Cardiovascular Flashcards
Blood Pressure Equation
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)
Cardiac Output Calculation
Stroke volume SV X Heart Rate HR
Frank-Starling Law
Stroke volume increases as ventricle volume increases
Increase of pressure = increase of cardiac output
Cardiac Output
The amount of blood ejected from the ventricles in one minuite
HR X SV = CO
4-6 L/min = normal for adult
Stroke Volume
Amount of blood ejected from ventricles each contraction
Systemic Vascular Resistance
Force of ventricle ejection against force of the arterial vessels
Normal values 900-1200 dyn/sec/cm5
Blood pressure control
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
Blood pressure control- different receptors
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
BP- RAAS system
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
SEPSIS
Life threatening organ dysfunction caused by a disregulated host response
SIRS- systemic inflammatory response syndrome
SEPTIC SHOCK
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%
SEPSIS MANAGEMENT
- Fluid review
- Low Tidal volume (6ml/kg)
- Steroids
- Glucose control <10
Fluid Resus
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
Electrical Activity of Heart
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
ECG Interpretation
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)
Blood flow through the heart
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
Main Veins
Jugular Subclavian Pulmonary Superior Vena Cava Inferior Vena Cava Hepatic Portal Hepatic Renal Iliac
Main Arteries
Jugular Subclavian Pulmonary Aorta Mesenteric Renal Iliac
Resting Potential
Isoelectric line on ECG
Maintained by Na+ pumps
No electrical activity
PQRS explained
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
T wave explained
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)
Important Electrolytes for myocardial function
K+
Mg++
Na+
Ca++
Hypokalaemia in Heart function
Low K+
Increases electrical potential
Increasing risk of early/premature contractions
ie AF etc
Hyperkalaemia in Heart function
Reduces electrical potential
can lead to asystole
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
QRS Complex
Represents conduction of ventricles
Spiked
Q= 0.04 (1small square)
QRS interval = <0.12 secs or 3 small squares
T wave
Represents repolarisation of Ventricles
Should start and end at isoelectric line
U Wave
Represents Bundle of His Repolarisation- mostly is not visible on ECG’s
small rounded positive deflection after T wave
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
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
Contractility
Strength of cardiac contraction/shortening
Cardiac Index
Normal CI 2.5-4.2L/min/m2
Physiological control of blood pressure
- Vasomotor (vessel control)
- Cardiovascular centre= (sympathetic/parasympathetic)
- Baroreceptors/chemoreceptors
- Higher brain centres
- Renin/Angiotensin
- Aldosterone/ADH
- Capillary fluid shift
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
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
Inotrope function
Increase contractility + HR= increased CO
Positive inotropes = increase contractility ie dobutamine and adrenaline
Negative= reduce contractility
Vasopressors Function
Cause vasoconstriction of vascular smooth muscle
indicated in hypotension and shock due to low SVR- ie sepsis
Short half life
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
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
Vasopressor Example
Meteraminol alpha 1 and some beta
Noradrenaline alpha 1 and beta 1
Phenyleprhine alpha 1
Hypovolaemic shock
causes: haemorrhage, trauma, poor hydration, insensible loss
signs: pale, clammy, HR elevated, low BP, oliguria
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
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
SIRS
Systemic inflammatory response syndrome
Indicates BUFALO
Sepsis Definition
Life threatening organ dysfunction caused by a dysregulated host response
MODS
Multiple organ dysfunction syndrome
potentially reversible physiologic derangement of 2 or more organ systems
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
Neurogenic Shock
Spinal chord injury
Cessation of sympathetic nervous control over vasculature
= vasodilation and reduced SVR
treatment= vasopressors
condition RARE
