Exam 4 (Pulmonary and Cardiac) Flashcards
Pnea
Breathing
Eupnea
Normal breathing
Hypopnea
Decreased breathing
Hyperpnea
Increased breathing
Apnea
No breathing
Dyspnea
Difficulty breathing
Orthopnea
Dyspnea lying down
AP diameter
Distance of chest front to back
What drives the body to breathe
Get CO2 out. NOT get O2 in because CO2 directly affects pH and we have a very narrow range of pH we can live at
Carbonic acid
H2CO3, formed when CO2 meets water in the lungs
Causes of hypoxia
ischemia - decreased blood flow
hypoxemia - decreased PaO2
Hemoglobin issues like anemia
Diffusion
Hemoglobin exchanging CO2 for O2 in the alveoli.
No ATP or carriers
Alveolar capillary membrane
Very thin with large SA.
Fluid line alveoli
Alveolar epithelium
Epithelial basement membrane
Fluid in interstitial space
Capillary endothelium
Endothelial basement membrane
What is directly proportional to rate of diffusion
Pressure
SA
Temp
Solubility
What is inversely proportional to rate of diffusion
Molecular size
Thickness of membrae
Can O2 or CO2 diffuse more easily
CO2
It is smaller and 24x more soluble.
Overall 20x better
Elastin
Important in lung recoil
Expiration
Passive
Longer
Decreases lung volume
Increases pressure to +1
Diaphragm ascends
Internal intercostals and abdominals used in forced expiration
Inspiration
Active
Shorter
Lung expands
Decreases pressure to -1
Sternoclediomastoid, serratus anterior, and scalene muscles used in forced inspiratoin
Flow in lungs
Volume of air per unit of time
(P1-P2)/Resistance
What part of lungs has greatest resistance
Bronchi
Does inspiration or expiration have most resistance
Expiration because airways are getting smaller
Intrapulmonary/intra-alveolar pressure
Can be positive or negative
Pressure inside the lungs.
Intrapleural/intra thoracic pressure
Always negative
Pressure between the two pleural layers
Pulls esophagus open increasing its volume and decreasing pressure until it becomes negative.
EQUAL to esophagus pressure
Normally -2 at end of expiration and -7 at end of inspiration.
Gets more negative as chest wall expands away from lung
Transpulmonary/Transmural pressure
Difference between intrapulmonary/intra-alveolar and Intrapleural/intra thoracic.
Always positive
Boyles law
Volume is inversely proportional to pressure
When is the lowest pressure in the lung
Mid-inspiration
When is the highest pressure in the lung
mid-expiration
What would happen if you were stabbed in a lung without negative pleural pressure
Lung collapses
Lung would recoil until relaxed and chest wall would expand until relaxed
Dead space of lung
Volume that does not undergo gas exchange
Anatomical space (conducting zone) of lung
1/3 of tidal volume that it takes to fill up conducting parts of lung
Physiological dead space
Anatomical deadspace + alveolar dead spaces (not normal.
Equals anatomical dead space in healthy
Conducting zone
No gas exchange
Nose
Nasal cavity
Pharynx
Trachea
Primary, secondary, and tertiary bronchi
Tidal volume
Amount of air breathed in and out on normal breath.
about 500 mL
Compliance
Change in V/change in P
Expansibility
Opposite to surface tension
Opposite to elasticity and recoil
Surfactant helps overcome surface tension
What causes recoil of lung
Surface tension
Elasticity (elastin and collagen)
Surfactant
Keeps aveoli and lung partially open so you don’t have to inflate lung from nothing.
Helps break surface tension of water in lungs to prevent lungs from collapsing and let air sink for gas exchange
Type 1 pneumanocytes
do gas exchange
Type 2 pneumanocytes
Function as stem cells and produce surfactant
What stimulates surfactant production
Cortisol
Thyroxin
Prolactin
Inspiratory reserve volume (IRV)
Amount of air that can be inspired above tidal volume.
About 3000 mL
Inspiratory capacity (IC)
Tidal volume + inspiratory reserve volume.
3500 mL
Expiratory Reserve Volume (ERV)
Amount of air that can be expired below the tidal volume.
1100mL
Residual Volume (RV)
Air that remains in lungs after maximal forced expiration.
Important to perform gas exchange because heart is sending more blood than you are breathing.
1200mL
Can’t be measured with spirometry
Functional residual capacity (FRC)
expiratory reserve volume + residual volume
2300mL
Vital Capacity (VC)
inspiratory reserve, tidal, and expiratory reserve volume.
(Everything but the residual volume)
Total lung capacity TLC)
Everything
5800 mL
COPD and asthma (obstructive lung disease)
Can get air in but it can’t get out.
Increased residual volume (RV)
RV/TLC ratio >30%
Average healthy RV/TLC ratio
21%
FEV1
Forced expiratory volume.
Amount of air you can forcibly exhale in one second
FVC
Forced vital capacity.
Amount of air you can forcibly exhale after maximal inhalation
FEV1/FVC ratio
Should be 80% (4L/5L)
Ventilation
Process of air getting into alveoli
AKA (V)
AKA PAO2
Perfusion
Blood flow to the lungs for gas exchange.
AKA (Q)
AKA PaO2
Aa gradient
Difference betwen PAO2 and PaO2
(oxygen in in alveoli vs in the arteries)
Or difference in PACO2 and PaCO2
PAO2
O2 in alveoli
105mmHg
PaO2
O2 In arteries
100 mmHg
PACO2
CO2 in alveoli
40 mmHg
PaCO2
40 mmHg
Alveolar ventilation perfusion ratio
Normally 0.8.
3 at apex of lung
0.6 at base of lung
Ventilation Defect
Air is unable to get to alveoli
So ventilation is lowered.
V/Q is decreased
Pulmonary shunt
Blood flowing past poorly ventilated alveoli doesn’t pick up oxygen and mixes with oxygenated blood.
Produces hypoxemia.
V/Q is decreased
Perfusion defect
Occurs when there is a prob with pulmonary artery or blood supply to lung.
V/Q is increased
Response to hypoxia in most organs
Blood vessels dialate to get more blood (and O2) to area
Lung response to hypoxia
Vessels constrict so other normal alveoli will get blood and effected area will not
Hypocapnea
Too little CO2.
Causes alkalosis
Is partial pressure of O2 in alveoli greater or less than that in blood
Greater.
Must be for O2 to diffuse across to capillaries to Hgb
Hemoglobin
4 subunits each with heme and iron molecule made of two alpha and two beta chains.
Each of the four iron atoms can reversibly bind to O2
O2 saturation
% of hemoglobin bound to O2.
Normal is 97%
What does the O2 binding curve/hemoglobin dissociation curve show
The more O2 thats on a heme, the easier it is to bind the next
Voluntary control of breathing
In cerebral cortex
Sends messages along the corticospinal tracts.
Automatic control breathing
In pre-Botzinger complex of medulla
Messages sent via cervical cord and activate diaphragm via phrenic nerve
What change is CSF most sensitive to
Change in hydrogen ion concentration
Normal PaCO2
34-45 mmHg
Central chemoreceptor
Monitor H+ concentrations in CSF
Peripheral chemoreceptors
Monitor pCO2 or pO2
Normal PaO2
80-100 mmHg
What does a left shift in the oxygen dissociation curve mean
Hemoglobin has increased affinity for O2
More difficult for O2 to unbind and perfuse the tissues.
Found in alveolus when CO2 is decreasing and pH is increasing (basic conditions)
What does right shift of oxygen dissociation curve mean
Hemoglobin has decreased affinity for oxygen.
Easier for oxygen to dissociate from hemoglobin to perfuse with tissues.
Found in peripheral tissue when CO2 increasing and pH is decreasing (acidic conditions)
2,3-diphosphoglycerate (2,3-DPG)
Inversely related to pH
Facilitates O2 transport within RBC
Increases at high pH, hypoxia, and low Hgb
Decreases at low pH
Normal arterial pH
7.35-7.45
Lung jobs as buffer
Maintain CO2 levels by either holding in or blowing off CO2
Kidney jobs as buffer
Regulates bicarbonate.
HCO3- + H+ <–> H2CO3
Metabolic acidosis
Decrease in serum HCO3- which means low pH
Metabolic alkalosis
Disorder that has high HCO3- which means there aren’t many H+ which means high pH
Respiratory acidosis
Disorder that has high arterial PaCO2 causing decreased pH
Respiratory alkalosis
Disorder that has low arterial PaCO2 causing increased pH
Normal HCO3- levels
22-26 mEq/L
Largest artery in the body
Aorta
Largest vein in the body
Inferior vena cava
Tunica Intima of artery
Inside
Exchange of gases and nutrients
Tunica Media of artery
Middle
Smooth muscle fibers of vascoconstriction/vasodilation
Tunica Externa of artery
Outside
Anchors and protects vessel, contains nerve fibers and lymphatics
Tunica Intima of veins
Inside
Endothelial tissue
Frictionless pathway for blood movement
Tunica Media of vein
Middle
Elastic and muscular tissue that vasoconstricts/dialates
Tunica Adventitia of Vein
Outer layer which provide support of vessel.
Are blood clots more commonly found in veins or arteries
Veins bc blood can pool.
Bc blood moved by muscle movement and has valves
What ion does most work in the heart
Calcium
Anneurism
Bulging of vessel wall from increased blood pressure/blockage
RAAS system
Renin
Angiotensin
Aldosterone
Causes vasoconstriction and Na/H2O retention
Angiotensin converted to Angiotensin I by Renin.
Angiotensin I converted to Angiotensin II by ACE
Angiotensin II causes Aldosterone and ADH to be released
What increase vasoconstriction/Na reabsorption/H2O retension/increase bloodflow
RAAS
ADH
Epi+NE
Endothelin’s
What causes Vasodilation/decrease Na/H2O Retension/decrease BP
Nitric oxide
CO2
Histamine
Acetylcholine
Prostaglandin
ANP
Cardiac output
Total volume ejected by ventricles per minute
Avg is 5L/min
Stroke volume x HR
Preload
end-diastolic volume created by venous return.
Volume in ventricles at end of diastole
Afterload
Fixed load cardiac muscle needs to overcome to shorten during contraction.
Pressure left ventricle must oppose to get blood out.
Affected by diameter of vessels
Contractility
Inotropy.
ability of heart to contract.
Directly related to ejection fraction
Ejection Fraction
stroke volume/end-diastolic volume
usually 50-70%
Positive inotropes
Increase contractility
Sympathetic
Negative inotropes
decrease contractility.
Parasympathetic
Pacemaker cells
Generate spontaneous action potentials and create conduction system in heart.
SA, AV, bundle of His, right and left bundle branches, Purkinje fibers
Contractile Cells
99% of myocardium.
Cardiac myocytes responsible for contraction of heart.
Rely on pacemaker cells to become depolarized
Cardiac index
Cardiac output relative to body surface area.
CI=CO/BSA
Invasive ways to measure cardiac output
Right heart catheterization
Indwelling swan ganz catheter
Indwelling pulmonary artery catheter
Noninvases ways to measure cardiac output
echocardiogram
Right Coronary Artery
On inferior wall
Provide blood to right ventricle, right atrium, SA, AV, and inferior heart.
What to do and look for with inferior right MI
Give lots of fluid and watch for slow HR bc pt is at higher risk for clots.
Left Anterior Decending Artery (LAD)
On anterior wall
Supplies about 60% of heart
Branches into left main coronary artery.
Perfuses septum (bundle of his and bundle branches), left ventricle, and apex
Left Circumflex artery (LCX)
Travels in left actrioventricular groove between left ventricle and left atrium.
Perfuses lateral and posterolateral walls of left ventricle
Three major types of cardiac muscle
Atrial muscle
Ventricular muscle
Specialized excitatory or conductive muscle fibers.
Synctium
Cardiac tissue in atria and ventricles form a unit
Three types of channels used in heart action potential
Fast sodium channels
Slow sodium-calcium channels
Potassium channels
Phase 0 of myocyte action potential
Sodium influx depolarizes cell
Phase 1 of myocyte action potential
potassium efflux makes it slightly less depolarized
Phase 2 of myocyte action potential
Calcium influx causing plateau
Phase 3 of myocyte action potential
Potassium eflux repolarizing the cell
Phase 4 of myocyte action potential
Resting potential
What determines heart rate
balance between inhibition of SA node by vagus nerve and stimulation of SA node by sympathetic nervous system
Heart conduction order
SA –> AV –> bundle of His –> Bundle branches –> Purkinje fibers
SA Node
Sinoatrial node
upper right atrium
Primary pace maker
60-100 bm
Bachman’s bundle
Conducts impulses from SA node to left atrium.
AV Node
Atrioventrcular node
In lower right atrium near interatrial septum.
Slows the conduction of electrical impulses from the SA node.
Tells SA node to chill out
40-60 BPM
Right and left bundle branches
20-40 BPM
Purkinje fibers
Conduct impulse to myocardial cells of ventricle causing ventricular depolarization.
20-40 BPM
Ventricle fire rate
30-40 BPM
Acetylcholine effect on HR
lowers
Baroreceptors
Nerve endings in aortic arch and carotid sinus that tell brain blood pressure and flow.
Adjust HR to fix pressure
Vagus nerve stimulation effect on cardiovascular system
Vasodilation and decrease in BP and HR
Vagal maneuvers
Slow HR
Cough
Bear down
Squat
Hold breath
gag
cold water on face
low up balloon
blow into syringe
Electrocardiogram
12 leads
12 diffeent views of heart
P wave
Atrial depolarization
QRS complex
Ventricle depolarization
T wave
Ventricle repolarization
Bronchodialaters
Short/long acting beta-2 agonist (-terol)
Short/long acting muscarinic antagonist (-ium)
Antiinflammatory
Inhaled corticosteroids (-sone)
LTD4-receptor blockers (-lukast)
Inhibitors of angiotensin
ACEi (-pril)
Ang II receptor blockers (-sartan)
Direct renin inhibitor (aliskiren)
Vasodilators
Dihydropyridine Calcium channel blockers with (-ipine)
Non-dihydropyridine (diltiazem and verapamin)
Beta-blockers (lol)
Allergic asthma physiology
Inflammation.
Bronchoconstriction
Mucus secretion
What does a beta 2 agonist cause
bronchodilation
Rapid relief
NO antiinflammatory effect
Also causes tachycardia and restlessness
What is used for maintenance of asthma
Inhaled corticosteroid.
Reduces inflammation
Beta-2 agonist mechanism of action
Bind to beta 2 receptor.
Activates G protein
Activates adenylyl cyclase.
Increase cAMP.
Inhibit Ca release.
Airway smooth muscle relaxation and dilation
Short acting Beta-2 agonist
-uterol.
acts quick.
short duration
NO anti-inflammatory effects
Long acting beta-2 agonist
-terol
Last up to 12 hrs.
Used with ICS for asthma or LAMA for COPD.
Given to pts with more freq asthma attacks
ACh effect on airway
Bind to M3 causing bronchoconstriction and increased mucus secretion.
Can also cause smooth muscle thickening and fibrosis
Muscarinic antagonist
-ium
Causes bronchodilation
Less effective than beta-2 agonist
Muscarinic antagonist method of mechanism of action
Completely blocks muscarinic receptors in lungs.
Block vagally mediated contraction of airway
Muscarinic antagonist adverse effects
Little systemic absorption.
Dy mouth
Urinary retention
Inhaled corticosteroids
-asone, -ide
Long-term control of persistant asthma.
Can be used by itself to treat asthma.
Decreases inflammatory cascade
Decreases mucus secretion
Decreases capillary permeability
Inhibits leukotriene release.
Reduce freq of exacerbations
Long term use decreases airway hyperresponsiveness
DO NOT relax airway smooth musle
Inhaled corticosteroids method of action
Block phospholipase A. –> Block arachidonic acid release. –> prevent leukotriene release
Inhaled corticosteroid adverse effects
Oropharyngeal candidiasis (yeast infection)
So pt should rinse mouth after use.
PO cortico steroid
For mild-moderate exacerbations
Prednisolone
Prednisone
Methylprednisolone
Parental corticosteroid
Used for severe exacerbations.
Methylprednisolone sodium succinate
LTD4 receptor blockers
-luk-
add on therapy for pts with asthma not well controlled on ICS.
Prevent allergic rhinitis and exercise-induced asthma.
No role in COPD
LTD4 receptor blockers method of action
Blocks Cys-LT1(an LTD4 receptor) receptor on mast cell –> decreased bronchial reactivity, decreased mucosal edema, decreased mucus secretion
LTD4 receptor blockers adverse affects
May stress liver and cause hepatic dysfunction
Mountelukast - neuropsychiatric effects on box
COPD
Chronic, progressive loss of pulmonary function.
Decreased SA for gas exchange.
Excessive mucus blocks airway.
Not fully reversible.
Pathophysiology of COPD
Caused by irritant, mostly cigs.
Changes epithelial cells and activates macrophages.
Fibrosis.
Narrowing of airways.
Inflammatory mediators destroy alveolar walls increasing mucus secretion.
COPD treatment
SABA, SAMA, and systemic steroid for acute
LABA, LAMA, and ICS for persistent.
ICS monotherapy NOT recomended
Most prevalent modifiable risk factor for CVD
BP
Baroreceptor reflexes for BP regulation
Maintain cardiac output and SVR
Moment to moment control via autonomic nerves.
Humoral mechanisms to regulate BP
Maintain cardiac output or long-term control of BP
Endothelin 1
constricts blood vessels
Nitric oxide
Dilates blood vessels
How do kidneys control BP
Controling sodium and water through RAAS system
ACE
Angiotensin converting enzyme.
Converts Ang I to Ang II.
Breaks down bradykinin
Angiotensin II
Bindst to angiotensin-1 receptor on blood vessel causing vasoconstriction.
Signal adrenal gland to release aldosterone
Signals pituitary to release ADH
Aldosterone
Signals kidney to increase Na and water reabsorption causing increased blood volume and therefore pressure.
ACE inhibitor and mechanism
-pril
Bind to ACE inhibiting conversion of ang I to ang II.
Decrease aldosterone secretion
Decreased Na and water retention, decreased sympathetic output.
Prevents breakdown of bradykinin causing increase in vasodilation
Decrease BP
Uses for ACEi
Control HTN.
Heart Failure
post heart attack
Prevention of kidney disease
ACEi adverse affects
Dry cough and angiodema from build up of bradykinin.
Hyperkalemia.
Orthostatic hypotension.
TETRATOGENIC ON BOX. can’t give to pregnant
Angiotensin II receptor blockers (ARBs) and mechanism
-sartan
Binds to angiotensin-1 receptor.
Decreases activation of AT1 receptor by ang II.
Causes vasodilation, decreased Na and water rentention, decreased sympathetic output.
No effect on bradykinin system.
More selective than ACEi
Uses of ARBs
HTN
Heart failure
TETRATOGENIC ON BOX. can’t use in pregnancy
Direct renin inhibitor
Aliskerin
Binds directly to renin.
Inhibits enzymatic effects of renin.
Reduces conversion of ang to ang I.
Causes vasodilation, decreased sodium and water retention. decreased sympathetic output.
Uses for direct renin inhibitor
Not used much
HTN only
Direct renin inhibitor adverse affects
Dry cough
Angiodema
hyperkalemia
renal impairment
diarrhea
TETRATOGENIC ON BOX. Can’t give to pregnant
Dhydropyridine
Subclass of calcium channel blocker.
-pine
Work in peripheral vasculature to lower BP.
Results in vasodilation in peripheral arterioles
Non-dihydropyridine
Verapamil, Diltiazem
Work in SA and AV node to fix arrhythmias.
Results in decreased cardiac conduction and contractility.
Decreases O2 demand
Calcium channel blockers mechanism
Bind and inhibit L-type (long acting) ca channels in heart an vascular smooth muscle
Decrease Ca intry into cells.
Ca channel blocker uses
HTN
Arrhythmias/dysrhythmias
Pulmonary hypertension
Migraine headaches
NOT heart failure
B1 receptor
in heart.
Epi and NE bind to increase contractility and HR thus increasing cardiac output.
On kidney, induces renin release
B2 receptor
In lungs.
Epi and NE bind causing relaxation of smooth muscles and dilation of bronchioles
B3 receptor
In adipose tissue
Beta Blockers
-lol
Antagonize Beta receptors.
Decrease HR and contractility thus decreased CO.
Decreased BP.
Decreased Renin secretion.
Some also block alpha 1 receptors causing vasodilation decreasing BP even more
Beta-blocker uses
HTN
Arrhythmias
Heart Failure
Beta blocker adverse effects
Bradycardia
Hypotension
May mask symptoms of hypoglycemia.
Insomnia
