Pathophysiology Flashcards
Stroke volume
Difference between end diastolic and end systolic
Amount of blood pumped out of heart with each beat
Cardiac output
Amount pumped in 1 min
=SVxHR
Affected by-
Tachycardia (ventricles can’t fill)
Contractility (decrease causes ventricle pressure to increase)
Preload (over stretch causes poor contractility
Afterload
Preload
Amount of cardiac muscle fibre and stretch that exists at the end of diastole (amount of blood in ventricle once atria contract)
Affected by amount of blood returning to heart
Afterload
Force ventricles must overcome to eject blood. Pressure in arterial system ahead of ventricles
Affected by hypertension and vascular contraction
Cardiac index
Body surface area divided by CO
Ejection fraction
Stroke volume divided by end diastolic volume
Normal range 50-70%
Peripheral/systemic vascular resistance
Determined by-
Blood viscosity, length of vessel, diameter of vessel
Affected by:
SNS- baroreceptors (aortic/carotid) signal SNS via cardiovascular control centre in medulla to increase HR/CO and constrict arterioles
Circulating adrenaline/noradrenaline from adrenal cortex
Renin-angiotensin-aldosterone system. Responds to renal perfusion, if drop occurs then renin is released which converts angiotensinogen to angiotensin 1, this is converted to angiotensin 2 (vasoconstrictor) by ACE in the lungs. Promotes sodium and water retention- increasing SVR and CO
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) released from atrial cells In response to stretching by excess blood volume- promotes vasodilation and water/sodium excretion
Adrenomedullin- peptide synthesised and released by endothelial and smooth muscle cells in blood vessels (vasodilator)
Vasopressin or ADH- promotes water retention and vasoconstriction
Local factors- inflammatory mediators and various metabolites promote vasodilation
Mean arterial pressure- measure of tissue perfusion
COx PVR 2x diastolic + systolic / 3 Normal 70-90 <50 organs not getting perfused >105 HT or vasoconstriction
Factors affecting BP
Sympathetic/parasympathetic systems
Baroreceptors/chemoreceptors
Kidneys-water level
Temperature- vasoconstriction/vasodilation
Chemicals/hormones/drugs
Dietary-salt, fat, cholesterol
Race, gender, age, weight, time of day, position, exercise, emotions
Cardiac adaptions
Franks starling- stroke volume increases when venous return increases
Hormones
Sympathetic Nervous system
Hypertrophy
Renin-angiotensin-aldosterone system
ADH- increase water reabsorption and thirst
Endothelin- vasoconstrictor peptides produced by vascular endothelium and cardiac myocytes
ANP (atria)/ BNP (ventricles)- tirggered by stretch in vessels- vasodilates, promotes water and sodium excretion
Nitric oxide- endothelial cells- vasodilator
Cardiac output compensations
Reduced CO stimulates aortic baroreceptor which stimulates sympathetic nervous system- release adrenaline
Adrenaline increases HR and vasoconstriction
Vasoconstriction increases venous return
Increased venous return increases myocardial stretch and force of contraction
If low CO then no renal perfusion as redistributed to brain/heart/lungs.
Kidneys activate renin-angiotensin-aldosterone system
Renin- released by kidney hypoperfusion, sympathetic nerve stimulation, reduced sodium in distal tubes. Activates angiotensin to be released and converted to angiotensin 2 by angiotensin converting enzyme (ACE-from the lungs)
Angiotensin 2- vasoconstriction, acts on adrenal cortex to releases aldosterone, stimulates vasopressin which acts on post pituitary to release ADH, stimulates thirst centre of brain, stimulates cardiac hypertrophy
Aldosterone- sodium/water retention
ADH- stops distal tubules from water excretion, and vasoconstriction
Counterbalance- stretch receptors in atria/ventricles release atrial natriuretic peptide and brain natriuretic peptide to produce sodium and water excretion and inhibit release of noradrenaline, renin and ADH
Receptors
Beta 1- heart and intestinal smooth muscle as well as platelets- increase HR, increased contractility, automacity, AV node conduction
Enhanced contractility through calcium through calcium mediated facilitation of the actin and myosin complex binding with troponin C
Enhanced chronicity through calcium channel
Increased platelet aggregation
Beta 2- bronchial vasculature, blood vessels, GI tract, skeletal muscle, liver, mast cells, and uterine smooth muscle- vasodilator and bronchial vessel vasodilation, dilation of small coronary arteries, relax GI tract, glyconeogenisis in liver, tremor in skeletal muscle, inhibition of histamine
Alpha 1- vascular smooth muscle- vasoconstrict due to catecholamines, activation of alpha 1 receptors on arterial vascular smooth muscle
Alpha 2- liver cells, platelets, smooth muscle of blood vessels
DA- renal and mesenteric vessels- vasodilation and increased blood flow to kidneys and mesenteric
V1- vascular smooth muscle -vasoconstriction
V2- renal collecting ducts - increases permeability of collection ducts and mediates water reabsorption
Coronary arteries
Left main coronary artery= anterior descending ( anterior interventricular septum and left ventricle), and circumflex (left lateral wall of left ventricle)
Right coronary artery ( right ventricle) , and posterior descending artery (posterior heart)
Cardiac drug responses
Automaticity- specialised fibres of conduction system (SA pacemaker cells) have inherent ability to spontaneously initiate electric impulse without nerve innovation
Conductivity- transmit action potential along its plasma membrane
Refractoriness- cardiac tissue non-responsive to stimuli
Post ganglionic fibres=sympathetic/noradrenaline(B1 receptors) - AV node, SA node, atria, ventricles= increased HR, automaticity, conduction velocity, force of contraction
Activation of SNS= HT, coronary artery disease, valvular disease- lead to heart failure
Vagal nerves- parasympathetic (acetylcholine)- SA node, AV node, atrial muscles= acts on muscarinic receptors and decrease HR, conduction velocity, limited reduction in contractility
Positive inotropic drugs- increase force of contraction (digoxin)
Negative inotropic drugs (decreases force of myocardial contraction (propranolol)
Positive chronotropic- accelerate HR by increasing impulse rate in SA node (adrenaline)
Negative chronotropic- slows HR (digoxin)
Positive dromotropic- increases conduction velocity (phenytoin)
Negative dromotropic- delays conduction (verapamil)
Electrical excitation
Sodium outside wants in and potassium inside wants out. Calcium combines with Troponin and tripomysin.
Phases:
0 (contraction/depolarisation)- sodium influx into cell via voltage dependant sodium channels (due to negative voltage in cell)
1 (repolarisation)- inactivation of sodium current
2 (repolarisation)- slow inward flow of calcium 2+ 40V via voltage sensitive calcium channels and small outflow of potassium
3 (repolarisation)- rapid potassium efflux from volatile gated potassium channels, calcium voltage closes voltage gates
4 (testing membrane potential/relaxed)- cell membrane actively transports sodium ions out and potassium ions in (requires ATP via sarcolemma)
