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Cardiology > CVS Physio > Flashcards

CVS Physio Flashcards

1
Q

CO =?

A

SV*HR

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2
Q

Ficks principle

A

CO=rate of O2 consumption/

arterial O2content-venous O2content

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3
Q

MAP=3

A

MAP=CO* TPR

MAP=PP+1/3 diastolic pr

MAP=1/3 sys p+2/3 Dias pr

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4
Q

Pulse pressure=
Proportionate to?
Inversely proportionate to?

A

SBP- DBP
SV
Compliance

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5
Q

SV=

A

SV=EDV-ESV

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6
Q

During exercise how’s the CO increased
Early
Late
Other changes

A

Early-increase HR and SV
late -SV plateus and HR increase

Reduce TPR

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7
Q

What happens when HR increase

Eg

A

Time of diastole reduce
Cardiac filling is compromised
Reduce CO
Eg-VT

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8
Q

Causes of increase pulse pressure 4

A

Hyperthyroid
Aortic regurgitation
Aortic stiffing -reduce compliance
OSA-increase sympathetic tone

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9
Q

Decrease PP Causes 4

A

AS
CHF
Cardiac tamponade
Carcinogenic shock

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10
Q

SV depends on 3

How

A

SV increase
High preload
high contractility
Low after load

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11
Q

Contractility increased by which factors and how 4

A

Catecoleamines-increase activity of Ca channels in SR.

High Intracellular Ca

Low extra cellular Na-inhibit Na Ca exchanger

Digoxin -inhibit Na K Atpase -increase Intracellular Na-inhibit Na Ca exchanger

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12
Q

Factors decreasing contractility 4

A 
Bblockers -reduce cAMP
Non dihydropiridine CCB
ischemia -MI
Hypoxia 
Hypercapnia
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13
Q

Myocardial O2 demand increase by which factors 4?

A

🍄myoCARDium

C-contractility
A-after load
R-rate
D-diameter(increase wall tension)

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14
Q

La Plases Law for wall tension

A

Tension=pressure *diameter/thickness of wall

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15
Q

Preload approximated by?
Depends on 2
Action of venodilators

A

EDV
venous return-venous tone
Blood vol
Reduce preload-nitrates

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16
Q

Afterload approx by
Vasodilators causes what

Drugs causing reduction of both pre and after load

A

MAP
Reduce afterload

ACEI ACRB

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17
Q

What happens to MAP in chronic HT

A

Increase MAP-increase afterload -increase wall tension-thickening to reduce tension

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18
Q

EF=
index of what?
What happens to it in sys HF and Dias HF

A

EF=SV/EDV-ESV

Index OF LV contractility

Sys HF-low EF
Dias HF -normal EF

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19
Q

Starlings curve
Draw
Explain
Changes with exercise and HF/digoxin

A

Refer book- x-EDV
Y-SV

Increase venous return
Increase EDV
Increase end diastolic fiber length which is proportionate to force of contraction
Increase SV

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20
Q 
^pressure=
What's Q and R
How to calculate Q
How to calculate R
R in series and parallel
A

Pressure difference=Q(volumetric flow rate)* TPR

Q=flow velocity/cross sectional area
R=P/Q
R=8nl/^r4(n-viscosity)

Series R =R1+R2…
Parallel R=1/R1+1/R 2..

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21
Q

Viscosity depends on?

Increase viscosity and decrease Vic’s eg

A

Hematocrite

Increase-high protein (MM),polycythemia
Decrease-anaemia

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22
Q

Highest cross sectional area in where?advantage?

Highest PR where ?
Lowest ?

Organ removal ep affects TOR how ?

A

Capillaries-low velocity

Arterioles
Veins

Increase-cause reduce CO
EG- nephrectomy

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23
Q

Cardiac function curve
Draw-x/y

Vascular functional curve
Draw-x/y

Joining point?means

Mean systemic pressure point is where?

A

Cardiac
X-EDV. Y-CO/SV

Vascular
X-RA pressure
Y-venous return

Cardiac operating point-when venous return=CO

Vascular curve join the x axis

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24
Q

Changes to each curve with

  1. ionotopes
  2. venuos tone and blood vol
  3. TPR

Eg-neg iono/pos venous tone/neg v tone/

A

Refer book for charts

Neg iono-narcotic overdose
Pos vt-sympathetic stimu
Neg vt-spinal analgesics

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25
Q

When does these changes occure to vascular and cardiac curves
How

A

To reinforce-exercise increase CO by reducing TPR

To compensate-in CHF (-ve ionotropic)to increase SV the is fluid retention

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26
Q

Pressure vol curves of LV
Draw with stages
Mark heart sounds
SV

Changes with
Increase preload
Increase afterload
Increase contractility

A

Refer book

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27
Q 
Cardiac cycle draw
Stages-7
LV pressure
aortic pressure
Heart sounds
Opening and closing of mitral and aortic valves
A

Refer book

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28
Q

Heart sounds
S1-heard when,best heard
S2-when ,where

A

S1-M/T valve closure
At apex

S2- A/P valve closure
At upper left sternal edge

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29
Q

S3
Heard when
Normal in who
Pathology with what

A

Rapid ventricular filling
Early diastole

Common in pregnancy and children

Dilated heart

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30
Q

S4
Heard when
Where
Pathology

A

Slow ventricular filling
Atrial systole

At apex on LLDP

Ventricular hypertrophy

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31
Q

Draw JVP waves

Occures when

A 
a-atrial contraction
c-isovol ventri contraction 
X-ventricular ejection
v-atrial filling with closed mitral valve
Y-opening of MV and atrial emptying
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32
Q

Types of splitting of second heart sound

A

Normal
Wide
Fixed wide
Paradoxical

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33
Q

Normal splitting explain

A

During inspiration the neg intra thoracic pressure causes more blood to return to R/heart.
Also reduces pulmonary vascular resisitance
RV empting takes longer
PV closes later than AV

During expiration this doesn’t happen
So both closes at the same time
No splitting

34
Q

Wide spitting explain

A

When there’s RV emptying probs
Eg-PS/RBBB

RV emptying is delayed in both inspiration and expiration
But more in inspiration
So exaggeration of the normal

35
Q

Wide fixed spitting

A

In ASD
Increase pulmonary blood flow
Wider spilt irrespective of breathing

So same widening in expiration and inspiration both

36
Q

Paradoxical spilt

A

With delaying in aortic valve closure
Eg-AS/LBBB

The spit is heard in expiration and not in inspiration

As the two sounds get closer in inspiration
No split

Aortic sound heard later than pulmonary in exp
So splitting

37
Q

What re the 6 auscultations sites

A 
Aortic
Pulmonary
Mitral 
Tricuspid
Left sternal edge
Left infracalivicular
38
Q

Murmurs heard in the aortic area

A

Systolic
AS
Aortic sclerosis
Flow murmurs

39
Q

Murmurs heard in the pulm area?

A

Systolic
PS
Flow murmurs

40
Q

Tricuspid area murmurs

A

Systolic
TR
VSD

Diastolic
TS
ASD

41
Q

Mitral area murmurs

A

Systolic
MR

Diastolic
MS

42
Q

Left sternal border murmurs

A

Diastolic
AR
PR

Sys
Hypertrophic cardiomyopathy

43
Q

I

Left infra clavicular

A

PDA

44
Q

ASD murmur types 3

Murmur from the defect

A

Pulm flow mumur
Tricuspid rumble

Later on with pul artery dialtaion-PR

No murmur from the defect

45
Q

Bed side maneuvers to change murmurs 4

Effect

A

Inspiration-increase preload
Hand grip-increase afterload
Vulvalva/standing - decrease preload
Rapid squatting-increase preload

46
Q

Inspiration change which mumurs

A

Increase all R heart murmurs

47
Q

Hand grip change which murmurs

A

Increase AR/MR/VSD
Decrease-HCM murmur
MVP-delayed click or murmur

48
Q

Vulsalva/standing change which murmurs

A

All murmurs reduce including AS
Increase HCM
MVP-late murmur

49
Q

Rapid squatting change which murmurs

A

Increase AS
Reduce HCM
MVP-delayed

50
Q 
AS
Time
Type
Best heard
Radiates to
Pulse
Symptoms 3
Causes 2
A 
Ejection systolic
Crescendo decresendo
Aortic area
Carotids
Weak with late peak
SAD-syncope/angina/dyspnoe with exertion

Age-calcification
Bicupid aortic valve -premature calcification

51
Q

MR/TR
Time
Type
Pitch

Site
Radiation
Causes

Both can occure in which diseases 2

A

Pansystiolic
Blowing
High pitched

MR-apex
Axilla
Post MI/MVP/LV dilation

TR-tricuspid area
R/sternal border
RV dilatatoin

RF
Infective endo

52
Q 
MVP
site
Time
Extra character,due to
Loudest before
Causes-common /eg
Other causes
Predispose to 
RX
A 
Apex
Crescendo
Mid systolic
Mid systolic click-tensing of corde tendine
S2
Myxomatus degeneration -primary/secondary (Marfans/ehlers dalos)
RF
Corde rupture

IE
IE priphylaxis

53
Q

VSD
Time
Type
Site

A

Pan systolic
Sea gull
Tricuspid

54
Q 
AR
Time
Type
Pitch
If chronic or severe what s additionally seen
Causes 4
Predispose to
A

Early diastolic
Decresendo
High pitched

Aortic root dilatation
RF
IE
BIcuspid av

LVF

55
Q 
MS
Time
Type
Additional feature,due to
If severe change
Commonest  cause
Predispose to
A 
Mid diastole 
Rumbling
Opening snap-sudden stoping of the valves
RHD
LA dilation
56
Q 
PDA
Type
Loudest when
Site
Causes 2
A

Continous machinary
At the s2
Infra clavi

Congenital rubella
Prematurity

57
Q

Myocardial action potential

  1. occurs in which structures
  2. draw
  3. phases
  4. ion channels involved
A

1.Ventricles /his bundle/perkingie fibers
2.refer book
3.0-voltage gated Na ch open-Na influx-rapid depolarization
1-Na ch close and K ch open-K flux-initial reporlaization
2-Ca ch open-ca influx-plateau
3-Ca ch close,K ch remain open -K efflux-rapid reporlaization
4- resting membrane potential -Na K Atpase and Na Ca exchanger

58
Q

In contrast to skeletal muscles

  1. presence of which phase
  2. contraction induced how
  3. cells are electrically coupled via
A
  1. plateau
  2. spontaneous depolarization
  3. gap junctions
59
Q

Pace maker action potential

  1. occurs where
  2. phases 3
  3. absent which phases 2
  4. Reason for absence
  5. phases and ion channels involved
  6. deporlarization slope indicates what
  7. factors affecting that?
A

1.SA /AV node
2.0- Ca ch opening-Ca influx
3-Ca ch close and K ch open-K eflux
4-deporlarization -If channels open-funny current-Na K influx

  1. no phase 1,2
  2. less negative resting mem potential deactivates the fast Na ch-conduction velocity is low so allows AV nodal delay

6.HR
7.increase -caticholamins/SNS
Decrease -Ach/Adenosine

60
Q

ECG
Components and durations
U waves seen when

A

P wave-atrial deporlarization-1,2

QRS-vent depolarization-

61
Q

Parts of the conduction system
Conduction velocity
Pace maker action

A 
SA 
AV
Bundle of His
R bundle-perkingie fibers
L bundle-left ant /left post-perkingie

Perkingie>atria >ventricles >AV

SA>AV>ventricles/his/perk

62
Q

Torsade Points

  1. what type of Arrythmia
  2. ECG pattern
  3. predisposes to
  4. caused by
  5. causes for prolong QT
  6. Drugs causing prolong QT
A

1.polymorphic VT
2.Sinosoidal pattern
3.VF and sudden death
4.low K
Low Mg
Drugs

5.ABCDE-
Antiarrythmic (1a,3)
Antibiotics (macroloides)
Antipsychotic (Halo)
Anti depressants(TCA)
Anti emetic (ondansetrone)

6.

63
Q

Congenital long QT syndromes 2

  1. Due to what
  2. Causes what
  3. Inheritance
  4. Phenotypes
  5. risk of
A

Romano-Ward syndrome-
AD
Cardiac only

ƒ Jervell and Lange-Nielsen syndrome-
AR
Also SND

Ion channel defect causing defective reporlarization

Risk of SCD

64
Q

Brugada syndrome

  1. Inheritance
  2. Commonly seen in
  3. ECG pattern 2
  4. Risk of
  5. Prevented by
A
  1. Autosomal dominant disorder
  2. most common in Asian males
  3. ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3
  4. risk of ventricular tachyarrhythmias and SCD. 5.Prevent SCD with implantable cardioverter-defibrillator (ICD).
65
Q 
WPW syndrome
1.What
2.Pathophysio 
3 ECG 3
4.Risk of
A

Most common type of ventricular pre- excitation syndrome

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing-AV node Ž ventricles begin to partially depolarize earlier Ž

characteristic delta wave
widened QRS complex
shortened PR interval

May result in reentry circuit Ž SVT

66
Q 
Atrial fibrillation 
1.ECG-
p waves
base line
QRS -shape/regularity
2.Causes
3.Complicaiton
4.MX-3
A 
1.No p waves
Irregular base line
QRS shape normal but irregular 
2.HT
RF
CAD
HF
Valvular dis
Hyperthyroidism

3.Stasis and thromboembolism

4.Mx-
anticoagulant (warfarin)
Rate control (BB/CCB/digoxin)
Rythem control(1c,3anti arryhthmics /cardioversion)

67
Q 
Atrial flutter
Pathophysio 
ECG
P waves
QRS-shape/rhythm 
Special name

Mx-palliative
Definitive

A

Rapid back to back atrial deporlarization
P waves saw tooth-regular
QRS-regular/normal

Mx-same as AF
Definitive-ablation therapy

68
Q

Heart blocks types

A

1AV blocks

2Bundle branch blocks

69
Q

AV Blocks types 3

A 
First degree
Second degree-mobitz type 1/2
Third degree(complete HB)
70
Q

First degree HB
ECG change
Symtopms
RX

A

Prolonged PR
Asymptomatic
No RX

71
Q 
Second degree -mobitz 1
Other name
ECG change 
RR interval
Symptoms
A

Wenckebach

Progressive increase in PR interval and sudden drop of QRS(p not followed by QRS)

RR interval different

Asymptomatic

72
Q

Mobitz 2
ECG changes/RR interval
Ca progress into
RX

A

Prolonged PR ,sudden drop of QRS
Same RR

Third degree HB
Pacemaker

73
Q 
Third degree HB
ECG-pp and RR 
Atrial rate and ventricular rate
RX
Infection causing this
A

No relationship bw p and QRS
PP same/RR same

Atrial rate faster

Pace maker

Lyme dis

74
Q 
ANP
Produce where
Due to what
Action where 
results in what
Acts via
A

Released from atrial myocytes

Increase blood volume and atrial pressure.

Acts via cGMP.

Causes vasodilation and  Na+ reabsorption at the renal collecting tubule.
Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism.

75
Q 
BNP
Produce where
Due to what
Action
Half life
Used clinically for 2
diagnostic value
A

Ventricular myocytes in response to  tension.

Similar physiologic action to ANP

longer half-life

BNP blood test used for diagnosing HF (very good negative predictive value)

Available in recombinant form (nesiritide) for treatment of HF.

76
Q 
Baroreceptors 
Site 2
Nerve conduction via
Impulse transmission to 
Stimulated by what
How
What's Cushins reaction
How does baro R contribute for it
A

Arch of aorta-vagus-solitary nucleus of medulla
Carotid sinus-glossy pharyngeal -solitary nucleus of medulla

Stimulated by BP changes

Low BP-less stretch of R-stimulate medulla-SNS activate/PSNS deactivates-vasoconstriction/contractility/high HR-high BP

Cushings-hypertension/bradycardia/resp depress

High ICP-cerebral arteriolar compression-hypoxia-chemo R activation-SNS activation-high BP-baro R activation -reflex bradycardia

77
Q

Chemo R types
Situated where
Response to what

A

ƒ Peripheral—
carotid and aortic bodies
stimulated by  Po2 (

78
Q

What’s pulmonary capillary wedge pressure
Approximation of
Eg for high PCWP
Monitored with what
Pressure values in RA/RV/LA/LV/aorta/pulm trunk

A

PCWP—pulmonary capillary wedge pressure (in mmHg) is a good approximation of left atrial pressure.

In mitral stenosis, PCWP > LV diastolic pressure.

Measured with pulmonary artery catheter (Swan-Ganz catheter).

RA-

79
Q 
What's auto regulation in organs
Auto regulation is done how in these organs
Heart
Brain
Kidney
Lungs
Skeletal muscles-during exercise /at rest
Skin for thermoregulation

Speciality of the lung

A

Mantaning a constant blood flow to the organs in wide range of perfusion pressures

Heart-
Local metabolites (vasodilatory): adenosine, NO, CO2,  O2

Brain-
Local metabolites (vasodilatory): CO2 (pH)

Kidney-
Myogenic and tubuloglomerular feedback

Lungs-
Hypoxia causes vasoconstriction

Skeletal muscle -
Local metabolites during exercise: lactate, adenosine, K+, H+, CO2

At rest: sympathetic tone

Skin-
Sympathetic stimulation most important mechanism: temperature control

Lung cause vaso constriction in hypoxia,all other organs Vasodilators in hypoxia

80
Q

Capillary fluid exchange
Which forces involved
Formula for net fluid flow
Causes for extra interstial fluid 4(edema)

A

Starling forces

Capillary hydrostatic pressure
Capillary oncotic pressure
Interstial hydro pressure 
Interstitial oncotic pressure
Permeability of the membrane

Jv =netfluidflow=Kf [(Pc −Pi)−ς(πc −πi)]
Kf = permeability of capillary to fluid
ς = permeability of capillary to protein

Edema—excess fluid outflow into interstitium commonly caused by: ƒ 

1.capillary pressure ( Pc; e.g., HF)
ƒ2.lowplasma proteins ( πc; e.g., nephrotic syndrome, liver failure)
ƒ3.highcapillary permeability ( Kf ; e.g., toxins, infections, burns)
ƒ4.high interstitial fluid colloid osmotic pressure ( πi; e.g., lymphatic blockage)

Cardiology (4 decks)

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