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VF1 - Block 3 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Endocarditis presentation

A
  • Fever
  • Night sweats
    • others
  • NEW STROKE in the stting of fever
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2
Q

Common complications of endocarditis

A
  • Embolism
    • Stroke
    • Infarction of the kidney
    • Can go anywhere
      *
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3
Q

Peripheral findings with endocarditis

A
  • Petechiae
  • Osler’s nodes
  • Splinter hemorrhages
  • Janeway lesions
  • Roth spots
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4
Q

How to diagnose endocarditis?

A
  • positive blood cultures from 2 separate cultures AND
  • abnormal cardiac findings
    • echocardiogram abnormal
    • new murmur
    • abscess
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5
Q

Medical Therapy of endocarditis

A

4-6 weeks of IV antibiotics

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6
Q

When do we use prophylactive antibiotics to prevent endocarditis?

A
  • High-risk individual + high-risk procedure

High risk individuals:

  • prosthetic cardiac valves
  • previous episode of endocarditis
  • transplant recipients with valve abnormalities

High risk procedures:

  • Dental procedures, including routine cleaning
  • Upper respiratory tract procedures, only if it involves incision or biopsy of mucosa
  • GI or GU procedures only if infection present
  • Procedures of infected skin
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7
Q

How to identify sinus rhythm on EKG?

A
  • p waves present
  • p waves upright in leads 1 and 2
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8
Q

Normal QRS complex basis

A
  • due to synchronous contraction of the ventricles
  • Equal to less than 2.5 boxes on EKG
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9
Q

Causes of wide QRS

A
  1. Bundle branch block = delay in ventricle contraction
  2. Ventricular Escape complex (3rd degree AV block)
  3. Wolff-Parkinson-White Syndorme
  4. Ventricular tachyarrhythmia
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10
Q

Location of conduction problem in right bundle branch block

A
  • His-Purkinje system
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11
Q

What does EKG look like for right bundle branch block?

A
  • QRS widened
  • V1 shows rsR’ pattern
  • V6 shows broad S-wave
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12
Q

Where is the conduction problem for a left bundle branch block?

A
  • His-Purkinje system
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13
Q

How does a left bundle branch block appear on EKG?

A
  • Wide QRS
  • V6 shows broad, sawtooth EKG
  • V1 shows broad S wave
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14
Q

Causes of left/right bundle branch block

A
  • Ischemic heart disease
  • Scarring of the heart tissue
  • Antiarrhythmic drugs
  • Hyperkalemia
  • MI infection
  • Trauma
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15
Q

First degree AV block

A
  • Every p wave has a QRS, but it takes longer than it should
  • PR interval is prolonged
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16
Q

Second degree AV block

A
  • Type 1 = “rubberband”
    • PR intervals get longer and longer and then QRS is blocked
    • n:n-1 pattern
  • Type 2 = fracture in the wire
    • Successive PR intervals are not longer, but you still get QRS block
    • n:n-1 pattern
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17
Q

Third degree AV block

A
  • There is no communication b/w p waves and QRS complexes
  • QRS rhythm is coming from an escape rhythm
  • You’ll still see a p-wave, but the QRS and p happen at different times
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18
Q

How do you tell where the escape rhythm is coming from in a 3rd degree AV block?

A
  • If QRS is narrow, then escape rhythm is coming from above the ventricles (AV junction escape rhythm)
  • If QRS is wide, the escape rhythm is coming from the ventricles
  • Evaluate the escape rhythm (QRS rhythm):
    • AV junction = 40-60 beats/min
    • Ventricles = 30-40 beats/min
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19
Q

AV junctional reentrant tachycardia

A
  • A type of supraventricular tachycardia
  • Inverted and retrograde p-wave on lead 2
    • Normal: upright p-wave in lead 2, before QRS
  • short, fixed PR interval
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20
Q

Orthodromic reentrant tachycardia

A
  • A type of supraventricular tachycardia
  • Accessory pathway reentrant tachycardia
  • Retrograde conduction via accessory pathway
  • Inverted, retrograde p-waves in lead 2
  • Short, fixed RP interval, but not as short as with AV-nodal reentry
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21
Q

Wolff-Parkinson-White Syndrome

A
  • Anterograde conduction through the accessory pathway
  • Shows a delta wave –> widened QRS
  • Occurs with a normal sinus rhythm, whereas orthodromic reentrant tachycardia does NOT show delta wave b/c accessory pathway is used retrogradely due to fast heart rate
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22
Q

Two things that can occur with an accessory pathway

A
  1. Orthodromic reentrant tachycardia
  • Tachycardia
  • Accessory pathway used retrogradely
  • See inverted p-wave after QRS
  1. Wolff-Parkinson-White syndrome
  • Normal sinus rhythms
  • Accessory pathway used anterogradely
  • See delta wave on EKG
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23
Q

Atrial tachycardia vs. supraventricular tachycardia

A
  • Atrial tachycardia has a variable RP interval
    • There is no real communication b/w atria and ventricles
    • This is b/c the AV node is not involved
  • SVT shows fixed RP interval
    • This is b/c the AV node is involved
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24
Q

Atrial flutter

A
  • Does not involve AV nodal tissue, completely confined to the atrium
  • Sawtooth pattern on EKG
  • Appears with a regular pattern, like 4:1 or 2:1
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25
Q

Atrial fibrillation

A
  • Focal point is point where pulmonary veins enter
  • Shows more flatline spots than in atrial flutter
  • No regular pattern like atrial flutter
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26
Q

Types of conduction problems involving the AV node vs. not involving AV node

A

Involves AV node:

  • AV nodal reentrant tachycardia
  • Orthodromic AV reentrant tachycardia

Does not involve AV node:

  • sinus tachycardia
  • atrial flutter
  • atrial fibrillation
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27
Q

Ventricular tachycardia

A
  • p-waves are often dissociated from QRS complex
  • Wide QRS b/c ventricle is getting a head start
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28
Q

Differentiating complete heart block from ventricular tachycardia

A
  • Complete heart block, the atria are beating faster than the ventricles b/c the sinus node is faster than the ventricular escape complex
    • See p-waves but no QRS
  • V. Tach shows faster ventricular rate and slower atrial rate
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29
Q

Cause of ventricular tachycardia

A
  • Prior MI –> reentrant circuits
  • Abnormal foci, usually ventricular outflow tracts
  • idiopathic dilated cardiomyopathy
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30
Q

Ventricular flutter

A
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31
Q

Ventricular fibrillation

A
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32
Q

Seizure vs. syncope

A

Duration:

  • Seizure lasts minutes
  • Syncope lasts second

Mental status

  • Returns quickly with syncope
  • Prolonged return with seizure

Cause:

  • Syncope = hypoperfusion to the brain
  • Seizure = CNS problems
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33
Q

Cardiovascular causes of syncope

A
  • Aortic stenosis
  • obstructive cardiomyopathy
  • mitral stenosis
  • aortic dissection
  • arrhythmias
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34
Q

neurocardiogenic cause of syncope

A
  • vasovagal response
    • hypotension due to vagal response
  • See bradycardia and vasodilation occur IN PARALLEL
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35
Q

Clinical features of neurocardiogenic syncope?

A
  • Nearly always a GI component, like nausea
  • warmth
  • once supine, consciousness returns fairly quickly
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36
Q

Holter monitor vs. event monitor vs. intracardiac electrophysiology studies

A
  • Holter monitor used for 24-48 hours
  • Event monitors used for days to weeks
    • Patient presses a button when symptoms appear
  • Intracardiac electrophysiology study
    • Catheterization –> leads inside the heart
    • Used for cardiac events that only occur every 6 months, for example
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37
Q

First steps in ER for STEMI

A

MONA

morphine, oxygen, nitro, aspirin

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38
Q

Inferior vs. anterior infarction vs. posterior infarction

A
  • Inferior: ST-elevation in leads 1, 2, avF
  • Anterior: ST-elevation in leads 1, 2, 3
  • Posterior: ST-DEPRESSION in leads 1, 2, 3
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39
Q

Vaughn Williams Classification

A
  • SoBePoCa
  • 1 = block sodium channels
  • 2 = beta blockers
  • 3 = potassium channel blockers
  • 4 = calcium channel blockers
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40
Q

Mechanism of Class 1 drugs

A
  • Interfere with Phase 0 of cardiac action potential
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41
Q

Quinidine

A
  • Class 1a antiarrhythmic
  • Increases length of AP, increases refractory period
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42
Q

Lidocaine

A
  • Class 1b antiarrhythmic
  • decreases length of action potential, decreases refractory period
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43
Q

Flecainide

A
  • Class 1c antiarrhythmic
  • Slows conduction velocity but no change to refractory period
  • Strongly associated with increased mortality
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44
Q

Main problem with class 1 antiarrhythmics

A

They can increase mortality

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45
Q

Mechanism of Class 2 antiarrhythmics

A
  • Beta blockers
  • Longer PR interval
  • Longer RR interval
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46
Q

Propanolol

A
  • Beta1 and beta2 blocker
  • Used for tachycardia, a fib, a flutter
  • Bronchospasms in asthmatics
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47
Q

Mechanism of Class 3 drugs

A
  • Block potassium channels
  • Increase length of AP, increase refractory period
  • Prolong QT interval
  • Prolong PR interval
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48
Q

Amiodarone

A
  • Class 3 drug
  • LOTS of side effects but it’s used VERY often
  • atrial flutter and atrial fibrillation
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49
Q

Mechanism of class 4 drugs

A
  • Block calcium channels
  • Prolong PR interval
  • Prolong RR interval
    • Slow HR
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50
Q

Verapamil

A
  • Class 4 antiarrhythmic
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51
Q

Diltiazem

A
  • Class 4 antiarrhythmic
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52
Q

adenosine

A
  • Used as an antiarrhythmic
  • Causes decrease in cAMP –> decrease AV node conduction velocity
  • Prolonged PR interval
  • Used for AV node reentrant tachycardia
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53
Q

Left vs. right bundle branch block

A
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54
Q

First, Second, and third degree block on EKG

A
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55
Q

Heart block poem

A
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56
Q

What is MVO2

A
  • Mixed venous oxygen saturation
  • A way of indirectly measuring how the heart is performing b/c it’s hard to measure cardiac output itself
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57
Q

What causes low MVO2?

A
  • Low cardiac output –> more time for oxygen extraction –> low MVO2
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58
Q

Relationship b/w mean arterial pressure and cardiac output

A

MAP - CVP = CO X SVR

  • MAP = mean arterial pressure
    • The pressure coming out of the heart
  • CVP = central venous pressure
    • A measure of preload
  • MAP - CVP = driving pressure for CO
  • SVR = systemic vascular resistance
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59
Q

What is shock?

A

Reduced effective circulation - i.e. inadequate perfusion

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60
Q

Factors that affect/lead to shock

A
  • Low Cardiac output
  • Vasodilation
  • Low blood volume (blood loss)
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61
Q

Pre-shock characteristics

A
  • Elevated lactate
  • No clinical symptoms
  • Reversible
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62
Q

Early shock characteristics

A
  • Tachycardia
  • Cool/clammy due to vasoconstriction
  • Reduced urinary output to conserve blood volume
  • Reversible
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63
Q

Progressive shock characteristics

A
  • Tachypnea
  • Altered mental status
  • End-organ damage
  • Possibly reversible
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64
Q

Refractory shock

A
  • Irreversible
  • Multi-system organ failure
  • high risk of death
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65
Q

4 types of shock

A
  1. distributive
  2. cardiogenic
  3. hypovolemic
  4. obstructive
66
Q

Distributive shock pathophysiology

A
  • Caused by profound vasodilation
  • SVR goes down
  • CO increases to compensate
  • CVP stays the same
  • MAP decreases
67
Q

Main clinical causes of distributive shock

A
  • SEPSIS
  • pancreatitis
  • burns
  • neurogenic shock
  • anaphylaxis
68
Q

Cardiogenic shock pathophysiology

A
  • Intracardiac pump failure –> low cardiac output
  • SVR increases to compensate
  • CVP increases b/c pump isn’t working so fluid gets backed up
  • MAP decreases
69
Q

Causes of cardiogenic shock

A
  • Decompensated Heart Failure
  • arrhythmias
  • cardiomyopathies
  • heart attack
  • VSD
70
Q

Hypovolemic shock pathophysiology

A
  • Loss of blood volume –> low preload
  • Reduced CVP is the cause
  • Causes reduced CO
  • SVR increases to compensate
  • MAP decreased
71
Q

Main causes of hypovolemic shock?

A
  • hemmorrhage
  • dehydration
72
Q

Obstructive shock pathophysiology

A
  • Something outside the heart is impairing its ability to pump
  • Block of flow –> reduced CO
  • SVR increases to compensate
  • CVP varies
  • MAP decreases
73
Q

Main causes of obstructive shock

A
  • Pulmonary embolism
  • Tension pneumothorax
  • Cardiac tamponade
74
Q

Treatment for shock

A
  • Vasopressors used in all to stabilize BP
  • IV fluids help when preload is low or normal
  • Inotropes help when CO is low
  • Afterload reduction helps when CO is low and SVR is high
75
Q

Definition of sepsis

A

A life-threatning organ dysfunction caused by a dysregulated host response to infection

76
Q

SIRS

A
  • Systemic inflammatory response syndrome
  • HR greater than 90
  • REspiratory rate greater than 20
  • Elevated WBC
  • Abnormal temp
77
Q

How have they operationalized sepsis?

A
  • SOFA score
  • qSOFA
    • altered mental status
    • increased respiratory rate
    • low blood pressure
78
Q

Tx of sepsis

A
  • antibiotics
  • IV fluids
  • Lactate measurement
  • Fix source of infection
  • Vasopressors
79
Q

What does a PT measure?

A
  • Extrinsic pathway factors
  • Factors 7, 10, 5, prothrombin, fibrinogen
  • UNIQUE to PT: factor 7
80
Q

What does a PTT measure?

A
  • Intrinsic pathway
  • 8, 9, 10, 11, 5, prothrombin, fibrinogen
  • UNIQUE to PTT: 8, 9, 11
81
Q

A factor 8 deficiency will show a prolonged PT or PTT?

A

PTT

82
Q

A deficiency in factor 5, 10, prothrombin, or fibrinogen will show a deficiency in PT, PTT, or both?

A

Both

83
Q

How does warfarin impact the PT or PTT?

A
  • Warfarin degrades factor 2, 7, 9, and 10
  • Results in PT being prolonged
84
Q

What is a mixing study used for?

A
  • When PT and PTT are both prolonged
  • You want to determine if the prolongation is due to a deficiency or an antibody binding one of the clotting factors
  • If mixing study –> PT/PTT normalizing, then patient has a deficiency
  • If mixing study –> PT/PTT still prolonged, then patient has an antibody/inhibitor present
85
Q

The most common cause of a prlonged PTT but normal PT?

A

Factor 8 inhibitor

86
Q

Common presentation of a bleeding disorder

A
  • Easy bruising
    • especially if this is NOT in the extremities
  • large bruises
  • Mucosal bleeding
    • including heavy periods
  • surgical hemorrhage
  • postpartum hemorrhage
  • joint/muscle bleeding
87
Q

DIC pathophysiology

A
  • disseminated intravascular coagulation
  • Shows both thrombosis and bleeding
  • acquired bleeding disorder caused by:
    • Trauma
    • placental rupture
    • infection
    • hemorrhage??
88
Q

Elevated D-dimer test indicates what?

A
  • Clots have been present
  • Formation of a clot –> fibrin cross-link –> generates D-dimer
  • Dissolution of a clot frees the D-dimers
89
Q

Vitamin K deficiency pathophysiology

A
  • Vitamin K is needed to activate factors 2, 7, 9, and 10
  • No vitamin K –> deficiency in these factors
90
Q

common cause of vitamin K deficiency

A
  • Warfarin
  • nutritional depletion
  • antibiotic administration
91
Q

Liver disease bleeding disorder pathophysiology

A
  • Liver producing lots of the clotting factors
  • Liver disease –> deficiency in clotting factors
92
Q

Test results of liver disease

A
  • Prolonged PT and PTT
  • **Elevated Factor VIII
    • Factor 8 is cleared by the liver
93
Q

How to tell the difference b/w vitamin K deficiency and liver disease?

A
  • Factor V will be low with liver disease, but not vitamin K deficiency
94
Q

Trauma associated coagulopathy

A
  • Diffuse bleeding from sites that were not injured
  • Failure to form clots in the capillary beds
  • Difficult to stop by just fixing the wound
95
Q

What is MAHA

A
  • Microangiopathic hemolytic anemia
  • Loss of red blood cells through increased destruction
  • Destruction of RBC’s is due to colliding with fibrin deposits or platelet aggregates
96
Q

How to identify MAHA

A
  • Shistocytes on peripheral blood smear
  • absence of platelets
97
Q

Differential diagnosis for MAHA?

A
  • DIC
  • Aortic stenosis
  • Heparin-induced thrombocytopenia
  • Other shit we haven’t learned yet
98
Q

Why is the intrapulmonary pressure negative?

A
  • The alveoli naturally want to collapse
  • The chest wall naturally wants to expand
  • Two opposing forces creates a negative pressure in the lung space
99
Q

Transpulmonary pressure

A
  • Alveolar pressure - intrapleural pressure
  • 0 - (-4) = 4 mmHg
  • Responsible for keeping our alveoli present at rest
100
Q

What causes inspiration?

A
  • Expand thoracic cavity –> pressure in the thoracic cage drops
  • Alveolar pressure drops below atmospheric pressure
  • Air rushes in
101
Q

What happens to transpulmonary pressure during tidal breathing?

A
  • Inspiration: increases
    • Intrapleural pressure becomes more negative during inspiration –> more positive transpulmonary pressure
102
Q

Definition of lung compliance

A
  • Transpulmonary Pressure vs. Lung volume
103
Q

Why is the lung compliance curve sigmoidal?

A
  • When transpulmonary pressure is small (i.e. the alveoli are not distended), there is more surface tension within the alveoli
  • As you blow up alveoli, surface tension is reduced
  • Like blowing up a balloon
104
Q

Conditions that alter normal lung compliance

A
  • Fibrosis: makes the lungs less compliant - need larger pressures for volume changes.
  • Emphysema: makes lungs more compliant b/c you lose elastin in the lungs
105
Q

Components in the work of breathing

A
  • Overcoming elastic forces
  • Overcoming surface tension in alveoli
  • Overcoming airway resistance
106
Q

Tidal volume

A
  • The volume of a regular passive breath
107
Q

Inspiratory reserve volume

A
  • The amount of volume you can take (above regular tidal volume) with a forceful inhale
108
Q

Expiratory reserve volume

A
  • The amount you can exhale with a forceful exhalation
109
Q

Vital Capacity

A
  • Total amount you can take in and blow out with a forced inhalation and forced exhalation
110
Q

Residual volume

A
  • the amount of air left in your lung no matter what
  • can’t measure directly
111
Q

Functional residual capacity

A
  • The amount of volume left in your lung at the end of normal tidal breathing
112
Q

spirometric measurements

A
113
Q

FEV1

A
  • Forced expiratory volume in one second
  • The amount of air you can forcefully exhale in one second
114
Q

FVC

A
  • Forced vital capacity
  • The amount you can forcefully exhale after a forceful inhale
115
Q

Normal FEV1/FVC ratio

A

0.8 - 1

116
Q

FEV1/FVC ratio for obstructive lung diseases

A
  • Less than 0.8
  • This is b/c it’s harder to get air OUT with obstructive diseases
117
Q

Obstructive lung diseases

A
  • Asthma
  • COPD
  • Emphysema
118
Q

How does flow volume loop appear in obstructive airway diseases?

A
119
Q

Intra-thoracic vs. extra-thoracic obstructions

A
  • Intrathoracic will show normal inspiration but flattened exhalation
    • b/c during inspiration your respiratory pathways open up and the obstruction is less noticable
  • extra-thoracic obstructions show problems with inspiration and the scooped exhalation
120
Q

intra-thoracic airway obstruction cause

A

masses

121
Q

extra-thoracic airway obstruction cause

A
  • vocal cord paralysis
  • tracheostomy scarring
122
Q

intrathoracic obstruction volume-flow loop

A
123
Q

extrathoracic volume-flow loop

A
124
Q

FEV1/FVC ratio for restrictive airway diseases

A
  • Normal or higher
125
Q

FVC for obstructive vs. restrictive diseases

A
  • FVC normal for obstructive
  • FVC lower for restrictive
126
Q

restrictive lung diseases

A
  • PAINT mnemonic
  • Pleural disease
  • abdominal
  • interstitial lung disease
  • neuromuscular
  • thoracic cage
127
Q

flow-volume loop for restrictive lung diseases

A
128
Q

FEV1/FVC decreased means…

A

obstructive lung disease

129
Q

FEV1/FVC normal means…

A

normal or restrictive lung disease

130
Q

FVC decreased means…

A

restrictive lung disease

131
Q

Tidal volume equation

A

VT = VD + VA

Tidal Volume = Dead Space + Alveolar Volume

132
Q

Minute Volume

A
  • The total amount of air we take in over the course of a minute
  • Directly proportional to alveolar ventilation
133
Q

Alveolar Ventilation Rate

A
  • Minute Volume - Dead space rate
  • This is the amount of air going to gas exchange
134
Q

Relationship between paCO2 and alveolar ventilation

A
135
Q

Normal paCO2 levels

A

40 mmHg (+/- 6)

136
Q

Hypoventilation

A

paCO2 > 46 mmHg

137
Q

Hyperventilation

A

paCO2 < 34 mmHg

138
Q

Why do you get more ventilation at the base of your lung than at the apex?

A
  • Pulmonary pressure at base of lung is more negative –> Alveoli at base of lung are smaller whereas alveoli at top of lung are already fairly distended
  • Alveoli at base are more compliant than alveoli at apex
139
Q

Why does ventilation increase during exercise?

A
  • To blow off more CO2 and maintain blood pH
140
Q

Why/when does paCO2 start to drop during exercise?

A
  • When you hit the peak of exercise
  • Ventilation rate goes up A LOT when you’re hitting your max threshold. That’s b/c lactic acid is building up, so you increase ventilation rate to maintain blood pH.
  • Increase ventilation –> lower paCO2
141
Q

Dalton’s Law of Partial Pressure

A
142
Q

Dalton’s Law predicts 160 mmHg of oxygen for the partial pressure. Why is it 150 mmHg in actuality?

A
  • About 47 mmHg are taken up by the partial pressure of water
  • 760 - 47 = 716 mmHg
  • 0.21 (716) = 150 mmHg
143
Q

Why is the partial pressure in our respiratory tract lower than in the atmosphere?

A
  • Due to humidification of the air –> there is a partial pressure in our respiratory tract due to water, whereas this is not the case in atmospheric air
144
Q

Concentration of oxygen in the blood

A
  • The concentration of oxygen is dependent on hemoglobin content, oxygen saturation, and the very small amount of oxygen that is dissolved in the blood
145
Q

Alveolar partial pressures

A
  • pACO2 = paCO2 = 40 mmHg
    • B/c CO2 freely dissolves in the blood
  • pAO2 = 100 mmHg
    • Calculate this based on alveolar gas equation, which is based on partial pressure of oxygen, barometric pressure, partial pressure due to water, and the alveolar partial pressure of CO2
    • This is lower than the 150 mmHg of oxygen in respiratory tract. Why?
      • B/c the partial pressure of CO2 is higher in the alveoli than in room air and oxygen has to share space with CO2
146
Q

Alveolar Gas Equation

A
  • Allows you to calculate alveolar oxygen (pAO2)
  • For normal ventilation, calculate pAO2 as follows:
    • paCO2 = pACO2 = 40 mmHg
  • pAO2 = 0.21 (760 - 47) - (40/0.8)
  • pAO2 = 100 mmHg
147
Q

Alveolar Oxygen partial pressure with hypoventilation

A
  • Use alveolar gas equation
  • Must first measure paCO2 = pACO2 = 80 mmHg
    • This will be given to you
  • pAO2 = 0.21 (760 - 47) - (80/0.8)
  • pAO2 = 50 mmHg
148
Q

Aa gradient

A
  • pAO2 - paO2
  • The difference between alveolar oxygen and arterial oxygen
149
Q

Normal Aa gradient

A
  • 12
150
Q

Widened Aa gradient tells you…

A

You’re not effectively getting oxygen from your lungs to your blood

151
Q

Two main mechanisms of hypoxia

A
  1. hypoventilation
  2. Aa gradient
152
Q

How to calculate the Aa gradient

A
  • Use alveolar gas equation to calculate what your alveolar oxygen should be
  • Take a blood gas to measure arterial oxygen
153
Q

Why is PVR much lower than SVR?

A
  • lung vessels are more distensible than systemic vessels
154
Q

Effect of lung volume on PVR

A
  • Extraalveolar vessels expand when you take a breath, reducing PVR
  • Vessels around alveoli get compressed during inspiration, increasing PVR
  • The balance b/w these two forces predicts overall PVR
155
Q

Effect of cardiac output on PVR

A
  • Resistance and cardiac output are inversely proportional
  • When CO goes up, resistance goes down
156
Q

What happens in lung vessels to accomodate increased CO?

A
  • Distension
  • Recruitment of more capillaries
157
Q

Impact of hypoxia on PVR

A
  • increases PVR due to pulmonary artery vasoconstriction
  • We don’t understand fully, but we think it is an evolutionary mechanism designed to divert blood flow away from an infection in the lungs
158
Q

Where is PVR lowest?

A
  • FRC = functional residual capacity
  • The end of your tidal exhalation
159
Q

Impact of positive pressure ventilation on PVR

A
  • Increases PVR b/c it distends alveoli –> compresses capillaries
160
Q

Effects of gravity on PVR

A
  • Higher PVR at the apex = less blood flow
    • Matches ventilation
  • Lower PVR at the base = more blood flow
    • Matches ventilation
161
Q

Cause of pulmonary edema

A
  • Increased hydrostatic pressure
    • Most commonly from left ventricular failure or valve disease
  • Decreased oncotic pressure
    • Most commonly from cirrhosis

VF1 - Block 3 (7 decks)

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