CV - Cardiovascular Reflexes Flashcards
(15 cards)
Describe the Relationship Between Arterial Blood Pressure and Cardiac Output:
Arterial BP Formula: BP = CO x TPR.
Systolic BP: Determined by cardiac output (CO), reflecting the force of heart contraction during systole.
Diastolic BP: Influenced by total peripheral resistance (TPR)
An increase in CO (at constant TPR) leads to increased ABP because more blood is ejected into the arterial system
A decrease in CO (at constant TPR) leads to decreased ABP, reducing perfusion to organs
Fcators affecting CO + ABP:
Preload - Increased preload → increased stroke volume → increased CO → increased ABP
myocardial contractility - Increased contractility (e.g., due to sympathetic stimulation or catecholamines) → increased stroke volume → increased CO → increased ABP
Afterload - Increased afterload (vasoconstriction) → increased ABP (can reduce stroke volume if excessive)
Describe the Factors Affecting Total Peripheral Resistance
Smooth Muscle Contractility in Arterioles: Primary determinant.
Influences on TPR:
Perfusion pressure (myogenic tone).
Vasodilation due to metabolic needs, circulating hormones, and nervous input.
Nervous Input Effects:
ACh → Vasodilation.
Adr/NA → Vasoconstriction (↑Diastolic BP).
Describe the Components of Cardiac Output and Venous return:
Formula: CO = Stroke Volume (SV) x Heart Rate (HR).
Stroke Volume Depends On:
Contractile force of left ventricle (e.g., inotropes like adrenaline).
Venous return (VR)
Key Factors Influencing VR:
Pressure gradient.
Thoracic pump and abdominal pump effects.
Muscle pump activity.
Venomotor tone (↑ Sympathetic activity → ↑ Venous tone → ↑ VR).
Blood volume
Describe heart rate regulation factors:
SA Node Depolarization Rate: Sets baseline HR.
AV Node Conduction Rate: Adjusts rhythm.
Right Atrium Stretch (Bainbridge Reflex): ↑Stretch → ↑HR.
Nervous Input:
Sympathetic (↑ HR).
Parasympathetic (↓ HR)
Describe the Bainbridge reflex:
A cardiovascular reflex where atrial stretch receptors respond to increased venous return
Location of Receptors: Junction of right atrium & vena cava, and pulmonary vein & left atrium
Mechanism:
Stretch receptors detect increased blood volume.
Vagus nerve signals medulla to inhibit vagus outflow to SA node → Increased Heart Rate (HR).
helps accommodate the increased venous return and prevent excessive atrial distension
May involve an intrinsic effect on pacemaker current
helps regulate heart rate in response to changes in blood volume
Counterbalances the baroreceptor reflex, which typically decreases HR in response to increased blood pressure
Describe the relationship between nervous reflexes and breathing pattern:
Respiratory Center → Cardiac Vagal Center:
- respiratory centre activity reduces vagal tone
- result is an increase in HR
Intrathoracic Pressure ↓ → Lung Volume Receptors Activated:
- lung stretch receptors signal cardiac vagal centre
- vagal tone decreases → HR increases
Intra-thoracic Pressure ↓ → Venous Return ↑:
- increased venous return stretches the right atrium
- atrial stretch triggers Bainbridge reflex, reducing vagal tone
- result is increased HR
ransient HR increase during inspiration (respiratory sinus arrhythmia) optimizes blood flow and cardiac efficiency
Describe the Bezold-Jarisch Reflex:
Cardiovascular and neurological processes which cause hypopnea (excessively shallow/rapid breathing) and bradycardia (abnormally low resting HR
Pressure receptors in the LV wall and trabeculae sense the underfilling and activate C-fibre afferent nerves which trigger paradoxicalbradycardia, decreased contractility and arterialhypotension
Triggered by stimulation of cardiac mechanoreceptors or chemoreceptors in the ventricles.
Stimuli: Ischemia, hypoxia, chemical agents (e.g., serotonin, bradykinin).
Response:
Bradycardia.
Hypotension.
Peripheral vasodilation.
Protective reflex to reduce cardiac workload
Describe Cushing’s reflex:
Triggered by ↑Intracranial Pressure (ICP).
Stimuli: Brain edema, hemorrhage, or space-occupying lesions.
Response:
- Hypertension: Maintains cerebral perfusion pressure.
- Bradycardia: Reflex vagal activation due to baroreceptor response to ↑BP.
- Irregular Respiration: Due to medullary compression.
Clinical Importance: Often indicates life-threatening conditions requiring immediate intervention.
Describe the chemoreceptor reflex:
Triggered by changes in blood gas levels (↓O2, ↑CO2, ↓pH).
Sensors: Peripheral chemoreceptors (carotid and aortic bodies).
Response:
- Severe Hypoxia:
↑Sympathetic activation → Vasoconstriction → ↑BP.
Activation of respiratory centers → Hyperventilation. - Hypercapnia (↑CO2):
Stronger respiratory drive.
Secondary effect: ↑Sympathetic tone → Vasoconstriction, ↑BP.
Describe the Regulation of Blood Volume by Cardiovascular Reflexes:
Baroreceptor reflex
Cardiopulmonary reflexes
Renin-Angiotensin-Aldosterone System
Vasopressin (Antidiuretic Hormone, ADH) Regulation
Atrial Natriuretic Peptide (ANP) & Brain Natriuretic Peptide (BNP)
Describe the Regulation of Arterial Blood Pressure by Reflex Mechanisms:
Baroreceptor reflex
Chemoreceptor reflexes
Bezold-Jarisch Reflex
Cushing’s reflex
Exercise and Emotional Reflexes (Central Command & Hypothalamic Control)
Describe the valsalva manoeuvre:
Valsalva manoeuvre (forced expiration against a closed glottis), increases the intrathoracic and intracranial pressure
Phase 1:
- forced expiration against a closed glottis increases intrathoracic pressure and also increases aortic pressure
- ↑ vagal outflow = ↓ HR
- baroreceptor reflex on
Phase 2:
- ↓VR = ↓ ventricular ejection = ↓BP = Baro off.
- ↓vagal activity & ↑ Symp = ↑HR ↑TPR and consequently ↑BP slightly
Phase 2b:
- With maintained higher intracranial pressure BP rises (Cushing’s reflex) HR then falls
Phase 3:
- relaxation
- when breath-hold is released, intrathoracic pressure rapidly normalises
- Sudden BP drop as the mechanical compression is relieved
- rebound ↑VR = ↑HR (Bainbridge)
Phase 4:
- Venous blood that was previously obstructed rushes back into the heart.
- This increases cardiac output and stroke volume significantly.
- The baroreceptor reflex responds to the sudden increase in BP
Describe the Renin-Angiotension-Aldosterone (RAA) System:
Hormonal system that regulates blood pressure (BP) and fluid balance
Renin Release Mechanism:
- juxtaglomerular cells located in the kidney’s afferent arteriole, sensitive to BP changes
High BP:
- Activates TRPV4 channels → Ca²⁺ influx → Inhibits Adenylate Cyclase V (AC-V)
- ↓cAMP production → Reduced Renin Release
Low BP:
- Reduced TRPV4 activation → Less Ca²⁺ influx
- ↑cAMP production → Increased Renin Release
renin converts angiotensin → angiotensin I → angiotensin II
Actions of Angiotensin II:
- Vasoconstriction Increases TPR → Raises BP
- Stimulates Aldosterone Secretion (Adrenal Cortex) which promotes Na⁺ and water reabsorption → increases blood volume
- Stimulates ADH Release (Posterior Pituitary) which enhances water retention.
Describe the relationship between Atrial Natriuretic Peptide and Blood volume:
ANP released by atrial myocytes in response to atrial distension (possibly via AngII Type 2 receptors - AT2R)
Released from the atria and ventricles in response to increased blood volume and atrial stretch
Systemic vasodilation - reducing total peripheral resistance (TPR) and lowering blood pressure
Improve GFR & filtration fraction
Inhibit renin release
↓ circulating Ang II & aldosterone
Inhibition of Vasopressin (ADH) – ANP reduces ADH secretion, decreasing water retention and promoting fluid loss
Natriuresis & Diuresis
ANP counteracts volume overload by reducing blood volume, central venous pressure, cardiac output, and arterial pressure, acting as a physiological antagonist to RAAS
What is the Baroreceptor reflex ?
baroreceptor reflex is the primary short-term mechanism regulating arterial blood pressure
Baroreceptors are mechanosensitive nerve endings located in the carotid sinus (CN IX, glossopharyngeal nerve) and the aortic arch (CN X, vagus nerve), which respond to stretch in the arterial wall
An increase in arterial pressure causes increased baroreceptor firing, which is relayed to the nucleus tractus solitarius (NTS) in the medulla oblongata
The NTS modulates autonomic output by;
- Increasing parasympathetic activity via the vagus nerve to the sinoatrial node, reducing heart rate (negative chronotropy)
- Inhibiting sympathetic output, reducing heart rate, contractility, and systemic vascular resistance
Conversely, a decrease in pressure reduces baroreceptor firing, resulting in enhanced sympathetic activity and reduced vagal tone
