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Critical Care Course > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Blood Pressure Equation

A

SV X HR X SVR = BP

SV= Stroke volume (blood in ventricle- PRELOAD) 60-120ml

HR= Heart rate (contractility, force and velocity of shortening and squeeze) 60-80bpm

SVR= Systemic vascular resistance (pressure during contraction- AFTERLOAD)

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2
Q

Cardiac Output Calculation

A

Stroke volume SV X Heart Rate HR

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3
Q

Frank-Starling Law

A

Stroke volume increases as ventricle volume increases

Increase of pressure = increase of cardiac output

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4
Q

Cardiac Output

A

The amount of blood ejected from the ventricles in one minuite

HR X SV = CO

4-6 L/min = normal for adult

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5
Q

Stroke Volume

A

Amount of blood ejected from ventricles each contraction

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6
Q

Systemic Vascular Resistance

A

Force of ventricle ejection against force of the arterial vessels
Normal values 900-1200 dyn/sec/cm5

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7
Q

Blood pressure control

A

Medulla Oblongata in brain stem

Cardiovascular centres:
Sympathetic increases HR and contractility
Parasympathetic decreases HR and contractility

Vasomotor centre- constriction control

Higher brain region- stress/anxiety

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8
Q

Blood pressure control- different receptors

A

Baroreceptors- detect pressure (stretch) in aortic arch/ R atrium

Chemoreceptors- monitor CO2/Po2 levels aortic arch

Higher Brain region in hypothalamus- fight/flight responses ie: stress or hot/cold

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9
Q

BP- RAAS system

A

Drop in BP
Reduced kidney perfusion
Kidneys secrete Renin
Renin in liver turns to Angiotensin 1
AG1 then converts into AG2 in lungs (where ACE is)
AG2 causes constriction to increase SVR and therefore CO= increase BP

AG2 also acts on adrenal cortex
Secretion of aldosterone
Reduced urine output and increases Na reabsorption

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10
Q

SEPSIS

A

Life threatening organ dysfunction caused by a disregulated host response

SIRS- systemic inflammatory response syndrome

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11
Q

SEPTIC SHOCK

A

Profound, circulatory, cellular and metabolic abnormalities

B- BLOOD CULTURE
U-URINE OUTPUT0.5ML/KG
F-FLUID RESUS 30ML/KG STAT
A-ANTIBIOTICS (within 1 hr)
L-LACTATE
O-OXYGEN 15L NRB SA02 >94%
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12
Q

SEPSIS MANAGEMENT

A
  • Fluid review
  • Low Tidal volume (6ml/kg)
  • Steroids
  • Glucose control <10
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13
Q

Fluid Resus

A

Osmolarity= hydration status/concentration osmotic particles
normally 275-300mmols/L

Isotonic fluid- Hartmans - same as inside and outside cell

Sodium Chloride- risk of hyperchloremic acidosis as Cl- is alkaloid, body removes by producing HC03 = free H+ ions (acidotic)

H+ + HCO3- = H2CO3 = H2O+O2

Hypotonic Fluid pulls fluid into cells

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14
Q

Electrical Activity of Heart

A

Sino Atrial node (SA) highest intrinsic rate -main pacemaker and influenced by Para and sympathetic system (75bpm)

Atrioventricular node (AV)- bridge between SA node- allows atrial contraction (40-60bpm)

Left and right bundle branch- allows ventricular contraction (20-40bpm)

Bundle of HIS

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15
Q

ECG Interpretation

A

p wave= atrial depolarisation <3ssq’s

QRS complex- ventricles depolarisation <3ssq’s

T wave= repolarisation of ventricles

U wave= bundle of his repolarisation

PR interval= delay in AV Node <3ssq’s

QRS if >3ssq’s - ventricle problem
Prolonged QT = sudden death/OHA (amiodarone can cause)

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16
Q

Blood flow through the heart

A 
Venacava brings blood to heart
through right atrium
through tricuspid valve
into right ventricle
out via pulmonary arteries
to lungs
Pulmonary veins bring blood back to heart from lungs
into left atrium
through mitral or bicuspid valve
into left ventricle 
through aortic valve
into aorta
out to rest of body
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17
Q

Main Veins

A 
Jugular
Subclavian
Pulmonary
Superior Vena Cava
Inferior Vena Cava
Hepatic Portal
Hepatic
Renal
Iliac
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18
Q

Main Arteries

A 
Jugular
Subclavian
Pulmonary
Aorta
Mesenteric
Renal
Iliac
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19
Q

Resting Potential

A

Isoelectric line on ECG
Maintained by Na+ pumps
No electrical activity

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20
Q

PQRS explained

A

SA node produces electrical impulse
This stops Na+ pump
So ions move across cells to create equilibrium
Like a Mexican wave- the electrical impulse passes from cell to cell
Depolarising (loosing +charge) as they go
Which creates an action potential = Depolarising
= PQRS complex

21
Q

T wave explained

A

As electrical impulse moves on, the previous cell which no longer has the impulse can reopen Na+ pump to produce an in equilibrium in + electrolytes out of the myocardial cells

This is repolarisation and is represented by the T wave (ventricle repolarisation)

22
Q

Important Electrolytes for myocardial function

A

K+
Mg++
Na+
Ca++

23
Q

Hypokalaemia in Heart function

A

Low K+
Increases electrical potential
Increasing risk of early/premature contractions
ie AF etc

24
Q

Hyperkalaemia in Heart function

A

Reduces electrical potential

can lead to asystole

25
P wave
P wave indicates atrial contraction Small, rounded and before QRS P-R interval 3-5 small squares (0.12-0.2 secs) PR interval delay in AV node
26
QRS Complex
Represents conduction of ventricles Spiked Q= 0.04 (1small square) QRS interval = <0.12 secs or 3 small squares
27
T wave
Represents repolarisation of Ventricles | Should start and end at isoelectric line
28
U Wave
Represents Bundle of His Repolarisation- mostly is not visible on ECG's small rounded positive deflection after T wave
29
Pre-Load
Stretch of ventricles at the end of diastole - meaning end diastolic volume So to Increase preload- increase stroke volume or cardiac output by More fluids or vasopressors To decrease preload - in cardiac failure patients maybe- diuretics and vasodilators GTN
30
Afterload
Pressure required for ventricles to pump the blood out of the heart To increase Afterload- need to increase SVR ie Vasopressors To decrease- vasodilators
31
Contractility
Strength of cardiac contraction/shortening
32
Cardiac Index
Normal CI 2.5-4.2L/min/m2
33
Physiological control of blood pressure
- Vasomotor (vessel control) - Cardiovascular centre= (sympathetic/parasympathetic) - Baroreceptors/chemoreceptors - Higher brain centres - Renin/Angiotensin - Aldosterone/ADH - Capillary fluid shift
34
Antidiuretic hormone (Vasopressin)
Reduction in plasma volume = Increase in osmotic pressure Receptors in heart and brain detect change ADH secreted by posterior pituitary gland Causes thirst kidneys conserve water to reduce urine output
35
Heart Rate on ECG
On ECG strip 5 large squares 1 seconds 30 large squares 6 seconds QRS complexes in 30 large squares X10= HR
36
Inotrope function
Increase contractility + HR= increased CO Positive inotropes = increase contractility ie dobutamine and adrenaline Negative= reduce contractility
37
Vasopressors Function
Cause vasoconstriction of vascular smooth muscle indicated in hypotension and shock due to low SVR- ie sepsis Short half life
38
Inotropes and Vasopressors
Usually catecholamines act on sympathetic nervous system Adrenoreceptors: Alpha 1= peripheries, renal and coronary = increase SVR Beta 1 = heart= Cardiac output Beta 2= lungs, peripheral and coronary = vasodilator reduce SVR
39
Inotrope Examples
Adrenaline- both alpha and beta 8mg in 100ml 5%dex 0-1mcg/kg/per Dobutamine Beta 1 and 2 can decrease after load 250mg in 50ml
40
Vasopressor Example
Meteraminol alpha 1 and some beta Noradrenaline alpha 1 and beta 1 Phenyleprhine alpha 1
41
Hypovolaemic shock
causes: haemorrhage, trauma, poor hydration, insensible loss signs: pale, clammy, HR elevated, low BP, oliguria
42
Cardiogenic Shock
Causes: MI, left ventricular failure and cardiac tamponade Signs: pale, clammy, cool, elevated HR, low BP, oliguria Reduces Stroke volume and cardiac output and increases SVR
43
Septic Shock
profound circulatory cellular and metabolic abnormalities Causes: meningitis, wound infections, pneumonia, bacteraemia signs: temp<36 >38.5, hr >90, tachypnoeic >20, altered mental state, hyperglycaemia, history or signs of infection, signs of organ dysfunction
44
SIRS
Systemic inflammatory response syndrome Indicates BUFALO
45
Sepsis Definition
Life threatening organ dysfunction caused by a dysregulated host response
46
MODS
Multiple organ dysfunction syndrome potentially reversible physiologic derangement of 2 or more organ systems
47
Anaphylactic Shock
Allergic reaction resulting in sudden drop in BP signs: flushed, warm, palpitations, difficulty breathing, wheeze, impending doom, bP low, sudden collapse causes a sudden drop in SVR and constriction in pulmonary bronchioles
48
Neurogenic Shock
Spinal chord injury Cessation of sympathetic nervous control over vasculature = vasodilation and reduced SVR treatment= vasopressors condition RARE

Critical Care Course (6 decks)

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