/stretched annulus (due to ventricular hypertrophy)

3. acute tear of valve
a rupture of the chorda tendinae/papillary muscle =>
partial eversion of a commissure
prolapse =
a complete eversion of both commisures
an acute tear of the valve =>
**immediate, huge rise in pressure of the LA**
effects of mitral insufficiency:

1. partly concentric, partly eccentric hypertrophy of LA

2. inc. EDV in ventricle
partly concentric, partly eccentric hypertrophy of LA =>
dec. pressure in LA => dec. pulmonary congestion
inc. EDV in LV (due to normal blood+regurgitated blood) =>
greater strength of contraction
***what's the most sheer-stressed area of the heart?***
the aorta
main cause of aortic stenosis:
wear and tear
you can narrow the aortic valve by __% before you see any resting symptoms
>50% narrowing of aortic valve =>

1. angina, esp. during exertion (due to dec. coronary artery perfusion)

2. inadequate flow to brain

3. HUGE increase in ventricular P

4. lower aortic BP
consequences of aortic stenosis:

1. **concentric** hypertrophy

2. **dec. coronary artery flow**

3. greater afterload for LA = > harder to fill LV
why is less compliance of the walls a bad thing?
makes the heart **harder to fill**
why is it harder for the LA to fill the LV when aortic stenosis occurs?
the LA has to push against a HUGE pressure in the LV
high EDV (due to failure to empty, b/c of more blood) => inc. LV pressure =>
inc. LA pressure to push blood in => *pulmonary congestion*
why is there a decrease in coronary artery flow with aortic stenosis?
decreased aortic pressure => decreased flow to coronary arteries
why does concentric hypertrophy ultimately fail?
**b/c the dec. coronary blood flow means blood can't get to the extra muscle that comes with hypertrophy**
exertional syncope is a characteristic of what kind of valve defect?
**aortic stenosis**

(inadequate perfusion to brain)
soln for aortic stenosis:
get new valve
cause of aortic insufficiency/regurgitation:
**acute tear** of the valve
acute tear of the aortic valve =>
big inc. in volume of LV =>=>

eccentric hypertrophy
consequences of aortic insufficiency:

1. dec. blood to system

2. inc. SP, => HUGE PP
(SP is great b/c of inc. EDV)

3. big dec. in aortic pressure

4. **murmur** right when aortic valve closes
soln for aortic insufficiency:
get a new valve
heart failure =
consequence of all these other problems
***there is no cure for HF, only***
treatments to dec. the pain.

HF is end-stage
forward HF vs. back HF
forward = inability of heart to develop enough SP to push blood out

"back" refers to HUGE increase in DP - heart can only pump blood with excessive filling
systolic (most cases) vs. diastolic HF
forward vs. back?

causes of HF:

1. dec. contractility

2. inc. afterload
dec. contractility is a result of:
(dead tissue)

(dec. ATP production)
inc. afterload is a result of:

1. aortic stenosis

2. hypertension

3. atherosclerosis
Frank-Starling mechanism =
greater preload => greater force of contraction
right HF is caused by:
1. left HF


2. pulmonary disease independent of the heart
right HF due to pulmonary problem only =
cor pulmonale
compensations for HF:

1. Frank-Straling mechanism

2. hormonal dec. of heart activity

3. baroceceptors to inc. vagal stimulation and dec. HR

4. RAA to increase blood volume

5. ADH to inc. blood volume
increasing blood volume via RAA or ADH is good for __________ __________, but bad when
inadequate filling

too much blood is the problem
clinical signs of Left HF:

1. breathlessness

2. inc. pulmonary venous pressure

3. dec. flow to brain - dull

4. low urine flow (due to low blood flow via low CO)

5. fatigue

6. orthopnia

7. backup of blood into systemic veins

8. inc. weight due to inc. fluid
orthopnia =
*exacerbated edema* as a result of lying down
backup of blood into systemic veins =>
edema in liver, lower legs, GI, ascites
treatments for left HF:

1. diuretics to get rid of excess fluid

2. vasodilators to inc. profusion

3. reduce HR

4. ACE inhibitors

5. anticoagulants
why is it important to decrease heart activity in order to treat HF?

1. ***so that each contraction is stronger due to greater filling***

2. to dec. O2 demand***
with HF, you WANT blood volume to dec., b/c
heart can't handle too much volume
Respiratory Rate is measured in
breaths per minute
normal RR =
12 breaths/min
normal TV =
500 ml/breath
Minute Ventilation equation:
MV = RR x TV
MV is measured in:
ml / min
normal MV =
6000 ml/min = 6 L/min
pathway for breath = trachea => bronchi =>
broncioles => alveolar ducts
***gas exchange occurs ONLY at***
the alveoli
Anatomical Dead Space =
volume of airways
normal ADS =
150 ml/breath
so amount of breath that is actually exchanged at the alveoli =
350 ml/breath
==> Alveolar Ventilation =
RR x (TV -ADS) =

12 x (500-150) = 4200 ml/min
**alveolar sac =
basketball within a thick net of capillaries
2 things about the barrier b/w caps and alveoli:
1. very thin

2. extensive - HUGE area of interaction (remember thick net)
thinness of the barrier b/w caps and alveoli, 0.5 micrometers, allows for
easy diffusion of O2
lungs taken out of body will immediately collapse, b/c:

1. elastic nature of lungs (elastin)

2. ST
***alveoli secrete a thin layer of
H2O mlcls that alveoli secrete associate with each other, causing:
the alveoli to collapse into small spheres
Pressure needed to keep alveoli uncollapsed =
2 ST / r
greater ST =>
need more pressure to keep alveoli up
greater radius of alveolus => less P to keep alveolus up, due to:
more separation b/w H2O mlcls
what kind of cells secrete surfactant?
Type II alveolar cells
major component of surfactant =
DPC, a phospholipid
DPC is ***amphipathic**:
has both phobic and philic part
the phobic tails of surfactant associate with:
the inner, O2-containing part of the alveoli
***philic portions of surfactant decrease ________________***
H-bonding b/w H2O mlcls***
dec. of H-bonding =>
dec. tendency to collapse
**surfactant's effect on water is greater when you've
why is surfactant more effective when you've breathed out?
b/c alveoli are smaller and sft's are close together/more concentrated
more-concentrated sft =>
much bigger dec. in ST, which dec. the pressure necessary to keep alveoli from collapsing
sft is critical for some infants b/c some don't
secrete as they should
so sft deficiency => infant _______ _________ __________
Respiratory Distress Syndrome

must be put on CPAP
**sft doesn't eliminate ST, but**
dec. it to a manageable amount
ST is greatest in:
the smallest alveoli
compliance =
how much Pressure is necessary to inc. Volume
when s/t is stiff, its compliance is

think new balloon
steep curve =
great compliance = easier to blow up
flat line =
very low compliance
what causes low compliance?
it's easier to deflate alveoli than it is to inflate them b/c of
alveolar recoil
a lung filled with fluid =>
***no more ST*** => huge inc. in compliance in BOTH directions

(inflate and deflate)
layers of the thorax:
parietal pleura / interpleural space / visceral pluera
parietal pleura is attached to
the chest wall
visceral pleura is
shrink-wrapped over lungs
lungs naturally have an inward collapse, which is prevented by
the pleura****
***both pleura secrete ***
H2O-based fluid ***
the fluid that pleura secrete =>
HUGE inc. in ST => ST makes lungs stick to pleura
what is the disease in which air gets into the interpleural space?
LOTS of air in the interpleural space =>
lung collapse

(in this case, called **atelolactasis**)
what is the disease in which LOTS of air in the interpelural space leads to lung collapse?
what is the disease in which air getting into **visceral** pleura more and more => collapse?
tension pneumothorax
"wind knocked out" =
brief separation of lungs from chest wall

will recover as pleura come together soon enough
Inspiration pushes diaphragm down, while elevating the the rib cage; external IC's pull up,
elevate ribs, expand the chest *anteriorly*
diaphragm ~ __% of breathing
in Expiration, muscles relax, abdomen pushes UP on diaphragm,
alveoli get smaller and push air out
expiratory muscles are all for active expiration; they are:

1. Internal IC's

2. ALL abdominals

3. SCM
Internal IC action:
compression of ribs
Ispiratory Reserve Volume =
volume inspired ABOVE normal inspiration
normal inspiration =
500 ml

(from 2500 ml to 3000 and back)
IRV often gets you up to ______ of inspired air
6000 ml

or, 6 L
ERV = volume expired more than normal =>
down to 1500 ml, from 2500

so 1000 ml extra
Vital Capacity =