CARDIOVASCULAR - PHYSIOLOGY (First AID 2020)

CARDIAC OUTPUT VARIABLES

STROKE VOLUME

Stroke Volume affected by

Contractility
Afterload
Preload
(SV CAP)

SV with:
Contractility (eg, anxiety, exercise)
Preload (eg, early pregnancy)
Afterload

A failing heart has SV (systolic and/or diastolic dysfunction)

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CONTRACTILITY

Contractility (and SV) with:

Catecholamine stimulation via β receptor:

Activated Protein Kinase A

Phospho Lamban phosphorylation

Active Ca2+ ATPase

Ca2+ storage in sarcoplasmic reticulum

Ca2+ channels phosphorylated

Ca2+ entry

Ca2+-induced Ca2+ release &

Intracellular Ca2+
Extracellular Na+ ( activity of Na+/Ca2+ exchanger)

Digitalis
Blocks Na+/K+ pump

Intracellular Na+

Na+/Ca2+ Exchanger activity

Intracellular Ca2+

Contractility (and SV) with:

β -blockade ( cAMP)
HF with systolic dysfunction
Acidosis
Hypoxia/hypercapnia ( PO2/ PCo2)
Non-dihydropyridine Ca2+ channel blockers

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PRE LOAD (PL)
Preload approximated by ventricular EDV;
Depends on venous tone and circulating blood volume.
Venous vasodilators (eg, Nitroglycerin) preload.

AFTER LOAD (AL)

Afterload approximated by MAP.
Wall tension (Laplace’s law) Pressure AL
LV compensates for AL by thickening (hypertrophy) in order to wall stress.

Arterial vasodilators (eg, hydralazine) Afterload.

ACE inhibitors and ARBs

Preload
Afterload

Chronic HTN ( MAP) LV hypertrophy.

MYOCARDIAL OXYGEN DEMAND

Myocardial O2 demand is by:

Contractility
AL (proportional to arterial pressure)
Heart Rate
Diameter of ventricle ( wall tension)

Wall tension follows Laplace’s law:

Wall tension = Pressure × Radius

Pressure × Radius
Wall stress = ---------------------------
2 × wall thickness

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CARDIAC OUTPUT EQUATIONS

STROKE VOLUME

SV EDV ESV

EJECTION FRACTION

SV EDV ESV
EF = ------- = --------------
EDV EDV

EF is an index of ventricular contractility

in systolic HF;
Usually normal in diastolic HF

CARDIAC OUTPUT

CO = SV × HR

Fick principle:
Rate of O2 consumption
CO = -------------------------------------
(arterial O2 content – venous O2 content)

EXERCISE
Early Stages: CO maintained by HR, SV
Later stages: CO maintained by HR only (SV plateaus)

Diastole is shortened with HR (eg, ventricular tachycardia)

Diastolic filling time SV CO

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PULSE PRESSURE

PP = SBP – DBP

PP
Directly proportional to SV
Inversely proportional to arterial compliance.

PP
Hyper thyroidism
AR
Aortic stiffening (isolated systolic HTN in elderly)
Obstructive sleep apnea ( sympathetic tone)
Anemia
Exercise (transient)

PP
AS
Cardiogenic shock
Cardiac tamponade
Advanced HF

MEAN ARTERIAL PRESSURE

MAP = CO × TPR

MAP (at resting HR)

DBP SBP
DBP PP

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STARLING CURVE

Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)

Contractility with
Catecholamines
Positive inotropes (eg, digoxin)

Contractility with
Loss of myocardium (eg, MI)
β-blockers (acutely)
Non-dihydropyridine Ca2+ channel blockers (NDHP CCB)
Dilated cardiomyopathy

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RESISTANCE PRESSURE FLOW

ΔP Q R

Similar to Ohm’s law: ΔV IR

Volumetric flow rate (Q) = flow velocity (v) × cross-sectional area (A)

Driving pressure (ΔP) η (viscosity) length

Resistance = ................................. = .........................................
Q πr

Total resistance of vessels in series:

RT = R1 + R2 + R3 . . .

Total resistance of vessels in parallel:

1 1 1 1
....... = ...... + ...... + .....
RT R1 R2 R3 ....

Capillaries have highest total cross-sectional area and lowest flow velocity.
Pressure gradient drives flow from high pressure to low pressure.

Arterioles account for most of TPR

Veins provide most of blood storage capacity.

Viscosity depends mostly on hematocrit.

Viscosity in
Hyper proteinemic states (eg, multiple myeloma)
Polycythemia

Viscosity in
Anemia

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CARDIAC & VASCULAR FUNCTION CURVES

Intersection of curves = operating point of heart

(ie, venous return and CO are equal, as circulatory system is a closed system).

INOTROPY
EFFECT:
Changes in contractility Altered SV Altered CO/VR and RA pressure (RAP).

EXAMPLES:
(1) Catecholamines, digoxin, exercise ⊕
(2) HF with reduced EF, narcotic overdose, sympathetic inhibition ⊝

VENOUS RETURN
EFFECT:
Changes in circulating volume Altered RAP Altered SV Change in CO.

EXAMPLES:
(3) Fluid infusion, sympathetic activity ⊕
(4) Acute hemorrhage, spinal anesthesia ⊝

TOTAL PERIPHERAL RESISTANCE

EFFECT:
Changes in TPR Altered CO.
Change in RAP unpredictable.

EXAMPLES:
(5) Vasopressors ⊕
(6) Exercise, AV shunt ⊝

NOTE: Changes often occur in tandem, and may be

Reinforcing (eg, exercise inotropy, TPR to maximize CO) or
Compensatory (eg, HF inotropy fluid retention to preload to maintain CO)

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PRESSURE VOLUME LOOPS & CARDIAC CYCLE

The black loop represents normal cardiac physiology.

PHASES - LEFT VENTRICLE:

(1) Isovolumetric contraction

- Period between MV closing and AV opening; period of highest O2 consumption
(2) Systolic ejection
- Period between AV opening and closing
(3) Isovolumetric relaxation
- Period between AV closing and mitral valve opening
(4) Rapid filling
- Period just after MV opening
(5) Reduced filling
- Period just before MV closing

HEART SOUNDS:

S1
MV and TV closure
Loudest at mitral area

S2
AV and PV closure
Loudest at left upper sternal border

S3
In early diastole during rapid ventricular filling phase.
A/w filling pressures (MR, AR, HF, Thyrotoxicosis)
MC in dilated ventricles
Can be normal in
Children
Young adults
Atheletes
Pregnant women

S4
In late diastole (“atrial kick”).
High atrial pressure.
Best heard at apex with patient in left lateral decubitus position
A/w - Ventricular noncompliance (eg, hypertrophy)
Left atrium must push against stiff LV wall
Consider abnormal if palpable.

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JUGULAR VENOUS PULSE:

a wave
atrial contraction
Absent in atrial fibrillation (AF)

c wave
RV contraction (closed tricuspid valve bulging into atrium)

x descent
Downward displacement of closed tricuspid valve during rapid ventricular ejection phase
Reduced or absent in TR and right HF because pressure gradients are reduced

v wave
Right atrial pressure due to filling (“villing”) against closed tricuspid valve

y descent
RA emptying into RV
Prominent in constrictive pericarditis, absent in cardiac tamponade

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PRESSURE VOLUME LOOPS & VALVULAR DISEASE

AS
LV pressure
ESV
No change in EDV
SV

Ventricular hypertrophy Ventricular compliance EDP for given EDV

MR
No true Isovolumetric phase
ESV due to resistance and regurgitation into LA during systole
EDV due to LA volume/pressure from regurgitation Ventricular filling
SV

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AR
No true isovolumetric phase
EDV
SV

MS
LA pressure
EDV because of impaired ventricular filling
ESV
SV

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 SPLITTING (S2)

NORMAL SPLITTING

Inspiration
Drop in intrathoracic pressure
Venous return
RV filling
RV stroke volume
RV ejection time
Delayed closure of pulmonic valve.

Pulmonary impedance ( capacity of the pulmonary circulation) also occurs during inspiration,
which contributes to delayed closure of pulmonic valve.

WIDE SPLITTING

Seen in conditions that delay RV emptying

Pulmonic stenosis
Right bundle branch block
Causes delayed pulmonic sound (especially on inspiration).
An exaggeration of normal splitting.

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FIXED SPLITTING

Heard in ASD
ASD
Left-to-right shunt
RA, RV volumes
flow through pulmonic valve
Delayed pulmonic closure (independent of respiration)

PARADOXICAL SPLITTING

Heard in conditions that delay aortic valve closure

AS
Left bundle branch block

Normal order of semilunar valve closure is reversed so that P2 sound occurs before delayed A2
sound.
On inspiration, P2 closes later and moves closer to A2, “paradoxically” eliminating the split.
On expiration, split can be heard (opposite to physiologic splitting).

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