Phase 1a Lauren Barker and Chiara Beck The Peer Teaching Society is not liable for false or misleading information…

Phase 1a

Lauren Barker and Chiara Beck

Cardiovascular

The Peer Teaching Society is not liable for false or misleading information…

• Anatomy– Surface Anatomy– Heart Borders

• Physiology– Muscle Contraction

• Filaments• Action Potential

– Cardiac Cycle• Nodes

– Regulation of MAP• Effectors of CO and TPR• Baroreceptors and Chemoreceptors


Aims







Aims


Surface Anatomy


Surface AnatomyLocation: L 3rd IC spaceAuscultation: Right sternal edge, 2nd IC space

Location: R 4th IC spaceAuscultation: R 5th IC space

Location: L 3rd CC Auscultation: L 2nd IC space

Location: L 4th CCAuscultation: APEX L 5th IC space, mid-clavicular line


Borders of the HeartSuperior: R 3rd CC L 2nd CC

Right: 3rd 6th CC (2/3cm from midline)

Left: 2nd IC space, 2/3cm from midline apex

Inferior: Sternal 6th CC apexAKA diaphragmatic surface

Anterior: sternocostal surface







Aims

• Different to normal muscle contraction– Extracellular calcium

ions– Sustains depolarisation

of cardiac muscle cells for longer


Physiology – Cardiac Contraction


Physiology – Sarcoplasmic Reticulum

The sarcoplasmic reticulum is the membrane network that surrounds the contractile proteins.Consists of sarcotubular network at the centre and the subsacrolemnal cisternae.


Physiology – Contraction

• Sliding of actin over myosin by ATP hydrolysis through the action of ATP-ase in the head of the myosin molecule.

• When Ca2+ floods in, it binds to troponin, therefore moving tropomyosin off actin, exposing the binding sites.

• The head of the myosin molecule forms crossbridges that interact with actin.


Physiology – Contraction


Physiology – Thick Filaments

• Myosin:– 2 heavy chains – alpha and beta myosin heads– 4 light chains– Perpendicular at rest– Bends towards the sarcomere centre during

contraction– Hydrolyses ATP, interacts with actin


Physiology – Thin Filaments

• Actin:– Globular protein– Double stranded helix– Both form F actin– Activates myosin ATP, interacts with myosin



• Tropomyosin:– Elongated molecule made of 2 helical peptide

chains– Regulates interaction!!



• Troponin:– TnI: inhibits actin and myosin binding– TnC: Ca2+ binding sites– TnT: binds troponin to tropomyosin– TnC drives away TnI allowing interaction


Physiology – Myosin ATP-ase

• ATP binds to the myosin head inducing a small conformational shift in the actin-binding site which reduces its affinity for actin causing the myosin head to release the actin filament.

• This causes the myosin head to ‘cock back’ into place. ATP is then hydrolysed leaving ADP and Pi bound to the myosin.

• Weak interactions with actin cause the myosin to release the Pi which triggers the ‘power stroke’.

• As myosin attaches, the ADP is released and it binds tightly to the actin.

Rigor Mortis: lack of ATP, therefore the myosin cannot detach from the actin, meaning the muscles stay contracted.


Physiology – Action Potential

• 4 resting membrane potential (diastole)

• 0depolarisation

• 1 transient outward partial repolarisation

• 2 plateau• 3 repolarisationHypocalcaemia?

Reduced refractory periodTetany: spasms of the hands, feet, larynx, and cramps.




– Cardiac Cycle• Nodes• Cycle



Aims


Physiology – Conduction System

• SA node:• Located near the entrance of the

SVC • “Pacemaker”

• AV node:• Located in the bottom of the right

atrium• Only electrical connection

between the atrium and ventricle• Slow propogation

• Bundle of His• Purkinje fibres

• Distributes the impulses throughout the ventricles


Physiology – Cardiac Cycle

3 main events:• LV contraction• LV relaxation• LV filling

Preload: load present before LV contraction has startedAfterload: load after the ventricle starts to contract

Sounds:• “Lub” – low pitched, closure of AV

valves, marks onset of systole• “Dub” – louder, closure of semilunar

valves, marks onset of diastole







Aims


Physiology – Regulation of MAP

MAP = CO X TPR

Average arterial blood pressure over a total cardiac cycle

The volume of blood each ventricle pumps

The sum of resistances to flow offered by all systemic blood vessels


Physiology – Effectors of CO

• Increase in sympathetic innervation to heart INCREASE in BP• vasoconstriction • increased myocardial contractility• increase plasma adrenaline

• Affects Heart Rate (HR) and Stroke Volume (SV)


Physiology – Effectors of TPR

• Vasodilators (decrease in TPR): • NO• CO2

• decrease in O2

• Inflammatory mediators• ANP (hormonal)

• Vasoconstrictors (increase in TPR):• Sympathetic nerves• ADH• Angiotensin II• Adrenaline


Physiology – Arterial Baroreceptors

• Stretch-sensitive receptors found in wall of carotid sinus and aortic arch

• Send neurons to medullary cardiovascular centre in brain• Key role in short-term regulation eg exercise• If becomes long term then adopt a new base line

pressure• Main control in long-term BP regulation is blood volume.• FEEDBACK LOOP• Sensitivity is affected by sympathetic

stimulation/hypertensionCarotid sinus: glossopharyngeal nerve (CN 9) – more sensitive as going to brainAortic arch: vagus nerve (CN 10)


Physiology – Arterial Baroreceptors

StimulusDecreased sympathetic outflow to kidneys

Increased renal blood flow and urine

Increased sympathetic outflow to SA node

Increased heart rate (HR)


Physiology – Chemoreceptors

• Small highly vascular bodies in the aortic arch and medial to carotid sinus.

• Stimulated by a fall in O2 and pH/increase in CO2

• Involved in the control of respiration and reflex vasoconstriction

• Less important than baroreceptors in the control of circulation

• CO2 and pH affect peripheral; O2 affects central• Increase in CO2 vasoconstriction, increase in PR and

BP


Pathology

• Atherosclerosis• Heart failure• Thromboembolism• Shock• Myocardial infarction• Arrhythmias:

– ECG


Atherosclerosis

1. Endothelia injury – increased permeability.2. LDL forms fatty streaks. 3. Monocytes attracted macrophages.4. Take up oxidised LDL to form foam cells.5. Adhesion of platelets to endothelium.6. Release cytokines and GF.7. Migration of smooth muscle cells from media

to intima stabilize growing region.


Atherosclerosis

• Plaque rupture: fibrous plaque ruptures exposing cholesterol etc.

• Strong clotting reaction in blood.

• Angina• Intermittent claudication• MI• Stroke


Complications

• Definition: heart is unable to pump enough blood to satisfy needs of metabolizing tissues.

• Breathlessness• Tiredness• Fatigue


Heart Failure

• CAUSES:– Myocardial dysfunction– Volume overload– Obstruction to outflow– Compromised ventricular filling – Altered rhythm


Heart Failure

• Symptoms: – Swollen ankles– Fatigue– Anorexia

• Signs:– Raised jugular venous pressure– Hepatomegaly– Pitting oedema – Ascitis


Right Heart Failure

• Symptoms: – Fatigue– Breathlessness– Dyspnoea, orthopnoea, paroxysmal nocturnal

dyspnoea. • Signs:

– Cardiomegaly– Added heart sounds– Tachycardia– Crackles in lung bases


Left Heart Failure

• Mixture of both left and right.• Almost always right secondary to severe left

heart failure.

• Cor Pulmonale?


Congestive Heart Failure

• Thrombus: blood clot forming inside vessel wall. • Thromboembolism: obstruction of a blood vessel by

a dislodged blood clot. • Embolus: detached, travelling, intravascular mass:


Thromboembolism

Examples: cholesterol, fat, air (gas) and tissue


Thromboembolism Stasis

Blood Constituents

Vessel Wall


Thromboembolism Arterial Venous

Characteristics High pressurePlatelet rich

Low pressureFibrin rich

Examples MIStroke

DVTPulmonary Embolism

Treatment Antiplatelets Anticoagulants

• Definition: failure of cardiovascular system to adequately perfuse tissues.

• Hypovolaemic shock • Distributive shock:

– Septic – Anaphylactic

• Cardiogenic shock


Shock

• Symptoms:– Faintness– Dizziness– Sweating– Pallor– Reduced level of consciousness


Shock

• Signs:– Pale, cold, clammy skin– Rapid, weak pulse– Tachycardia, decreased stroke volume– Rapid, shallow breathing– Impaired urine output– Confusion


Shock

• Fall in circulating blood volume: blood or fluid.

• Loss of blood:– Trauma– Acute GI bleed– Haemorrhage– Operations

• Loss of fluid:– Severe burns– Dehydration– Pancreatitis – Vomiting– Diarrhoea


Hypovolaemic Shock

• Class I-III: increasing in severity:– Pulse increases– Respiratory rate increases– Urine output decreases– Mental status declines


Hypovolaemic Shock

• ‘Pump Failure’• Interruption of cardiac function.• Heart unable to maintain circulation.

– MI– Cardiac tamponade– Myocarditis – Pulmonary embolism– Valve failure – endocarditis – Fluid overload – poor left ventricular function

• Obstructive shock? The Peer Teaching Society is not liable for false or misleading information…

Cardiogenic Shock

• Sepsis: systemic inflammatory response associated with an infection.

• Septic shock: sepsis complicated by persistent inappropriate hypotension.

• Unresponsive to fluid resuscitation.• Treatment with vasoconstrictors.


Septic Shock

• Hypersensitivity reaction.• Massive release of histamine.• Peripheral vasodilatation – hypotension.• Vascular permeability – loss of plasma.• Bronchial muscle contraction – dyspnoea. • Oral, laryngeal and pharyngeal oedema.


Anaphylactic Shock

• Definition: necrosis of heart muscle due to impaired oxygen supply.

• Usually occlusion of coronary artery by unstable atherosclerotic plaque.


Myocardial Infarction

• SYMPTOMS: – Chest pain– Radiates to neck and arm– Shortness of breath– Sense of anxiety– Profuse sweating– Nausea– Vomiting– Light-headed



• Consequences: – Arrhythmia– Heart failure– Pericarditis – Rupture:

• Muscle• Walls• Valves




Coronary Arteries


Coronary ArteriesLeft Coronary Artery Right Coronary Artery

• Left posterior aortic sinus.• Behind pulmonary trunk.• Circumflex: left AV groove. • LAD: diagonal arteries.

• Left atrium• Most of left ventricle• Part of right ventricle• Most of IV septum• SA node (40%)• AV node (10%)

• Right anterior aortic sinus. • Right AV groove.• Posteriorly in sulcus on diaphragmatic base. • Posterior descending artery in IV groove.

• Right atrium• Most of right ventricle. • AV septum.• SA node (60%)• AV node (90%)

Widow Maker?


ECG

• Definition: abnormality of cardiac rhythm. – Sudden death– Syncope – Dizziness– Palpitations– No symptoms

• Bradycardia: <60bpm• Tachycardia: >100bpm


Arrhythmias


Atrial Fibrillation

• First degree: – Delayed AV conduction.– Prolonged PR interval: >0.22s

• Second degree:– Some atrial impulses fail to reach ventricles.– Some P waves followed by QRS complex.

• Third degree:– Complete heart block.– All atrial activity fails to reach ventricles. – No association between atrial and ventricular activity.– P waves and QRS complex occur independently.

• Bundle branch block: loss of synchronized ventricles. The Peer Teaching Society is not liable for false or misleading information…

Heart Block


Cardiovascular Therapeutics - Antiplatelets

ASPIRIN• NSAID• Decreased prostaglandin

synthesis• Decreased platelet

aggregation• Causes gastric ulceration• Causes bleeding

• Need to know Clopidogrel/prasugrel AND GP IIb/IIIa antagonists


Cardiovascular Therapeutics - Thrombolytics

STREPTOKINASE• Plasminogen plasmin• Plasmin destroys

clots/thrombus• 1% risk of stroke


Cardiovascular Therapeutics - Anticoagulants

WARFARIN• Anticoagulant• Inhibits vitamin K

dependant synthesis of coagulation factors II, XII, IX, X

• Takes time to work (2-3 days)

• Bleeding

• Need to learn LMW heparin/fondaparinux


Cardiovascular Therapeutics – Hypertension Drugs

ACE INHIBITORS• - pril• Act on the RAA system• eg Ramiprilß – BLOCKERS• Beta-1 receptors in myocardium• Lowers heart rate, CO, LV contractility, oxygen demand =

lower BP• Beta-2 receptors in smooth muscle, therefore

contraindicative in asthmatics• Need to know calcium channel blockers, loop/thiazide

diuretics, aldosterone antagonists, nitrates, digoxin, angiotensin receptor blockers, etc


Cardiovascular Therapeutics – Cholesterol Lowering Drugs

STATIN• Used to prevent hyperlipidaemia• Reduces the formation of atherosclerotic plaques• - statin• eg simvastatin

Drug that can be used for pulmonary hypertension if all else fails?

Viagra – vasodilator, relaxes arterial wall therefore reducing resistance and pressure


Topics we didn’t cover

• Blood disorders (RBC + WBC)• Haematology (blood groups)• Cardiovascular genetics• Detailed cardiovascular histology• Don’t forget veins!

• Histology – PDF• Revise from lectures!!!

– Recommended reading?• Past papers!!!• Formative assessments• Arteries and nerves!

– If all else fails – recurrent laryngeal. • Public health, stats, screening!• Definitions!!• Handwrittentutorials.com


Tips

Documents

Phase 1a Lauren Barker and Chiara Beck The Peer Teaching Society is not liable for false or misleading information…