CARDIOVASCULAR PHYSIOLOGY Dr Poland Room 3 007 Sanger

CARDIOVASCULAR PHYSIOLOGY Dr. Poland Room 3 -007, Sanger Hall Phone: 828 -9557 E-mail: poland@hsc. vcu. edu

HEART (PUMP) REGULATION CARDIOVASCULAR SYSTEM VESSELS (DISTRIBUTION SYSTEM) AUTOREGULATION NEURAL HORMONAL RENAL-BODY FLUID CONTROL SYSTEM

PULMONARY CIRCULATION 1. LOW RESISTANCE 2. LOW PRESSURE (25/10 mm. Hg) SYSTEMIC CIRCULATION 1. HIGH RESISTANCE 2. HIGH PRESSURE (120/80 mm. Hg) PARALLEL SUBCIRCUITS UNIDIRECTIONAL FLOW

ARTERIES (LOW COMPLIANCE) HEART DIASTOLE VEINS CAPACITY VESSELS 80 mm. Hg 120 mm. Hg SYSTOLE CAPILLARIES

THE SYSTEMIC CIRCULATION CAPACITY VESSELS

NORMAL

AUTOMATICITY Na+ K+ Gradually increasing PNa Na+ + K -70 m. V THRESHOLD RESTING -0

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

MEMBRANE POTENTIAL (m. V) 0 PHASE 0 = Rapid Depolarization Mechanical Response (inward Na+ current) 1 1 = Overshoot 2 2 = Plateau (inward Ca++ current) 3 = Repolarization + current) (outward K 0 4 = Resting Potential 3 4 -90 TIME

MEMBRANE POTENTIAL (m. V) ACTION POTENTIALS 0 VENTRICULULAR CELL 1 2 SAN 0 0 -50 0 3 -50 4 -100 4 3

SINGLE VENTRICULAR ACTION POTENTIAL ENDOCARDIAL FIBER ATRIAL FIBER EPICARDIAL FIBER R 1 m. V ECG P T QS Repolarization 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: a. VR = (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: a. VR = (LA-LL) vs. RA(+) a. VL = (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: a. VR = (LA-LL) vs. RA(+) a. VL = (RA-LL) vs. LA(+) a. VF = (RA-LA) vs. LL(+) LL

6 PRECORDIAL (CHEST) LEADS Spine V 6 V 5 Sternum V 1 V 2 V 3 V 4

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 a. VR = (LA-LL) vs. RA(+) a. VL = (RA-LL) vs. LA(+) a. VF = (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.

THE CARDIAC CYCLE DIASTOLE ISOMETRIC VENTRICULAR RELAXATION VENTRICULAR EJECTION LATE DIASTOLE ATRIAL SYSTOLE ISOMETRIC VENTRICULAR CONTRACTION

EJECTION PRESSURE (mm. Hg) ISOVOLUMETRIC RELAXATION RAPID INFLOW ISOVOLUMETRIC DIASTASIS CONTRACTION ATRIAL SYSTOLE AORTIC PRESSURE ATRIAL PRESSURE VOLUME (ml) VENTRICLE PRESSURE ECG PHONOCARDIOGAM SYSTOLE DIASTOLE SYSTOLE

MEASUREMENT OF CARDIAC OUTPUT THE FICK METHOD: VO 2 = ([O 2]a - [O 2]v) x Flow Spirometry (250 ml/min) VO 2 Flow = [O 2]a - [O 2]v Pulmonary Artery Blood (15 ml%) Arterial Blood (20 ml%) CARDIAC OUTPUT PULMONARY BLOOD FLOW VENOUS RETURN PERIPHERAL BLOOD FLOW

. VO 2 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 70 beats/min = 1. 6 m 2 = 0. 0714 L or 71. 4 ml = 3. 1 L/min/m 2

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 Mitochondria Sarcolemma T-tubule SR Fibrils

T-tubule SARCOLEMMA 20% 80% Mitochondria 10% Ca++ SR 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 Fast Heart Rate Ca++ Ca++

SERIES ELASTIC ELEMENTS CONTRACTILE COMPONENT PARALLEL ELASTIC ELEMENTS (ACTIVE TENSION) (PASSIVE TENSION) TOTAL TENSION

LENGTH-TENSION CURVE TOTAL TENSION ACTIVE TENSION EQUILIBRIUM LENGTH PASSIVE TENSION OPTIMAL LENGTH (Lo) RESTING LENGTH

TENSION SARCOMERE LENGTH ( )

CARDIAC MUSCLE TOTAL TENSION ACTAIVE TENSION PASSIVE TENSION MUSCLE LENGTH

HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase PRESSURE After-load Isovolumetric Phase Stroke Volume Pre-load End Systolic Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

HEART D Y E IT S A IL E SYSTOLIC PRESSURE CURVE R CT C IN TRA N O C Isotonic (Ejection) Phase PRESSURE After-load Isovolumetric Phase Stroke Volume Pre-load End Systolic Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

HEART D Y E S IT A E TIL SYSTOLIC PRESSURE CURVE R C AC E D TR N O C Isotonic (Ejection) Phase PRESSURE After-load Isovolumetric Phase Stroke Volume Pre-load End Systolic Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

IN C FI RE LL A IN SE G D HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase PRESSURE After-load Isovolumetric Phase Stroke Volume Pre-load End Systolic Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

CARDIAC FUNCTION CURVE STROKE VOLUME Cardiac Output = Stroke Volume x Heart Rate If: Constant Then: CO reflects SV DIASTOLIC FILLING Right Atrial Pressure (RAP) reflects Diastolic Filling

CARDIAC FUNCTION CURVE 15 - 10 Pressure CARDIAC OUTPUT (L/min) THE FRANK- STARLING “LAW OF THE HEART” 5 - Volume -4 0 +4 RAP mm. Hg +8

CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) THE FRANK- STARLING “LAW OF THE HEART” 15 - Inc Co rease ntr d act ilit y 10 - 5 - -4 0 +4 RAP mm. Hg +8

CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) THE FRANK- STARLING “LAW OF THE HEART” 15 - De c Co reas ntr ed act ilit y 10 - 5 - -4 0 +4 RAP mm. Hg +8

CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) THE FRANK- STARLING “LAW OF THE HEART” 15 - Inc He rease art d Ra te 10 - 5 - -4 0 +4 RAP mm. Hg +8

CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) THE FRANK- STARLING “LAW OF THE HEART” 15 - De c He reas art ed Ra te 10 - 5 - -4 0 +4 RAP mm. Hg +8

P 1 > P 2 P 1 mm Hg FLOW P 2 P = FLOW x R FLOW = P R R= L/min or ml/sec P FLOW mm Hg ml/sec Peripheral Resistance Units (PRU)

LAMINAR or STREAMLINE FLOW P 1 P 2 P 1 > P 2 -Cone Shaped Velocity Profile -Not Audible with a Stethoscope

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 = R A + R C + R V RESISTANCES IN PARALLEL Flow. T = Flow 1 + Flow 2 + Flow 3 P = P + P RT R 1 R 2 R 3 1 = 1 + 1 RT R 1 R 2 R 3 RT = 1 1 + 1 R 2 R 3 R 1 PV PA R 2 R 3

If: R 1 = 2; R 2 = 4; R 3 = 6 PRU’s Then a series arrangement gives: RT = R 1 + R 2 + R 3 RT = 12 PRU’s But a parallel arrangement gives: 1 RT = 1 =1. 94 PRU’s 1 1 + + R 1 R 2 R 3

Poiseuille's Law v = Pr 2 /8 l P Flow = R Q = v r 2 P r 4 Q = 8 l R = 8 l/ r 4

TOTAL PERIPHERAL RESISTANCE SYSTEMIC CIRCULATION: TPR = Aortic Pressure - RAP FLOW TPR = 100 - 0 mm. Hg = 1. 2 PRU’s 83. 3 ml/sec (5 L/min) PULMONARY CIRCULATION: Pul. R. = Pul. Art. P. - LAP FLOW Pul. R. = 15 - 5 mm. Hg = 0. 12 PRU’s 83. 3 ml/sec

PRESSURE (mm. Hg) VASCULAR COMPLIANCE V C= P Arteries Ca = 250 ml =2. 5 ml/mm. Hg 100 - Sym Cv = 300 ml = 60 ml/mm. Hg 5 mm. Hg Sym Cv = 24 x Ca Veins Sym 1 2 3 VOLUME (L) Sym 4

PRESSURE (mm. Hg) MEAN CIRCULATORY PRESSURE Unstressed Volume Stressed Volume 7 MCP = 7 mm. Hg 1 2 3 4 VOLUME (L) 5 6

CAPILLARIES • Pressure inside is 35 to 15 mm. Hg • 5% of the blood is in capillaries • exchange of gases, nutrients, and wastes • flow is slow and continuous

Arteriole Precapillary Sphincters Capillaries 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) 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

DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID Plasma Proteins BLOOD INTERSTITIAL FLUID CELL O 2 CO 2 Glucose active transport

PRESSURE (mm. Hg) FLUID BALANCE Filtration vs. Reabsorption 40 Outward Forces: 1. Capillary blood pressure (Pc = 35 to 15 mm. Hg) 302. Interstitial fluid pressure (PIF = 0 mm. Hg) 3. Interstitial fluid colloidal 20 osmotic pressure ( IF = 3 mm. Hg) 100 - TOTAL = 38 to 18 mm. Hg Inward Force: 1. Plasma colloidal osmotic pressure ( C = 28 mm. Hg)

CAPILLARY FLUID SHIFT Pout > c Pc FAVORS FILTRATION Pout < c Pc FAVORS REABSORPTION PULMONARY CIRCULATION

FLUID BALANCE PRESSURE (mm. Hg) Filtration vs. Reabsorption 4030 Via lymphatics 20 - Filtration Reabsorption 10 RADIAL FLOW 0 -

LYMPHATIC CAPILLARY 2 - 4 L/day ( 125 ml/hr) Anchoring Filaments “PUMP” Compression Smooth muscle contraction

Effects of gravity on arterial and venous pressures. Each cm of distance produces a 0. 77 mm. Hg 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) CO = PBF RAP 7 mm. Hg ARTERIES 7 mm. Hg Peripheral Blood Flow

RELATIONSHIP BETWEEN RAP and PBF Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR (mm. Hg) (PRU’s) (ml/sec) 7 0 7 6 5 4 3 7 31 55 79 103 0 25 50 75 100 1. 2 1. 2 0 20. 8 41. 7 62. 5 83. 3 (5 L/min)

THE VASCULAR FUNCTION CURVE 10 PBF or VENOUS RETURN 5(L/min) 0 - -4 0 +4 RAP (mm. Hg) +8

WAYS TO ALTER THE VASCULAR FUNCTION CURVE • CHANGE THE MEAN CIRCULATORY PRESSURE • CHANGE BLOOD VOLUME • CHANGE VENOUS CAPACITY • CHANGE TOTAL PERIPHERAL RESISTANCE

PRESSURE (mm. Hg) MEAN CIRCULATORY PRESSURE 7 - Unstressed Volume Infusion Normal Stressed Volume Hemorrhage 1 2 3 4 5 BLOOD VOLUME (L) VOLUME MCP 6

MEAN CIRCULATORY PRESSURE (mm. Hg) VENOCONSTRICTION Unstressed Volume 7 - Stressed Volume Normal 1 2 3 4 5 BLOOD VOLUME (L) 6

MEAN CIRCULATORY PRESSURE (mm. Hg) VENODILATION Unstressed Volume 7 - Stressed Volume Normal 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 (mm. Hg) (PRU’s) (ml/sec) 7 0 MCP 8 0 7 6 5 4 3 7 31 55 79 103 0 25 50 75 100 1. 2 1. 2 0 20. 8 41. 7 62. 5 83. 3 (5 L/min) 8 7 6 5 4 3 8 32 56 80 104 128 0 25 50 75 100 125 1. 2 1. 2 0 20. 8 41. 7 62. 5 83. 3 (5 L/min) 104. 2 (6. 25 L min

THE VASCULAR FUNCTION CURVE 10 PBF or VENOUS RETURN 5(L/min) Blood Volume or Venodilation 0 - MCP Blood Volume or Venoconstriction MCP -4 0 +4 RAP (mm. Hg) +8

RELATIONSHIP BETWEEN RAP and PBF Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR (mm. Hg) (PRU’s) (ml/sec) 7 0 TPR 7 0 7 6 5 4 3 7 31 55 79 103 0 25 50 75 100 1. 2 1. 2 0 20. 8 41. 7 62. 5 83. 3 (5 L/min) 7 6 5 4 3 7 31 55 79 103 0 25 50 75 100 2. 0 2. 0 0 12. 5 25. 0 37. 5 50. 0 (3 L/min)

THE VASCULAR FUNCTION CURVE Vasodilation 10 PBF or VENOUS RETURN 5(L/min) Vasoconstriction 0 - TPR -4 0 +4 RAP (mm. Hg) +8

CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15 OUTPUT or 10 - PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mm. Hg +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

MOTOR CORTEX HYPOTHALAMUS Chemosensitive Area Glossopharyngeal Nerve Sympathetic Nervous System VASOMOTOR CENTER PRESSOR AREA DEPRESSOR AREA CARDIOINHIBITORY AREA Baroreceptors Carotid Sinus Aortic Arch Chemoreceptors Carotid Bodies Aortic Bodies Atrial Receptors Vagus HEART Arterioles Veins Adrenal Medulla 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 76 Fluid 5 Intake (x normal) 4 - 3 x Normal 321 - Normal -8 -7 -6 Uninary -5 Output -4 (x normal) -3 P alone -2 -1 50 100 150 ARTERIAL BLOOD PRESSURE (mm. Hg)

HYPERTENSION (140/90 mm. Hg) 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 Pressure 7 MCP CO or PBF 1 2 3 4 5 (L/min) Blood Volume (L) -4 CO BP 0 +4 +8 RAP (mm. Hg)

CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15 OUTPUT or 10 Response to Hemorrhage HR & Contractility Venoconstriction ( MCP) Vasoconstriction ( TPR) PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mm. Hg +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, Renin. Angiotensin-Aldosterone) • Restore plasma proteins & hematocrit

SYNCOPE (FAINTING) Postural syncope (Blood pooling in the extremities) Vasovagal syncope Carotid sinus syncope

PRESSURE (mm. Hg) SYNCOPE (FAINTING) Blood pooling in the extremities Unstressed Stressed Volume 7 - Normal Syncope (Fainting) 1 2 3 4 5 BLOOD VOLUME (L) Unstressed Vol. Stressed Vol. MCP 6

SYNCOPE (FAINTING) Blood pooling in the extremities Pressure 7 MCP CO or PBF 1 2 3 4 5 (L/min) Blood Volume (L) -4 CO BP 0 +4 +8 RAP (mm. Hg)

CARDIAC & VASCULAR FUNCTION CURVES CARDIAC 15 OUTPUT or 10 - Response to Syncope (Fainting HR & Contractility Venoconstriction ( MCP) Vasoconstriction ( TPR) PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4 0 +4 RAP mm. Hg +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 15 OUTPUT or SYMPTOMS: Systemic Edema Pulmonary Congestion Enlarged Heart 10 - PERIPHERAL BLOOD FLOW [Venous Return] 5 - Adjustments to Failure Cardiac Failure (L/min) -4 0 +4 RAP mm. Hg +8

C A I E D R UR A C IL FA HEART SYSTOLIC PRESSURE CURVE Isotonic (Ejection) Phase PRESSURE After-load Isovolumetric Phase Stroke Volume Pre-load End Systolic Volume DIASTOLIC PRESSURE CURVE 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 Upper limit of survival? Heat stroke Brain lesions Fever therapy Febrile disease and Hard exercise Usual range of normal Temperature regulation impaired 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 HOT 70% 30% * * *

SKIN HYPOTHALAMUS Preoptic Area W Warm Receptors Set W point W Cold Receptors Sweating Vasodilation C Vasoconstriction Shivering

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 Heat Stroke: Temperature regulation lost Symptoms: high body temperature NO sweating dizziness or loss of consciousness Body temperature MUST be lowered!

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 Reference Temperature or Set Point Onset of Fever Sweating Vasodilation Actual Core Temperature Fever Breaks