Cardiac Output and Blood Pressure Flashcards

1
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2
Q

What is the cardiac cycle?

A

The cardiac cycle is the sequence of events from the beginning of one heartbeat to the start of the next. It includes phases such as atrial contraction, isovolumetric contraction, ventricular ejection, isovolumetric relaxation, and ventricular filling.

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3
Q

Define cardiac output (CO) and provide its formula.

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Cardiac output (CO): The volume of blood pumped by the heart per minute.

Formula: CO = Heart Rate (HR) × Stroke Volume (SV)

Normal Values: Approximately 5–6 L/min at rest; up to 25–30 L/min during exercise.

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4
Q

What is stroke volume (SV) and how is it determined?

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Stroke volume: The volume of blood ejected by a ventricle during one heartbeat.

Determination: SV = End-Diastolic Volume (EDV) − End-Systolic Volume (ESV)

EDV: The volume in the ventricle immediately before contraction (after filling).
ESV: The volume remaining in the ventricle after contraction.

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5
Q

Explain the ejection fraction (EF) and its significance.

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Ejection fraction: The percentage of the end-diastolic volume that is ejected during a contraction.

Calculation: EF = (SV / EDV) × 100%

Significance: Used to assess the pumping efficiency of the heart; low EF is a key indicator of heart failure.

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6
Q

How does cardiac output change during exercise?

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During exercise: Cardiac output increases significantly (from about 5–6 L/min at rest up to 25–30 L/min) to meet the body’s higher oxygen demands.

Mechanism: Primarily due to an increased heart rate and, to a lesser extent, increased stroke volume.

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7
Q

What is preload and what are its surrogate markers?

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Preload: The tension or stretch in the ventricular wall just before contraction (end-diastole).

Surrogate Markers: Left Ventricular End-Diastolic Volume (LVEDV), Left Ventricular End-Diastolic Pressure (LVEDP).

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8
Q

What is Starling’s Law of the Heart?

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Starling’s Law: An increase in ventricular end-diastolic volume (preload) increases the stretch of the cardiac muscle fibers, leading to a stronger contraction.

Implication: Up to a certain limit, more filling (greater preload) results in a higher stroke volume; however, overstretching (as in heart failure) impairs contraction.

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9
Q

Define afterload and list the factors that affect it.

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Afterload: The force or resistance that the ventricles must overcome to eject blood during systole.

Factors: Arterial blood pressure: Higher pressures increase afterload. Vascular resistance: Narrower or less compliant arteries (e.g., due to aging or smoking) increase afterload.

Effect: Increased afterload can reduce stroke volume and lower cardiac output.

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10
Q

What does inotropy refer to and how does it impact the heart?

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Inotropy: The contractility or intrinsic strength of the heart muscle’s contraction.

Impact: An increase in inotropy boosts stroke volume and cardiac output.

Influences: Increased by sympathetic stimulation (e.g., adrenaline) and drugs such as digitalis.

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11
Q

What are chronotropic effects in the context of heart function?

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Chronotropic effects: Changes in the heart rate.

Examples: Positive chronotropes: Increase heart rate (e.g., adrenaline). Negative chronotropes: Decrease heart rate (e.g., beta-blockers).

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12
Q

How does the autonomic nervous system influence heart function?

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Parasympathetic (Vagus Nerve): Acts on the SA node to slow the heart rate. Sympathetic System: Acts on the SA node and myocardium to increase heart rate and contractility via β₁-adrenergic receptors. Blood-borne Adrenaline: Also increases heart rate and contractility throughout the myocardium.

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13
Q

What are the two major circulations in the cardiovascular system?

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Systemic Circulation: Originates from the left heart; supplies oxygenated blood to the body. Arteries: Moderate size with thick, muscular walls.

Pulmonary Circulation: Originates from the right heart; sends deoxygenated blood to the lungs. Arteries: Larger diameter with thin, elastic walls.

Key Principle: Both circulations must maintain equal cardiac outputs to prevent blood accumulation.

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14
Q

Define systolic blood pressure (SBP).

A

Systolic BP: The maximum arterial pressure during ventricular contraction.

Normal Value: Approximately 120 mmHg in the brachial artery.

Clinical Guidelines: >140 mmHg: Stage One Hypertension (intervention based on risk factors). >160 mmHg: Definite intervention threshold.

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15
Q

Define diastolic blood pressure (DBP).

A

Diastolic BP: The minimum arterial pressure during ventricular relaxation.

Normal Value: Approximately 80 mmHg in the brachial artery.

Clinical Guidelines: >90 mmHg: Stage One Hypertension (with risk factor considerations). >100 mmHg: Definite intervention threshold.

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16
Q

What is pulse pressure (PP) and how is it calculated?

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Pulse Pressure: The difference between systolic and diastolic blood pressures.

Formula: PP = SBP − DBP

Example: For a BP of 120/80 mmHg, PP = 40 mmHg.

Note: Pulse pressure may rise with age due to arterial stiffening.

17
Q

How is mean arterial blood pressure (MAP) estimated using SBP and DBP?

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MAP Formula: MAP = DBP + (1/3) × (SBP − DBP)

Example: For 120/80 mmHg, MAP ≈ 80 + (1/3) × (40) ≈ 93−94 mmHg.

18
Q

What is total peripheral resistance (TPR)?

A

TPR (or Systemic Vascular Resistance, SVR): The cumulative resistance offered by all blood vessels in the systemic circulation.

Key Determinant: Mainly determined by the arteriolar diameter.

Role: A key factor in determining MAP, as per the equation: MAP ≈ CO × TPR.

19
Q

How does peripheral resistance relate to blood pressure?

A

Blood pressure is influenced by the product of cardiac output and total peripheral resistance: MAP = CO × TPR.

A decrease in peripheral resistance (e.g., due to vasodilation) leads to a lower MAP, which can result in hypotension.

20
Q

Describe the procedure for accurate blood pressure measurement.

A

Preparation: Patient should be seated quietly for at least 5 minutes. The patient’s arm should be supported, outstretched, and at heart level.

Equipment: Use an appropriately sized cuff.

Manual (Auscultatory) Method: Palpate the radial pulse to check for regularity. Inflate the cuff 20–30 mmHg above the point where the pulse disappears. Deflate slowly (around 2 mmHg per second). Record the first Korotkoff sound as SBP and the disappearance of sound as DBP.

Notes: Measure in both arms and take at least two readings. Be aware of “white coat hypertension.”

21
Q

What is the concept of venous return and why is it important?

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Venous Return: The process by which blood returns from the peripheral tissues to the heart.

Key Principle: The heart can only pump out the blood it receives; therefore, venous return directly limits cardiac output.

22
Q

What mechanisms aid venous return?

A

Skeletal Muscle Pump: Muscle contractions compress veins, pushing blood toward the heart. One-way valves in the veins prevent backflow.

Abdomino-Thoracic Pump: During Inspiration: The diaphragm moves downward, increasing abdominal pressure and decreasing intrathoracic pressure, which draws blood into the thoracic cavity. During Exhalation: The diaphragm moves upward, slightly reducing the pressure gradient and potentially impeding venous return.

23
Q

How does a decrease in peripheral resistance contribute to hypotension?

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Mechanism: A decrease in peripheral resistance reduces the mean arterial pressure, as given by the equation: MAP = CO × TPR.

Causes: Conditions like sepsis, anaphylaxis, neurogenic shock, or the use of vasodilator medications can lower TPR.

Result: Lower blood pressure (hypotension) can lead to inadequate blood flow and oxygen delivery to tissues.

24
Q

What is orthostatic hypotension?

A

Definition: A significant drop in blood pressure when moving from a sitting or lying position to standing.

Mechanism: Gravity reduces venous return when standing, which decreases stroke volume and cardiac output. In healthy individuals, compensatory mechanisms (vasoconstriction and increased heart rate) usually counteract this drop.

Clinical Note: More common in older adults or those on certain blood pressure medications.

25
Q

List some clinical consequences of hypertension.

A

Consequences: Increased risk of heart disease and eventual heart failure. Higher risk of stroke (cerebrovascular accidents). Kidney damage. Damage to retinal vessels in the eyes. Potential for atherosclerotic plaque rupture leading to thrombus formation or embolism. Aneurysm formation (e.g., in the abdominal aorta).

26
Q

What are the two primary systems that regulate blood pressure?

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Neuronal (Fast-Acting) System: Mediated by the autonomic nervous system, which quickly adjusts heart rate and vascular tone.

Hormonal (Slower-Acting) System: Involves hormones such as those in the renin–angiotensin–aldosterone system (RAAS) that regulate blood volume and vascular resistance over a longer period.