First Aid - Cardiovascular - General Physiology

Front 1

Variable coronary vascular supply

Back 1

Variable coronary vascular supply:

Posterior Descending/interventricular artery
-supplies posterior septum / LV

*80% of time from RCA
*20% of time from CFX

Front 2

MC site of CA occlusion?

Back 2

MC site of CA occlusion?

LAD - supplies anterior interventricular septum

Front 3

LA enlargement?

Back 3

LA enlargement?

*LA is most posterior

-dysphagia - compression of esophagus
-hoarseness - compression of recurrent laryngeal nerve

Front 4

Cardiac Output

Back 4

Cardiac Output

CO = SV x HR

Fick's principle:
CO = rate O2 consumption / [arterial O2 content - venous O2 content]

Front 5

Pulse Pressure

Back 5

Pulse pressure

systolic pressure - diastolic pressure
approximated ~ stroke volume

SV = CO / HR = EDV-ESV

Front 6

CO during exercise

early
late

Back 6

CO during exercise

early - maintained by SV
late - maintained by HR

Front 7

Effect of acidosis on contractility / SV?

Back 7

Effect of acidosis on contractility / SV?

decreases

Front 8

How to decrease preload?
How to decrease afterload?

Back 8

How to decrease preload?
-venodilators (nitroglycerin)

How to decrease afterload?
-vasodilators (hydrAlAzine)

Front 9

Starling curve (Frank-Starling relationship)

Back 9

Starling curve (Frank-Starling relationship)

increasing preload causes increased force of contraction, & thus increased SV

**asumes on ascending limb of starling curve - CHF goes past

Front 10

Ejection Fraction (EF)

Back 10

Ejection Fraction (EF)

nl >= 55%
decreases in systolic heart failure

EF = SV / EDV = [EDV - ESV] / EDV

Front 11

Causes of increased blood viscosity

Back 11

Causes of increased blood viscosity

1.) polycythemia
2.) hyperproteinemic states (multiple myeloma)
3.) herditary spherocytosis

Front 12

What vessels account for most of the total peripheral resistance?
What is the significance?

Back 12

What vessels account for most of the total peripheral resistance?
**arterioles

What is the significance?
**regulate capillary flow

Front 13

Calculating resistance

Back 13

Calculating resistance

R = pressure / flow = 8*n*l / (pi*r^4)

n = viscosity; increases resistance
l = length; increases resistance
r = radius; exponentially decreases resistance

series vs parallel resistors

Front 14

Graphing cardiac cycle

Back 14

Graphing cardiac cycle

typically done for Left ventricle

X-axis --> volume
Y-axis --> pressure

Front 15

During what phase does LV consume most oxygen?

Back 15

During what phase does LV consume most oxygen?

Phase 1 - isovolumetric contraction following mitral valve closure preceding aortic valve opening

Front 16

S3

Back 16

S3

early diastole
hear immediately after S2 "I believe"
associated w/increased filling pressure (MR, CHF)
more common in dilated ventricles (dilation - 3 syllables, S3)
normal in children & pregnancy

Front 17

S4

Back 17

S4

"atrial kick"
late diastole; immediately preceding S1 "believe me"
high atrial pressure
associated w/ventricular hypertrophy (4 syllables)
[LA must push against stiff LV wall]

Front 18

Diagrams - see pg 283

Back 18

Diagrams - see pg 283

Front 19

Normal S2 splitting

Back 19

Normal S2 splitting

aortic valve closes before pulmonic
inspiration increases difference

(think expanded lungs, neg intrathoracic pressure, increased capacitance, more blood enters lungs so pulm valve closes later)
(aortic valve closes sooner b/c less return to left heart from lungs)

Front 20

Wide S2 splitting

Back 20

Wide S2 splitting
**delayed RV emptying

pulmonic stenosis
right bundle branch block

Front 21

Fixed S2 splitting

Back 21

Fixed S2 splitting

Atrial Septal Defect
**left to right shunting
**increased flow thru pulmonic valve, closure greatly delayed regardless

(don't confuse w/VSD)

Front 22

Paradoxical S2 splitting

Back 22

Paradoxical S2 splitting
**delayed LV emptying
**pulmonic closure still is delayed with inspiration, but this moves it towards aortic valve closure b/c order is reversed w/aortic delay

aortic stenosis
left bundle branch block

Front 23

pulsus parvus et tardus

Back 23

pulsus parvus et tardus

Aortic Stenosis
-weak pulse compared to heart sounds

Front 24

Crescendo-decrescendo systolic, followed by ejection click

Back 24

Crescendo-decrescendo systolic, followed by ejection click

Aortic stenosis
-click - abrupt halting of valve leaflets
-LV pressure >> aortic during systole
-radiates to carotids

Front 25

pulsus parvus et tardus

Back 25

pulsus parvus et tardus

Aortic Stenosis
-weak pulse compared to heart sounds

Front 26

Holosystolic, harsh-sounding murmur; tricuspid area

Back 26

Holosystolic, harsh-sounding murmur; tricuspid area

VSD

Front 27

Late systolic crescendo murmur, midsystolic click, loudest at S2

Back 27

Late systolic crescendo murmur, midsystolic click, loudest at S2

Mitral proplapse
-Most frequent valvular lesion
-usually benign
-mid click due to sudden tensing of chordae tedinaea
-can predispose to infective endocarditis

Possible causes:
-myxomatous degeneration
-rheumatic fever
-chordae rupture

Front 28

Immediate, high-pitched "blowing" diastolic murmur

Back 28

Immediate, high-pitched "blowing" diastolic murmur

Aortic regurgitation (AR)
-wide pulse pressure when chronic
-bounding pulses / head bobbing

Possible causes:
-often due to aortic root dilation
-bicuspid aortic valve
-rheumatic fever

Front 29

delayed late diastolic rumbling murmur

Back 29

delayed late diastolic rumbling murmur

Mitral stenosis
-follows opening snap (abrupt half in leaflet motion, after rapid opening, due to fusion at leaftips)
-LA >> LV during diastale

Possible causes:
-2ndary to rheumatic fever
-chronic MS --> LA dilation

Front 30

continuous machine-like murmur

Back 30

continuous machine-like murmur

PDA
-loudest at S2
-often due to congenital rubella
-prematurity

Front 31

Ventricular action potential

-phases & ion channels

Back 31

Ventricular action potential (pg 286 diagram)

-phase 0: rapid depolarization
**Na channels open

-phase 1: initial repolarization (small)
**inactivation of Na channels
**K channels begin opening

-phase 2: plateau'd depolarization
**Ca++ channels, influx maintains depolarization
**K+ channels open; balanced by Ca

-phase 3: rapid repolarization
**K channels - massive K efflux due to slow channels opening
**closure of Ca channels

-phase 4: resting potential
**high K+ permeability

Front 32

Pacemaker action potential

-which cells?
-differences from Ventricular AP

Back 32

Pacemaker action potential

-which cells?
**SA node
**AV node

-differences from Ventricular AP
**phase 0 - upstroke due to voltage gated Ca++ channels (not Na)
[Na channels permanently inactivated b/c of resting potential; Ca channels slower, pacemakers use this to prolong transmission]

**phase 1 (absent)

**phase 2 - absent (no plateau)

**phase 3 - repolarization; inactivation of Ca++ & activation of K+ channels

**phase 4 - slow diastolic depolarization
---membrane spontaneously depolarizes as Na+ conductance increases (If, not Ina)
---accounts for autamaticity
---slope of phase 4 determines HR - ACh/adenosine decrease, catecholamines increase
---[sympathetic stim increases chance If channels are open]

Front 33

ANP

-stimulated by?
-MOA?

Back 33

ANP
-causes generalized vascular relaxation

-stimulated by: increased blood volume & atrial pressure

-MOA
**constrict renal efferents, dilate afferents (cGMP)
**promotes diuresis, escape from aldosterone

Front 34

Aortic Arch receptors

Back 34

Aortic Arch receptors

respond only to INCREASED blood pressure
signal via vagus nerve to medulla

Front 35

Carotid Sinus receptors

Back 35

respond both to increase & decrease in BP
signals via glossopharyngeal nerve to solitary nucleus of medulla

Front 36

What is central control of BP/HR sensitive to?

Back 36

responds to changes in:
**pH
**pCO2 of brain interstitial fluid (influenced by arterial pCO2)

Front 37

What does CO2 do to cerebral arteries?

Back 37

CO2 causes cerebral arteries to vasodilate
if hyperventilate a patient --> low CO2 causes cerebral arteries to constrict
**can decrease ICP this way

Front 38

Cushing's triad?
Cushing's Reaction?

Back 38

triad = hypertension, bradycardia, respiratory depression

incrased intracranial pressure constricts arterioles --> cerebral ischemia --> hypertension --> reflex bradycardia

Front 39

Circulation: peculiarities of specific organs

Back 39

Circulation: peculiarities of specific organs

Liver - largest share of systemic CO
Kidney - highest flow per gram tissue
Heart - largest AV O2 difference; O2 extraction is always ~100%

Front 40

How is increased O2 demand in the heart met?

Back 40

How is increased O2 demand in the heart met?

-increased coronary blood flow
-O2 extraction is always ~100%, so cannot increase this, must be done by flow

Front 41

Normal Pressures:

RA -->
RV -->
Pulmonary Artery -->
LA -->
LV -->
Aorta -->

Back 41

Normal Pressures:

RA --> 5
RV --> 25/5
Pulmonary Artery --> < 25/10
LA --> < 12
LV --> 130/10
Aorta --> 130/90

Front 42

What if PCWP > LV diastolic pressure?

Back 42

Mitral Stenosis (Swan-ganz findings)

Front 43

Autoregulation of blood flow

Heart -->
Brain -->
Kidneys -->
Lungs -->
Skeletal mm -->
Skin -->

Back 43

Autoregulation of blood flow

Heart --> CO2, adenosine, NO
Brain --> CO2 (pH)
Kidneys --> myogenic / tubuloglomerular feedback
Lungs --> hypoxia causes vasoconstriction [unique]
Skeletal mm --> lactate, adenosine, K+
Skin --> stimulation most important, temp control

Front 44

Starling Forces Equation

Back 44

Starling Forces Equation
**positive is defined as efflux of fluid from vessel

Pnet = [Pcap - Pinterstit] - [Oncotic cap - Oncotic intersit]

Net fluid flow = Kf * Pnet

Front 45

Causes of Edema

Back 45

Causes of Edema

1.) increased capillary pressure (CHF)
2.) decreased plasma prtns (nephrotic syndrome; liver failure)
3.) increased capillary permeability (toxins, infections, burns)
4.) increased interstitial osmotic pressure (lymphatic blockage)