Physiology of the Cardiovascular & Pulmonary Systems Flashcards
1
Q
Why does the first part of the P-wave represent R atrial depolarization and the second part L atrial depolorization
A
- Sinus node is located n the R atrium and therefore begins to depolarize before the L atrium & finishes earlier as well
2
Q
What is the role of the Bachman bundle
A
- Allows for rapid activation of the L atrium from the R
- May be implicated in atrial fibrillation
3
Q
What is the pause the separates the conduction from the atria into the ventricles
A
- Wave of depolarization is briefly held up at the AV node
- Permits the atria to empty their volume of blood completely into the ventricles before the ventricles contract
- Seen on EKG/ECG following the P-wave
4
Q
What is repolarization
A
- After myocardial cells depolarize, they pass through a brief refractory period during which they are resistant to further stimulation
5
Q
Describe the difference b/w the PR interval and PR segment
A
- Interval: includes the P-wave & the horizontal line connecting it to the QRS complex; measures the time from the start of atrial depolarization to the start of ventricular depolarization
- Segment: measures the time from the end of atrial depolarization to the start of ventricular depolarization
6
Q
What does the ST segment measure
A
- Measures the time from the end of ventricular depolarization to the start of ventricular repolarization
7
Q
What does the QT interval measure
A
- Measures the time from the beginning of ventricular depolarization to the end of ventricular repolarization
8
Q
What does the QRS interval measure
A
- Measures the duration of ventricular depolarization
9
Q
What 3 factors effect stroke volume
A
- Preload
- Contractility
- Afterload
10
Q
Describe the sympathetic and parasympathetic impact on heart rate
A
- Sympathetic: release of epinephrine from the adrenal medulla of the adrenal gland and norepinephrine from the sympathetic axons open channels of the pacemaker cells of the SA node and increase the rate of depolarizations, resulting in an increase in heart rate
- Parasympathetic: release of acetylcholine released by vagus nerve endings that bind to acetylcholine receptors, slowing down the rate of action potential production at the level of the SA node, thereby depressing heart rate
11
Q
What is preload correlated with
A
- End diastolic volume (EDV) which is the max amount of blood that can be in the ventricles at the end of diastole immediately before contraction
12
Q
What is the Frank-Starling mechanism of preload
A
- Strength of ventricular contraction increases as the pre contractile myocardial cell length increases (influenced by ventricular filling)
13
Q
What intrinsic factors effect contractility
A
- Degree of myocardial stretch caused by change sin the EDV
- Force frequency relationships: higher HR (>120 bpm) and increased availability of calcium ions allows for excitation-contraction coupling & a resultant stronger contraction
14
Q
What extrinsic factors effect contractility
A
- Epinephrine from adrenal medulla & norepinephrine from sympathetic nerve endings produce pos. ionotropic effect (increased contractility) by promoting an influx of calcium available to the sarcomeres of the myocardial cells
- Reduction in sympathetic stimulation/reduction in HR results in reduced myocardial contractility
15
Q
Describe what afterload is
A
- Pressure generated within the ventricle must exceed the pressure within the systemic vasculature
-Total peripheral resistance: pressure within arterial system during the diastolic phase of the cardiac cycle while the heart is filling; presents a hindrance to the ejection of blood from the ventricles - Afterload is inversely proportional to stroke volume (increase in after load/total peripheral resistance reduces the amount of blood ejected with each contraction)
16
Q
What si the best indicator of cardiac function
A
- Ejection fraction
- Percentage of the volume of blood ejected out of the ventricles relative to the volume of blood received by the ventricles before contraction
- EF = stroke volume/end diastolic volume
17
Q
Describe normal, reduced, and preserved ejection fraction
A
- Normal = 60-70%
- Heart failure w/reduced EF = systolic dysfunction (can’t squeeze)
- Heart failure w/preserved EF = diastolic dysfunction (can’t fill/stretch): due to HTN, hypertrophy
18
Q
What is end systolic volume
A
- Volume of blood that remains in the ventricle following contraction
- ~30% of the end diastolic volume
19
Q
What hormones do vasoconstriction
A
- Norepinephrine
- Epinephrine,
- Angiotensin II: potent vasoconstrictor released from kidneys when arterial pressure decreases
- Vasopressin (antidiuretic hormone aka ADH): more powerful than angiotensin II, formed by hypothalamus & secreted by the posterior pituitary gland
20
Q
What are the two ways that Vasopressin acts in
A
- Potent vasoconstrictor when circulating in blood
- Greatly increases water reabsorption in the kidney effectively increasing circulating blood volume & pressure
21
Q
What agents are vasodilators
A
- Bradykinin
- Histamine: released throughout the body in response to damage & inflammation
22
Q
The most important endothelial-derived relaxing factor is
A
- Nitric oxide (NO): potent vasodilator released in response to chemical/physical stimuli of the endothelium
23
Q
When endothelial cells are damaged by chronic HTN what can it lead to
A
- Impaired NO synthesis & increased endothelia release contributing to excessive vasoconstriction/worsening HTN & the progression of atherosclerotic disease
24
Q
What 2 factors dictate the rate at which the right atrium fills with venous blood
A
- Total blood volume
- Pressure within the venous vasculature
25
Q
Blood returned to the heart is primarily returned because of venous pressure
A
- Venous pressure higher distal versus proximal
26
Q
What factors influence venous return
A
- Venous pressure
- Musculature pump
- SNS
- Thoracic pressure
- Positioning: Trendelenburg & elevation of LEs
27
Q
Describe coronary blood flow
A
- Perfusion to myocardium occurs more during diastolic/relaxation phase of each cardiac cycle
- Sympathetic hormone epinephrine that affects the β-adrenergic receptors on the coronary arteries, producing vasodilatation
- Myocardial tissue has a higher capillary density than skeletal muscle tissue
28
Q
What happens to the blood flow during exercise
A
- Norepinephrine related by sympathetic nerve fibers stimulate the α-adrenergic receptors along the blood vessels of the digestive organs and kidneys
- Vascular resistance increases due to vasoconstriction while the blood vessels to the active muscles vasodilate
- At the level of the working muscles, epinephrine released by the adrenal medulla stimulates the β-adrenergic receptors within the blood vessel of the muscle to produce vasodilation and increase blood flow to the active muscles.
29
Q
What is Boyle’s law
A
- P (pressure) = 1/V (volume)
30
Q
Define the ventilation terms
A
- Tidal Volume: Approximately 350 to 500 mL of air is inhaled or exhaled at rest with each breath
- Minute Ventilation: total volume of air that is inhaled or exhaled in 1 minute= (RR x TV)
Inspiratory Reserve Volume: additional volume of air that can be taken into the lungs beyond the normal tidal inhalation - Expiratory Reserve Volume: additional volume of air that can be let out beyond the normal tidal exhalation
- Residual Volume: volume of air that remains in the lungs after a forceful expiratory effort
- Inspiratory Capacity: sum of the tidal and inspiratory reserve volumes= (TV + IRV)
- Functional Residual Capacity: sum of the expiratory reserve and RV= (ERV + RV); it is the amount of air remaining in the lungs at the end of a normal tidal exhalation
- Vital Capacity: sum of the inspiratory reserve, tidal, and expiratory reserve volumes; it is the maximum amount of air that can be inhaled following a maximum exhalation. VC= IRV + TV + ERV
- Total Lung Capacity: maximum volume to which the lungs can be expanded; it is the sum of all the lung volumes.
31
Q
What structures are involved in the involuntary control of ventilation
A
- Medulla oblongata: produce inspiration/expiration neurons with forced expiration
- Sensations of pain & alterations in emotion alter ventilation through input to brainstem from limbic system & hypothalamus
- Chemoreceptors detect alterations in blood pH, CO2, and O2 levels: increased ventilation with increased CO2 (hypercapnia) and decreased O2 in blood (hypoxia)
- Pons: Pneumotaxic center in the upper pons maintains the rhythm of ventilation; Apneustic center in the lower pons facilitates sustained or prolonged breathing patterns
32
Q
What structures are involved in voluntary control of ventilation
A
- Controlled by frontal lobe & motor cortex
- More difficult to coordinate
- Requires practice: Pursed lip breathing and Diaphragmatic breathing
33
Q
What are the 3 main lung receptors
A
- Irritant receptors: These receptors are found within the epithelial layer of the conducting airways and respond to various noxious gases, particulate matter, and irritants, causing them to initiate a cough reflex
- Stretch receptors: These receptors are located along the smooth muscles lining the airways and are sensitive to increasing size and volume within the lung
- J receptor: The juxtapulmonary receptors (J receptors) are located near the pulmonary capillaries and are sensitive to increased pulmonary capillary pressures
34
Q
What is a normal ventilation response to exercise
A
- Twofold increase in minute ventilation noted
- An initial abrupt increase followed by a secondary gradual increase in ventilation
35
Q
Define the 3 main properties of lungs
A
- Compliance: allows lung tissue to stretch during inspiration
- Elasticity: allows passive expiration to occur
- Surface tension: allow the lung to get smaller during expiration
36
Q
What are the main functions of surfactant
A
- Lowering surface tension at the air-liquid interface & thus preventing alveolar collapse at end-expiration
- Interacting with & subsequent killing of pathogens or preventing their dissemination
- Modulating immune responses
37
Q
Atmospheric air is a mixture of gases containing
A
- ~79% nitrogen
- ~21% oxygen
- 0.03% carbon dioxide
38
Q
Define perfusion
A
- Blood flow to the lungs available for gas exchange
- Pulmonary arterioles constrict when partial pressures of oxygen in alveoli are low and dilate when alveolar partial pressures for oxygen increase
39
Q
Describe partial pressures of gases and diffusion for gas exchange
A
- Partial pressures of gases: each gas exerts a pressure in proportion to it’s concentration; Dalton’s law = sum of partial pressures; Henry’s law = gas dissolves in fluid
- Diffusion: alveolar capillary membrane; PO2 higher in alveoli than capillary and PCO2 higher in capillary than alveoli
40
Q
How does the ventilation & perfusion (V/Q) matching change based on position
A
- Upright: gravity allows for greater perfusion to the base of the lungs and greater ventilation to the alveoli/apices of the lungs
- To improve ventilation to the posterior bases of the lungs one must position an individual in prone
- Example: beer with foam; beer = perfusion/blood, foam = mixing of blood/air, air/empty glass = ventilation
41
Q
What is a normal V/Q match and what does it mean if it is low versus high
A
- Normal: 4/5 or 0.8
- If V/Q is >0.8 means ventilation exceeds perfusion: causes include blood clot, heart failure, emphysema, or damage to the pulmonary capillaries
- If V/Q is <0.8 means perfusion exceeds ventilation: causes include aspiration, blockage of bronchi by foreign object, pneumonia, severe asthma, pulmonary edema, or COPD
42
Q
Describe the oxyhemoglobin dissociation curve
A
- O2 on Y-axis vs PaO2 on X-axis
- Increasing pH shifts the curve to the left
- Rapid fluctuations in pH or core temp. are not well tolerated
- Increasing tissue temp. during exercise shifts the curve to the right
- Decreasing the pH of the blood shifts the curve downward and to the right
- The curve flattens at peak SaO2 when partial pressure of O2 in the blood is 80 mmHg or above
43
Q
What are the key take aways from the oxyhemoglobin dissociation curve
A
- 95-100% SpO2= 80-100 mmHg PaO2
- PaO2 <80 mmHg= hypoxemia
- PaO2 <60 mmHg= respiratory distress
44
Q
What is the Bohr effect
A
- More O2 is released to those tissues with higher carbon dioxide concentrations
- Lower affinity for O2 secondary to increases in the partial pressure of CO2 and/or decreased blood pH: enhances unloading of O2 into tissues to meet the O2 demand
45
Q
Describe how CO2 is transported in the blood
A
- CO2 diffuses out of the muscle cell
- CO2 binds with H2O to form H2CO3 (unstable)
- H2CO3 dissociates into H+ and HCO3-
- H+ binds to deoxyhemoglobin in RBC: unloading of O2 increases in peripheral tissues as more H+ ions are released to create greater amounts of deoxyhemoglobin for H+ ion to bind to
- HCO3- diffuses out of RBC into plasma
- Positively charged RBC results in chloride shift and Cl- diffuses into RBC to replace HCO3-
46
Q
Describe the acid-base balance within the blood
A
- HCO3- from plasma travels to the lungs and enters the RBC
- Cl- exits the RBC (reverse chloride shift)
- Deoyghemoglobin is converted to oxyhemoglobin with lower affinity for H+
- H2CO3 dissociates into CO2 & H2O (facilitated by carbonic anhydrase)
- CO2 diffuses from pulmonary capillary into alveolus which is exhaled during expiration
47
Q
How are metabolically produced acids largely eliminated
A
- Eliminated from the body via the lungs in the form of CO2 bc major blood acid and carbonic acid are volatile & can vary b/w a liquid or gas state
- Other blood acids are regulated by the kidneys & the liver
