CVS Physio Flashcards
1
Q
CO =?
A
SV*HR
2
Q
Ficks principle
A
CO=rate of O2 consumption/
arterial O2content-venous O2content
3
Q
MAP=3
A
MAP=CO* TPR
MAP=PP+1/3 diastolic pr
MAP=1/3 sys p+2/3 Dias pr
4
Q
Pulse pressure=
Proportionate to?
Inversely proportionate to?
A
SBP- DBP
SV
Compliance
5
Q
SV=
A
SV=EDV-ESV
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
7
Q
What happens when HR increase
Eg
A
Time of diastole reduce
Cardiac filling is compromised
Reduce CO
Eg-VT
8
Q
Causes of increase pulse pressure 4
A
Hyperthyroid
Aortic regurgitation
Aortic stiffing -reduce compliance
OSA-increase sympathetic tone
9
Q
Decrease PP Causes 4
A
AS
CHF
Cardiac tamponade
Carcinogenic shock
10
Q
SV depends on 3
How
A
SV increase
High preload
high contractility
Low after load
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
12
Q
Factors decreasing contractility 4
A
Bblockers -reduce cAMP Non dihydropiridine CCB ischemia -MI Hypoxia Hypercapnia
13
Q
Myocardial O2 demand increase by which factors 4?
A
🍄myoCARDium
C-contractility
A-after load
R-rate
D-diameter(increase wall tension)
14
Q
La Plases Law for wall tension
A
Tension=pressure *diameter/thickness of wall
15
Q
Preload approximated by?
Depends on 2
Action of venodilators
A
EDV
venous return-venous tone
Blood vol
Reduce preload-nitrates
16
Q
Afterload approx by
Vasodilators causes what
Drugs causing reduction of both pre and after load
A
MAP
Reduce afterload
ACEI ACRB
17
Q
What happens to MAP in chronic HT
A
Increase MAP-increase afterload -increase wall tension-thickening to reduce tension
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
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
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..
21
Q
Viscosity depends on?
Increase viscosity and decrease Vic’s eg
A
Hematocrite
Increase-high protein (MM),polycythemia
Decrease-anaemia
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
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
24
Q
Changes to each curve with
- ionotopes
- venuos tone and blood vol
- 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
25
When does these changes occure to vascular and cardiac curves
How
To reinforce-exercise increase CO by reducing TPR
| To compensate-in CHF (-ve ionotropic)to increase SV the is fluid retention
26
Pressure vol curves of LV
Draw with stages
Mark heart sounds
SV
Changes with
Increase preload
Increase afterload
Increase contractility
Refer book
27
```
Cardiac cycle draw
Stages-7
LV pressure
aortic pressure
Heart sounds
Opening and closing of mitral and aortic valves
```
Refer book
28
Heart sounds
S1-heard when,best heard
S2-when ,where
S1-M/T valve closure
At apex
S2- A/P valve closure
At upper left sternal edge
29
S3
Heard when
Normal in who
Pathology with what
Rapid ventricular filling
Early diastole
Common in pregnancy and children
Dilated heart
30
S4
Heard when
Where
Pathology
Slow ventricular filling
Atrial systole
At apex on LLDP
Ventricular hypertrophy
31
Draw JVP waves
| Occures when
```
a-atrial contraction
c-isovol ventri contraction
X-ventricular ejection
v-atrial filling with closed mitral valve
Y-opening of MV and atrial emptying
```
32
Types of splitting of second heart sound
Normal
Wide
Fixed wide
Paradoxical
33
Normal splitting explain
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
Wide spitting explain
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
Wide fixed spitting
In ASD
Increase pulmonary blood flow
Wider spilt irrespective of breathing
So same widening in expiration and inspiration both
36
Paradoxical spilt
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
What re the 6 auscultations sites
```
Aortic
Pulmonary
Mitral
Tricuspid
Left sternal edge
Left infracalivicular
```
38
Murmurs heard in the aortic area
Systolic
AS
Aortic sclerosis
Flow murmurs
39
Murmurs heard in the pulm area?
Systolic
PS
Flow murmurs
40
Tricuspid area murmurs
Systolic
TR
VSD
Diastolic
TS
ASD
41
Mitral area murmurs
Systolic
MR
Diastolic
MS
42
Left sternal border murmurs
Diastolic
AR
PR
Sys
Hypertrophic cardiomyopathy
43
I
| Left infra clavicular
PDA
44
ASD murmur types 3
| Murmur from the defect
Pulm flow mumur
Tricuspid rumble
Later on with pul artery dialtaion-PR
No murmur from the defect
45
Bed side maneuvers to change murmurs 4
| Effect
Inspiration-increase preload
Hand grip-increase afterload
Vulvalva/standing - decrease preload
Rapid squatting-increase preload
46
Inspiration change which mumurs
Increase all R heart murmurs
47
Hand grip change which murmurs
Increase AR/MR/VSD
Decrease-HCM murmur
MVP-delayed click or murmur
48
Vulsalva/standing change which murmurs
All murmurs reduce including AS
Increase HCM
MVP-late murmur
49
Rapid squatting change which murmurs
Increase AS
Reduce HCM
MVP-delayed
50
```
AS
Time
Type
Best heard
Radiates to
Pulse
Symptoms 3
Causes 2
```
```
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
MR/TR
Time
Type
Pitch
Site
Radiation
Causes
Both can occure in which diseases 2
Pansystiolic
Blowing
High pitched
MR-apex
Axilla
Post MI/MVP/LV dilation
TR-tricuspid area
R/sternal border
RV dilatatoin
RF
Infective endo
52
```
MVP
site
Time
Extra character,due to
Loudest before
Causes-common /eg
Other causes
Predispose to
RX
```
```
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
VSD
Time
Type
Site
Pan systolic
Sea gull
Tricuspid
54
```
AR
Time
Type
Pitch
If chronic or severe what s additionally seen
Causes 4
Predispose to
```
Early diastolic
Decresendo
High pitched
Aortic root dilatation
RF
IE
BIcuspid av
LVF
55
```
MS
Time
Type
Additional feature,due to
If severe change
Commonest cause
Predispose to
```
```
Mid diastole
Rumbling
Opening snap-sudden stoping of the valves
RHD
LA dilation
```
56
```
PDA
Type
Loudest when
Site
Causes 2
```
Continous machinary
At the s2
Infra clavi
Congenital rubella
Prematurity
57
Myocardial action potential
1. occurs in which structures
2. draw
3. phases
4. ion channels involved
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
In contrast to skeletal muscles
1. presence of which phase
2. contraction induced how
3. cells are electrically coupled via
1. plateau
2. spontaneous depolarization
3. gap junctions
59
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?
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
3. no phase 1,2
4. 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
ECG
Components and durations
U waves seen when
P wave-atrial deporlarization-1,2
| QRS-vent depolarization-
61
Parts of the conduction system
Conduction velocity
Pace maker action
```
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
Torsade Points
1. what type of Arrythmia
2. ECG pattern
3. predisposes to
4. caused by
5. causes for prolong QT
7. Drugs causing prolong QT
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
Congenital long QT syndromes 2
1. Due to what
2. Causes what
3. Inheritance
4. Phenotypes
5. risk of
Romano-Ward syndrome-
AD
Cardiac only
Jervell and Lange-Nielsen syndrome-
AR
Also SND
Ion channel defect causing defective reporlarization
Risk of SCD
64
Brugada syndrome
1. Inheritance
2. Commonly seen in
3. ECG pattern 2
4. Risk of
5. Prevented by
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
```
WPW syndrome
1.What
2.Pathophysio
3 ECG 3
4.Risk of
```
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 ventricles begin to partially depolarize earlier
characteristic delta wave
widened QRS complex
shortened PR interval
May result in reentry circuit SVT
66
```
Atrial fibrillation
1.ECG-
p waves
base line
QRS -shape/regularity
2.Causes
3.Complicaiton
4.MX-3
```
```
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
```
Atrial flutter
Pathophysio
ECG
P waves
QRS-shape/rhythm
Special name
```
Mx-palliative
Definitive
Rapid back to back atrial deporlarization
P waves saw tooth-regular
QRS-regular/normal
Mx-same as AF
Definitive-ablation therapy
68
Heart blocks types
1AV blocks
| 2Bundle branch blocks
69
AV Blocks types 3
```
First degree
Second degree-mobitz type 1/2
Third degree(complete HB)
```
70
First degree HB
ECG change
Symtopms
RX
Prolonged PR
Asymptomatic
No RX
71
```
Second degree -mobitz 1
Other name
ECG change
RR interval
Symptoms
```
Wenckebach
Progressive increase in PR interval and sudden drop of QRS(p not followed by QRS)
RR interval different
Asymptomatic
72
Mobitz 2
ECG changes/RR interval
Ca progress into
RX
Prolonged PR ,sudden drop of QRS
Same RR
Third degree HB
Pacemaker
73
```
Third degree HB
ECG-pp and RR
Atrial rate and ventricular rate
RX
Infection causing this
```
No relationship bw p and QRS
PP same/RR same
Atrial rate faster
Pace maker
Lyme dis
74
```
ANP
Produce where
Due to what
Action where
results in what
Acts via
```
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
```
BNP
Produce where
Due to what
Action
Half life
Used clinically for 2
diagnostic value
```
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
```
Baroreceptors
Site 2
Nerve conduction via
Impulse transmission to
Stimulated by what
How
What's Cushins reaction
How does baro R contribute for it
```
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
Chemo R types
Situated where
Response to what
Peripheral—
carotid and aortic bodies
stimulated by Po2 (
78
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
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
```
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
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
Capillary fluid exchange
Which forces involved
Formula for net fluid flow
Causes for extra interstial fluid 4(edema)
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:
1.capillary pressure ( Pc; e.g., HF)
2.lowplasma proteins ( πc; e.g., nephrotic syndrome, liver failure)
3.highcapillary permeability ( Kf ; e.g., toxins, infections, burns)
4.high interstitial fluid colloid osmotic pressure ( πi; e.g., lymphatic blockage)
