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BS2 > Cardiopulmonary > Flashcards

Cardiopulmonary Flashcards

1
Q

Cardiac Output/Blood Flow Equation

A

HR x Stroke Volume

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2
Q

What type of blood is found in fetal circulation?

A

Mixed Blood (both oxygenated and deoxygenated)

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3
Q

Fetal Circulation Anatomy

A

1) Ductus Venosus: shunts oxygenated blood from liver to inferior vena cava
2) Foramen Ovale: mixed blood travels from right to left atrium
3) Ductus Arteriosus: mixed blood shunted from pulmonary artery to aorta to send out to body
4) Umbilical Arteries: bring oxygenated blood back to placenta

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4
Q

Cardiac Muscle Anatomy/Physiology

A

1) Intercalated discs (increase closeness of fibers for transmitting excitation quickly)
2) Syncytial (“all or nothing” function, all fibers twitch at same time)
3) Larger T-tubules (propogate action potentials)
4) Calcium induced calcium release ( unique bc K+ drives skeletal muscle)
5) Less work required vs skeletal muscle
6) Twitches generate output
7) Never fatigues or rests

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5
Q

Tissue Layers of Heart (Superficial to Deep)

A

1) Pericardium (fibrous layer)
2) Myocardium (contractile layer)
3) Endocardium (endothelial layer)

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6
Q

Landmarks for
1) Listening to HR
2) Apex location

A

1) Listening to HR: second intercostal space
2) Apex location: midclavicular line of 5th intercostal space

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7
Q

Right vs Left Side of Heart

A

· Left Side: receives oxygenated blood from lungs and pumps to body
· Right Side: Receives deoxygenated blood from body and pumps to lungs

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8
Q

Systemic vs Pulmonary Circulation

A

· Systemic:
- delivers oxygenated blood to organs and muscles
- returns deoxygenated blood to heart
· Pulmonary:
- delivers deoxygenated blood to lungs
- returns oxygenated blood to heart

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9
Q

Opening and Closing of Valves (passively)

A

· Open: upstream pressure > downstream
· Close: downstream pressure > upstream

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10
Q

Chordae Tendinae Function

A

Provide tension for AV Valves (Tricuspid and Mitral) to prevent prolapse

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11
Q

Clinical Relevance of Heart Valve Sounds

A

·S1 (Lub): End of Diastole/ventricular filling
- Tricuspid and Mitral Valves close

·S2 (Dub): End of blood ejection
- Pulmonary and Aortic Valves close

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12
Q

Cardiac Cycle Events

A

1) AV Valves Open (Diastole)
- ventricles fill
2) AV Valces Close (Systole)
- Isovolumetric Ventricular Contraction (all valves close)
3) Semilunar Valves Open (Systole)
- ventricular ejection
4) Semilunar Valves Close (Diastole)
- Isovolumetric Ventricular Relaxation (all valves closed)

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13
Q

Cardiac Performance Factors

A

1) Volume
2) Pressure
3) Flow

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14
Q

Starling’s Law/ Length- Tension Relationship

A

↑ Volume (Preload/EDV) then ↑ Stretch

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15
Q

Contractility

A

· Intrinsic property of cardiac muscle and therefor NOT effected by volume or pressure
· Does effect preload/EDV
· Can change based on preload and what is needed to reach a certain SV
- ex: If contractility is ↓ then preload must be ↑ to achieve a certain SV
* Usually assumed as a constant measure but realistically functions to help balance what is needed

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16
Q

Hydrostatic Pressure

A

Change in Pressure relative to gravity

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17
Q

Transmural Pressure

A

· Difference in pressure between the inside and outside of a vessel
· Pressure must be greater inside > outside or else vessel would collapse

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18
Q

Type of relationship between cross-sectional area and velocity?

A

· Inverse relationship
· Ex: If ↑ CSA then ↓ Velocity (in capillaries)

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18
Q

Relationship between Flow and Driving Pressure, Radius, Viscosity, and Length

A

· Flow is directly proportional to driving pressure and radius but inversely proportional to viscosity and length
· Ex: ↑ Flow :
- ↑ Driving Pressure
- ↑ Radius
- ↓ Viscosity
- ↓ Length

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18
Q

Is pressure greater in systemic or pulmonary circulation?

A

· Systemic (left side of heart) > Pulmonary (right side of heart)

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19
Q

Relationship between Resistance to Blood Flow and Radius

A

· Resistance is directly proportional to viscosity and length but inversely proportional to (fourth power) radius
· Ex: ↑ Resistance :
- ↑ Viscosity
- ↑ Length
- ↓ radius ^4
·

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20
Q

STEMI vs. NSTEMI

A

1) STEMI (ST Elevation Myocardial Infarction): transmural, full thickness ischemia
* Myocardial injury more severe usually

2) Non-ST Elevation Myocardial Infarction: subendocardial, partial ischemia

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21
Q

What can happen during the super-normal refractory period?

A

Another impulse can cause ventricles to depolarize again

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22
Q

What happens if QT Interval is greater than half the R-R Interval?

A

Another Heartbeat can happen before ventricles have repolarized which can lead to lethal arrhythmias

23
Q

What part of the EKG would reflect damage to the atria conduction system?

A

P-wave

24
Q

What dysfunction would a widened QRS complx represent?

A

His-Purkinje network

25
Q

Normal Capillary Pressure Factors

A

Maintained when pre-capillary resistance> post-capillary resistance

26
Q

How do you increase capillary pressure?

A

Decrease pre-capillary resistance which leads to more flow and thus an increase in pressure

27
Q

· What happens to pre-capillary resistance during Arteriole Dilation (or venular constriciton)

· Arteriole Constriction?

A

· Arteriole Dilation: ↓ Pre-capillary Resistance

· Arteriole Constriction: ↑ pre-capillary resistance thus decreasing flow and decreasing pressure in the capillary

28
Q

Distensibility

A

Describes the change in volume for a given change in pressure

29
Q

Convection

A

· Capillary exchange of water
· Dependent upon the balance of pressures between capillary and interstitial

30
Q

Cardiac Action Potentials

A

· Na+ Current: rapid depolarization
· Ca2+: triggers cardiac contraction
· K+ Current: repolarization

31
Q

Nitroglycerin (Cardiac Medication)

A

· Powerful vasodialator that decreases afterload thus decreasing the work of the heart

32
Q

How do pacemakers decrease heart rate? (3 ways)

A

1) Decrease rate of depolarization
2) Shift maximum daistolic potential to start out more negative
3) Increase threshold (thus more time required to reach a positive threshold)

33
Q

Inotropic Agents (Cardiac Medications)

A

· Modify contractility independent of pre/afterload and by raising/lowering Ca+ levels
· Positive Inotropic Agent: ↑ contractility and work of the heart by ↑ Ca+
· Negative Inotropic Agent: ↓ contractility and work of the heart by ↓ Ca+

34
Q

Where does gas exchange occur?

A

· Blood-air barrier (due to vessels lining the alveoli)
· Type 1 Cells
· Lung parenchyma

35
Q

Visceral vs Parietal Pleura and Plueral Space

A

· Visceral Pleura: covers surface of lung and is inseperable from lung tissue
· Parietal Pleura: covers inner surface of chest wall and exposed part of diapragm
· Pleural Space: thin serous film that separates the 2 pleura and has an airtight seal to enhance lung expansion

36
Q

Bohr’s Method

A

· Expired CO2 comes from alveolar gas not dead space
· Ex: Increase dead space means decreased expired CO2

37
Q

How to decrease pulmonary vascular resistance (PVR)

A

· 2 Methods
1) Recruitment- opening of previously closed vessels
2) Distention- increase in the caliber of vessels that were already open

38
Q

Alveolar Hypoxia

A

· Constriction of small pulmonary arteries as a way to direct blood flow away from poorly ventilated areas of the lungs

39
Q

Hypoxemia

A

Drop in partial pressure of O2 in arterial blood

40
Q

What can change ventilation or perfusion?

A

1) Intrapulmonary Shunt- no ventilation occurs
2) Alveolar Dead Space- no perfusion occurs

41
Q

Respiratory Alkalosis

A

· Result of Hyperventilation causing a decrease in CO2 and thus an increase in pH

42
Q

Compliance

A

· Ability to generate a certain volume at a certain pressure

43
Q

Hysteresis

A

· Amount of pressure generated for a given volume
· At a given pressure, volume during expiration > inspiration

44
Q

What does surfactant affect?

A

· Reduces Surface tension to equalize pressure
· Produced by Type 2 Pneumocytes
· Decreased surfactannt can lead to difficulty inflating the lungs and potential of atelectasis (alveolar collapse)

45
Q

Regulated variables in breathing?

A

Arterial blood gases (O2 and CO2) and pH

46
Q

What has a greater influence of changing breathing- CO2 or O2?

A

CO2> O2

47
Q

Obstructive vs Restrictive Patterns

A

1) Obstructive: decrease in expiratory airflow
- decreased elastic recoil results in air trapping in lungs
2) Restrictive: decrease in lung volume

48
Q

COPD Characteristics and 2 Main Types

A

Characteristics
· ↓ elasticity
· ↑ airway resistance
· Air trapping

2 Main Types:
1) Chronic Bronchitis
2) Emphysema

49
Q

Atherosclerosis

A

· Progressive hardening and narrowing of the arteries, occurs within the arterial walls
* Cause of most heart and vascular diesases

50
Q

Orthostatic Hypotension Diagnostic Requirements

A

· Drop in SBP >20 mm Hg
· Drop in DBP >10 mm Hg
· Increase in HR > 15bpm

51
Q

Composition of Whole Blood

A

· Plasma (liquid) (47-64%)
· Red Blood Cells (formed elements)
· WBCs and platelets (buffy coat)

52
Q

Hemoglobin vs Hemotocrit

A

· Hemoglobin: O2 carrying protein
· Hemotocrit: % of whole blood that is composed of RBCs

53
Q

Thrombocytopenia vs Thrombocytosis

A

· Thrombocytopenia: decrease in platelet count below 70,000
- increased risk for bruising
· Thrombocytosis: increase in platelet count
- due to hemostasis problem

54
Q

Erythrocyte Function

A

1) Carry O2 to tissues
2) Carry CO2 to lungs
3) Buffer to maintain pH balance
* Key factor is Hb

55
Q

Oxygen Saturation

A

· Amount of Hb actually bound to O2
· Females: ~ 14.0 g/dL
· Males: ~ 15.5g/dL

56
Q

Screening for a DVT (Wells Clinical Decision Rules:DVT)

A

· Scored based on clinical liklihood of a DVT
· Score of 0 or less = DVT unlikely
· Score of 3+ = DVT highly likely

57
Q

Normal Hb Ranges, Hematocrit, pH, PaCO2, PaO2

A

· Male: 14-18 g/dL
· Female: 12-16 g/dL

Hematocrit:
· Males: 42-52%
· Females: 37-47%

pH:
· 7.35-7.45

PaCO2:
· 35-45 mm Hg

PaO2:
· 80-100 mg Hg

BS2 (7 decks)

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