CV - Cardiac Output 1 Flashcards
Define cardiac output and direct way of measuring
Cardiac output (CO) is the volume of blood pumped per minute
Cardiac output = stroke volume x heart rate
CO = SV x HR
Flowmetry probe inserted into mouth of aorta accessed from a peripheral artery.
Highly invasive and cannot be used in patients
Describe indirect ways of measuring cardiac output:
Fick principle - Based on uptake or release of a substance in the body which is dependent on blood flow
Dye dilution - based on the addition of a dye to the blood
Thermodilution - based on the addition of a cooled substance to the blood
Doppler flow echocardiography - Based on the Doppler shift of an ultrasound beam when reflected back off RBCs moving through the aortic valve or descending thoracic aorta
Define:
- diastole
- systole
- preload
- afterload
Diastole - relaxation
Systole - contraction
Preload;
- wall tension at end of diastole
- depends on volume in the chamber – greater volume = greater preload
- end diastolic volume depends on venous return (VR)
Afterload:
- wall tension during systole
- produced by resistance of the vessels through which the blood is being push
- depends on Total peripheral resistance (TPR)
Define:
- inotropic state
- stroke volume
- ejection fraction
- chronotropy
Inotropic state:
- contractile strength of the heart muscle (myocardium)
- positive inotropy increases the force of contraction, while negative inotropy decreases it
- controlled by sympathetic nervous system, calcium
Stroke volume:
- volume of blood ejected by one ventricle during a single heartbeat
- SV=EDV−ESV
- EDV: End-Diastolic Volume (blood in the ventricle at the end of filling)
- ESV: End-Systolic Volume (blood remaining in the ventricle after contraction)
Ejection fraction:
-% of blood ejected from the ventricle during each contraction relative to the ED
- SV/ EDV x 100
- key measure of heart function
Chronotropy - heart’s ability to adjust its rate of contraction in response to metabolic factors
Explain Starlings Law:
The force of contraction of the cardiac muscle increases as the cardiac muscle fibers are stretched, up to an optimal length
Preload:
Refers to the volume of blood filling the ventricles at the end of diastole (end-diastolic volume, EDV).
Increased preload stretches the ventricular muscle fibers.
Tension and Contraction:
As the muscle fibers stretch, the actin and myosin filaments align more optimally for cross-bridge formation.
This results in a stronger contraction and greater stroke volume (SV).
Output Matching:
Starling’s Law ensures that the heart pumps out the volume of blood it receives (venous return = cardiac output).
This mechanism maintains balance between the right and left sides of the heart to prevent blood pooling or backflow.
Starling’s Law is intrinsic to the heart; it does not rely on external neural or hormonal control.
It is critical for adapting cardiac output to changes in venous return (e.g., during exercise or changes in posture).
Overstretching of the fibers (e.g., in heart failure) can impair this mechanism, reducing contractility and cardiac efficiency.
Describe the factors influencing venous return in pre-load:
Pressure gradient - difference in pressure (higher in veins, lower in the heart) pushes blood back to the heart and maintains venous return (VR
Thoracic pump - negative pressure in the thoracic
cavity pulls blood from the body
Abdominal pump - pushes blood out of splanchnic reservoir
Muscle pump - squeezes blood up from legs
Venous tone:
- venoconstriction caused by sympathetic stimulation which reduces venous compliance, pushing blood toward the heart and increasing venous return
- venodilation reduces venous return, lowering preload
Blood volume:
- increase blood volume = raised venous return + higher preload
- decreased blood volume = reduced venous return + lowering preload
Venous valves - prevent back flow of blood
Describe graphical representation of Starling’s law:
Starling’s law of the heart states that the force of cardiac contraction is directly proportional to the initial length of myocardial fibers
Axis
X axis - Measures ventricular preload
Y axis - Measures cardiac output
The relationship between stroke volume and end-diastolic volume is shown as a curve:
Ascending Limb: Increased EDV leads to increased SV due to greater stretch and stronger contraction.
Plateau: Beyond an optimal stretch length, further increases in EDV do not enhance SV, and excessive stretch may reduce contractility.
In pathological conditions (such as heart failure), the curve shifts downward and to the right, indicating reduced cardiac efficiency
Describe Doppler flow electrocardiography and CO:
A non-invasive technique that combines Doppler ultrasound and electrocardiography (ECG) to assess blood flow velocity and cardiac function
Doppler ultrasound:
- measures the velocity of blood flow based on the Doppler effect,
- shift in the frequency of the reflected waves (Doppler shift) is proportional to the velocity of blood flow as the beam is reflected back off moving RBCs
- shows velocity and directionality of flow through the aortic valve or LVOT
Electrocardiography:
- records electrical activity of the heart to provide timing information for different phases of the cardiac cycle
Describe the regulatory influences on cardiac output:
Mechanical factors;
Preload - initial stretching of the cardiac myocytes prior to contraction, dependent on venous return, increases right atrial pressure
Afterload - the load the heart must eject blood against
Nervous + humoral factors:
Chronotropic - enhance cardiac function by increasing heart rate (HR)
Inotropic - length independent activation of myocardial contractility eg by increasing Ca2+ release
Describe the inotropic effects on stroke volume:
Positive inotropes:
- increase contractility by either increasing Ca2+ entry or Ca2+ release
Negative inotropes:
- decrease contractility
- drugs used to decrease the cardiac workload
- e.g beta blockers, L-type Ca channel inhibitors
Describe coupling cardiac and vascular function:
Cardiac function is intrinsically linked to vascular function through preload, afterload, and venous return
The interaction between cardiac output (CO) and vascular function, which determines systemic blood flow and blood pressure regulation
Frank Starling mechanism - Increased venous return enhances stroke volume due to increased sarcomere stretch
Mean Systemic Filling Pressure (MSFP): The pressure that drives venous return when the heart is stopped
Increased mean systemic filling pressure → increased venous return → increased CO
Afterload increase = Increases total peripheral resistance (TPR) → reduces stroke volume
Effects of Resistance Changes:
Increased total peripheral resistance (TPR) → Decreases venous return and cardiac output.
Decreased TPR → Enhances venous return and cardiac output.
Describe the pressure volume loop for the left ventricle vs the cardiac cycle:
The Pressure-Volume (PV) loop graphically represents the mechanical function of the left ventricle during a single cardiac cycle
It provides insights into stroke volume (SV), ventricular compliance, and myocardial contractility
describe the adaptations in cardiac output during exercise:
Increased sympathetic activity (β1-adrenergic activation) → increases heart rate and contractility.
Vasodilation in muscles (metabolic demand) → decreases systemic vascular resistance (SVR).
CO increases up to 4-6 times resting levels due to increased stroke volume and heart rate.
Redistribution of blood flow:
↑ to skeletal muscles, heart, skin
↓ to splanchnic organs and kidneys
describe the adaptations in cardiac output during pregnancy:
↑ Blood volume (~40-50%) due to increased plasma volume.
↑ Cardiac output (~30-50%) due to:
Increased stroke volume (↑ preload)
Increased heart rate (~10-20 bpm higher)
Decreased systemic vascular resistance (SVR) due to progesterone-mediated vasodilation.
describe the adaptations in cardiac output during a heart attack;
Reduced contractility → lower stroke volume and CO.
Compensatory mechanisms:
Increased sympathetic activation → tachycardia, vasoconstriction.
Increased renin-angiotensin-aldosterone system (RAAS) → fluid retention, increased preload.
Chronic HF leads to remodeling (hypertrophy, fibrosis).
Describe the cardiac cycle:
Phase 1 - Ventricular Filling:
- diastole
- mitral valve is open, allowing blood to flow from the left atrium into the left ventricle
- pressure remains low as ventricle fills passively (early diastole) and actively (late diastole)
- End-diastolic volume (EDV) is reached at the end of this phase
Phase 2 - Isovolumetric Contraction:
- mitral valve closes (first heart sound) and ventricle contracts without volume changes as both mitral and aortic valves are closed
- Ventricular pressure rises steeply, preparing for ejection
Phase 3 - Ejection Phase:
- systole
- when ventricular exceeds aortic pressure, aortic valve opens allowing blood into systemic circulation
- Stroke volume (SV) is determined by the difference between end-diastolic volume (EDV) and end-systolic volume (ESV)
- The peak of the pressure-volume loop corresponds to maximum ventricular pressure
Phase 4 - Isovolumetric Relaxation:
- aortic valve closes (second heart sound, S2), and the ventricle relaxes without volume change since both valves are closed
- Once ventricular pressure falls below atrial pressure, the mitral valve opens, restarting the cycle
describe the adaptations in cardiac output during shock:
Shock is a state of inadequate tissue perfusion due to circulatory failure, leading to cellular hypoxia
SNS activation - ↑ Heart rate (tachycardia) to maintain or increase CO, positive ionotropy, Peripheral vasoconstriction
Types:
Hypovolemic: Blood loss reduces preload.
Cardiogenic: Heart failure (MI, arrhythmias).
Distributive (septic, anaphylactic, neurogenic): Vasodilation reduces SVR.
Obstructive: Cardiac tamponade, PE.
Describe the Nervous and Humoral Factors Influencing Cardiac Output
Neural Regulation (Autonomic Nervous System):
- Sympathetic Nervous System (SNS) (via β1-adrenergic receptors):
↑ Heart rate (chronotropic effect).
↑ Contractility (inotropic effect).
↑ Conduction velocity (dromotropic effect). - Parasympathetic Nervous System (PNS) (via vagus nerve, M2 receptors):
↓ Heart rate (negative chronotropic effect).
Minimal effect on contractility.
Humoral Factors (Hormonal Regulation)
- Epinephrine (from adrenal medulla)
β1 stimulation → increases HR, contractility.
β2 stimulation → vasodilation in skeletal muscle. - Renin-Angiotensin-Aldosterone System (RAAS)
Angiotensin II → vasoconstriction, increases afterload.
Aldosterone → Na+ retention, increases preload. - Atrial Natriuretic Peptide (ANP)
Released from atria when stretched → vasodilation, natriuresis (reduces preload). - Thyroid Hormones
Increase β-adrenergic sensitivity, leading to increased heart rate and contractility.
- Thyroid Hormones
