TSP Study

Overdampened Arterial line

flat looking wave form

Underdampened arterial line waveform

overly sharp

What does CVP measure

R) atrial and ventricular end diastolic pressure + venous return (preload)

Cardiac Conduction pathway

SA node
AV node
bundle of HIS
bundle branch
purkinje fibres

P wave represent + measurements

atrial depolarisation
<3 small squares

PR interval

time for conduction through atria to purkinje fibres
0.12-0.20

QRS

depolarisation of ventricles
normal <0.12

J point

junction between QRS and start of ST segment

ST elevation

infarct - tissue death

ST depression

ischaemia - mismatch of oxygen supply and demand

Lateral Leads

I

Inferior leads

II

Septal leads

V1

anterior leads

V3

junctional escape

40-60bpm
regular
abnormal P wave
PR <0.12
narrow QRS

ventricular escape/ idioventricular

20-40
absent p wave
no PR
wide QRS
accelerate >50

1st degree HB

constant prolonged PR interval

Second Degree Type 1 = Wenckebach

progressively lengthened PR

2nd Degree Type 2 - Mobitz 2

constant PR

complete heart block

no relationship between P and QRS

Inotrope

relates to force of contraction

chronotrope

relates to rate of contraction

dromotrope

speed of electrical impulse through AV node

vasopressor

drugs that cause vasoconstriction

what is BP made up of

cardiac output x systemic vascular resistance

What is cardiac output

amount of blood ejected from heart per minute
SV x HR

what is stroke volume

amount of blood ejected from LV per beat
preload

what is preload

amount of myocardial stretch at the end of diastole due to volume

what is contractility

force of myocardial contraction

what is afterload

amount of resistance ventricles must overcome to eject blood each beat

where are alpha 1 receptors located

blood vessels

where are beta 1 +2 receptors

beta 1 - heart
beta 2 - lungs + blood bessels

adrenaline MOA

mixed alpha and beta agonist
+ve inotrope

noradrenaline MOA

alpha 1 agonist
-ve inotrope

metaraminol MOA

potent alpha 1 agonist
mild beta 1 agonist
+inotrope

isoprenaline MOA

beta agonist
+ve chronotrope

dobutamine MOA

beta 1 agonist
+ve chronotrope and inotrope
vasodilation

vasopressin MOA

synthetic antidiuretic hormone

what is a shunt

alveoli cannot ventilate due to lack of area

what is a dead space

some alveoli are ventilated but not well perfused

cardiac blood flow

SCV - RA - TCV - RV - PValve- PA
PVein - LA- MV - LV - AV - Aorta

what is peep + benefits

amount of pressure left in the alveoli at the end of expiration
splints alveoli
increases alveolar surface area
increased FRC

what is pressure support + benefits

flow of gas that augments a patients spontaneously initiated breath
supports work of breathing

what is shock

inadequate delivery of oxygen to tissues causing anaerobic metabolism

initial stage of shock

imbalance between oxygen demand and supply leading to tissue hypoperfusion

compensatory phase

compensatory mechanisms activated to maintain CO

progressive phase

failure of compensatory mechanisms to maintain CO

refractory stage

MODS + irreversible tissue damage and cell death

RAAS System

kidneys release renin in response to low BP
stimulates liver to release angiotensin
angiotensin converted to angiotensin1
lungs secrete ACE
converts angiotensin 1 to angiotensin 2
angiotensin 2 causes adrenal glands to release ADH

hypovolemic shock

loss of circulating volume
decreased venous return + preload
decreased SV
decreased CO
decreased tissue perfusion

cardiogenic shock

abnormal cardiac function
myocardial insult
decreased pump efficiency
low SV

Hypovolaemic shock signs

high HR
low BP
low CO
high SVR
low CVP

cardiogenic shock signs

high hr
low BP
low CO
high SVR
high CVP

obstructive shock

obstruction or compression of heart interfering with filling or emptying
PE
tamponade
tension pneumothorax

obstructive shock signs

high HR
low BP
low CO
high SVR
high CO

septic shock signs

high HR
low BP
low CO
low SVR
low CVP

anaphylactic shock

high hr
low BP
low CO
low SVR
low CVP

neurogenic shock

spinal injury above T8 leading to dysregulated autonomic system

neurogenic shock signs

low HR
low BP
low CO
low SVR
low CVP

STEMI

occluded coronary artery which involves full thickness of myocardial tissue damage

NSTEMI

coronary artery becomes blocked - partial thickness myocardial wall damage

unstable angina

ischaemic chest pain occurring at rest

Angina

cardiac oxygen demand is greater than supply

6 'r's for ACS management

recognise
relieve symptoms
reperfusion
reduce complications
reduce recurrent events
rehabilitation

R) sided heart failure

inability to pump blood to lungs leading to build up of fluid in peripheries

L sided heart failure

inability to pump blood to peripheries

Systolic heart failure

HFrEF
LVEF <50%

Diastolic heart failure

HFpEF= LVEF >50%

frank starlings law

increased preload will equate to greater SV and greater CO

MV complications

barotrauma

s/s raised ICP

decreased conscious state

cushings triad - sign of increased ICP

systolic hypertension

circle of willis

A circle of arteries at the base of the brain that supply blood to the brain

layers of the brain outer to inner

dura matter
subdural space
arachnoid membrane
subarachnoid space
pia matter

focal seizures

start in area of network of cells
focal motor - convulsive
focal non-motor - non- convulsive

generalised seizures

occurs in both sides of the brain
generalised motor - tonic clonic
generalised non-motor - absent

monro-kellie hypothesis

volume-pressure relationship in the skull as it is a fixed space. There is 80% tissue

CPP formula

MAP-ICP

MAP formula

SBP+2(DBP)/3

causes of raised ICP

cerebral oedema

ALS adrenaline

administer immediately on non-shockable pathway
administer on second shock
ongoing every second round for both

HYPOXIA causes and treatment ALS

airway obstruction
respiratory failure
ventilate with BVM/ adjuncts
intubate

ALS HYPOVOLAEMIA causes and treatment

fluid loss
bleeding
burns
shock states
control fluid loss
replace like with like

ALS HYPER/HYPOKALAEMIA

Potassium chloride 5mmol slow push
Calcium Chloride 10mmol slow push CVC
Calcium gluconate 10mmol slow push peripheral
10U actrapid in 50ml 50% glucose

Symptomatic Bradycardia

Atropine 500-600mcg per bolus
Adrenaline infusion low dose
Isoprenaline infusion low dose

fixed pacing vs demand pacing

fixed paces the heart regardless of intrinsic activity

SVT

valsalva maneuver
adenoside 6mg/12mg/12mg
SCV

Kidney function

excretion of waste

Pre- renal AKI

impaired perfusion: cardiac failure

intra-renal AKI

direct damage to the kidneys by inflammation

post -renal AKI

urinary calculi

DKA

hyperglycaemia

manifestations of DKA

polyuria

HHS

hyperglycaemic state without presence of ketones

function of the pancreas

controls digestive process and blood sugar levels

pancreatitis

inflammation of the pancreas caused by premature activation of enzymes
most common causes are alcohol and gallstones

liver function

production of bile

Cirrhosis

diffuse fibrosis of the liver

hydrostatic pressure

push of fluid through capillary wall into interstitial space

oncotic pressure

pressure that pulls fluid into capillary