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

Na
Gradually increasing PNa

AUTOMATICITY

+
K+

Na+

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

MEMBRANE POTENTIAL (mV)

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 3 4 = Resting Potential

-90 TIME

4

ACTION POTENTIALS

MEMBRANE POTENTIAL (mV)

0

VENTRICULULAR CELL 1 2

SAN 0 0 3

-50

0

3 4

-50

4

-100

-100

SINGLE VENTRICULAR ACTION POTENTIAL ENDOCARDIAL FIBER EPICARDIAL FIBER R 1 mV ECG P T QS Repolarization of ventricles Depolarization of ventricles

ATRIAL FIBER

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

Sternum V1 V2 V3

V6 V5 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 VENTRICLE PRESSURE ECG PHONOCARDIOGAM SYSTOLE DIASTOLE SYSTOLE

VOLUME (ml)

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

. CARDIAC OUTPUT (Q) = =

VO2 [O2]a - [O2]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 Mitochondria Sarcolemma

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

EQUILIBRIUM LENGTH LENGTH LENGTH

PASSIVE TENSION OPTIMAL LENGTH (Lo) RESTING LENGTH

TENSION

SARCOMERE LENGTH (µ )

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 End Diastolic Volume

Pre-load End Systolic Volume

HEART D Y SE IT EA TIL SYSTOLIC PRESSURE CURVE CR AC IN R NT CO Isotonic (Ejection) Phase
After-load

PRESSURE

Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

Pre-load End Systolic Volume

HEART ED TY AS ILI SYSTOLIC PRESSURE CURVE RE CT C A DE TR ON C Isotonic (Ejection) Phase
After-load

PRESSURE

Isovolumetric Phase Stroke Volume

Pre-load End Systolic Volume

DIASTOLIC PRESSURE CURVE

End Diastolic Volume

IN C FI RE LL A I N SE G D

HEART
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase After-load

PRESSURE

Isovolumetric Phase Stroke Volume DIASTOLIC PRESSURE CURVE End Diastolic Volume

Pre-load End Systolic 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-

10-

5-

Pressure
Volume -4 0 +4 RAP mmHg +8

CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min)

15-

10-

Inc Co rease ntr d act ilit

y

5-

-4

0 +4 RAP mmHg

+8

CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min)

15-

10-

De c Co reas ntr ed act ilit y

5-

-4

0 +4 RAP mmHg

+8

CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min)

15-

10-

Inc He rease art d Ra te

5-

-4

0 +4 RAP mmHg

+8

CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min)

15-

10-

De c He reas art ed Ra te

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 R3 PA

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 / 8η l Q= vπ r2 Q= ∆ Pπ r
4

8η l R= 8η l/π 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 Ca = 250 ml 100 mmHg =2.5 ml/mmHg 100- ↑Sym Cv = 300 ml = 60 ml/mmHg 5 mmHg ↓Sym Cv = 24 x Ca Veins ↑Sym 1 ↓Sym 2 3 VOLUME (L) 4

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 Metarteriole Precapillary Sphincters

?

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 BLOOD INTERSTITIAL FLUID CELL Plasma Proteins

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 (µ IF = 3 mmHg) 100TOTAL = 38 to 18 mmHg Inward Force: 1. Plasma colloidal osmotic pressure (µ C = 28 mmHg)

PRESSURE (mmHg)

CAPILLARY FLUID SHIFT
Pout > π
c

Pout < π

c

↑Pc

↓Pc

FAVORS FILTRATION

FAVORS REABSORPTION PULMONARY CIRCULATION

FLUID BALANCE Filtration vs. Reabsorption 40-

PRESSURE (mmHg)

30Via lymphatics 2010RADIAL FLOW 0Filtration Reabsorption

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 10PBF 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 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 ↑ MCP 8

0

THE VASCULAR FUNCTION CURVE 10PBF or VENOUS RETURN 5(L/min) ↓ Blood Volume or Venodilation 0↑ MCP ↑ Blood Volume or Venoconstriction

↓ MCP -4 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 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 ↑ TPR 7

0

THE VASCULAR FUNCTION CURVE 10PBF or VENOUS RETURN 5(L/min) Vasoconstriction 0Vasodilation ↓ TPR

↑ 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 Arterioles

Sympathetic Nervous System

Baroreceptors Carotid Sinus Aortic Arch Chemoreceptors Carotid Bodies Aortic Bodies Atrial Receptors

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 76Fluid 5Intake (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 (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) -4

Pressure

↓MCP

↓CO ↓BP

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) -4

Pressure

↓MCP

↓CO ↓BP

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 Cardiac Failure

PERIPHERAL BLOOD FLOW [Venous Return] 5(L/min) -4

0 +4 RAP mmHg

+8

C IA E RD UR CA IL FA

HEART
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase After-load

PRESSURE

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 Temperature regulation impaired Temperature regulation lost

Upper limit of survival? Heat stroke Brain lesions Fever therapy Febrile disease and Hard exercise Usual range of normal

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% 30% * HOT ↓ ↑ * *

SKIN

HYPOTHALAMUS Preoptic Area W Set W point W C Vasoconstriction Shivering Sweating Vasodilation

Warm Receptors

Cold Receptors

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 Reference Temperature or Set Point

Sweating Vasodilation

Actual Core Temperature

Onset of Fever

Fever Breaks

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