Cardiology Physiology Flashcards Preview

Year 1 Body Systems > Cardiology Physiology > Flashcards

Flashcards in Cardiology Physiology Deck (70)

Action potential in the T tubules of cardiac myocytes triggers calcium entry in which 2 ways?

1) L type channels - voltage sensitive Ca2+ channels
2) Calcium induced calcium release - Calcium released from SR


What protein does calcium interact with to induce contraction?



What is the resting potential and threshold potential of pacemaker cells?

Resting = -60mV
Threshold = -40mV


What is the resting potential and threshold potential of cardiac myocytes?

Resting = -90mV
Threshold = -65mV


What is the TFR of a cardiac myocyte?

ARP (absolute refractory period) + RRP (relative refractory period)


In an ECG what direction does the depolarisation go in a +ve and -ve deflection?

Towards an electrode = +ve deflection
Away from an electrode = -ve deflection


What are Einthoven's 6 leads?

Lead I - LA -RA
Lead II - LL-RA
Lead III - LL-LA
Augmented limb leads (recorded with respect to 0)
aVR = RA
aVL = LA
aVF = LL


What are Virchows leads?

Chest leads (V1-V6) Unipolar leads recorded with respect to 0


What leads is the electrical axis of the heart to do with?

Einthovens's leads


What is the electrical axis of the heart?

Max current produced by an ECG - normally lead II (60 degrees) but can be anywhere between -30 and 90 degrees (einthoven's leads)


What would left deviation (-150 - -30) and right deviation (+90 - -150) tell you?

Left deviation - left ventricular hypertrophy
Right deviation - right ventricular hypertrophy


What is the left ventricular axis and which leads is it to do with?

To do with Virchows leads
Max current generated by ECG - towards V6


What are the 4 phases of the heart beat?

1) Diastolic ventricular filling (passive phase followed by active phase when atria contract)
2) Isovolumic contraction (semilunar valves closed by ventricles contracting)
3) Systolic ejection ( 2nd phase of ventricular systole - ventricles contracting and blood ejecting - during this phase atria relax and fill with blood)
4) Isovolumic relaxation (ventricles relax, semilunar valves close, atria continue to fill)


What is cardiac power and how is it calculated?

Rate of work done by the heart
Cardiac power = pressure x flow rate


What is EDV?

End diastolic volume


What is ESV?

End systolic volume


How is stroke volume calculated?



How is ejection fraction (LVEF) calculated?



What is the main source of ATP for the heart?

Free fatty acids


What does the difference between LV and aortic pressure tell us?

The extent of aortic stenosis


What is V (blood velocity)?

Distance travelled per particle per unit of time


What is the equation linking pressure, blood flow and resistance?

Pressure = blood flow x resistance


What is the difference between the action potential in cardiac and skeletal muscle and what is the purpose of this difference?

Presence of plateau caused by Ca2+ ions in the cardiac myocyte action potential
Maintains contractile period during depolarisation


What happens to the troponin tropmyosin complex during systole?

Calcium binds to troponin, troponin-tropomyosin complex moves and myosin can now dock onto the exposed binding sites


What happens to the longitudinal and horizontal and circumferential filaments during systole?

Longitudinal filament shortening
Horizontal and circumferential filament thickening


In which 2 ways can heart rate be increased?

1) Sympathetic innervation
2) Adrenaline - beta 1 agonism


In which 2 ways can stroke volume be increased?

1) Increase pre load
2) Sympathetic input - prolonged opening of Ca2+ channels, enhances calcium action in excitation/contraction coupling mechanisms


What happens to the LVEF of a failing heart?



What is the physiological LVEF and the LVEF in exercise?

Physiological LVEF - 50-75%
LVEF in exercise - can reach 90%


Why would ischaemia and viral infection/alcohol lead to a heart which contracts with less force?

Ischaemia - scarred myocardium
Viral infection/alcohol - wall thinning


In heart failure how does you body try to compensate for the weaker contraction of the heart and what does this lead to?

1) SNS overactivates
2) RAAS kicks in
Both these measures increase the pre load and the LV stretch exceeds physiological levels - go onto descending limb of the curve


What 3 treatments would be given to a patient with heart failure and pulmonary oedema?

1) High flow O2
2) Morphine - relax pulmonary vessels to reduce preload and relieving pain
3) Furosemide - diuretic


How is preload measured?

End diastolic volume using an echocardiogram


What 6 ways can stroke volume be increased?

1) Increased central venous pressure - increased by increased circulatory volume
2) Decreased venous compliance
3) Increased atrial filling or contraction
4) Decreased heart rate - prolongs diastole and filling
5) Increased ventricular compliance - more can get in
6) Increased aortic or pulmonary pressure - need more blood to generate enough pressure to open valves


What is the bowditch effect?

Another curve, up to a point, increased heart rate = increased force of contraction


What organs does the parasympathetic nervous system have no effect on?

Adrenal glands and kidneys


What are the 4 effects of SNS on heart?

1) positive chonotropy - SA node
2) positive dromotropy - AV node
3) positive inotropy - atria and ventricles
4) positive lusitropy - atria and ventricles


What are the actions of RAAS (ie. angiotensin II, aldosterone and vasopressin)?

Increased Na+ and H2O retention
Vasopressin release
Aldosterone release
Increased Na+ and H2O retention
Increased water retention


What are the PNS actions on the heart?

1) negative chonotropy - SA node
2) negative dromotropy - AV node
3) negative inotropy - Only ATRIA - no effect on ventricles


Epinephrine is released into the blood from the adrenal medulla in response to sympathetic innervation what 3 effects does it have in terms of the cardiovascular system?

1) Causes kidneys to release renin
2) Causes vasoconstriction
3) Acts directly on the heart to increase heart rate and stroke volume


How does the renal juxtaglomerular system work?

Macula densa cells in the distal convaluted tubule located next to the glomerulus sense a drop in NA concentration (lower transglomerular pressure - less filtered out - indicates BP) and signals to granular cells to secrete renin


Where are baroceptors located and how do they control BP?

Carotid sinuses and aortic arch
Decreased arterial pressure - decreased firing - increase in sympathetic tone and decrease in parasympathetic tone
Increased arterial pressure - increased firing - decrease in sympathetic tone and increase in parasympathetic tone


What is the anaerobic threshold in cardiopulmonary exercise testing?

Time when anaerobic respiration begins


What does cardiopulmonary exercise testing measure?

O2 consumption at rest and during exercise


What are the 6 consequences of uncontrolled hypertension?

1) Stroke - hameorrhagic/ischaemic
2) LV hypertrophy - diastolic dysfunction, AF, heart failure
3) Hastened atherosclerosis
4) Vascular disease - coronary, peripheral, arterial
5) Retinopathy
6) Renal failure


Where the cardiovascular center located in the brain?

Medulla oblongata of the brain stem - region known as the tractus solitarius


What are the 4 inputs to the cardiovascular center in the brain?

1) Higher brain centers
2) Proprioreceptors - monitor joint movements
3) Baroreceptors - monitor blood pressure
4) Chemoreceptors - monitor blood acidity


What are the outputs from the CV center in the brain?

1) Vagus nerves - heart (decreased rate)
2) Sympathetic nerves - heart (increased rate and contractility) and blood vessels (vasoconstriction)


What is orthostatic or postural hypotension?

Decreased BP on standing


Which 2 hormones lead to increased BP through increasing cardiac rate and contractility?



What 4 hormones lead to increased BP through vasoconstriction?

1) Angiotensin 2
2) Vasopressin
3) Norepinephrine
4) Epinephrine


What 2 hormones lead to increased circulatory volume and thus increase in BP?

1) Vasopressin
2) Aldosterone


What hormone leads to decreased circulatory volume and thus a decrease in BP?

1) Atrial natiuretic peptide


What structures can pass through fenestrated capillaries and where are they found?

Small, lipophillic molecules
Intestinal villi, endocrine glands, kidney glomeruli


What substances can pass through sinusoidal capillaries and where are they found?

Red blood cells and large hydrophillic molecules
Liver, bone marrow and spleen


What is Starling's law of the capillaries?

Hydrostatic pressure out and osmotic pressure in
At arterial end net pressure is out
At venous end net pressure is in


What are the 3 types of blood flow?

1) laminar flow
2) Turbulent flow
3) Single file flow


What is the flow in the aorta?

Pulsating laminar flow during early systole
Turbulence during peak velocity of flow


Why is velocity of blood lowest in capillaries?

Velocity = Flow rate/cross sectional area
Flow rate must be the same throughout circulation
Capillaries have the largest cross sectional area and thus the lowest velocity


What 3 parameters determine resistance?

1) Length of blood vessel
2) Radius of the vessel
3) Viscocity of blood


The levels of what 4 substances rise in the blood during exercise and cause local vasodilation by relaxation of vascular smooth muscle?

1) H+
2) CO2
3) K+
4) Adenosine (ATP-ADP-AMP-Adenosine)


Why does NO have a protective effect against thrombosis?

Causes relaxation of vascular smooth muscle and thus vasodilation reducing blood pressure
It makes the blood less prone to clotting


By what process is increased NO formed in endothelial cells during exercise?

1) Increased blood flow through capillaries
2) Ca2+ moves into endothelial cell
3) Ca2+ causes the conversion of Larginine to NO
4) NO moves into vascular smooth muscle and causes relaxation


Why is NO given in GTN spray to relieve angina?

Causes vascular smooth muscle relaxation and thus vasodilation


Why does atheroma formation occur frequently at arterial junctions?

These are stress points
They have high flow rates and more turbulent flow in these regions


What are the 3 main stages of atheroma formation?

1) Endothelial damage
2) Uptake of LDL particles, adhesion and infiltration of macrophages
3) Smooth muscle proliferation and formation of a fibrous cap


What 4 factors promote atheroma formation?

1) Sheer stress - hypertension
2) Toxic damage, chemicals - cigarette smoke
3) High levels lipids - familial hypercholesterolaemia, diabetes
4) Viral or bacterial infection - chlamydia pneumoniae


What causes proliferation of smooth muscle and deposition of collagen in a atheromatous plaque?

Growth factors are released by the damaged endothelium which cause proliferation of smooth muscl and deposition of collagen


What forms a fibrous cap over an atheromatous plaque and why is the fragility increased?

Collagen forms a fibrous cap
Fragility is increased because of calcification of the plaque


What triggers the formation of a thrombus in atheroscelrosis?

Rupture of fibrous cap exposes collagen and TF to the blood which triggers the formation of a thrombus