The document provides an overview of cardiovascular physiology, including:
1. It describes the basic components and regulation of the cardiovascular system, including the heart, vessels, and regulatory mechanisms.
2. It discusses the pulmonary and systemic circulations in terms of pressure, resistance, and flow.
3. It covers the structure and function of the heart as a pump, including cardiac cycle, regulation of contractility, and the Frank-Starling mechanism.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
The epsilon wave is a small positive deflection (‘blip’ or ‘wiggle’) buried in the end of the QRS complex.
Epsilon waves are caused by postexcitation of the myocytes in the right ventricle.
Epsilon waves are the most characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD).
Here myocytes are replaced with fat, producing islands of viable myocytes in a sea of fat.
This causes a delay in excitation of some of the myocytes of the right ventricle and causes the little wiggles seen during the ST segment of the ECG.
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
The epsilon wave is a small positive deflection (‘blip’ or ‘wiggle’) buried in the end of the QRS complex.
Epsilon waves are caused by postexcitation of the myocytes in the right ventricle.
Epsilon waves are the most characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD).
Here myocytes are replaced with fat, producing islands of viable myocytes in a sea of fat.
This causes a delay in excitation of some of the myocytes of the right ventricle and causes the little wiggles seen during the ST segment of the ECG.
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Basic hemodynamic principles viewed through pressure volume relationsInsideScientific
The goal of this webinar is to provide an overview of the fundamental principles of preload, afterload, contractility and lusitropy (diastolic properties), how these are quantified on the pressure-volume diagram, and how they are affected in heart failure. Links are made to underlying properties of cardiac muscle and ventricular structure. After establishing basic concepts, it will be demonstrated how pressure-volume analysis can lead to a quantitative understanding of how heart and vasculature interact to determine stroke volume, cardiac output and blood pressure. The implications for understanding therapeutic effects will also be discussed.
Key Topics:
- Preload, Afterload, Contractility and Lusitropy
- Cardiac Muscle and Ventricular Structure
- Understanding Heart-Vasculature Interactions
- PV Loops in Heart Failure
- Understanding Therapies and Their Effects on Cardiac Pump Performance
A closed system of the heart and blood vessels
The heart pumps blood
Blood vessels allow blood to circulate to all parts of the body
The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide and other waste products
2 hearts, each with 2 chambersLeft heart to all body except lungs (systemic)Right heart to lungs (pulmonary)Systemic arteries: oxygenated bloodPulmonary arteries: deoxygenated bloodSystemic veins: deoxygenated bloodPulmonary veins: oxygenated bloodAtria: receive blood from veinsVentricles: pump blood to arteries
ecg basics made easy, with description of most common ecg types especially in emergency situation.
easy to memorize points and mnemonics included.
approach to ecg diagnosis.
sample ecgs.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
13. SINGLE VENTRICULAR ACTION POTENTIAL ECG P Q S T R 1 mV Repolarization of ventricles Depolarization of ventricles Depolarization of atria ENDOCARDIAL FIBER EPICARDIAL FIBER ATRIAL FIBER
14. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+)
15. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+) II = RA vs. LL (+)
16. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+)
17. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+) 3 Augmented Limb Leads: aVR = (LA-LL) vs. RA(+)
18. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+) 3 Augmented Limb Leads: aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+)
19. LA RA LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+) 3 Augmented Limb Leads: aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+) aVF = (RA-LA) vs. LL(+)
20. V 1 V 2 V 3 V 4 V 5 V 6 6 PRECORDIAL (CHEST) LEADS Spine Sternum
21. ECG Recordings: (QRS vector---leftward, inferiorly and posteriorly 3 Bipolar Limb Leads I = RA vs. LA(+) II = RA vs. LL(+) III = LA vs. LL(+) 3 Augmented Limb Leads aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+) aVF = (RA-LA) vs. LL(+) 6 Precordial (Chest) Leads: Indifferent electrode (RA-LA-LL) vs. chest lead moved from position V 1 through position V 6 .
22. LATE DIASTOLE ATRIAL SYSTOLE ISOMETRIC VENTRICULAR CONTRACTION VENTRICULAR EJECTION ISOMETRIC VENTRICULAR RELAXATION THE CARDIAC CYCLE DIASTOLE
24. MEASUREMENT OF CARDIAC OUTPUT THE FICK METHOD: VO 2 = ([O 2 ] a - [O 2 ] v ) x Flow Flow = VO 2 [O 2 ] a - [O 2 ] v Spirometry (250 ml/min) Arterial Blood (20 ml%) Pulmonary Artery Blood (15 ml%) CARDIAC OUTPUT PERIPHERAL BLOOD FLOW VENOUS RETURN PULMONARY BLOOD FLOW
25. CARDIAC OUTPUT (Q) = VO 2 [O 2 ] a - [O 2 ] v 250 ml/min 20 ml% - 15 ml% = = 5 L/min . Q = HR x SV . SV = Q HR . = 5 L/min 70 beats/min = 0.0714 L or 71.4 ml CARDIAC INDEX = Q m 2 body surface area . 5 L/min 1.6 m 2 = = 3.1 L/min/m 2
26.
27. CARDIAC OUTPUT = STROKE VOLUME x HEART RATE Autoregulation (Frank-Starling “Law of the Heart”) Contractility Sympathetic Nervous System Parasympathetic Nervous System
28. STRIATED MUSCLE CARDIAC MUSCLE SKELETAL MUSCLE - Functional Syncytium - Automaticity - Motor Units - Stimulated by Motor Nerves
29. STRUCTURE OF A MYOCARDIAL CELL Mitochondria Sarcolemma T-tubule SR Fibrils
41. CARDIAC FUNCTION CURVE STROKE VOLUME DIASTOLIC FILLING Cardiac Output = Stroke Volume x Heart Rate Constant If: Then: CO reflects SV Right Atrial Pressure (RAP) reflects Diastolic Filling
42. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 0 +4 +8 Volume Pressure THE FRANK- STARLING “LAW OF THE HEART”
43. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 0 +4 +8 THE FRANK- STARLING “LAW OF THE HEART” Increased Contractility
44. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 0 +4 +8 THE FRANK- STARLING “LAW OF THE HEART” Decreased Contractility
45. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 0 +4 +8 THE FRANK- STARLING “LAW OF THE HEART” Increased Heart Rate
46. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 0 +4 +8 THE FRANK- STARLING “LAW OF THE HEART” Decreased Heart Rate
47. P 1 P 2 P 1 > P 2 FLOW FLOW = P R P = FLOW x R R = mm Hg L/min or ml/sec mm Hg ml/sec Peripheral Resistance Units (PRU) P FLOW
48. LAMINAR or STREAMLINE FLOW P 2 P 1 P 1 > P 2 -Cone Shaped Velocity Profile -Not Audible with a Stethoscope
49. MEASURING BLOOD PRESSURE TURBULENT FLOW 1. Cuff pressure > systolic blood pressure--No sound. 2. The first sound is heard at peak systolic pressure. 3. Sounds are heard while cuff pressure < blood pressure. 4. Sound disappears when cuff pressure < diastolic pressure.
50. RESISTANCES IN SERIES R T = R A + R C + R V RESISTANCES IN PARALLEL R 1 R 2 R 3 P A P V Flow T = Flow 1 + Flow 2 + Flow 3 P R T P R 1 P R 2 P R 3 = + + 1 R T 1 R 1 1 R 2 1 R 3 = + + 1 R 1 1 R 2 1 R 3 R T 1 + + =
51. If: R 1 = 2; R 2 = 4; R 3 = 6 PRU’s Then a series arrangement gives: R T = R 1 + R 2 + R 3 R T = 12 PRU’s But a parallel arrangement gives: R T = =1.94 PRU’s 1 1 R 1 1 R 2 1 R 3 + +
52. v = Pr 2 /8 l Q = v r 2 Poiseuille's Law P r 4 8 l Q = P R Flow = R = 8 l/ r 4
53. TOTAL PERIPHERAL RESISTANCE TPR = Aortic Pressure - RAP FLOW TPR = 100 - 0 mmHg 83.3 ml/sec (5 L/min) = 1.2 PRU’s SYSTEMIC CIRCULATION: PULMONARY CIRCULATION: Pul. R. = Pul. Art. P. - LAP FLOW Pul. R. = 15 - 5 mmHg 83.3 ml/sec = 0.12 PRU’s
54. VASCULAR COMPLIANCE C = V P PRESSURE (mmHg) VOLUME (L) 1 2 3 4 Arteries Veins 100- Sym Sym C v = 24 x C a C a = =2.5 ml/mmHg C v = = 60 ml/mmHg 250 ml 100 mmHg 300 ml 5 mmHg Sym Sym
58. VASOMOTION = Intermittent flow due to constriction- relaxation cycles of precapillary shpincters or arteriolar smooth muscle (5 - 10/min) AUTOREGULATION OF VASOMOTION: 1. Oxygen Demand Theory (Nutrient Demand Theory) O 2 is needed to support contraction (closure) 2. Vasodilator Theory Vasodilator substances produced (via O 2 ) e.g. Adenosine Heart CO 2 Brain Lactate, H + , K + Skeletal Muscle 3. Myogenic Activity
59. DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID Plasma Proteins BLOOD O 2 CO 2 Glucose INTERSTITIAL FLUID CELL active transport
60. FLUID BALANCE 40- 30- 20- 10- 0- PRESSURE (mmHg) Filtration vs. Reabsorption Outward Forces: 1. Capillary blood pressure (P c = 35 to 15 mmHg) 2. Interstitial fluid pressure (P IF = 0 mmHg) 3. Interstitial fluid colloidal osmotic pressure ( IF = 3 mmHg) TOTAL = 38 to 18 mmHg Inward Force: 1. Plasma colloidal osmotic pressure ( C = 28 mmHg)
61. CAPILLARY FLUID SHIFT P out > c P out < c P c P c FAVORS FILTRATION FAVORS REABSORPTION PULMONARY CIRCULATION
62. FLUID BALANCE 40- 30- 20- 10- 0- PRESSURE (mmHg) Filtration vs. Reabsorption Filtration Reabsorption Via lymphatics RADIAL FLOW
64. Effects of gravity on arterial and venous pressures. Each cm of distance produces a 0.77 mmHg change. Sphincters protect capillaries VENOUS PUMP keeps P V < 25 mm Hg Veins Arteries 190 mm Hg 100 mm Hg 0
66. C v = 24 x C a P RAP P v P a P= P a - P v TPR PBF=TPR (mmHg) (mmHg) (mmHg) (mmHg) (PRU’s) (ml/sec) 7 7 7 0 1.2 0 6 31 25 1.2 20.8 5 55 50 1.2 41.7 4 79 75 1.2 62.5 0 3 103 100 1.2 83.3 (5 L/min) RELATIONSHIP BETWEEN RAP and PBF
67. THE VASCULAR FUNCTION CURVE 10- 5- 0- PBF or VENOUS RETURN (L/min) -4 0 +4 +8 RAP (mmHg)
77. CHANGES IN CARDIOVASCULAR PERFORMANCE BY ALTERING THE CARDIAC FUNCTION CURVE - CHANGING CONTRACTILITY - CHANGING HEART RATE BY ALTERING THE VASCULAR FUNCTION CURVE - CHANGING MEAN CIRCULATORY PRESSURE Blood Volume Venous Capacity - CHANGING TOTAL PERIPHERAL RESISTANCE
78. MOTOR CORTEX HYPOTHALAMUS VASOMOTOR CENTER PRESSOR AREA DEPRESSOR AREA CARDIOINHIBITORY AREA Vagus HEART Arterioles Veins Adrenal Medulla Baroreceptors Carotid Sinus Aortic Arch Chemoreceptors Carotid Bodies Aortic Bodies Bainbridge Reflex ( Heart Rate) Atrial Receptors Volume Reflex ( Urinary OUTPUT) a. Vascular Sympathetic Tone b. ADH Secretion c. Aldosterone Secretion Chemosensitive Area Glossopharyngeal Nerve Sympathetic Nervous System
79. BP (Kidney) Renin Angiotensinogen (renin substrate) Angiotensin Aldosterone Kidney sodium & water retention Vasoconstriction Venoconstriction RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
80.
81. Hypothalamic Osmoreceptors BP via Posterior Pituitary Vasopressin (ADH) (Atrial Receptors) Vasoconstriction Water Venoconstriction Retention VASOPRESSIN (ANTIDIURETIC HORMONE) X X
82. RENAL--BODY FLUID CONTROL MECHANISM 8- 7- 6- 5- 4- 3- 2- 1- -8 -7 -6 -5 -4 -3 -2 -1 Uninary Output (x normal) Fluid Intake (x normal) 50 100 150 Normal ARTERIAL BLOOD PRESSURE (mmHg) P alone All Mechanisms 3 x Normal
83. HYPERTENSION (140/90 mmHg) Secondary Hypertension (10%) [e.g., Pheochromocytoma] Essential Hypertension (90%) - Normal cardiac output - Cardiac hypertrophy [left ventricle] - “Resetting” of the baroreceptors - Thickening of vascular walls ARTERIAL PRESSURE-URINARY OUTPUT THEORY Hypertension causes thickening of vascular walls NEUROGENIC THEORY Thickening of vascular walls causes hypertension TREATMENT: Reduce stress Sympathetic blockers Low sodium diet Diuretics
84. HEMORRHAGE Pressure 7- 1 2 3 4 5 Blood Volume (L) MCP -4 0 +4 +8 RAP (mmHg) CO or PBF (L/min) CO BP
96. Upper limit of survival? Heat stroke Brain lesions Fever therapy Febrile disease and Hard exercise Usual range of normal Temperature regulation seriously impaired Temperature regulation efficient in febrile disease health and work Temperature regulation impaired Temperature regulation lost Lower limit of survival?
97. HEAT PRODUCTION BASAL METABOLIC RATE - Catecholamines -Hyperthyroidism FOOD INTAKE (Specific Dynamic Action) -lasts up to 6 hours after a meal PHYSICAL ACTIVITY -Exercise (20 x BMR) -Shivering (5 x BMR)
98. HEAT LOSS COOL HOT RADIATION CONDUCTION 70% CONVECTION VAPORIZATION 30% Insensible Water Loss * * Sweating *
99. SKIN HYPOTHALAMUS Sweating Vasodilation Vasoconstriction Shivering W W W Set point C Warm Receptors Cold Receptors Preoptic Area
100. Interaction Between Peripheral & Central Sensors Cooling the skin raises the set point above which sweating begins. Warm skin--sweating occurs above 36.7 C Cold skin--sweating occurs above 37.4 C The body is reluctant to give off heat (sweat) in a cold environment. Warming the skin lowers the set point below which shivering begins. Cold skin: shivering occurs at 37.1 C Warm skin: shivering occurs at 36.5 C The body is reluctant to produce heat (shiver) in a warm environment.
101. LIMITS TO TEMPERATURE REGULATION Heat Exhaustion: Inadequate water/salt replacement Body temperature may be normal Symptoms: cerebral dysfunction nausea fatique Vasodilaton causing fatigue or fainting Heat Stroke: Temperature regulation lost Symptoms: high body temperature NO sweating dizziness or loss of consciousness Body temperature MUST be lowered!
102. FEVER FEVER = an abnormally high body temperature PYROGEN = a fever producing substance PYROGEN WBC bacterial toxins, leukocytes, viruses, pollen, + monocytes = endogenous pyrogen proteins, dust Arachidonic Acid Prostaglandins Aspirin RAISES THE “SET POINT”
103. Actual Core Temperature Onset of Fever Fever Breaks Reference Temperature or Set Point Shivering Vasoconstriction Sweating Vasodilation