Ian La Grice Flashcards
What happens to the venous return when the mean right atrial pressure increases?
It decreases due to the increased pressure.
What does equilibrium of the vascular system and heart mean?
It means that the heart and vascular system must work together to increase cardiac output. Blood vessels must increase venus return and heart function must increase togeher, such as when exercising. The autonomic nervous system and the endocrine system connects these two.
What controls the cardiovascular system?
Intrinsic
1) stretch
Extrinsic
1) neural (PNS, SNS)
2) endocrine - Adrenaline, RAS, ADH, NP
What does the adrenal medulla do?
Prduces and stores endogenous catacholamines, including adrenaline and noradrenaline. The adrenal medualla recieves sympathethic innervation, which causes the release of NA and adrenaline into the blood stream.
What is renin releasd in response to?
Sympathetic stimulation via beta 1 receptors.
Decreased pressure in the afferent arterioles
Decreased sodium load in the macula densa
What does angiotensin II do?
a potent vasoconstrictor.
It penetrates the blood brain barrier and activates the hypothalamus pathways which modulate sympathetic outflow to the cardiovascular system and adrenal medulla.
It also stimulates ADH synthesis and induces thirst.
Increases synthesis and release of NA from sympathetic nerve terminals -> to the heart and vessels.
Causes constriction of smooth muscle
Increased release of aldosterone from the adrenal cortex -> reabsorption of Na by the renal tubules.
What is the function of ADH?
Increases water reabsorption
Can also induce vasoconstriction
What are natriuretic peptides?
Synthesised by the heeart, brain and other organs.
Release by the heart is stimulated by atrial and ventricular distension, angiotensin II, endothelin and sympathetic stimulation (beta adrenoceptor mediated) and by neurohormonal stimuli, usually in response to heart failure.
ANP is released in response to hypervoluemic staes and chronic heart failure.
ANP and BNP (brain-type natriuretic peptide)
What are the functions of BNP and ANP?
ATRIAL Naturetic Peptide - atria production
BNP - ventricles
BNP is a sensitive marker for heart failure.
Opposite roles to angiotensin II. - ANG II stimulates this negative feedback.
They cause : Natriuresis Diuresis Increase GFR and filtration fraction Inhibit renin release - decrease circulation angiotensin II and aldosterone Systemic vasodilation Arterial hypotension Reduced venous pressure Reduced pulmonary capillare wedge presure.
This: Decreases blood volume decreases arterial pressure Decreases central venous pressure Decreases pulmonary capillary wedge pressure Decreases cardiac output
Therefore, this system counter regulates RAAS
Neural endopeptidase degrades natriuretic peptides.
What maintains the sinus rhythm?
Suppression of the lower pacemakers
Coordinated excitation via specialised conduction system
Existence of a prolonged refractory period in the myocardium
There are two periods during an action potential when it is difficult to create a new action potential. What are those called
Relative refractory period
Supernormal period
Need a larger or smaller stimulus than normal but they generate a slow conduction action potential.
What is an arrhythmia?
1) Disorder of impulse formation - early discharge of a pacemarker by an unstable resting membrane potential in working myocardial cells. tachycardia and bradycardia
2) Disorders of impulse conduction - Conduction abnormalities such as partial or complete AV block, left or right bundle branch block and reentry. The first gives rise to a slow heart rate or bradycardia, while the others alter the time course of the ventricular spatial or temporal dispersion of repolarization.
What are the types of reentrant arrhythmias?
Atrial flutter - fast regular ,atrial rate (250-350 bpm). Organised (same) action potentials. Heart block may develop
Atrial fibrillation - Raid disorgansied atrial activation (350-600 bpm). Not all impulses conducted to ventricles. Rapid disorganized ventricular rhythm. Risk of embolisation. due to blood stasis.
Ventricular tachycardia: rapid ventricular activation (110-250 bpm) Impaired mechanical function and risk of ventricular fibrillation..(wide QRS)
Ventricular fibrilation - chaotic ventricular rhythm leads to circulatory arrest and death.
What cases the prolonged refractory period in cardiac cells?
The dependence on the Na channels for the membrane potential to decrease before they can be refired.
What does increased vulnerability to recurrent activation increase with?
Decreased conduction velocity
Decreased refractory period - a smaller refractory period means that the cells can reset and be stimulated earlier (in time for the conduction to induce activation)
What do you need for re-entrant activation?
A circuit Slow conduction or short effective refractory period Unidirectional block (so conduction doesn't go both way A trigger (something to set the conduction off).
Reentrant circuits can be functional or anatomical.
What is a potential complication with wolf-parkinson white syndrome?
If atrial flutter or fibrilation develops then there is nothing preventing the action potential from going straight into the ventricles.
What determines the rate of propagation of electrical activation?
Electrical properties of the myocytes -increased electrical coupling between myocytes increases propagation rate. Propagation is greatest in large diameter cells.
Inward current during excitation - density and status of Na channels is important - greater current faster propagation.
Ca channesl are slow at influx and that is why the SA and AV nodes are slow conduction.
What does myocardial ischaemia result in?
A potential for an arrhythmia. This is what causes death.
Myocardial ischaemia causes
1) slow conduction
2) reduced AP duration
3) non-uniform repolarization
4) ectopic activation
Need a reduced wavelength caused by reduced conduction rate and reduced refractory period. Then a trigger.
Slow conduction:
a) ischaemic tissue is low in ATP
b) Na/K ATPase reduced
c) transmembrane Na, K gradients reduced
d) partial membrane depolarization
e) inactivation of Na channels
f) reduced gap junctions coupling (low pH due to regional metabolic acidosis).
Reduced action potential duration
a) Na/K ATPase reduced
b) transmembrane Na, K
c) inactivation of Na channels
d) hyperkalaemia outside of the cell -> activates a potassium channel that repolarises the cell
Ectopic activation -delayed after depolarisation - impaired Ca homeostasis in myocardial ischaemia leads to elevated intracellular Ca2+ from SR.-> spontaneous release. Na/Ca exchanger then tries to remove 1Ca bringing in more 3Na -> depolarising current -> start of arrhythma.
Non-uniform repolarization - conduction block
If ventricle tachycardia develops this causes an increased energy demand that further increases the ischaemia and leads to ventricular fibrilation
What is an issue for someone with a past MI?
Monomorphic VT generated from the damaged tissue.
How does heart failure generate arrhythmia?
Heart failure is associated with an increased risk of VT and VF becauee it is associated with remodelling, fibrosis, scaring, altered ANS and cellular electrical properties.
a) Atria are dilated -> increased duration of circuit -> reentrant circuit can develop.
b) Increased atrial pressure stimulates stretch receptors
c) Heart failure causes atrial fibrosis - slowing of conduction
d) Altered expression of Na/Ca exchanger
e) ANS inputs change
f) AF promotes more AF
g) HF has increased risk of VT and VF
What is an early after depolarization and what is the risk?
Early after depolarizations are caused by prolonged action potentials which enable the calcium channels to re-activate. This promotes the T wave.
Long QT syndrome prolongs the action potential duration. This prolongs the vulnerable period for arrhythmia and can cause an early after depolarisation.
Increased action potentials are caused by:
a) drugs - amiodarone (is supposed to prolong the action potentials to prevent reentrant circuits)
b) Reduced extracellular potassium concentration - decreases channel function
c) potassium ion channel mutation leading to reduced effectiveness of the delayed rectifier
d) Na ion channel mutations that affect inactivation of the channel.
They can result in continuously varying polymorphic VT (torsade de pointes. May resolve spontaneously or progress to VF.
What order to you check a ECG?
Rate, rhythm, P wave, PR interval, QRS, QRS axis, Q wave, ST segment, T wave, QT interval.
What are the possible causes of polymorphic ventricular tachycardia?
Long QT syndrome -
Signs:
family history, presyncope, and ECG showing QT interval and VT morphology
Why is VT caused by long QT polymorphic?
Because it is not anchored by structural abnormalities. Activation drifts around the heart.
What advice do you give someone with long QT syndrome?
Avoid lifestyle modifications and medications that prolong QT.
LQT1 - stress, exercise
LQT2 - auditory stimuli, stress
LQT3 - rest and sleep
Beta blockers and ICD
How do you treat someone with long QT syndrome?
Lifestyle modifications.
Beta blockers and implantable cardioventer defribulator placement
Why is their a low blood pressure with VT?
VT leads to reduced ventricular filling
VT leads to impaired pump function
Poor coordination of ventricle
These cause reduced CO and therefore, the mean artrial pressure is low. This leads to poor brain perfusion.
What do you do for monomorphic ventricular tachycardia?
Defibrillator
Antiarrhythmia medication
Ablation of reentrant circuits
What affects the inotropic state?
The magnitude and rate of Ca released from SR
Amount of Ca in the SR
Affinity of troponin C for Ca
