cardiovascular physiolgy

CARDIOVASCULAR PHYSIOLOGY Dr. Poland Room 3-007, Sanger Hall Phone: 828-9557 E-mail: poland@hsc.vcu.edu HEART (PUMP) AUTOREGULATION NEURAL HORMONAL RENAL-BODY FLUID CONTROL SYSTEM REGULATION CARDIOVASCULAR SYSTEM VESSELS (DISTRIBUTION SYSTEM) PULMONARY CIRCULATION 1. LOW RESISTANCE 2. LOW PRESSURE (25/10 mmHg) SYSTEMIC CIRCULATION 1. HIGH RESISTANCE 2. HIGH PRESSURE (120/80 mmHg) PARALLEL SUBCIRCUITS UNIDIRECTIONAL FLOW ARTERIES (LOW COMPLIANCE) HEART DIASTOLE VEINS CAPACITY VESSELS 80 mmHg 120 mmHg SYSTOLE CAPILLARIES THE SYSTEMIC CIRCULATION CAPACITY VESSELS NORMAL AUTOMATICITY Na+ Gradually increasing PNa Na+ K+ + K -0 -70 mV THRESHOLD RESTING Atrio-ventricular (AV) node Sino-atrial (SA) node BUNDLE BRANCHES PURKINJE FIBERS INTERCALATED DISC (TIGHT JUNCTION) PACEMAKERS (in order of their inherent rhythm) • • • • • Sino-atrial (SA) node Atrio-ventricular (AV) node Bundle of His Bundle branches Purkinje fibers 0 PHASE 0 = Rapid Depolarization Mechanical Response (inward Na+ current) 1 1 = Overshoot 2 2 = Plateau (inward Ca++ current) 3 = Repolarization (outward K+ current) 0 4 = Resting Potential 3 -90 TIME 4 ACTION POTENTIALS MEMBRANE POTENTIAL (mV) VENTRICULULAR CELL 1 2 SAN 0 0 0 3 -50 0 3 -50 4 4 -100 -100 SINGLE VENTRICULAR ACTION POTENTIAL ATRIAL FIBER ENDOCARDIAL FIBER EPICARDIAL FIBER R 1 mV ECG P T QS Repolarization of ventricles Depolarization of ventricles Depolarization of atria ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA I = RA vs. LA (+) LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA I = RA vs. LA (+) II = RA vs. LL (+) LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+) LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA I = RA vs. LA (+) II = RA vs. LL (+) III = LA vs. LL (+) 3 Augmented Limb Leads: aVR = (LA-LL) vs. RA(+) LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA 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(+) LL ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly) 3 Bipolar Limb Leads: RA LA 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(+) LL 6 PRECORDIAL (CHEST) LEADS Spine V6 V5 Sternum V1 V2 V3 V4 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 V1 through position V6. THE CARDIAC CYCLE DIASTOLE LATE DIASTOLE ISOMETRIC VENTRICULAR RELAXATION ATRIAL SYSTOLE VENTRICULAR EJECTION ISOMETRIC VENTRICULAR CONTRACTION ISOVOLUMETRIC RELAXATION RAPID INFLOW ISOVOLUMETRIC DIASTASIS CONTRACTION ATRIAL SYSTOLE PRESSURE (mmHg) EJECTION AORTIC PRESSURE ATRIAL PRESSURE VOLUME (ml) VENTRICLE PRESSURE ECG PHONOCARDIOGAM SYSTOLE DIASTOLE SYSTOLE MEASUREMENT OF CARDIAC OUTPUT THE FICK METHOD: VO2 = ([O2]a - [O2]v) x Flow Spirometry (250 ml/min) VO2 Flow = [O2]a - [O2]v Pulmonary Artery Blood (15 ml%) Arterial Blood (20 ml%) CARDIAC OUTPUT PULMONARY BLOOD FLOW VENOUS RETURN PERIPHERAL BLOOD FLOW . VO2 CARDIAC OUTPUT (Q) = [O ] - [O ] 2 a 2 v = 250 ml/min 20 ml% - 15 ml% = 5 L/min . Q = HR x SV . Q SV = HR . CARDIAC INDEX = Q 2 m body surface area = 5 L/min 5 L/min 70 beats/min = 1.6 m2 = 0.0714 L or 71.4 ml = 3.1 L/min/m2 THE HEART AS A PUMP • REGULATION OF CARDIAC OUTPUT – Heart Rate via sympathetic & parasympathetic nerves – Stroke Volume • Frank-Starling “Law of the Heart” • Changes in Contractility • MYOCARDIAL CELLS (FIBERS) – Regulation of Contractility – Length-Tension and Volume-Pressure Curves – The Cardiac Function Curve Autoregulation (Frank-Starling “Law of the Heart”) CARDIAC OUTPUT = STROKE VOLUME x HEART RATE Contractility Sympathetic Nervous System Parasympathetic Nervous System CARDIAC MUSCLE - Functional Syncytium - Automaticity STRIATED MUSCLE SKELETAL MUSCLE - Motor Units - Stimulated by Motor Nerves STRUCTURE OF A MYOCARDIAL CELL Sarcolemma Mitochondria T-tubule SR Fibrils SARCOLEMMA T-tubule 20% 80% SR Mitochondria 10% Ca++ THICK MYOFILAMENT THIN MYOFILAMENT REGULATAION OF CONTRACTILITY • Recruitment of motor units • Increase frequency of firing of motor nerves • Calcium to trigger contraction INCREASING HEART RATE INCREASES CONTRACTILITY Normal Heart Rate Ca++ Ca++ Fast Heart Rate Ca++ Ca++ Ca++ Ca++ SERIES ELASTIC ELEMENTS PARALLEL ELASTIC ELEMENTS (PASSIVE TENSION) CONTRACTILE COMPONENT (ACTIVE TENSION) TOTAL TENSION LENGTH-TENSION CURVE TOTAL TENSION TENSION ACTIVE TENSION PASSIVE TENSION EQUILIBRIUM LENGTH LENGTH LENGTH OPTIMAL LENGTH (Lo) RESTING LENGTH TENSION SARCOMERE LENGTH () CARDIAC MUSCLE TOTAL TENSION ACTAIVE TENSION TENSION PASSIVE TENSION MUSCLE LENGTH HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase After-load PRESSURE Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE Pre-load End Systolic Volume End Diastolic Volume HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase After-load PRESSURE Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE Pre-load End Systolic Volume End Diastolic Volume HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase After-load PRESSURE Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE Pre-load End Systolic Volume End Diastolic Volume HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase After-load PRESSURE Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE Pre-load End Systolic Volume End Diastolic Volume CARDIAC FUNCTION CURVE Cardiac Output = Stroke Volume x Heart Rate STROKE VOLUME If: Constant Then:  CO reflects SV DIASTOLIC FILLING Right Atrial Pressure (RAP) reflects Diastolic Filling CARDIAC FUNCTION CURVE THE FRANK- STARLING “LAW OF THE HEART” CARDIAC OUTPUT (L/min) 15- 10Pressure Volume -4 0 +4 RAP mmHg +8 5- CARDIAC FUNCTION CURVE THE FRANK- STARLING “LAW OF THE HEART” CARDIAC OUTPUT (L/min) 15- 10- 5- -4 0 +4 RAP mmHg +8 CARDIAC FUNCTION CURVE THE FRANK- STARLING “LAW OF THE HEART” CARDIAC OUTPUT (L/min) 15- 10- 5- -4 0 +4 RAP mmHg +8 CARDIAC FUNCTION CURVE THE FRANK- STARLING “LAW OF THE HEART” CARDIAC OUTPUT (L/min) 15- 10- 5- -4 0 +4 RAP mmHg +8 CARDIAC FUNCTION CURVE THE FRANK- STARLING “LAW OF THE HEART” CARDIAC OUTPUT (L/min) 15- 10- 5- -4 0 +4 RAP mmHg +8 P1 > P2 P1 mm Hg FLOW = P R R= L/min or ml/sec FLOW P2 P = FLOW x R P FLOW mm Hg ml/sec Peripheral Resistance Units (PRU) LAMINAR or STREAMLINE FLOW P1 P1 > P2 -Cone Shaped Velocity Profile -Not Audible with a Stethoscope P2 MEASURING BLOOD PRESSURE TURBULENT FLOW 1. 2. 3. 4. Cuff pressure > systolic blood pressure--No sound. The first sound is heard at peak systolic pressure. Sounds are heard while cuff pressure < blood pressure. Sound disappears when cuff pressure < diastolic pressure. RESISTANCES IN SERIES RT = RA + RC + RV RESISTANCES IN PARALLEL FlowT = Flow1 + Flow2 + Flow3 P = P + P + P RT R1 R2 R3 1 = 1 + 1 + 1 RT R1 R2 R3 RT = 1 1 + 1 + 1 R1 R2 R3 R1 PV R2 PA R3 If: R1 = 2; R2 = 4; R3 = 6 PRU’s Then a series arrangement gives: RT = R1 + R2 + R3 RT = 12 PRU’s But a parallel arrangement gives: 1 RT = 1 1 + 1 =1.94 PRU’s + R1 R2 R3 Poiseuille's Law P Flow = R v = Pr2 /8l Q = vr2 Pr4 Q = 8l R = 8l/r4 TOTAL PERIPHERAL RESISTANCE SYSTEMIC CIRCULATION: TPR = Aortic Pressure - RAP FLOW TPR = 100 - 0 mmHg = 1.2 PRU’s 83.3 ml/sec (5 L/min) PULMONARY CIRCULATION: Pul. R. = Pul. Art. P. - LAP FLOW Pul. R. = 15 - 5 mmHg = 0.12 PRU’s 83.3 ml/sec VASCULAR COMPLIANCE PRESSURE (mmHg) V C= P Arteries ml Ca = 250 mmHg =2.5 ml/mmHg 100 100Sym Cv = 300 ml = 60 ml/mmHg 5 mmHg Sym Cv = 24 x Ca Veins Sym 1 2 3 Sym 4 VOLUME (L) MEAN CIRCULATORY PRESSURE PRESSURE (mmHg) Unstressed Volume 7MCP = 7 mmHg Stressed Volume 1 2 3 4 VOLUME (L) 5 6 CAPILLARIES • Pressure inside is 35 to 15 mmHg • 5% of the blood is in capillaries • exchange of gases, nutrients, and wastes • flow is slow and continuous Arteriole Capillaries Precapillary Sphincters Metarteriole ? Venule VASOMOTION = Intermittent flow due to constrictionrelaxation cycles of precapillary shpincters or arteriolar smooth muscle (5 - 10/min) AUTOREGULATION OF VASOMOTION: 1. Oxygen Demand Theory (Nutrient Demand Theory) O2 is needed to support contraction (closure) 2. Vasodilator Theory Vasodilator substances produced (via  O2) e.g. Adenosine  Heart CO2  Brain Lactate, H+, K+  Skeletal Muscle 3. Myogenic Activity DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID Plasma Proteins BLOOD INTERSTITIAL FLUID CELL O2 CO2 Glucose active transport FLUID BALANCE Filtration vs. Reabsorption 40Outward Forces: 1. Capillary blood pressure (Pc = 35 to 15 mmHg) 302. Interstitial fluid pressure (PIF = 0 mmHg) 3. Interstitial fluid colloidal 20osmotic pressure (IF = 3 mmHg) 10TOTAL = 38 to 18 mmHg Inward Force: 1. Plasma colloidal osmotic pressure (C = 28 mmHg) PRESSURE (mmHg) 0- CAPILLARY FLUID SHIFT Pout > c Pout < c Pc Pc FAVORS FILTRATION FAVORS REABSORPTION PULMONARY CIRCULATION FLUID BALANCE Filtration vs. Reabsorption 40PRESSURE (mmHg) 30Via lymphatics 20- Filtration 10- Reabsorption RADIAL FLOW 0- LYMPHATIC CAPILLARY 2 - 4 L/day ( 125 ml/hr) “PUMP” Compression Smooth muscle contraction Anchoring Filaments Effects of gravity on arterial and venous pressures. Each cm of distance produces a 0.77 mmHg change. Veins Arteries 0 100 mm Hg 190 mm Hg Sphincters protect capillaries VENOUS PUMP keeps PV < 25 mm Hg HEART  Art. BP VEINS (RAP) 7 mmHg  CO = PBF  RAP ARTERIES 7 mmHg Peripheral Blood Flow RELATIONSHIP BETWEEN RAP and PBF Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR (mmHg) (mmHg) (mmHg) (mmHg) (PRU’s) (ml/sec) 7 7 6 5 4 3 7 31 55 79 103 0 25 50 75 100 1.2 1.2 1.2 1.2 1.2 0 20.8 41.7 62.5 83.3 (5 L/min) 0 THE VASCULAR FUNCTION CURVE 10- PBF or VENOUS RETURN 5(L/min) 0-4 0 +4 RAP (mmHg) +8 WAYS TO ALTER THE VASCULAR FUNCTION CURVE • CHANGE THE MEAN CIRCULATORY PRESSURE • CHANGE BLOOD VOLUME • CHANGE VENOUS CAPACITY • CHANGE TOTAL PERIPHERAL RESISTANCE MEAN CIRCULATORY PRESSURE PRESSURE (mmHg) Unstressed Volume Infusion Normal Hemorrhage Stressed Volume  VOLUME  MCP  VOLUME  MCP 7- 1 2 3 4 5 BLOOD VOLUME (L) 6 MEAN CIRCULATORY PRESSURE VENOCONSTRICTION PRESSURE (mmHg) Unstressed Volume 7Normal Stressed Volume 1 2 3 4 5 BLOOD VOLUME (L) 6 MEAN CIRCULATORY PRESSURE VENODILATION PRESSURE (mmHg) Unstressed Volume 7Normal Stressed Volume 1 2 3 4 5 BLOOD VOLUME (L) 6 RELATIONSHIP BETWEEN RAP and PBF Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR (mmHg) (mmHg) (mmHg) (mmHg) (PRU’s) (ml/sec) 7 7 6 5 4 3 8 7 6 5 4 3 0  MCP 8 7 31 55 79 103 8 32 56 80 104 128 0 25 50 75 100 0 25 50 75 100 125 1.2 1.2 1.2 1.2 1.2 1.2 1.2 1.2 1.2 1.2 1.2 0 20.8 41.7 62.5 83.3 (5 L/min) 0 20.8 41.7 62.5 83.3 (5 L/min) 104.2 (6.25 L min 0 THE VASCULAR FUNCTION CURVE 10 Blood Volume or Venoconstriction PBF or VENOUS RETURN 5(L/min)  Blood Volume or Venodilation 0-4  MCP  MCP 0 +4 RAP (mmHg) +8 RELATIONSHIP BETWEEN RAP and PBF Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR (mmHg) (mmHg) (mmHg) (mmHg) (PRU’s) (ml/sec) 7 7 6 5 4 3 7 6 5 4 3 0  TPR 7 7 31 55 79 103 7 31 55 79 103 0 25 50 75 100 0 25 50 75 100 1.2 1.2 1.2 1.2 1.2 2.0 2.0 2.0 2.0 2.0 0 20.8 41.7 62.5 83.3 (5 L/min) 0 12.5 25.0 37.5 50.0 (3 L/min) 0 THE VASCULAR FUNCTION CURVE 10- Vasodilation  TPR PBF or VENOUS RETURN 5(L/min) Vasoconstriction 0-  TPR -4 0 +4 RAP (mmHg) +8 CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15OUTPUT or 10- PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mmHg +8 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 Chemosensitive Area MOTOR CORTEX HYPOTHALAMUS Glossopharyngeal Nerve VASOMOTOR CENTER PRESSOR AREA DEPRESSOR AREA CARDIOINHIBITORY AREA Vagus HEART Sympathetic Nervous System Baroreceptors Carotid Sinus Aortic Arch Arterioles Veins Adrenal Medulla Chemoreceptors Carotid Bodies Aortic Bodies Atrial Receptors Bainbridge Reflex ( Heart Rate) Volume Reflex ( Urinary OUTPUT) a.  Vascular Sympathetic Tone b.  ADH Secretion c.  Aldosterone Secretion RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM Angiotensinogen (renin substrate)  BP (Kidney) Renin Angiotensin Vasoconstriction Venoconstriction Aldosterone Kidney  sodium & water retention HORMONAL REGULATION • Epinephrine & Norepinephrine – From the adrenal medulla • Renin-angiotensin-aldosterone – Renin from the kidney – Angiotensin, a plasma protein – Aldosterone from the adrenal cortex • Vasopressin (Antidiuretic Hormone-ADH) – ADH from the posterior pituitary VASOPRESSIN (ANTIDIURETIC HORMONE) Hypothalamic Osmoreceptors  BP via Posterior Pituitary  Vasopressin (ADH) X (Atrial Receptors) X Vasoconstriction  Water Venoconstriction Retention RENAL--BODY FLUID CONTROL MECHANISM 8- All Mechanisms 76Fluid 5Intake 4(x normal) 3- 3 x Normal 21- Normal -8 -7 -6 Uninary -5 Output -4 (x normal) -3 P alone -2 -1 50 100 150 ARTERIAL BLOOD PRESSURE (mmHg) 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 HEMORRHAGE 7CO or PBF 1 2 3 4 5 (L/min) Blood Volume (L) Pressure MCP CO BP -4 0 +4 +8 RAP (mmHg) CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15OUTPUT or 10Response to Hemorrhage  HR & Contractility Venoconstriction ( MCP) Vasoconstriction ( TPR) PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mmHg +8 RESPONSE TO HEMORRHAGE •  Sympathetic tone via baroreceptor reflex –  Heart rate and contractility – Venoconstriction ( MCP) – Vasoconstriction ( arterial BP & direct blood to vital organs) • Restore Blood Volume – Capillary fluid shift ( BP favors reabsorption) –  Urinary output ( Arterial BP, ADH, ReninAngiotensin-Aldosterone) • Restore plasma proteins & hematocrit SYNCOPE (FAINTING) Postural syncope (Blood pooling in the extremities) Vasovagal syncope Carotid sinus syncope SYNCOPE (FAINTING) Blood pooling in the extremities PRESSURE (mmHg) Unstressed Volume 7Normal Syncope (Fainting)  Unstressed Vol.  Stressed Vol.  MCP Stressed Volume 1 2 3 4 5 BLOOD VOLUME (L) 6 SYNCOPE (FAINTING) Blood pooling in the extremities 7CO or PBF 1 2 3 4 5 (L/min) Blood Volume (L) Pressure MCP CO BP -4 0 +4 +8 RAP (mmHg) CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15OUTPUT or 10Response to Syncope (Fainting  HR & Contractility Venoconstriction ( MCP) Vasoconstriction ( TPR) PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mmHg +8 CARDIAC FAILURE CAUSES: Impairment of electrical activity Muscle damage Valvular defects Cardiomyopathies Result of drugs or toxins PROBLEM: Maintaining circulation with a weak pump ( Cardiac output & cardiac reserve;  RAP) SOLUTIONS:  Sympathetic tone via baroreceptor reflex - Heart rate and contractility -Venoconstriction ( MCP) -Vasoconstriction ( Arterial BP) Fluid retention ( MCP) -Capillary fluid shift -ADH -Renin-angiotensin-aldosterone CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15OUTPUT or 10SYMPTOMS: Systemic Edema Pulmonary Congestion Enlarged Heart Adjustments to Failure PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 Cardiac Failure 0 +4 RAP mmHg +8 HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase After-load PRESSURE Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE Pre-load End Systolic Volume End Diastolic Volume TEMPERATURE REGUALTION • • • • Body Temperature Heat Production Heat Loss Temperature Regulation – Heat Exhaustion – Heat Stroke – Hypothermia • Fever WARM COLD Temperature regulation seriously impaired Temperature regulation efficient in febrile disease health and work Temperature regulation impaired Upper limit of survival? Heat stroke Brain lesions Fever therapy Febrile disease and Hard exercise Usual range of normal Temperature regulation lost Lower limit of survival? 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) HEAT LOSS COOL RADIATION CONDUCTION CONVECTION VAPORIZATION Insensible Water Loss Sweating 70% HOT   * * 30% * SKIN HYPOTHALAMUS Preoptic Area W Set W point Sweating Vasodilation Vasoconstriction Shivering Warm Receptors W Cold Receptors C 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. 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 Temperature regulation lost Symptoms: high body temperature NO sweating dizziness or loss of consciousness Body temperature MUST be lowered! Heat Stroke: FEVER FEVER = an abnormally high body temperature PYROGEN = a fever producing substance PYROGEN WBC bacterial toxins, leukocytes, viruses, pollen, + monocytes proteins, dust = endogenous pyrogen Arachidonic Acid Prostaglandins Aspirin RAISES THE “SET POINT” Shivering Vasoconstriction Sweating Vasodilation Reference Temperature or Set Point Actual Core Temperature Onset of Fever Fever Breaks