PCS-Revision-Cardiology PDF

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CARDIOLOGY REVISION – Cardiac cycle (L) CAR CARDI DI DIAC AC CYC CYCLE LE

CAR CARDI DI DIAC AC CO COND ND NDUC UC UCTI TI TION ON

 Heart conduction is myogenic.  Myocardial cells are el- linked by intercalated discs so that the heart beats as syncytium.  Conduction through the heart is at ~1m per second, but 3.5-5m/sec in purkinje fibres so that ventricles contract same time.  Cardiac AP = 150-300msec.  The whole cardiac cycle is ~800msec  AP of heart is longer to allow contract.  Excitation of myocardial cell causes contration and repolarisation of membrane causes relaxation.

1. AP at SA node 2. AP spreads through atria via interatrial bands to the AV node travelling at 1m/sec 3. AP passes slowly thr AVN at 0.05m/sec t atria time to contract. 4. AP passes down the AV bundle and then into the left and right branches of the interventricular septum. 5. The AP now spreads to the base and up the purkinje fibres below the endocardium, up the ventricular walls 6. This allows the ventricles to contract in unison.

SYSTOLE = 0.3sec DIASTOLE = O.5sec 1. EARLY DIASTOLE = The heart is relaxed, the semilunar valves (pulmonary and aortic) have just closed. The pressure in atria > ventricles so AV vales are open and blood is flowing into ventricles. 2. DIASTOLE = AP is generated at SA node causing the atria depolarise (P wave) 3. SYSTOLE = Atria depolarising causes them to contract and push the remaining 30% of blood into the ventricles. 4. SYSTOLE = Ventricular pressure > atrial pressure so AV valves shut, (S1 after R) 5. SYSTOLE/ISOVOLUMETRIC CONTRACTION = 0.02 sec the AV and SL valves are shut and ^ pressure but no change in volume. 6. SYSTOLE = AP has spread to the AV node . The ventricles depolarise as the atria repolarise (QRS) and the ventricles contract. 7. SYSTOLE/EJECTION = When ventricular pressure > arterial pressure the SL valves open and blood leaves the ventricles. 8. DIASTOLE = Ventricles repolarise (T wave) and relax. The SL are open and AV closed. As ventricles relax the pressure in arteries>ventricles so SL valves close. (S2 at end of T wave). 9. DIASTOLE/ISOVOLUMETRIC RELAXTION = Both valves are closed and there is a decrease in pressure but no volume change. 10. DIASTOLE = When pressure in the atria>ventricles the AV valves open and ventricles begin to fill again.

The long AP in purkinje fibres is to ensure unidirectional impulse and prevents excitation immediately after.

CARD CARDIA IA IAC CA AP P (SA N NOD OD ODE E) Phase 4 = pacemaker potential; Na+ goes into cell through slow Na+ channels (funny currents). Phase 0 = upstroke; AP is generated as T-type Ca2+ channels open until -40mv then L-type Ca2+ channels open and Ca2+ floods into the pacemaker cell. Phase 3 = downstroke; L-Ca2+ channels shut and lots of voltage-gated K+ channels open and K+ floods out. Membrane is repolarised. K+ channels shut.  Slope of phase 4 determines heart rate.  Change pacemaker potential by SNS stim (changes slope), or hyperpolarising the cell by PSNS stimulat. Hyperpolarises & change slope with strong vagal stimulation. Resting potential = ~ -60mv Threshold = ~ -50/40mv Peak = ~ 0mv

CARD CARDIA IA IAC CA AP P (VE (VENTRI NTRI NTRICLE CLE CLESS) Phase 0 = upstroke upstroke; an AP causes depolarisation of ventricular myoctes. This is because Na+ channels open and Na+ floods in. Phase 1 = peak; inactivation Of Na+ channels. K+ channels open and K+ goes out.

P wave (depolarisation of atria) causes atria to contract (a wave), small ^ ventricle vol. QRS compl complex ex (depolarisation of ventricles) causes ventricle contraction. Valves open and there is a decrease in ventricular vol. T wa wave ve is the ventricles depolarising and relaxing (see vnetric pressure). Also causes SL valves shut. Isovolum relax then AV valves open; ^ventricular volume. Yellow highlighted area shows increase in ventricular pressure but not volume (isovolumetric contraction). Heart sounds S1 – closure of the AV valves, heard during R/S S2 – closure of the SL valves, heard just after T wave Murmers are due to turbulent flow and can be benign or pathological. S3 and S4 are gallop rhythms heart during heart failute/pulmonary oedema.

Phase 2 = plateau; only occurs in ventricular AP. Ca2+ is released from the sarcoplasmic reticulum (calcium induced calcium release). It is the balanced flow of Ca2+ inward, and K+ out. It allows for a sustained contraction. Voltages cancel = plateau. Ca2+ comes in through slowly activating channels, and K+ out through fast-voltage gated channels. Contraction of myocytes. Phase 3 = downstroke; repolarisation due to opening of K+ channels and closure of Ca2+ channels. Phase 4 = rest; the resting memb potential in ventricles is ~-90mv. High potassium permeability.

CARDIOLOGY REVISION – Haemostasis (L) LEA LEARN RN RNIN IN ING GO OUT UT UTCO CO COME ME MESS a) describe the histological features of arteries, arterioles, capillaries and veins b) identify the form and function of the main constituents of blood, with particular reference to plasma proteins and lipoproteins c) describe the role of platelets in haemostasis d) identify the function of the components of the normal coagulation pathway, and explain their involvement in the intrinsic and extrinsic pathways of coagulation

CON CONSTI STI STITUE TUE TUEN NTS OF B BLO LO LOO OD RBCs (38 (38-54%), -54%), WBCs and platelets. WBCs can be granulocytes: neutrophils, eoisonophils or basophils. Or agranulocytes: monocytes or lymphocytes. Blood serum/b serum/blood lood plasma – blood serum is plasma without the clotting factors (e.g. fibrinogen) or the cells. Blood plasma makes up 55% of blood volume and holds the cells in suspension. Contains albumin, globulins, fibrinogen, clotting factor, CO2, hormones and electrolytes. Plasma proteins Albumin is a small protein that maintains colloid osmotic pressure. -ve so attracts counterions. Osmotic pressure has to be = on both sides to prevent net movement of fluid; albumin maintains this. True function is to transport insoluble FA, steroids and bilirubin. Kwashikor is swollen stomach due to fluid movement into abdomen due to `’ protein intake and therefore `’ albumin. Globulins/globular proteins act as enzymes and components of the immune system/transporters etc. Fibrinogen is synthesised in the liver as a glycoprotein, thrombin converts it into fibrin in the blood for clot formation. Clotting factors are syn in the liver and are vitamin K dependent. They convert fibrinogen to fibrin in cascade. Platelets They are involved in everyday wear and tear; they adhere to the site of damage and secrete thromboxane A and ADP to increase platelet adhesion and form a platelet plug. They help with vascular integrity and small-scale damage. They also secrete growth factors. Too much causes thrombosis and too little causes excessive bleeding. Lipoproteins Made of proteins and lipid and they transport TAGs and cholesterol in the blood. HDL goes from fat to liver and LDL from liver to fat. The hydrophobic groups face out (cholesterol and phospholipids) and the lipid is emulsified on the inside. Coagulatio Coagulation n factors Bind because aggregated platelets in plug are –ve, then Ca2+ binds to these, and then coag factors (-ve) bind to Ca2+.

CO COAGU AGU AGULLATI ATION ON CA CASC SC SCAD AD ADE/ E/ E/PAT PAT PATHW HW HWAY AY 1. Vasoconstrictio Vasoconstriction n - SM in vessels causes them to narrow when there is damage to endothelium. 2. Platelets – fall through gap and adhere to site of damage. Endothelial cells release VWF (von willebrand factor), this causes platelets to bind to VWF and exposed collagen. Adhered platelets secrete ADP and thromboxane A causing more platelets to adhere. Collagen on wall causes platelets to adhere via glycoprotein 1a. This aggreg and adhesion causes PLATELET PLUG. 3. Blood coagulat coagulation ion – Intrinsic is sower and is when blood comes into contact with collagen from damaged wall. Extrinsic is faster and is when damage tissue releases thrombopl thromboplastin. astin.

Note that Ib/IX complex is a receptor Vwf and thrombin Iib/IIIa is a receptor for fibrinogen and Vwf Platelets bind to collagen via glycoprotein 1a which is expressed on collagen Fibrin forms a mesh like structure that binds the vessel together. There is cross linking covalent bonds for strength. It is a fibrous, non-globular protein. Fibrin mesho overlies the platelet plug and factor 13 completes the cross-linking. ∞ ∞ ∞ ∞ ∞

∞

All of these clotting factors require Vit K for production and the ones in green require Ca2+. Blue arrows slow that the buddy factors (in purple) require thrombin for formation. Antithrombin 2 is activated by heparin and interferes with the formation of fibrin from activated thrombin. Antithrombin binds to factors 2 and 10. Haemophil Haemophillia lia is the loss of factor 8 from the intrinsic pathway. Factor 8 needed as cofactor with 9a to form 10a. Clot retraction is when the blood clot is issolved by the enzyme plasm plasmin. in. Thrombin causes Ca2+ in the platelets to be released causing contraction. Pseudopodia pull on the fibrin and release serum causing the clot to shrink. Functions of b blood: lood: carriage of nutrients, communication (hormones), defence and temperature. Haematocrit (PCV)

CARDIOLOGY REVISION – Control and reg of CO (SG) FRA FRANKNKNK-ST ST STA ARLIN RLING G

LEA LEARN RN RNIN IN ING GO OUT UT UTCO CO COME ME MESS

Fick’s principle = CO. The increa increase se in cardiac stretch (i (increasing ncreasing muscle le length) ngth) increase increasess the strength of contractio contraction. n. - Non nervous and nonhormonal - E.g. increasing venous return increases stretch of the myocardium and therefore stroke volume E.g. standing up decreases central venous pressure and therefore decreases venous return, decreasing stroke volume and so decreasing the cardiac output. Exercise ^ venous return and so ^ CO. Frank-starling m mechanism echanism is an intrinsic contr control ol of cardiac out output. put.

a) define and distinguish the physiological mechanisms which change cardiac output from rest to exercise, b) including Starling’s law c) describe and interpret how haemodynamics and cardiac output affect arterial blood pressure d) identify and apply the physical laws underlying haemodynamics e) describe mechanisms which may lead to cardiac failure

CAR CARDIA DIA DIAC C OU OUTP TP TPUT UT CARDIAC OUT OUTPUT PUT = the volume of blood pumped from ventricle per minute. STROKE VO VOLUME LUME = the volume of blood pumped from the heart each beat. CO = HR x SV Regulated by iintrinsic ntrinsic and e extrinsic xtrinsic mechanism mechanisms: s: INTRINSIC = non-nervous and non-hormonal (Frank Starling). They affect stroke volume and force of contraction. Determined by stretch of fibres. Also all about pre-load and after load; to increase stroke volume the heart may increase pre-load. EXTRINSIC = Controlled by ANS (and hormones) & factors affect heart rate (ionotropic). ~ The SA and AV nodes have SNS and PSNS innervation but the ventricles only have SNS. ~ Basically SNS increases ionotropic state of the heart by sympathetic nerves or aderenaline/NA ~ B1 adrenergic receptors of the heart &SNS cause +ve ionotropic effect. ~ +ve ionotropic agents increase Ca2+ release: Thyroxine, Ca2+ and caffeine. ~ --ve iontropic agents decrease force of contraction. This is important as there is no PSNS control of contraction force. Low PH, Ca2+ channel blockers, propanolol, barbituates. As HR increases time for ventricular filling falls so SV doesn’t proportionally ^ with HR. It levels off when CO is 50% above max level

LA LAMIN MIN MINAR AR VS. TU TURBU RBU RBULE LE LENT NT FLO FLOW W Laminar flo flow w is when fluid flows in parallel layers. Turbulent flow is when blood flows chaotically, it often occurs in arch of aorta, stenotic valves, stenotic arteries and branching points. Turbulence increases the perfusion pressure need to drive flow. Therefore turbulence decreases flow and also increases risk of atheroma etc forming due to the damage it causes. Also causes eddie currents/bruits.

EXCI EXCITA TA TATION TION TION-C -C -CON ON ONTR TR TRAC AC ACTION TION C COU OU OUPLIN PLIN PLING G IN CA CARDI RDI RDIAC AC TIS TISSU SU SUE E 1) AP is generated in SA node, conducted to AV node via gap junctions. 2) AP travels via T-tubules and causes L-type Ca2+ channels to open and small increase in intracellular Ca2+. 3) Ryanodine receptors (on SR) detect increase in Ca2+ and cause SR to release Ca2+ (calcium induced calcium release). 4) Calcium binds to troponin C, moves tropomyosin complex off actin binding site allowing myosin to bind to actin. 5) Using ATP hydrolysis the myosin head pulls the actin towards centre of sarcomere. 6) SERCA pumps Ca2+ back into SR using ATP. 7) Some Ca2+ is pumped out of cell via Na+/Ca2+ cotransport. 8) Lower Ca2+ levels cause troponin covers actin binding site once more.

DEFI DEFINITI NITI NITION ON ONSS Jugular pulse - as there are no valves between jugular vein and RA, pressure changes in RA are reflected in jugular vein. Preload – is when the ventricles fill in diastole. It is the ^ tension placed on the fibres caused by ^pressure and stretch before contraction. AKA endvolumet pressure. Afterload – the tension developed in the wall of the LV during ejection. It is dependent on aortic pressure. Larger volume means the heart has more to pump / a greater load so there is higher afterload. Hypertrophied heart has more muscle, more strength and less volume so lower afterload. How much pressure the heart has to generate to eject blood. Venous retu return rn is the volume of blood returning to the heart fromt eh vasculature every minute. Central ve venous nous pressure – as the end of diastole when the pressure in the RA is equal to that in the S+IVC. Perfusion pressure – the difference in pressure of arteries and veins drives the movement of blood. Blood flow - Perfusion p pressure ressure / Vasc Vascular ular resistance Mean arterial p pressure ressure - average of whole cycle = 90mmHg. Low as more time spent in diastole than systole Pulse pressu pressure re = systolic – diastolic pressure Mean BP = C CO O X TPR

CARDIOLOGY REVISION – Control and reg of CO and the ECG (SG) ECG

EXT EXTRIN RIN RINSI SI SIC CC CON ON ONTR TR TROL OL OF THE HE HEART ART

P = atrial depolarisation Q = invasion of the septum, it’s positive because the left ventricle > mass than RV R = invasion of the ventricular walls S = ventricular depolarisation at the base of the heart T = ventricular repolarisation

Changes the heart chronotropicall chronotropicallyy (HR) Parasympathetic The vagal nerve has post-gang fibres that release ACh onto the SAN and AVN. This decreases the excitability of the SA node slowing heart rate. The Ach increases the permeability of the pacemaker cells to K+, hyperpolarising them and decreasing the pacemaker slope. Vagal tone is normal and naturally decreases the HR of the SA node from 100bpm to the more normal 60-100 Sympathetic Varicosities of post-gang fibres release NA onto B1 receptors increasing contractility and decreases duration in systole. Increases permeability of SA node to Na+ and Ca2+ therefore pacemaker cells can reach threshold moe quickly. The pacemaker potential slope is short.

P-R = atrial contraction S-T = ventricular contraction Atrial repolarisation is masked byt eh QRS complex Atrial flutter – AV node cannot transmit all of the impulses causing a long P-R interval Atrial fibril fibrillation lation – irregular atrial contractions meaning the heart cannot properly fill with blood Heart block – damage to the AV node, if 1st deg causes a long PR wave, if 2nd not all of impulses get to ventricles, if 3rd – cells make their own rhythm.

NO NOTES TES Control of CO is intrinsic (determined by force of contraction) or extrinsic (autonomic nerves) Capillaries: According to Poisuielle’s law capillaries should have a lot of resistance. Poisuielle’s law says that radius and length of vessels determines flow. But because they have a massive cross-sectional area for flow there is little resistance. Also don’t have SM so they cannot vasoconstrict. The most imp graph tor ememebr is the F-S one where it plots a curved graph of end-diastolic volume against stroke volume. End-diast End-diastolic olic volume also affects CO – this is either from outside or inside the heart. Outside the heart it is due to gravity, intrathoracic pressure and respiration, or due to central venous pressure. Central ve venous nous pressure is when at the end of diastole, the pressure in the RV is equal to the pressure in the S+IVC. It is affected by vasoconstriction, increasing venous return and CO. Axial st streaming reaming is the way that RBCs have a tendancy to flow along the middle of the BVs. The higher the haematocrit, the higher the viscosity and the harder the heart has to pump to get blood around the body. This is true at high altitudes and with polycythemia (^ RBC breakdown). +ve ionotropes Thyroxine, Ca2+ and caffeine all act to increase intraceullar calcium or stim Ca2+ release from store. -ve ionotropes This is an important mechanism because there is little/no PSNS innervation in the heart to decrease the force of contraction. Affected by low blood PH, Ca2+ channel blockers, barbiturates and propranolol.

A BI BITT M MORE ORE ON IINTR NTR NTRIN IN INSIC SIC CO CONTR NTR NTROL OL OF HE HEART ART Basically the F-S relationship but also…. Pre Pre-load -load – occurs when the ventricles are filling with blood in diastole, it is the tension in the myocardial fibres due to tension and stretch. Afterload – the tension developed in the LV wall during ejection and the load that the heart has to pump against. The aorta is the load against which the heart must pump

The SA and AV nodes have SNS and PSNS innervation, however the ventricles only have SNS.

EFFE EFFECTS CTS O OFF TH THE E NE NERV RV RVOU OU OUSS SY SYSTE STE STEM M ON TH THE EH HE EART SNS ^ vasoconstriction ^ venous return ^ preload ^ force of ventricular contraction => ^ stroke volume => ^CO SNS ^ pacemaker slope => ^HR => ^CO

PSNS `’ force of atrial contraction `’ preload `’ force of ventricular contraction `’ CO and venous return PSNS `’ slope of pacemaker potential `’ HR `’ CO `’ venous return

HAE HAEM MODY ODYNA NA NAMI MI MICS CS Is the relationship between blood pressure and blood flow. The flow of blood is driven by the difference in pressure between arteries and veins (p perfusion p pressure). ressure). Blood flow = p perfusion erfusion pressu pressure re / vas vascular cular resist resistance ance When fluid flows through a tube the velocity is inversely proportional to the cross sectional area of the tube. So basically increasing the SA, decreases the velocity. V α 1/A Pouiseuill Pouiseuille’s e’s law – relates blood flow through a tube to pressure, essentially increasing diameter ^ flow rate. Increasing the diameter, decreases the resistance so increases the flow.

CARDIOLOGY REVISION – Modifying HR & autonomic control of heart LEA LEARN RN RNIN IN ING GO OUT UT UTCO CO COME ME MESS     

NOT NOTES ES

describe the sympathetic and parasympathetic control of heart rate explain how changes in heart rate affect cardiac output identify the effects of the ANS on the Frank-Starling relationship, identify the mechanisms by which the ANS alters the inotropic state of the heart identify the mechanisms by which the ANS affects lucitropy

SYM SYMPA PA PATH TH THETI ETI ETIC C INN INNER ER ERVA VA VATI TI TION ON ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞ ∞

Mainly in the heart and vasculature NT = noradrenaline Actions: ^HR and conduction velocity ^ contractility via B1 receptors Vasoconstriction via 1 receptors Vascular beds in SM vasodilate via B2 receptors Noradrenaline mainly works on 1 and B2 receptors; but a higher affinity for  receptors There is a mix of constriction and dilation in diff parts of the vasculature Activation of the SNS causes release ...