final rcp Flashcards
Ventilation
process of moving gas into and out of the lungs
Respiration
process of moving oxygen and carbon dioxide
Respiratory System
The upper airways Chest wall respiratory muscle the lower airways pulmonary blood vessels supporting nerves lymphatics
Sniffing position
extending neck and pulling chin anteriorly
Glottis
narrowest part of the adult upper airway
characteristics of obstructive sleep apnea
obesity fatigue snoring short neck daytime sleepiness pharyngeal muscles relax when we sleep
imbalance between mucus water content and airway humidity of the mucous sheet
thick, dehydrated
infected
immobile
impairment of the mucociliary clearnance system
air pollution
dehydration
smoking
neutrophillic inflammation of the airways
cystic fibrosis
COPD
asthma
smokers
BTPS
body temperature 37C
pressure 760
water saturation at AH 44mg/L
water vapor saturation 47mg/L
anatomical shunt
deoxygenated blood from the pulmonary arteries mixes with oxygenated blood from the pulmonary veins 1%-2%
Purpose of surfactant
reduces surface tension
reduces work of breathing
increases lung compliance
ACM
Type 2 cells Type 1 Cells basement membrane interstitial space capillary endothelial cell plasma erythrocyte
impact of anatomical shunt
systemic arterial blood can never have the same partial pressure of oxygen as alveolar gas, gives rise to the normal PAO2
natural mechanism of brochodilation
neurotransmitter: norepinephrine
B2 receptors located
airway smooth muscle
vascular smooth muscle
submucosal glands
airway epithelium
parasympathetic
increase viscosity
thick secretions
sympathetic
thin, watery secretions
Phrenic nerve
diaphragm innervated by somatic innervation
primary muscles of quiet breathing
diaphragm
parasternal intercostals
scalenes
assessory muscle of inspiration and expiration
scalenes - inspiration
sternomastoids - inspiration
pectoralis major - inspiration
abdominals - expiration
thoracic cavity enlargement
the downward movement of the diaphragm
causes the flattening of the diaphragm
if the lungs fail to empty normally during exhalation
emphysema
High compliance low elasticity low recoil force air trapping pursed lip breathing longer expiratory time
pulmonary fibrosis
Low compliance high elasticity high recoil force rapid, shallow breathing shorter expiratory time
pulmonary surfactant
to prevent lung collapse by lowering the surface tension in the alveoli
benefits of surfactant
reduces WOB
reduces the distending pressure required to keep small alveoli open
provides a stabilizing influence alveoli of different sizes
Laplaw Law
if the collapsing force of alveolar surface tension is opposed by an equal counter pressure, the alveolus remains in an inflated state
Poiseuille Law
16 X more work if the airway diameter is cut in half
Auto-PEEP
if the lungs do not have enough time to empty, pressure may still be positive in slowly emptying alveoli and still be positive at the end of expiration when the next inspiration begins, air trapping
air-trapping
asthma
emphysema
weak lung recoil force
Alveolar Ventilation
TV-(dead space per pound)
ex. TV = 700
weight 200 Lb
= 500
slow deep breathing will improve
partial pressure of oxygen in atmosphere
21%
149 mmHg
alveolar pressure
- inspiration
0 rest
+ expiration
hysteresis
lung volume is greater during deflation than inflation
time constants
compliance and airway resistance is the time constant expressed in seconds, how rapidly the source pressure and lung pressure equalize
time constant less = less compliant
time constant more = more compliant
surface tension
70%
normal % of the minute ventilation in dead space
30%-40%
pressure
pressure in lungs is above pressure in the atmosphere, this is how we breathe naturally
anatomical dead space
150mL
total volume of the conducting airways from the nose to the terminal bronchioles
partial pressure of inspired air
159mmHg
partial pressure of conducting airway
149mmHg
alveolar air equation
PAO2 = (pressure-H2Op) X FiO2 - 40/ 0.8 ex. PAO2 = 760 - 47 X (40) - 0.8 713(.21) - 50 149.73 - 50 =99.73 mmHg
FICKS LAW
A - surface area
D - diffusion solubility
P1-P2 - diffusion gradient
T - membrane thickness
if membrane thickness increases diffusion through ACM increases
DLCOab
diffusion capacity of the lungs for carbon monoxide
normal is 20-30mL/min/mmHg
21
25
DLCO
What affects it: body size age lung volume exercise body position
oxygen is found
bound to hemoglobin on the erythrocyte
oxygen content in blood
Hb carries 20 m/dL of oxygen content = 100mmHg PaO2
Hb concentration of 15 g/dL
normal cardiac output
5 L/min
oxygen delivery to oxygen consumption
arterial blood deliver 1000 mL/O2/min
tissue consumes 250 mL/O2/min
25%
Oxygenated Hb
97% @ 100mmHg
mixed venous oxygen saturation
75% @ 40mmHg
Hb equillibrium curve
OHEC
steep 20-60mmHg
small changes in PaO2
flat 60-100mmHg
large changes in PaO2
P50 @ 27mmHg
left shift
- lower P50
- lower PCO2
- lower 2,3 DPG
- lower temperature
- higher pH
right shift
- higher P50
- higher PCO2
- higher 2,3 DPG
- higher temperature
- lower pH
Hb affinity for oxygen
increase in affinity
- left shift OHEC curve
- decrease P50/PO2
- increase SO2 for every PO2
decrease affinity
- right shift OHEC cruve
- increase P50/PO2
- decrease SO2 for every PO2
Bohr effect
the decreased affinity or Hb for oxygen
Haldane effect
Hb release of oxygen takes up carbon dioxide
affinity for carbon dioxide increases
widening of (C(a-v)O2)
increase in oxygen extraction, decrease in cardiac output
anerobic metabolism
oxidative metabolism in body tissues is the sole source of the blood’s CO2
DOcrit
blood fails to satisfy the demands of the tissue for oxygen
lactate produced
ion gap increases
low O2 delivery
carboxyhemoglobin
carbon monoxide poisoning
anemia
low Hb content of 5g/dL
may not look blue but is hypoxic
polycythemia
too much blood volume, thickening of blood, will look blue without being hypoxic
treating acute CO2 poisoning
an Fio2 of 1.0 (100%) greatly decreases the half life
half life = time required to cut COHb blood level in half
major forms of carbon dioxide transport
dissolved CO2 = 8%
H2CO3 = 80%
carbamino compounds = 12%
reaction between carbon dioxide and H2O
combination
slow reaction in blood plasma
faster reaction in the erythrocyte
chloride shift
HCO3 leaves the RBC and leaving the erythrocyte electropositive
CO2 transport in blood
HCO3 transports majority of the CO2 in blood
ventilation
CO2 is the main stimulus
buffers
decrease acidity as it transports CO2
10 fold change
a change in 1 pH unit corresponds to a 10 fold change in H+
10X
volatile acid
carbonic acid
fixed acid - nonvolatile
sulfuric acid
phosphoric acid
lactic acid (anaerobic)
20:1
kidneys (20) fixed
lungs (1) volatile
bicarbonate
open system
fixed (nonvolatile)
plasma bicarb
erythrocyte bicarb
nonbicarbonate
closed system volatile (carbonic) fixed hemoglobin organic phosphates inorganic phosphates plasma protein
compensations
chronic acidemia
chronic alkalemia
fully compensated - pH normal, HCO3/CO2 not
partially compensated - opposite outside
uncompensated
acute acidemia
acute alkalemia
combined
both same outside normal limits
metabolic alkalosis
most complicated to treat - electrolyte imbalance
elevated HCO3 may be renal compensation for resp. acidosis
occurs: loss of fixed acid, gain of blood buffer base
causes: vomiting - loss of hydrochloric acid nasogastric suctioning hypochloremia hypokalemia (low K+) weakness latrogenic - diuretic, low-salt diet (medically induced) volume depletion - high urine output
compensation:
hypoventilation
-anxiety, pain, infection, fever
correction:
restore fluid/ electrolyte imbalance
-KCL infusion
Metabolic acidosis
occurs: accumulation of fixed acid in blood excessive loss of HCO3 in body -lack of blood flow ---tissue hypoxia, anaerobic metabolism, lactic acid severe diarrhea
anion gap >16
causes:
severe diarrhea
pancreatic fistules
hyperchloremic acidosis
compensation:
hyperventilation
rapid central chemoreceptor response
manifestations: increase in minute ventilation - complaint of dyspnea - extreme: stupor/ coma - hyperpnea
Severe:
diabetic ketoacidosis
- kussmaul breathing
–deep/ gasping
Anion Gap
plasma electrolyte
determines if metabolic acidosis is caused by gain of fixed acids or loss of base (HCO3)
ignores K+
High anion gap indicates increase in fixed acid
- lactic acid
- ketoacid
- uremic acid
normal anion gap indicates loss of HCO3
Respiratory acidosis
hypoventilation
hypercapnea (inadequate ventilation)
causes: COPD (most common) drug-induced CNS depression extreme obesity neurological disorder
compensation:
renal (increase in HCO3)
masks the problem by maintaining normal pH
neuromuscular weakness: shallow, rapid, short breath
CNS depression: slow, shallow, possibly apnea
increase in PaCO2: increase ICP myoclonus asterixis mental confusion
abrupt increase of PaCO2 70mmHg = coma
COPD / chronic hypercapnia can tolerate higher CO2 levels
correction: restore ventilation -secretion mobilization -bronchodilator drugs -endotracheal intubation -mechanical ventilation
respiratory alkalosis
hyperventilation
decreased PaCO2/ hypocapnia
causes: hypoxia pulmonary disease - pneumonia - edema CNS disease high altitude acute asthma general anxiety fever latrogenically - agressive ventilation (medically induced)
anxiety:
panic - vision impaired / speaking difficulty
- rebreather therapy
correction:
remove stimulus causes hyperventilation
- hypoxia O2 therapy
compensation:
slow renal excretion of HCO3
rise in HCO3
every 10mmHg rise = 1 mEq/L rise in HCO3
ex. 40mmHg rises to 70mmHg = increase in 3 mEq/L
lab value to indicate tissue hypoxia
lactic acid
chronic hypoxemia
increase cardiac output
increase RBC
increase tissue perfusion
hypoxic hypoxia
increase in PAO2 hypoventilation shunt V/Q mismatch aim to ventilate alveoli reduces O2 delivery to tissue
Anemic hypoxia
low Hb concentration
Hb not binding chemically to oxygen
CO poisoning
-reduce O2 delivery to tissue
stagnant hypoxia
low blood flow, low BP lung function can be normal low oxygen delivery rate -shock low blood volume -hemorrhage -severe dehydration O2 therapy cardiac arrest = restore blood flow
histotoxic hypoxia
blocked oxidative metabolism -cyanide poisoning -smoke inhalation 100% oxygen inhaled *methemoglobin
physiological shunt
in bronchial vasculature
bronchial blood flow is only 1%-2% of the cardiac output
catheter flow
right atrium (CVP) 2-4
Right ventricle S/D
Pulmonary artery 25/8 systole
PCWP 4-12
thermodilution
most useful in evaluating cardiac output
what substances are eliminated by the kidneys
urea creatine uric acid bilirubin various toxins foreign substances metabolites of assorted hormones
what structures compose the nephron
bowmans capsule proximal convoluted tubule loop of henle (ascending, discending) distal convoluted tubule collecting duct
what substance is secreted at the juxatoglomerular apparatus when systemic blood pressure decreases
renin, an enzyme that activates angiostensin, which leads to widespread system arteriole constriction
what substances, when excessive, does the nephron clear from the plasma
sodium
potassium
chloride
how much of the glomerular filtrate is reabsorbed into the blood
99%
gloerular filtrate is the same as plasma except it does not contain what substances
proteins
what substances are almost totally reabsorbed from the tubules
sodium
potassium
chloride
bicarbonate
what is the most important autoregulatory mechanism of renal blood flow
afferent vasodilator mechanism
what part of the nephron is highly impermeable of water
thick portion of the loop of henle
assending loop of henle
thin
descending loop of henle
thick
the hormones inhibit the effects of aldosterone
renin secretion results in angiotensin II formation, which causes the cortex of the adrenal gland to secrete aldosterone -> ANH & BNP -> inhibit aldosterone (promote loss of Na+ in urine
what type of urine is excreted by the kidneys, under the influence of ADH
low volume
high concentration
what is the best clinical indicator of perfusion adequacy
urine output
osmotic diuretic
mannitol - proximal tubules, elevates osmotic pressure of the filtrate, keeping water inside the tubules to be excreted as urine, decreases ICP in cerebral edema by decreasing brain swelling and ICP
diuretic
loop diuretic
furosemide
-lasix
toresimide
-dernadex
ethacynic
-edearin
block Cl- and Na- out of ascending henle loop to promote diuresis (K+ loss)
useful in treating edema related to CHF and can increase urine output by 25Xs
diuretic that is effective in treating edema of CHF
loop diuretic
categories of acute renal failure
decreased blood supply
- heart failure, hemorrhage
intrarenal failure
- abnormalities within kidney
postrenal failure
- obstruction of urine outflow
increased BUN, creatinine, sodium, potassium, fixed acids
renal failure
metabolic acidosis
pulmonary manifestation of nephortic syndrome
interstitial edema
pleural effusion
pericardial effusion
ascites
characteristics of goodpasture syndrome
autoimmune disease
hemoptysis
hematuria
targets kidney and lung alveoli
normal range for BUN
8-20 mg/dL
normal range for creatine
0.6-1.2 mg/dL
diseases associated with increased blood creatinine
kidney and muscle disease
renal failure
when BUN and creatinine are elevated in renal failure which acid-base disturbance
metabolic acidosis
why is a patient gaining weight on mechanical ventilation
fluid retention
causes of pulmonary edema
increased hydrostatic pressure -left ventricular failure (CHF) -hypervolemia -mitral stenosis increased capillary membrane decreased plasma oncotic pressure insufficent lymphatic drainage
edema associated with high PCWP
cardiogenic pulmonary edema
major effect of V/Q mismatch
hypoxemia
chronic hypercapnia
V/Q mismatch
P(a-A)O2 when 100% oxygen is breathed
50-60mmHg
when breathing room aire
7-14mmHg
conditions associated with dead space
pulmonary embolism
severe hypotension
alveolar overdistension
Auto-PEEP
PaO2/PAO2
most reliable indicator of shunt in stable conditions
Qt/Qs
most reliable indicator of shunt in unstable conditions
Thiazides
chlorothiazide
inhibit reabsorption of Na+
mild
blood pressure control
effects if acute renal failure
- decreased blood supply, heart failure or hemmorrhage
- intrarenal failure, or abnormalities with the kidneys
- postrenal failure, obstruction of urine outflow from the kidneys
chronic renal failure
decrease of number of functional nephrons
pyelonephritis - bacteria causes
arteriosclerotic - decreases renal blood flow and ichemiac nephrons
physiological effects of chronic renal failure
general edema, salt and water retention
nephrotic syndrome
goodposture syndrome
metabolic acidosis because the kidneys cant excrete fixed acids
high blood concentrations of nitrogenous compounds like urea, creatine, and uric acid (uremia), phenols, sulfates, phosphates, potassium.
azotemia
patients may progress to a confused mental state that can progress to uremic coma (acidosis)
renal clearance blood tests
BUN - blood urea nitrogen
pyelogram
creatinine
PMI
point of maximal impact
fifth intercostal space and midclavicular line
repeated impact of heart beat on chest wall
sympathetic receptors are mainly
(adrenergic) B1 - they increase myocardial force of contraction and heart rate
parasympathetic receptors are mainly
(cholinergic) alpha 1 - they slow heart rate
drugs that block Ca++
decrease heart force of contraction
clinical indicator of heart attack
troponin 1
all or none principle
if one fiber of the syncytium contract then all fibers contract
Frank-Starling
the greater the diastolic volume of the heart the greater the force of contraction - increase in sarcomere length
when does most of blood perfusion happen
during diastole
preload
the precontraction length of the sarcomere
if preload is good you will contract well
overdistended heart stretched
CHF
cardiac cycle
0.8 seconds
atrial kick
20%
80% passive
decrease heart rate
vagal stimulation
normal pulse pressure
40 mmHg
venous
veins are 64% of total blood volume
venous return
- cardiac pumping of large leg muscles
- sympathetic venous contraction
- cardiac pumping action
- thoracic pump
blood flow is determined by
- driving pressure
- vascular resistance
mean blood pressure
stroke volume
arterial compliance
arterial resistance
High BP
systolic over 135
diastole over 90
detrimental effects of high BP
- high workload on heart, leading to heart failure
- rupture of blood vessel in brain, stroke, CVA
venous blood flow (CVP) increases if
- increased blood volume
- venous tone increases
- arteriolar dilation occurs
normal RAP
0-5 mmHg
peripheral edema
RAP increases above 6 mmHg and effects PVP
JVD hepatomegaly ascites pedal edema anasarca enlarged spleen
adenosine
most important local vasodilator
cycling
vasomotion
oxygen demand theory
lack of oxygen dilates precapillary sphincters and arterioles, blood flow increases
central control
autonomic system
sympathetic division
vasoconstriction/ vasodilation - depends on adrenergic receptors
B2
vasodilation
A
vasoconstriction
baroreceptors
responsive to stretch
when stretched by high BP they send impulses to the glossopharyngeal and vagus nerve and causes vasodilation and slows the heart rate, low BP
RAAS
controls low BP
holds onto fluid and stimulates renin from kidneys
renin produces
angiotensin 1
angiotensin 1
produces ACE
ACE produces
aldosterone
aldosterone
causes kidneys to reabsorb water and sodium
ADH
low BP
holds onto water / fluid
raises BP
BNP
response to high BP
BNP inhibits aldosterone and RAAR secretion
promotes sodium loss and decreases BP
diagnostic marker for heart failure
BNP
helps differentiate between cardiac and pulmonary causes of dyspnea
P WAVE
arterial depolarization
positive
PR interval
AV node to bundle of His
0.12-0.20
isoelectric
QRS
ventricular depolarization
less than 0.10
ST segment
depressed >0.5mm = myocardial ischemia
elevated >2mm = myocardial injury
MCV
60 degrees
normal axis 0-90 degrees
normal range -30 - 120 degrees
MCV deviations
change in heart position
hypertrophy in one ventricle
myocardial infarction
bundle branch conduction block
right axis deviation
COPD
cor pulmonale
left axis deviation
CHF
reading heart rate on ECG
# of large squares between 2 QRS intervals divide number of squares by 300
12 lead ECG
bipolar limb leads - anterior / posterior view
uniploar limb leads - anterior / posterior view
chest leads - horizontal / sagittal view
bipolar limb leads
lead 1 right arm to left arm
lead 2 right arm to left leg
lead 3 left arm to left leg
unipolar limb leads
aVr right arm
aVL left arm
aVf left leg/ foot
extreme right axis deviation
lead 1 negative
aVf negative
aVf
90 degrees
right axis deviation
lead 1 negative
aVf postive
left axis deviation
lead 1 positive
aVf negative
normal
lead 1 positive
aVf positive
V1
fourth intercostal , right of sternum
V2
fourth intercostal, left of sternum
V4
fifth intercostal, midclavicular
V3
between V2, V4 centered
V5
fifth intercostal
V6
fifth intercostal, midaxillary
high amplitude P WAVE
enlarged atrium
pulmonary valve stenosis
cor pulmonale
COPD
O2 content of 100mL of apical blood
20.5 mL
PO2 130 mmHg @ 100%
O2 content of 100mL of basal blood
19.1
PO2 85 mmHg @ 94%
absolute shunt
40 mmHg PAO2
45 mmHg PACO2
Low V/Q
zone 3 basal
normal
PAO2 80-100 mmHg
PACO2 35-45 mmHg
V/Q 1:1
zone 2
absolute dead space
PAO2 150 mmHg
PACO2 0
High V/Q
zone 1
MAP
110 mmHg
intrapulmonary/ physiological shunt
pneumonia
pneumothorax
pulmonary edema
bronchial occlusion
hallmark of intrapulmonary shunt
refractory hypoxemia
shunted blood
can not take up oxygen or release carbon dioxide
supraventricular (atrial) (base) arrythmias
sinus tachycardia
atrial fibrillation
atrial flutter
PAC
ventricular arrythmias
ventricular tachycardia
torsades de pointes
ventricular fibrillation
PVC
Brady arrythmias
sinus bradycardia
1,2,3 degree block
Tachycardia
HR >100
Causes: exercise fever anxiety pain smoking b-anergenic drugs hypoxia anemia shock
treatment:
b-blocker drugs
vagal stimulation (decrease HR)
bradycardia
HR < 60
causes:
normal in physically fit, or sleeping individuals
vagal stimulation
- pharynx , trachea instrumentation
symptoms: hypotension weakness sweating synscope
treatment:
atropine
pacemaker
abnormal sinus arrythmia
bradycardia - expiration
tachycardia - inspiration
no treatment
non pathological
1st degree AV block
conduction time is slow
PR interval >0.2 seconds
2nd degree AV block
MOBITZ 1 - treated with drugs
MOBITZ 2 - pacemaker
3rd degree AV block
pacemaker 15 bpm
stokes adams syndrome
- heart block, fainting, loss of consciousness
PAC
compensatory pause
PWAVE close to SA +
PWAVE close to AV -
causes: stress alcohol tobacco electrolyte imbalance sympathetic stimulation
treatment:
quinidine
verapamil
Atrial conditions
CHF
mitral valve stenosis
pulmonary vascular resistance
atrial fibrillation
300-600 bpm
loss of atrial kick 20%
fine F waves
causes: increased atrial pressure enlarged atrium thromboembolism longer depolarization time
treatment:
anticoagulant (do first)
Ca++ blocker
electrical cardioversion
T wave
vetricular repolarization
QT interval
<0.40 seconds
atrial flutter
F waves saw toothed
200-350 bpm
symptoms: palpitations nervousness anxiety synscope
treatment:
Ca++ blocker
electrical cardioversion
PVC
> 0.12 seconds and bizzare
single life threatening arrhythmia
causes: stress tobacco caffeine sympathetic stimulation
diseases: hypoxia acidosis hypokalemia myocardial irritability MULTI focal
treatment:
lidocaine
amiodarone
VT
runs of PVC
110-250 bpm
may not feel a pulse - pulse deficit
treat as emergency can progress to VF
treatment:
lidocaine
amiodarone
electrical cardioversion
torsades de pointes “ twisting of the points “
causes: electrolyte imbalance antiarrhythmic drugs low Ca++ Low Mg++
VF
most lethal
cardiac arrest
code blue
no drugs can treat
circus reentry mechanism
shock
CPR
junctional escape rhythm
if the SA node fails to generate impulses the AV junction may assume the role of the pacemaker
DRG
inspiratory neurons
primary stimulus for inspiration
VRG
expiratory
inspiration ramp signal
neurons that switch off
- pneumotaxic center
- pulmonary stretch receptors
apneustic breathing
prolonged inspiratory gasps interrupted by occasional expirations
damage to pons
pneumotaxic center
controls the length of inspiration
hering-breurer deflation reflex
hyperpnea
increase RR
hering-breurer inflation relflex
slowing adapting receptors
stretch receptors
stops further inspiration when stretched
activated by large tidal volumes of 800-1000mL
heads paradoxical reflex
rapidly adapting receptors
maintains large tidal volume during exercise
prevents atelectasis
first breath of newborn
**periodic deep sighs during quiet breathing
rapidly adapting irritant receptors
vagocagel reflex - ETT - airway suctioning - bronchoscopy inhaled irritants
sensory reflex
laryngospasm
bronchospasm
coughing
decrease HR
motor reflex
bronchoconstriction coughing sneezing tachypnea narrow glottis
central chemoreceptors
repsonds to H+
arrises from the reaction between dissolved CO2 and H2O in the CSF
CO2 diffuses from blood brain barrier to CSF to form H+
CO2 diffusion
ventilation increases 2-3L/min for every mmHg in PaCO2 rise
maximal hyperventilation
PaO2 can not rise over 130 mmHg
peripheral chemoreceptors
20%-30% of ventilation responds to PaCO2 rise 5X quicker than central
carotid bodies
exert much more influence over the respiratory center than aortic - high blood flow rate
glossopharyngeal - carotid
vagus - aortic
hypoxia
doesnt stimulate ventilation until PaO2 decreases less than 60 mmHg or less
normal ICP
<10mmHg
normal CBF`
60 mmHg
exercise
onset
period of adjustment
steady state
J receptors
rapid-slow breathing , sensation of dyspnea
cheyne-stokes
increase RR and volume by gradual decrease in RR to complete apnea
CHF
biot
RR and tidal volume increase with volume at the same depth
lesions of the PONS
central reflex hypernea
continuous deep breathing
central reflex hypopnea
respiratory centers do not respond to appropriate ventilation stimuli such as CO2 - hypoventilation
brain trauma
narcotic depression