• Examine Pulse th

• Apical (5 IC space, mid clavicular)

DEFINATION-
PERICARDIUM- Double walled sac fibrous outer layer Function- protects against infection and trauma.
EPICARDIUM-outermost layer of cardiac wall, cover surface of heart and great vessels. Function- protects against infection and trauma.
MYOCARDIUM- Central layer of thick muscular tissue. Provides major pumping force of the ventricles.
ENDOCARDIUM- thin layer of endothelium and connective tissue. Lines the inner surface of the heart, valves, chondrae tendiness and
papillary muscle.
RIGHT ATRIUM- heart chamber. Receive blood from venous system.
TRICUSPID VALVE- atrioventricular valve between right atrium and ventricle.Prevent back flow of blood from the left ventricle to the atrium
during ventricular systole.
RIGHT VENTRICLE- heart chamber pump bloods to the pulmonary circulation.
Pulmonary valve- semilunar valve
bw rt ventricle and pulmonary artery. Prevent back flow of blood from the pulmonary artery to the right ventricle during distance
Understand Changes in Vitals in all
conditions.
1. HR – 60 to 100 beats per minute
2. BP
3. SV- stroke volume- amount of
4. blood coming out in every beat
from left ventricle.
Factors that increase or decrease sv- heart rate, viscosity, strength of contraction, blood pressure. Medicine- digitials can increase
stroke volume, by changing conduction speed from atria to ventricles, short qt – cause by digitialis.
5.

CO- HEART
EG HR=120 BPM, total amount of blood
IS BEATING twicecoming out inFAST,
per second a minute. CO- HR
VENTRICLE NOTX SV HR= CO/SV,
EXPANDING HRinUP,
less blood SV DOWM.
ventricles, LVEDV-preload decrease.
HR- 60 bpm- higher lvedv it has one second to contract relax, ventricle dilating more, LVEDV more. SV more. Lvedv directly proportional to
stroke volume.
Overall stroke volume decrease, if heart rate goes up.

6. RR- 12 to 20 breaths per minute

7. LVEDV/preload/ left ventricle diasystolic volume-
amount of blood in ventricle just before it contracts. Lvedv decides stroke volume. Eg-marathon training u can increase the blood
volume or increase lvedv. Some people don’t do exercise less blood volume entering and then moving out.
 8. EF- ejection fraction, IMP use for heart failure, percentage of blood coming out from ventricle in every beat from total volume of
blood in ventricle. Like 55percent out of 100 FORMULA - to see SV good or bad. Factors that control EF are- if ventricle muscle are
strong eject normal ef but weak will not eject normal ef. Normal- 70 percent
Sa nodes- natural pacemaker. We have to install pacemaker because with age cardiac muscle get weak. Pacemaker generates impulses
Weaken cardiac muscle weak because of cardiac injury For example, myocardial infarction- means myocardium dead, weaker than counterpart,
after load can contribute to weaking of muscle, for eg aortic stenosis or high bp for whole life, muscle go weak, they may lose strength. Muscle
weak ef will go down.
Cardiac muscle strong with aerobic exercises or activity, marathon runner have good cardiac muscle, high stroke volume.
Who will have higher ef- a. HR= NORMAL- 60-100, BELOW 60, BRADYCARDIA, ABOVE 100- TRADYCARDIA,
ATHLETES will lower heart rate, if ur heart beating at 82 bpm that means ur heart is beating 82 times, to meet the need of body. If somebody
heart beating at 46 beats per minute times then heart is beating 46 times able to produce enough blood cardiac output to meet the need of
athletes. That means SV, CO everything is very high, but in 70 yrs old man , heart beating at 46, is not normal he need pacemaker.

If u check ur heart rate- lower heart rate is better. If u exercise for one month and ur heart rate goes down, that’s good sign, ur muscle
strengthen.- aerobic training.

9. CI- CARDIAC INDEX-

10. Heart sound
11. RPP
12. MAP
13. ECG
14. Auscultation of valves
 15. Scales
16. X ray
17. Labs

Sympathetic system means part of nervous system that increase heart rate, bp, breathing pattern, pupil size control krda - can increase
contractility of ventricles.
Beta blockers block or decrease contractility of sympathetic system, slow down heart or decrease stroke volume, pulmonary drugs, sympathetic
momatic stimulate sympathetic system.
AFTER LOAD- force against which left ventricle has to contract . Aortic valve there, strength of contraction should be good enough to open the
valve and blood can move forward.

FACTOR THAT INCREASE STRESS ON LEFT VENTRICLE

decrease cardiac output or stroke volume -

1. Imagine aortic stenosis - calcium build up at valve, decrease flexibility of tissue, condition called rheumatic fever in which calcium build up
at valves but has problem in 50 yrs. If u have extra fat, it can deposit on valve. Common in children

2. DIABETIC MILETUS- High blood viscosity/ thick blood( diabetic people, bcz of high blood sugar blood stay more viscous)
Imagine ventricle has to open the gate of aorta and push all blood forward, if left ventricle not strong enough a soon as blood can come back
from aortic valve to left ventricle, resulting in heart failure or aortic regurgitation.

Shortness of breath connect with high blood viscosity. Eg if u have viscous blood in the aortic valve, less blood is going to muscles, resulting in
more tiredness while running bcz less blood is going to muscles bcz of viscosity.
 Haemodynamics

A) Heart rate
B) Stroke Volume
a) Preload:- Amt of blood in Ventricle at the end of Diastole (LVEDV). Diastole means phase of heart beat when the heart
muscles relax and allow the chambers to fill the blood.
b) Afterload:- It is the pressure against which the ventricles must work to eject blood during
systole
• How does high Afterload alters cardiovascular mech.
• (Impact on SV –Dec, CO -Dec, BP-- INC, eventually on parasympathetic nervous system--activates)
• What happens to afterload in CHF, MI, CAD >>>
• How to Decrease afterload ?
• Example _ athletes:- expands more – Preload more >>> SV is more
• Which Drug can increase afterload ?

B) Cardiac Output :- HR x SV
• CO relation with HR – Directly proportional
• CO relation with SV - Directly proportional
• SV relation with HR – IN Directly proportional
 C) Cardiac Index :- CO/Body surface area
Think of all factors (afterload, drugs) , conditions (CHF, MI) that can dec CO >>> will
eventually decrease Cardiac index
• To check whether the Cardiac output is enough or notWhat does it mean ?
• Fatigue, SOB, Poor activity tolerance
D) Ejection fraction :- SV/ LVEDV Normal EF – 60-70
% of LVEDVLower EF = ?
DeC EF:- caused by >>> High Periph resistance, Cardio myopathy,
Conditions when EF is altered :- Systolic CHF, Cardiomyopathy, MI, (When cardiac
muscles are bad)
DD Cardiac Index vs Ejection fraction
E) MVO2

Reserve end volume – at systole and diasystole

Stroke Volume

SV depends on 2 things :-

1. How much blood left ventricle receives

2. How much blood left ventricle pumps out
a) Strength of ventricle contraction
b) Peripheral resistance from blood in aorta ---
i. Increases with vasoconstriction
ii. Dec with vasodilation

• Causes :-
For low SV
• Mitral stenosis
• Aortic stenosis
• Poor venous return(Low LVEDV)
• High Afterload(Low Ef)
• Cardiac Output :_ All the cause of low SV will lead to low CO
• Then EF :- cause of EF, low or high
• Will the factors leading to low SV like – low return, will cause low EF.
• Give example - - LVED = 60 ml and SV is 36 ml, though SV is low but EF is normal as it is still 60%.

Frank sterling law

• Frank-Starling’s law of the heart describes this phenomenon appliedto the myocardium.
• More preload :- More Output
Effect of
Position-
Standing, u fall due to hypotension- go supine because of higher venous return, in standing valves has to pump strongly to contract
in
• Body position affects circulatory dynamics. Cardiac output and strokevolume reach the highest and most stable levels in a
horizontal position.
• Near maximal stroke volume occurs at rest in a horizontal positionand increases only slightly during exercise.
• In contrast, gravity’s effect in the upright position counters venousreturn and lowers stroke volume
• Swimmer has higher SV than Running on treadmill at same intensity.

• Which position to prefer during episode of Hypotension

• Horizontal (Supine)
Heart valves

Beta blocker decrease contractility

Ef=15% heart
failure.

Where to palpate these valves?1

Questions.
 Valves auscultation-
IMP

• Aortic – Rt 2nd Intercostal space, from aortic, aorta is coming out

• Pulmonic – Lt 2nd Intercostal space, vessels to the lungs

• Tricuspid – Lt 4th Intercostal space,

sternal border
• Mitral – Lt 5th Intercostal space , Midclavicular line
(Apex beat)
- Regurgitation, heart sound change
With location of mitral vale- ausculate heart sound
Hypotensive response

• Hypotensive response during exercise : A decrease of SBP below thepretest resting value or by >10 mm Hg after a
preliminary increase, particularly in the presence of other indices of ischemia, is abnormaland often associated with
• myocardial ischemia,
• left ventricular dysfunction
• increased risk of subsequent cardiac events
Lmp- blood pressure number
• RPP = MVO2
• Energy cost to the myocardium/Myocardial O2 demand
• Directly proportional to HR and SBP
• RPP = HR x SBP
• Typical values for RPP range from 6000 at rest (HR, 50 bmin1; SBP, 120 mm Hg) to 25K
– 40k during intense exercise (HR, 200 bmin1; SBP, 200 mm Hg
• High and Low RPP means what :-

• MAP = Mean arterial pressure

• Arterial pressure within the large arteries.
• MAP = 1/3 (SBP – DBP) + DBP
• High and Low MAP means what :-
Brainstorming

• High and Low RPP means what :-

• HR
• BP
• Stress on heart :- Inc or dec

• High and Low MAP means

what :-
• High RPP is an indicator of CAD –
Angina.
Identify the arteries- TO CHECK ABI
Radial- palpating purpoe- to check peripheral, brachial- medial side, blood pressure
At legs pulses, groin area- femoral, next popliteal at knee, dorsl pedius and post tibial artery.
Ankle brachial index- check blood circulation, proximal and distal.
ABI superficial = systolic bllod pressure in lower extremity/systolic bp in upper extremity ,
idea is blood pressure should be same in upper and
lower both , if answer 1 – consider normal, pressure in arm and lower extremity normal, ankle blood pressure we check, post tibial we check
bp, ankle brachialis index,

• A)
Temporal-
• B) Carotid
• C) Radial
AT ELBOW – BRACHIAL
 Heart Sounds
• A) S1 (Lub) :- Beginning of Ventricular systole
• AV valve closure, (Mitral and tricuspid)
• To prevent backflow of blood into
atrium
• B) S2 (Dub) :- End of ventricular systole
• Semilunar valves close (Aortic and
pulmonic )
• To prevent backflow of blood into
ventricles
• C) S3 :- Occurs soon after S2, Assoc with
Ventricular filling
• Due to rapid ventricular filling, also causing vibrations in theventricles, producing ,
(Vibration by mov of blood between ventricular walls in a distended ventricles)
• At the end of S2, when semilunar valves close, AV valves openand allows a strong gush
of blood to ventricles , producing S3
• Also called – S3 gallop or Ventricular gallop
S3- SYSTOLIC HEART FAILURE
S4- DIASTOLIC HEART FAILURE

• D) S4 :- Assoc with ventricular filling and Atrial contraction, Justbefore S1. Indicates :- MI, Aortic stenosis,
Hypertension.
• Bruit :- A blowing sound of arterial or venous origin due to narrowingof vessels (Atherosclerosis)
S1-----------------S2 S3 --------------------S4 S1 S2 S3 ---- S4
Start –Vent Systo End Start Vent diast End Ventricular sytole Ventricular diastole
Ventricular diastole

• Ventricular Diastole has 3 stage

• Early ventricular diastole
• Initial part – At the beginning of ventricular diastole, blood stored in Atria after opening of AVvalves, rush to the
ventricles as soon as it opens. That initial rush of blood causes S3 gallop Sound.
• Middle ventricular diastole
• Middle part of ventricular diastole, some blood enter from systole to diastole,
• Late ventricular diastole
• In the last part, atria has to contract more strongly to push the remaining blood from atria toventricles, in order to
fully fill the ventricles- This produces S4 (ventricular stiffened,MI)
• Reason atria has to contract more strongly in the last part of ventricular filling is – either ventricular
tissues are stiffened, not relaxing, expanding, dilating easily :-
• seen in Myocardial infarction, when due to dead cells they don’t stretch completely leading to stiffened
Ventricles
• Aortic stenosis--- since there is already some blood in ventricles as it is not going out, making it hard foratria
to completely drain its fluid,so atria has to contract strongly to push the remaining blood to ventricles
 • D
S3 vs
S4 i
• S3 • S4 l
• 2 things needed to produce a
S3 t
• Ventricles should
be e
pliable/distension c
capability d
• Rapid blood flow a
• Early phase of ventricular
filling in distended r
ventriclesproducing o
ventricular vibrations d
m
• Also called Ventricular y
gallop i
o
• Seen in p
• Pregnancy
• CHF a
• Mitral valve regurgitation
(backflow from ventricles, t
causes excessive blood in
atria h
, which is then rapidly
pushed y
to ventricless)
 v Angine/(CAD), MI >>> cardiac fibres
does not relax/stretch welldue to poor
e bld supply >>> producing S4
• n • Restricted cardiomyopathy
• Later phase of ventricular filling, t IN S4
by atrial strong
contractions, leading to r
ventricular vibrations i
• Atrial gallop due to strong
atrial contractions c
l
• Stiffened ventricles are vibrating due to atrial
contractions e
• Eg • Hypertrophied/ Stiffened ventricles
• Aortic stenosis _ ventricle s
partially filled , making it
hard for atria to drain s
completely, atria contracts • S
strongly in lastphase of vent i
diastole se
• Chronic hypertension :- c
Inc peripheral resistance v
h
forces the ventricles to e
workstrongly, leading to a e
m
development of i
ventricular hypertrophy ra
>>> increasing stiffness of /
e
• For sounds (S3-S4) created by left ventricles
• We hear them at the
• apex beat with bell lightly applied
• During expiration,
• lungs go on the side, and apex beat comes more close to the chest
• Also during expiration , lungs recoil,which compress the pul vessels, forcing more blood to be
pushed to the left heart,

• For sounds (S3-S4) created by Rt ventrciles

• We hear them at the –
• Left lower para sternal border at 4th intercostal space
• During inspiration becoz inc venous return on the right , so more chances to hear.
• During inspiration, abdo veins r compressed (vena cava) due to diaphragm contraction and
more intake of air, focing them to push blood to Rt atrium
Blood pressure during Aerobic and
AnaerobicExc.
B
P
Exercise tolerance test

• Purpose :-
• To determine stress on heart during exercise
• as an outcome measure post cardiac Rehab

• Importance ?
• Test mode :- ?
• Types :-
• a) Max ETT – To the Point of HRmax , HRR
• b) Submax ETT _ Symptom limited, Used to test recovery post cardiac problems – MI,
CAD,CABG
• a) Continous - Proper stress test protocol
• b) Discontinous – For more pronounced CAD
• Positive vs negative ETT
Examination during Exercise

• A) HR
• C) RPP – Myocardial oxygen consumption
• D) RPE
• E) Pulse oxymetry
• F) ECG
• G) Signs of exertional intolerance
• Persistent dyspnea, Excessive fatigue
• Dizziness, Confusion, Angina, Claudication
 Heartfailure
Types
• Diastolic heart
failure
• Systolic heart failure • Poor ventricular filling due
toreduced ventricular diastole
• Poor ejection fraction
• Heart unable to
• Weak Cardiac contractility relax/distendcompletely
• Ventricular walls
• High Peripheral resistance hypertrophy
• Chronic hypertension
• High afterload • Myocardial infarction history
• High BP • Chronic aortic stenosis
 Frequency Intensity Time Type
Aerobic 3-5 times/wk • Vo2max 40-80% 30-60 min
• HRR – 40-80%
If no HR values
available -
• RPE – 12-
16
Or
• HR 20-30 mins
above resting
HR(standing)

Flexibility 2-3 times/wk • TO the point of • Static

slight and
discomfort dynamic
• Atleast 15
secs hold
Resistance 2-3 • 40-70% of 1 RM • 10-15 reps
times/wk After • RPE 11-13 of each
4 weeksof Exercises
aerobic • Less for UE &
• 2-4 sets
more for LE

How to progress during aerobic & resistive exercises