Applied Surgical Physiology Vivas - part 1 pdf

What happens to the stroke volume when standing up after a period of lying supine?. Explain why this change occurs Standing up increases the venous pooling of blood in the most dependent

Applied Surgical Physiology

Vivas

Applied Surgical Physiology Vivas

Mazyar Kanani BSc (Hons) MBBS (Hons) MRCS (Eng)

British Heart Foundation

Paediatric Cardiothoracic Clinical Research Fellow

Cardiac Unit Great Ormond Street Hospital for Children

London, UK

Martin Elliott MD FRCS

Consultant Cardiothoracic Surgeon

Chief of Cardiothoracic Surgery

Director of Transplantation and Tracheal Services Great Ormond Street Hospital for Children

London, UK

  

Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press

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2005

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A P P L I E D S U R G I C A L P H Y S I O L O G Y V I V A S

Muscle I – Skeletal and Smooth Muscle 97

Pancreas I – Endocrine Functions 111 Pancreas II – Exocrine Functions 115

Proximal Tubule and Loop of Henle 121

Stomach II – Applied Physiology 152

Synapses I – The Neuromuscular Junction (NMJ) 158 Synapses II – Muscarinic Pharmacology 161 Synapses III – Nicotinic Pharmacology 164

Ventilation/Perfusion Relationships 174

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LIST OF ABBREVIATIONS

ACh Acetylcholine

AChE Acetylcholinesterase

ACTH Adrenocorticotrophic hormone

ADH Antidiuretic hormone

ADP Adenosine diphosphate

ALT Alanine aminotransferase

ANP Atrial natriuretic peptide

ANS Autonomic nervous system

APTT Activated partial thromboplastin time

ARDS Adult respiratory distress syndrome

AST Aspartate aminotransferase

ATP Adenosine triphosphate

AV Atrioventricular

AVP Arginine vasopressin

BBB Blood-brain barrier

BMR Basal metabolic rate

BP Blood pressure

cAMP Cyclic adenosine monophosphate

CAT Choline acetyl transferase

CBF Coronary blood flow

CCK Cholecystokinin

cGMP Cyclic guanosine monophosphate

CNS Central nervous system

CO Cardiac output

COPD Chronic obstructive pulmonary disease

CPAP Continuous positive airway pressure

CRTZ Chemoreceptor trigger zone

CSF Cerebrospinal fluid

CVP Central venous pressure

DAG Diacylglycerol

DCT Distal convoluted tubule

DHEA Dehydroepiandrosterone

DOPA Dihydroxyphenylalanine

ECF Extracellular fluid

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LIST OF ABBREVIA

ECG/EKG Electrocardiogram

EGF Epidermal growth factor

EPSP Excitatory postsynaptic potential ERV Expiratory reserve volume FiO 2 Fraction of inspired oxygen FEV Forced expiratory volume FFA Free fatty acid

FRC Functional residual capacity FVC Force vital capacity

GDP Guanosine diphosphate

GFR Glomerular filtration rate GTP Guanosine triphosphate

IC Inspiratory capacity

ICF Intracellular fluid

IP 2 Inositol diphosphate

IP 3 Inositol triphosphate

IPSP Inhibitory postsynaptic potential IRV Inspiratory reserve volume IVC Inferior vena cava

MAP Mean arterial pressure

MEN Multiple endocrine neoplasia

MI Myocardial infarction

NMJ Neuromuscular junction

NO Nitric oxide

PAH Para-aminohippuric acid

PAP Pulmonary artery pressure PCT Proximal convoluted tubule PDGF Platelet-derived growth factor PNS Parasympathetic nervous system

PT Prothrombin time

PVR Pulmonary vascular resistance R-A-A Renin-angiotensin-aldosterone RBF Renal blood flow

RES Reticuloendothelial system RPF Renal plasma flow

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RV Residual volume

SIADH Syndrome of inappropriate ADH

SLE Systemic lupus erythematosus

SNS Sympathetic nervous system

SR Sarcoplasmic reticulum

SVR Systemic vascular resistance

TCA Tricarboxylic acid

TLC Total lung capacity

TLV Total lung volume

TSH Thyroid-stimulating hormone

VC Vital capacity

V/Q Ventilation/perfusion ratio

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To my daughter, Edel Roya Kanani

A well-known doctor once told me that “learning is the noblest form of begging” This is certainly what it feels like just before the MRCS exam when the brain labours with the weight of temporary information Physiology is not an inher-ently difficult subject – only made so by the unholy trinity of

a bad night on-call, dwindling time and a thick textbook

I hope that this book is the remedy to this unfortunate com-bination, and helps a little to play the game.

M.K M.J.E

January 2004

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A CHANGE IN POSTURE

Below is a set of graphs showing some cardiovascular

parameters during a change in posture from supine to

standing, and then to supine again.

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1 What happens to the stroke volume when standing

up after a period of lying supine? Explain why this

change occurs

Standing up increases the venous pooling of blood in

the most dependent parts of the body (Veins are, after

From Smith J, Bush J, Weidmeier V and Tristani Application of

impedance cardiography to study of postural stress Journal of

Applied Physiology, 29:133 The American Physiological Society, 1970

Time (min)

Systolic

Diastolic

1.0

1.0

0.8

0.6

1.0

60

100

Supine

Heart

rate

(beats/min)

Relative

stroke

volume

(ratio)

Relative

cardiac

output

(ratio)

Blood

pressure

(mmHg)

Relative

total

peripheral

resistance

(ratio)

Standing Supine

1.2

1.4

80

120

all, capacitance vessels.) This redistribution of blood causes a reduction in the intrathoracic blood volume returning to the heart Through the Frank-Starling mechanism, this causes a reduction in the stroke volume (by 30–40%) This rises again when going back to the supine position, in response to increased venous return

2 What happens to the arterial pressure during this period?

Despite changes in the physiologic environment and stroke volume, reflex responses ensure that there is little change in the arterial pressure

3 What is the physiologic relationship between the cardiac output (CO) and the arterial pressure

normally?

The arterial pressure is defined as the product of the

CO and the systemic vascular resistance (SVR) and may

be considered as the afterload An increase of this places

a negative feedback on any further rise in the CO

4 What physiologic mechanisms ensure that the arterial pressure is maintained after standing?

The changes that occur may be understood by considering the relationship of the arterial pressure to the heart rate and SVR

Arterial pressure⫽ CO ⫻ SVR

where CO⫽ heart rate ⫻ stroke volume

Arterial pressure⫽ heart rate ⫻ stroke volume ⫻ SVR

There is a fall in the stroke volume, so in order to main-tain the blood pressure (BP), the heart rate and the SVR

must increase

䊉 Carotid baroreceptor stimulation is reduced

following a fall in the pulse pressure on standing

∴

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This causes a reduction of vagal cardiac stimulation,

and an increase in sympathetic nervous system

(SNS) stimulation of the heart and peripheral

vasculature

䊉 There is, therefore, an increase in the heart rate by

15–20 beats per minute

䊉 Increased peripheral SNS activity stimulates

arteriolar vasoconstriction – increasing the SVR

䊉 There is also some venoconstriction, limiting the

amount of peripheral blood pooling

䊉 There is a sympathetically-mediated inotropic

effect on the myocardium, limiting the fall in the

stroke volume and CO

䊉 As a result of increases in the heart rate and SVR,

the arterial pressure may actually rise slightly on

standing

5 Give some common causes for postural hypotension.

䊉 Failure to increase the CO during standing

䊏 Simple vaso-vagal syncope

䊏 Fixed heart rate or bradycardia: ␤-blockers,

heart block, sick sinus syndrome

䊏 Myocardial diseases: cardiomyopathy, other

cardiac failure

䊉 Reduced stroke volume

䊏 Fixed afterload: aortic stenosis, pulmonary

embolism

䊏 Dehydration, diuretics

䊉 Reduced SVR

䊏 Vasodilator drugs, e.g ␣-blockers, nitrates,

antidepressants

䊏 Pregnancy

䊏 Sepsis

䊏 Autonomic failure, e.g chronic diabetes mellitus

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ACID-BASE

1 Define the pH.

The pH is ⫺log10[H⫹]

2 What is the pH of the blood?

7.36–7.44

3 Where does the Hⴙin the body come from?

Most of the H⫹in the body comes from CO2generated

by metabolism This enters solution, forming carbonic acid through a reaction mediated by the enzyme car-bonic anhydrase

Acid is also generated by

䊉 Metabolism of the sulphur-containing amino acids cysteine and methionine

䊉 Anaerobic metabolism, generating lactic acid

䊉 Generation of the ketone bodies: acetone,

acetoacetate and ␤-hydroxybutyrate

4 What are the main buffer systems in the intravascular, interstitial and intracellular compartments?

In the plasma the main systems are:

䊉 The bicarbonate system

䊉 The phosphate system (HPO4⫺⫹ H⫹S H2PO4⫺)

䊉 Plasma proteins

䊉 Globin component of haemoglobin

Interstitial: the bicarbonate system

Intracellular: cytoplasmic proteins.

5 What does the Henderson–Hasselbalch equation describe, and how is it derived?

This equation, which may be applied to any buffer sys-tem, defines the relationship between dissociated and

CO2⫹H2OSH CO2 3 SH+⫹HCO⫺3

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undissociated acids and bases It is used mainly to

describe the equilibrium of the bicarbonate system

The dissociation constant,

Therefore

Taking the log10

Taking the negative log, which expresses the pH, and

where ⫺log10K is the pK

Invert the term to remove the minus sign:

The [H2CO3] may be expressed as pCO2⫻ 0.23, where

0.23 is the solubility coefficient of CO2(when the pCO2

is in kPa)

The pK is equal to 6.1

pH⫽pK⫹log HCO⫺

H CO

10

3

pH

HCO

⫽pK⫺log10 H CO2 ⫺3

3

HCO

⫹

⫺

⫽log K10 ⫹

3

HCO

⫹

⫺

⫽K

3

H CO

⫽[ ⫹][ ⫺]

3

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Thus,

6 Which organ systems are involved in regulating acid-base balance?

The main organ systems are:

䊉 Respiratory system: this controls the pCO2through alterations in the alveolar ventilation Carbon

dioxide indirectly stimulates central chemoceptors (found in the ventro-lateral surface of the medulla oblongata) through H⫹released when it crosses the blood-brain barrier (BBB) and dissolves in the cerebrospinal fluid (CSF)

䊉 Kidney: this controls the [HCO3 ⫺], and is important for long-term control and compensation of acid-base disturbances

䊉 Blood: through buffering by plasma proteins and

haemoglobin

䊉 Bone: H⫹may exchange with cations from bone mineral There is also carbonate in bone that can be used to support plasma HCO3⫺levels

䊉 Liver: this may generate HCO3 ⫺and NH4 ⫹(ammonia)

by glutamine metabolism In the kidney tubules, ammonia excretion generates more bicarbonate

7 How does the kidney absorb bicarbonate?

There are three main methods by which the kidneys increase the plasma bicarbonate:

䊉 Replacement of filtered bicarbonate with

bicarbonate that is generated in the tubular cells

䊉 Replacement of filtered phosphate with bicarbonate that is generated in the tubular cells

䊉 By generation of ‘new’ bicarbonate from glutamine molecules that are absorbed by the tubular cell

pCO

0 23

10 2

.

+

×

3

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