LESSON 3
CARDIODYNAMICS & HEMODYNAMICS
HEMODYNAMICS
• Is the study of the forces the heart
develops to circulate blood through the
cardiovascular system.
• These forces are demonstrated as blood
pressure and blood flow.
• The focus is on systemic hemodynamics
(the output of the left heart). HEMODYNAMIC CONCEPTS
HEART ANATOMY & CARDIAC CYCLE BLOOD PRESSURE:
• SYSTOLIC: peak pressure during
CHAMBERS & FLOW: ventricular contraction.
• RIGHT SIDE: deoxygenated blood • DIASTOLIC: lowest pressure during
enters the right atrium via the vena ventricular relaxation.
cavae → flows through the tricuspid • PULSE PRESSURE: difference between
valve into the right ventricle → is systolic and diastolic pressure
ejected through the pulmonary valve to • MEAN ARTERIAL PRESSURE (MAP):
the lungs for oxygenation. average pressure driving blood to
• LEFT SIDE: Oxygenated blood returns organs. MAP > 60mmHg indicates
to the left atrium via pulmonary veins → adequate perfusion.
flows through the mitral valve into the o Formula: S + D x
thick-walled left ventricle → is ejected CARDIAC OUTPUT (CO) & CARDIAC INDEX
through the aortic valve into the aorta (CI):
and systemic circulation. • CO: Volume of blood ejected by the left
ventricle per min (4-8 L/min).
• CI: CO adjusted for body surface area
(2.8 – 4.2 L/min/m2), making it a better
indicator for different body sizes.
• Formula: CO = Heart rate x Stroke
Volume
o Tachycardia/Bradycardia: both
can reduce CO by limiting
PRIMARY FUNCTION ventricular filling time of the
The core function of this system is tissue number of ejections.
perfusion. STROKE VOLUME (SV):
DIASTOLE (FILLING PHASE): Volume of blood ejected per heartbeat (60-100
• Passive Phase: Heart at rest, blood mL). Determined by:
flows from atria into ventricles. • PRELOAD: The stretch of the ventricular
• Active Phase (“Atrial Kick”): Atria muscle at end-diastole (“filling
contract, contributing 20-30% of pressure”).
ventricular filling. This is triggered by o Increased by: volume overload,
the P wave on an ECG. heart failure, valve stenosis.
• Clinical Note: Loss of atrial kick can lead o Decreased by: hypovolemia
to decreased cardiac output. (bleeding, dehydration), loss of
SYSTOLE (EJECTION PHASE): atrial kick (afib), venodilation
Ventricles contract after filling. (nitroglycerin), increased
• Mitral/tricuspid valve close; intrathoracic pressure
aortic/pulmonic valves open. (mechanical ventilation)
• Blood is ejected into the pulmonary and ELEVATED DECREASED
systemic circulations. Systemic • Hypertension • Septic shock
vascular • Vasopressor • Anaphylacti
resistance use c shock
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, • Aortic stenosis • Neurologic SVI SV/BSA 30-65
• Hypothermia shock mL/beat/m2
• Use of SVR MAP – CVP/RA 900-1400
vasodilators X 80 ÷ CO dynes/s/cm-5
• S/E of some SVRI SVR ÷ BSI 2000-2400
meds dynes/s/cm-5
Pulmonary • Pulmonary • Use of PVR PA mean – 100-250
vascular hypertension vasodilators PCWP X 80 ÷ dynes/s/cm-5
resistance • Hypoxia • S/E of some CO
• Pulmonary meds PVRI PVR ÷ BSI 255-315
embolism dynes/s/cm-5
• Pulmonary
stenosis OXYGEN SUPPLY & DEMAND BALANCE
GOAL: Adequate tissue perfusion requires a
FRANK-STARLING LAW: balance between oxygen supply and demand:
• Increased preload (end-diastolic Oxygen supply is determined by:
volume) stretches the heart muscle, • OXYGEN CONTENT OF BLOOD:
leading to a more forceful contraction o Hemoglobin (Hb) level: the
and increased stroke volume, up to a primary carrier of oxygen.
physiological limit. o Arterial oxygen saturation
• The core principle: “The heart pumps (Sa02): percentage of Hb
what it receives” saturated with oxygen
• The law states that the force of the (measured by Sp02 or ABG).
heart’s contraction is directly o Dissolved oxygen (Pa02): a
proportional to the initial length of the small fraction measured via
cardiac muscle fiber at the end of arterial blood gas.
diastole. • CARDIAC OUTPUT (CO): the delivery
PRELOAD (THE “STRETCH”): mechanism that carries the oxygen
This is the “initial length” of the muscle fibers. content to tissues.
In clinical practice, preload is equivalent to the CAUSES OF ELEVATED AND DECREASED
end-diastolic volume (EDV) – the amount of CONTRACTIBILITY
blood in the ventricle just before it contracts. ELEVATED DECREASED
• The greater the EDV, the more the • Hypercalcemia • Hyperkalemia
ventricular walls are stretched. • Administration of • Hypocalcemia
STROKE VOLUME (THE “FORCEFUL positive inotropic • Myocardial
CONTRACTION”): medications ischemia
This is the volume of blood ejected from the • Sympathetic • Administration of
ventricle with each heartbeat. The Frank- stimulation negative inotropic
Starling mechanism states that increased medications
preload leads to increased stroke volume. • Hypercapnea
• Hypoxia
HEMODYNAMIC CALCULATIONS • Acidosis
PARAMETER CALCULATION NORMAL
VALUES OXYGEN DEMAND
Mean Arterial (S) + (D X 2) 70–105 Oxygen demand is the amount of oxygen
Pressure c3 mmHg required by the blood’s tissues to produce
(MAP) energy (in the form of ATP) through aerobic
Cardiac Heart rate x 4–8 L/min metabolism.
Output stroke volume Think of the body as a car engine:
Cardiac Cardiac output 2.8-4.2 • Oxygen is the fuel
Index ÷ body surface L/min/m2 • Glucose and fatty acids are the raw
area materials.
Stroke Cardiac output 60-100 • ATP (adenosine triphosphate) is the
Volume x 1000 x heart mL/beat/m2 usable energy produced.
rate • The metabolic rate is the engine’s RPMs.
BALANO | 2
CARDIODYNAMICS & HEMODYNAMICS
HEMODYNAMICS
• Is the study of the forces the heart
develops to circulate blood through the
cardiovascular system.
• These forces are demonstrated as blood
pressure and blood flow.
• The focus is on systemic hemodynamics
(the output of the left heart). HEMODYNAMIC CONCEPTS
HEART ANATOMY & CARDIAC CYCLE BLOOD PRESSURE:
• SYSTOLIC: peak pressure during
CHAMBERS & FLOW: ventricular contraction.
• RIGHT SIDE: deoxygenated blood • DIASTOLIC: lowest pressure during
enters the right atrium via the vena ventricular relaxation.
cavae → flows through the tricuspid • PULSE PRESSURE: difference between
valve into the right ventricle → is systolic and diastolic pressure
ejected through the pulmonary valve to • MEAN ARTERIAL PRESSURE (MAP):
the lungs for oxygenation. average pressure driving blood to
• LEFT SIDE: Oxygenated blood returns organs. MAP > 60mmHg indicates
to the left atrium via pulmonary veins → adequate perfusion.
flows through the mitral valve into the o Formula: S + D x
thick-walled left ventricle → is ejected CARDIAC OUTPUT (CO) & CARDIAC INDEX
through the aortic valve into the aorta (CI):
and systemic circulation. • CO: Volume of blood ejected by the left
ventricle per min (4-8 L/min).
• CI: CO adjusted for body surface area
(2.8 – 4.2 L/min/m2), making it a better
indicator for different body sizes.
• Formula: CO = Heart rate x Stroke
Volume
o Tachycardia/Bradycardia: both
can reduce CO by limiting
PRIMARY FUNCTION ventricular filling time of the
The core function of this system is tissue number of ejections.
perfusion. STROKE VOLUME (SV):
DIASTOLE (FILLING PHASE): Volume of blood ejected per heartbeat (60-100
• Passive Phase: Heart at rest, blood mL). Determined by:
flows from atria into ventricles. • PRELOAD: The stretch of the ventricular
• Active Phase (“Atrial Kick”): Atria muscle at end-diastole (“filling
contract, contributing 20-30% of pressure”).
ventricular filling. This is triggered by o Increased by: volume overload,
the P wave on an ECG. heart failure, valve stenosis.
• Clinical Note: Loss of atrial kick can lead o Decreased by: hypovolemia
to decreased cardiac output. (bleeding, dehydration), loss of
SYSTOLE (EJECTION PHASE): atrial kick (afib), venodilation
Ventricles contract after filling. (nitroglycerin), increased
• Mitral/tricuspid valve close; intrathoracic pressure
aortic/pulmonic valves open. (mechanical ventilation)
• Blood is ejected into the pulmonary and ELEVATED DECREASED
systemic circulations. Systemic • Hypertension • Septic shock
vascular • Vasopressor • Anaphylacti
resistance use c shock
BALANO | 1
, • Aortic stenosis • Neurologic SVI SV/BSA 30-65
• Hypothermia shock mL/beat/m2
• Use of SVR MAP – CVP/RA 900-1400
vasodilators X 80 ÷ CO dynes/s/cm-5
• S/E of some SVRI SVR ÷ BSI 2000-2400
meds dynes/s/cm-5
Pulmonary • Pulmonary • Use of PVR PA mean – 100-250
vascular hypertension vasodilators PCWP X 80 ÷ dynes/s/cm-5
resistance • Hypoxia • S/E of some CO
• Pulmonary meds PVRI PVR ÷ BSI 255-315
embolism dynes/s/cm-5
• Pulmonary
stenosis OXYGEN SUPPLY & DEMAND BALANCE
GOAL: Adequate tissue perfusion requires a
FRANK-STARLING LAW: balance between oxygen supply and demand:
• Increased preload (end-diastolic Oxygen supply is determined by:
volume) stretches the heart muscle, • OXYGEN CONTENT OF BLOOD:
leading to a more forceful contraction o Hemoglobin (Hb) level: the
and increased stroke volume, up to a primary carrier of oxygen.
physiological limit. o Arterial oxygen saturation
• The core principle: “The heart pumps (Sa02): percentage of Hb
what it receives” saturated with oxygen
• The law states that the force of the (measured by Sp02 or ABG).
heart’s contraction is directly o Dissolved oxygen (Pa02): a
proportional to the initial length of the small fraction measured via
cardiac muscle fiber at the end of arterial blood gas.
diastole. • CARDIAC OUTPUT (CO): the delivery
PRELOAD (THE “STRETCH”): mechanism that carries the oxygen
This is the “initial length” of the muscle fibers. content to tissues.
In clinical practice, preload is equivalent to the CAUSES OF ELEVATED AND DECREASED
end-diastolic volume (EDV) – the amount of CONTRACTIBILITY
blood in the ventricle just before it contracts. ELEVATED DECREASED
• The greater the EDV, the more the • Hypercalcemia • Hyperkalemia
ventricular walls are stretched. • Administration of • Hypocalcemia
STROKE VOLUME (THE “FORCEFUL positive inotropic • Myocardial
CONTRACTION”): medications ischemia
This is the volume of blood ejected from the • Sympathetic • Administration of
ventricle with each heartbeat. The Frank- stimulation negative inotropic
Starling mechanism states that increased medications
preload leads to increased stroke volume. • Hypercapnea
• Hypoxia
HEMODYNAMIC CALCULATIONS • Acidosis
PARAMETER CALCULATION NORMAL
VALUES OXYGEN DEMAND
Mean Arterial (S) + (D X 2) 70–105 Oxygen demand is the amount of oxygen
Pressure c3 mmHg required by the blood’s tissues to produce
(MAP) energy (in the form of ATP) through aerobic
Cardiac Heart rate x 4–8 L/min metabolism.
Output stroke volume Think of the body as a car engine:
Cardiac Cardiac output 2.8-4.2 • Oxygen is the fuel
Index ÷ body surface L/min/m2 • Glucose and fatty acids are the raw
area materials.
Stroke Cardiac output 60-100 • ATP (adenosine triphosphate) is the
Volume x 1000 x heart mL/beat/m2 usable energy produced.
rate • The metabolic rate is the engine’s RPMs.
BALANO | 2
