Cardiovascular Flashcards
Electrocardiography is a representation of what?
The electrical events of the cardiac cycle.
Name 6 conditions that electrocardiography can help identify.
Arrhythmias. Myocardial ischaemia and infarction. Pericarditis. Chamber hypertrophy. Electrolyte disturbances. Drug toxicity.
Name a drug which may cause arrhythmia.
Digoxin.
Name the dominant pacemaker of the heart.
The sinoatrial node.
What is the intrinsic rate of the SAN?
60-100bpm.
What is the name for a cardiac rhythm in which depolarisation of the cardiac muscle begins at the SAN?
Sinus rhythm.
What is the function of the AVN.
To manage electrical activity from the atria to the ventricles and act as a back-up pacemaker.
What is the intrinsic rate of the AVN?
40-60bpm.
In addition to the AVN, what also functions as a back-up pacemaker?
Ventricular cells.
What is the intrinsic rate of ventricular cells?
20-45bpm.
Describe the conduction pathway of the heart.
SAN to AVN to Bundle of His to Bundle branches to Purkinje fibres.
On an ECG trace, the P wave represents what?
Atrial depolarisation.
On an ECG trace, the PR interval represents what?
The time between atrial depolarisation and electrical activation through the AVN.
On an ECG trace, the QRS complex represents what?
Ventricular depolarisation.
On an ECG trace, the ST segment represents what?
The period between depolarisation and repolarisation.
On an ECG trace, the T wave represents what?
Ventricular repolarisation.
Why doesn’t atrial repolarisation appear on the trace?
It is hidden by the QRS complex.
Define tachycardia.
An elevated heart rate, >100 bpm.
Define bradycardia.
A reduced heart rate, <60 bpm.
Define dextrocardia.
The heart is on the right hand side of the chest instead of the left.
Define acute anterolateral myocardial infarction.
Elevated ST segment in the anterior (V3 and V4) and lateral (V5 and V6) leads.
Define acute inferior myocardial infarction.
Elevated ST segment in the inferior (I, III, aVF) leads.
On ECG paper, what does one large box represent horizontally?
0.2 seconds.
On ECG paper, what does one small box represent horizontally?
0.04 seconds, 40ms.
On ECG paper, what does one large box represent vertically?
0.5mV.
Describe the location where the left ventricle can be palpated.
The left, 5th intercostal space on the mid-clavicular line.
What is the left ventricle responsible for?
The apex beat.
Define stroke volume.
The volume of blood ejected from each ventricle during systole.
Define cardiac output.
The volume of blood ejected from each ventricle as a function of time.
Define total peripheral resistance.
The total resistance to blood flow in the systemic blood vessels (between the aorta and the vena cava).
Which blood vessels have the highest resistance to blood flow.
Arterioles.
Define preload.
The volume of blood in the left ventricle before left ventricular contraction (end-diastolic volume).
Define afterload.
The pressure the left ventricle must overcome to eject blood during contraction.
Define contractility.
The force of contraction and change in myocardial fibre length.
Define cardiac elasticity.
The ability of the muscle to recover to its normal shape after systole.
Define diastolic dispensability.
The pressure required to fill the ventricles to the same diastolic volume.
Define cardiac compliance.
How easily the heart chamber expands when filled with blood.
What is Starling’s law?
The contractility of the heart is directly proportional to the end-diastolic volume.
Explain why stroke volume decreases as you stand up.
The effect of gravity reduces venous return, reducing end-diastolic volume
The first heart sound is produced from which event in the cardiac cycle?
The closure of the mitral and tricuspid valves.
The second heart sound is produced from which event in the cardiac cycle?
The closure of the aortic and pulmonary valves.
The third heart sound occurs when during the cardiac cycle?
In early diastole during rapid ventricular filling.
The third heart sound is normal in which patients?
Children and pregnant women.
What conditions is the third heart sound associated with?
Mitral regurgitation and heart failure.
The fourth heart sound occurs because of what?
Blood being forced into a stiff hypertrophic ventricle.
When does the fourth heart sound occur in the cardiac cycle?
Late diastole.
Name the condition associated with the fourth heart sound.
Left ventricular hypertrophy.
Give another name for ischaemic heart disease.
Coronary heart disease.
Give examples of ischaemic heart disease.
Stable angina. Unstable angina. Myocardial infarction. Cardiac arrest.
Describe the mechanism by which ischaemic heart disease develops.
Atherogenesis causes atherosclerosis.
Define atherogenesis.
The formation of fatty deposits in the arteries.
Define atherosclerosis.
The narrowing of an artery due to a build up of plaque.
Atherosclerosis commonly develops in which three arteries?
The circumflex, left anterior descending and right coronary artery.
Name seven risk factors for atherosclerosis.
Age. Smoker. High serum cholesterol. Obesity. Diabetes. Hypertension. Family history.
Why is diabetes a risk factor for atherosclerosis?
Hyperglycaemia damages endothelium.
Why is smoking a risk factor for atherosclerosis?
Smoking cause endothelial erosion.
What is the first step of the development of an atherosclerotic plaque?
Damage to endothelium.
How does damage to the endothelium contribute to atherosclerosis.
Damaged endothelium releases chemoattractants.
What is the function of chemoattractants?
To attract leukocytes.
Give examples of chemoattractants involved in atherosclerosis.
IL-1
IL-6
IFN gamma
How do leukocytes contribute to atherosclerosis?
They accumulate and migrate into the vessel wall.
Atherosclerosis begins as which type?
Fatty streak.
At what age can fatty streaks be found in the body?
Less than 10 years old.
What are fatty streaks composed of?
Lipid-laden macrophages and T-lymphocytes in the intimal layer of vessel wall.
Lipid-laden macrophages are called what?
Foam cells.
Fatty streaks develop into what?
Intermediate lesions.
What are intermediate lesions composed of?
Layers of foam cells, vascular smooth muscle cells and T-lymphocytes.
Other than cells, what also contributes to intermediate lesions?
Adhesion and accumulation of platelets to the vessel wall.
Intermediate lesions develop into what?
Fibrous plaques.
What are fibrous plaques composed of?
Smooth muscle cells.
Foam cells.
Red blood cells.
T-lymphocytes.
The components of a fibrous plaque are covered by what?
A dense fibrous cap made of extracellular matrix proteins.
Name two proteins that form the cap of a fibrous plaque.
Collagen.
Elastin.
The cap of the fibrous plaque keeps what contained?
Lipid core and necrotic debris.
Describe the two possible outcomes of atherosclerotic development.
Plaque grows and occludes the vessel, restricting blood flow.
Plaque ruptures, forming thrombus and causing death.
What condition is caused when a plaque occludes a blood vessel and restricts blood flow?
Angina.
How does angina present?
Chest tightness/heaviness that radiates to the arms, neck, jaw and teeth. Precipitated by exertion. Relieved by rest / GTN spray.
Angina is a result of what?
Reversible myocardial ischaemia causing a mismatch of blood supply and metabolic demand.
What is myocardial ischaemia?
Inadequate blood supply (due to narrowing of the coronary arteries, reducing blood and therefore oxygen supply).
How is stable angina characterised?
Induced by effort/exertion and relieved by rest.
How is unstable angina characterised?
More sever and more frequent. Occurs at minimal exertion or even at rest.
Unstable angina is associated with an increased risk of what?
Myocardial infarction.
Other than stable and unstable, name another type of angina?
Prinzmetal’s angina.
How is Prinzmetal’s angina characterised?
Caused by coronary artery spasm.
Other than mismatch of supply and demand, what else is responsible for angina?
Ischaemic metabolites stimulate nerve endings and cause pain.
Gender.
Give nine risk factors for angina.
Smoking. Sedentary lifestyle. Obesity. Hypertension. Diabetes. Family history. Genetics. Age. Hypercholesterolaemia.
How do arteries accommodate the growth of plaques?
By arterial remodelling.
What is arterial remodelling?
Arterial vessel growth.
At what point is arterial remodelling unable to accommodate plaque growth?
When the plaque is greater than 50% of the lumen size.
Give examples of a differential diagnosis of angina.
Pericarditis. Pulmonary embolism. Chest infection. Dissection of the aorta. GORD.
How is angina diagnosed on an ECG?
ECG typically normal but may show ST segment depression, a flat/inverted T wave or signs of past MI.
Other than the use of an ECG, give four other methods for diagnosing angina.
Treadmill test.
CT scan calcium scoring.
SPECT.
Cardiac catheterisation.
How does a CT scan for calcium scoring help diagnose angina?
The CT scan identifies calcium - a marker for atherosclerosis (calcified plaque).
How does SPECT help diagnose angina?
A radio-labelled tracer is injected into the patient, which is taken up the coronary arteries to highlight areas of good blood supply (and inversely poor blood supply - as a result of atherosclerosis).
Angina treatment can be separated into which three categories?
Modify risk factors.
Pharmacological intervention.
Surgical intervention.
Give five pharmacological options for the treatment of angina.
Aspirin. Statin. Beta-blockers. Glyceryl trinitrate spray. Calcium channel antagonists.
Describe two ways by which aspirin helps treat angina.
Inhibits platelet aggregation - avoiding platelet thrombosis.
Inhibits COX.
How does COX inhibition help treat angina?
By reducing prostaglandin synthesis thereby reducing platelet aggregation.
Describe how statins help treat angina.
Reduce cholesterol production by the liver.
Describe how beta-blockers help treat angina.
By slowing the heart and reducing the force of contraction - lower oxygen demand.
Give five contra-indicators for treating angina with beta-blockers.
Asthma. Hypotension. COPD. LVF. Bradycardia.
Describe how glyceryl trinitrate spray helps to treat angina.
GTN sprays are venodilators, meaning they dilate the systemic veins. Venodilation reduces the venous return and reduces preload, therefore the force of contraction decreases and the heart has a lower oxygen demand.
Describe how calcium channel antagonists help to treat angina.
Calcium channel antagonists are arteriodilators, meaning they dilate the systemic arteries. Arteriodilation reduces the blood pressure and reduces afterload, therefore the force of contraction decreases and the heart has a lower oxygen demand.
Give two surgical options for the treatment of angina.
Percutaneous transluminal coronary angioplasty (or percutaneous coronary intervention).
Coronary artery bypass graft.
Describe how percutaneous transluminal coronary angioplasty helps to treat angina?
Atheromas are dilated by inflating a balloon within a vessel, then removing the balloon to leave behind a stent.
Give risks and benefits of percutaneous transluminal coronary angioplasty.
Risk of stent thrombosis.
PCTA is minimally invasive and has a short recovery time.
Describe how a coronary artery bypass graft can help treat angina.
The left internal mammary artery is used to bypass a proximal narrowing in the left anterior descending artery.
What are negatives of the use of coronary artery bypass grafts?
An invasive procedure with a long recovery time.
What is acute coronary syndrome?
A syndrome due to decreased blood flow in the coronary arteries, leading to improper functioning or death of the heart muscle.
How is acute coronary syndrome characterised?
With central chest pain lasting greater than 20 minutes.
ACS characteristic chest pain is associate with what other signs/symptoms?
Sweating, nausea, vomiting, dyspnoea and fatigue.
Chest pain may not present in which patients with ACS?
Diabetics and the elderly.
How may ACS present in diabetic and elderly patients?
Syncope, pulmonary oedema, epigastric pain and vomiting.
Give five examples of signs of ACS other than chest pain.
Distress and anxiety. Pallor. Increased pulse and reduced blood pressure. Reduced fourth heart sound. Tachy/bradycardia.
Give six risk factors for ACS.
Age. Male. Family history of IHD. Smoking. Hypertension, diabetes mellitus, hyperlipidaemia. Obesity.
Describe how ACS develops.
Rupture/erosion of fibrous cap of coronary artery plaque leads to platelet aggregation and adhesion. Platelets cause vasoconstriction and localised thrombosis which results in reduced blood flow and ischaemia.
The risk of rupture of a coronary artery plaque increases due to which factors?
Presence of rich lipid pool beneath the fibrous cap.
The fibrous cap is thin.
What are the three types of ACS?
STEMI.
NSTEMI.
UA.
What is STEMI?
ST-elevation myocardial infarction is full thickness damage of heart muscle that occurs due to the complete occlusion of a major coronary artery.
How is STEMI diagnosed using ECG?
ST elevation. New left bundle branch block. Pathological Q wave will be present some time (days) after MI. Hyperacute T waves.
What is NSTEMI?
Non-ST-elevation myocardial infarction is partial thickness damage of heart muscle due to partial occlusion of a major coronary artery or complete occlusion of a minor coronary artery.
How is NSTEMI diagnosed?
Retrospectively after troponin results are available.
How may NSTEMI present on an ECG?
ST depression and/or T wave inversion. Hyperacute T waves.
What is UA?
Unstable angina of recent onset (less than 24 hours). A deterioration of previously stable angina.
What is the difference between NSTEMI and UA?
In NSTEMI an occluding thrombus causes myocardial necrosis and increased serum troponin or CK-MB.
What is myocardial infarction?
Myocyte death due to myocardial ischaemia.
What is Type 1 MI?
Spontaneous MI with ischaemia due to a primary coronary event.
Give three examples of a primary coronary event.
Plaque rupture. Fissuring. Dissection.
What is Type 2 MI?
MI secondary to ischaemia due to increased oxygen demand or decreased supply.
What conditions may lead to a decreased supply of oxygen to cause ischaemia?
Coronary spasm.
Coronary embolism.
Anaemia. Arrhythmia. Hyper/hypotension.
What is Type 3 MI?
MI due to sudden cardiac death.
What is Type 4 MI?
MI related to PCI (including stent thrombosis).
What is Type 5 MI?
MI related to CABG.
Give six possible differential diagnosis’ of ACS.
Angina. Pericarditis. Myocarditis. Aortic dissection. Pulmonary embolism. Oesophageal reflux.
Name three biochemical markers of ACS.
Troponin T & I.
CK-MB.
Myoglobin.
Which biochemical marker is the best for diagnosing ACS?
Troponin T & I.
The most sensitive and specific markers of myocardial necrosis.
How are Troponin T & I used to diagnose ACS?
3 to 12 hours from the onset of chest pain, serum Troponin T & I levels will be increased.
When do Troponin T & I levels peak?
24 to 48 hours after the onset of chest pain.
When do Troponin T & I levels return to baseline?
Over a period of 5 to 14 days.
Give another use, other than identifying ACS, for measuring Troponin T & I levels.
Peak levels can be used as prognostic indicator for risk of mortality. As well as determining which patients would benefit the most from aggressive medical therapy and early coronary revascularisation.
What is CK-MB?
A creatine kinase isoenzyme mainly found in heart muscle.
How is CK-MB used to diagnose ACS?
3 to 12 hours from the onset of chest pain, serum CK-MB levels will increase.
When do CK-MB levels peak?
Within 24 hours from the onset of chest pain.
When do CK-MB levels fall to baseline?
After 48 to 72 hours.
How is myoglobin used to diagnose ACS?
1 to 4 hours from onset of chest pain, serum myoglobin levels will increase.
Why is myoglobin unreliable?
It isn’t specific. Myoglobin is also found in skeletal muscle.
How can a chest x-ray be used to diagnose ACS?
Identification of pulmonary oedema, cardiomegaly and widened mediastinum.
Suggest nine groups of treatments that may be used to treat ACS?
Pain relief. Antiemetic. Oxygen. Anti-platelet. Beta-blockers. Statins. ACE inhibitors. Coronary revascularisation. Modifiable risk factors.
What options are available for pain relief treatment for ACS?
GTN spray.
IV opioid.
What is the purpose of an antiemetic?
Effective against nausea and vomiting.
What is an ideal oxygen saturation?
94-98%
What is an ideal oxygen saturation for a patient with COPD?
88-92%
Give three examples of antiplatelet therapies.
Aspirin.
P2Y12 inhibitors.
Glycoprotein IIa/IIIb antagonists.
What is the route of administration of P2Y12 inhibitors?
Oral.
Name three drugs that are P2Y12 inhibitors and used in the treatment of ACS.
Clopidogrel.
Prasugrel.
Ticagrelor.
What is a side effect of using P2Y12 inhibitors?
Increased risk of bleeding.
What is a caution for using P2Y12 inhibitors?
Avoid if CABG planned.
When are glycoprotein IIa/IIIb inhibitors used?
In combination with aspirin and P2Y12 inhibitors in patients with ACS undergoing PCI.
Name three drugs that are glycoprotein IIa/IIIb inhibitors and used in the treatment of ACS.
Abciximab.
Tirofiban.
Eptifbatide.
What is a side effect of using glycoprotein IIa/IIIb inhibitors?
Increased risk of major bleed.
How are glycoprotein IIa/IIIb inhibitors administered?
By IV only.
Name two beta-blockers used in the treatment of ACS.
Atenolol.
Metoprolol.
How are beta-blockers administered?
By IV then orally.
Explain the use of statins in the treatment of ACS.
HMG-CoA inhibitors inhibit cholesterol production.
Name three statins used in the treatment of ACS.
Simvastatin. Pravastatin. Atorvastatin.
Name two ACE inhibitors used in the treatment of ACS.
Ramipril. Lisonopril.
Ramipril and lisonopril are administered by which route?
Orally.
What is the incidence of ACS in the UK per year?
5/1000.
Define acute myocardial infarction.
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of an artery by thrombus.
Of deaths, how many people die from STEMI per annum?
5/1000.
STEMI has a worse prognosis in which groups of patients?
The elderly.
Those with left ventricular failure.
Give examples of risks for acute myocardial infarction.
Premature ménopause. Those with CHD. Age. Male. Hyperlipidaemia. Hypertension. Diabetes mellitus. Family history of IHD. Obesity. Smoking.
Describe how acute myocardial infarction occurs.
Rupture/erosion of a vulnerable fibrous cap of coronary artery plaque. Platelet accumulation, adhesion, localised thrombosis, vasoconstriction result in distal thrombus embolisation - arterial occlusion.
Myocardial necrosis occurs how long after complete arterial occlusion?
15 to 30 minutes.
Infarction initially affects which area following complete coronary artery occlusion?
Sub-endocardial myocardium.
If ischaemia continues after initially affecting sub-endocardial myocardium, which area becomes affected?
Sub-epicardial myocardium.
What is the difference between the endocardium and the epicardium?
The endocardium is the inner layer of the heart wall.
The epicardium is the outer layer of the heart wall.
What can the MI be called when infarct zone spreads to the epicardium?
Transmural Q wave MI.
Define transmural.
Occurs across the entire wall of the organ.
How may regions of the myocardium be salvaged after MI?
Early reperfusion.
How does MI present?
Severe central chest pain lasting greater than 20 minutes.
How is the pain of MI described?
Substernal pressure. Sharp. Squeezing. Aching. Burning.
How effective is GTN spray for treating MI pain?
Pain doesn’t usually respond.
Other than chest pain, how else does MI present?
Breathlessness. Distress and anxiety. Significant hypotension. Fatigue. Tachy/bradycardia. Pale, clammy and marked sweating.
How does STEMI present on an ECG?
ST elevation.
Hyperacute T waves.
LBBB.
T wave inversion and pathological Q wave follow.
An anterior infarct causes what changes on an ECG?
ST elevation in leads V1 to V3. ????????
An inferior infarct causes what changes on an ECG?
ST elevation in leads I, III and aVF.
A lateral infarct causes what changes on an ECG?
Leads I, AVL and V5 to V6 show change.
A posterior infarct causes what changes on an ECG?
ST depression V1 to V3.
ST elevation V5 to V6.
Dominant R wave.
A subendocardial infarct causes what changes on an ECG?
Any change.
Why is continuous ECG monitoring required after MI.
Likelihood of significant cardiac arrhythmia.
Minutes after STEMI: what does the ECG show?
T waves tall, pointed and upright.
ST elevation.
Hours after STEMI: what does the ECG show?
T waves invert.
Q waves develop as the R wave voltage increases.
Days after STEMI: what does the ECG show?
ST segment returns to normal.
Weeks/months after STEMI: what does the ECG show?
T waves may return upright.
Q waves remain.
Other than ECG, what investigation could be performed to confirm MI?
Transthoracic echocardiography.
What can transthoracic echocardiography show?
Wall motion abnormalities.
How is prehospital MI treated?
Aspirin 300mg chewable.
GTN.
Morphine.
How is hospital MI treated?
IV morphine.
Oxygen.
Betablockers - atenolol.
P2Y12 inhibitor - clopidogrel.
Give two other options, other than pharmacological intervention, for the treatment of MI?
Coronary revascularisation (including percutaneous transluminal coronary angioplasty and coronary artery bypass graft) or fibrinolysis.
Describe how fibrinolysis is used as a treatment of MI?
To enhance the breakdown of occlusive thromboses by activation of plasminogen to form plasmin.
What are modifiable risk factors of MI?
Stop smoking. Increase exercise. Lose weight. Eat a healthier diet. Alcohol intake within recommended limits.
What drugs are used for secondary prevention post MI?
Statins. Aspirin. Beta-blockers. ACE inhibitors. Warfarin (if large MI).
Give a possible complication within hours of MI.
Sudden death.
Sudden death post MI is due to what?
Ventricular fibrillation.
Why may persistent pain occur post MI?
Due to progressive myocardial necrosis.
How soon may persistent pain occur following MI?
12 hours to days after.
Why may arrhythmias occur post MI?
Due to electrical instability following infarction, pump failure and excessive sympathetic stimulation.
Explain why heart failure may occur following MI.
Muscle necrosis causes ventricular dysfunction, reducing cardiac output to a level that is insufficient to meet metabolic demands.
What is mitral incompetence?
Failure of the mitral valve to close properly allowing the regurgitation of blood back from the left ventricle into the left atrium. (Mitral regurgitation).
Why does mitral incompetence occur following MI?
Myocardial scarring prevents valve closure.
Why may pericarditis occur following MI?
A transmural infarct would cause inflammation of the pericardium.
Early cardiac rupture is a result of what?
Shearing between mobile and immobile myocardium.
Late cardiac rupture is a result of what?
Weakening of the wall following muscle necrosis and acute inflammation.
What is a ventricular aneurysm?
Inward bulging of the ventricular wall. Begin from a weakened area of the ventricular wall - filled with blood.
Why are ventricular aneurysms concerning?
Although they won’t usually rupture they can block passageways out of the heart and reduce blood flow.
Why may ventricular aneurysms occur post MI?
Due to stretching of newly formed collagenous scar tissue.
What is cardiac failure?
The inability of the heart to deliver blood (and therefore oxygen) at a rate that is commensurate with the requirements of the body’s metabolising tissues.
What is the mortality rate of cardiac failure following diagnosis?
25% to 50% mortality within the five years following diagnosis.
What is the prevalence of cardiac failure among the population?
1% to 3%.
What is the prevalence of cardiac failure among elderly patients?
10%.
Give six causes of cardiac failure.
Ischaemic heart disease. Cardiomyopathy. Valvular heart disease. Cor pulmonale. Hypertension. Alcohol excess.
What is cardiomyopathy?
Disease of the heart muscle, which becomes enlarged, thick and stiff.
What is cor pulmonale?
Pulmonary heart disease. Enlargement and failure of the right ventricle.
What causes cor pulmonale?
Increased pulmonary resistance (due to pulmonary stenosis or pulmonary hypertension) puts the right ventricle under greater stress - eventually it fails.
Give five risk factors for cardiac failure.
Aged over 65. Of African descent. Obesity. Male. People with a history of MI.
Heart failure brings about what kind of physiological changes?
Compensatory changes.
Why does heart failure cause compensatory changes?
Compensatory changes try to negate the effect of heart failure.
Compensatory changes for heart failure aim to maintain what?
Cardiac output.
Peripheral perfusion.
How does the progression of heart failure effect the compensatory changes?
Further progression overwhelms the compensatory changes.
What term describes the state when the compensatory changes are overwhelmed?
Decompensation.
What are the four compensatory mechanisms?
Venous return (preload).
Outflow resistance (afterload).
Renin-angiotensin system.
Sympathetic stimulation.
Describe how preload is a compensatory mechanism for heart failure.
During heart failure the volume of blood ejected from the heart decreases (more blood remains) so preload increases. According to Starling’s law, greater preload increases the force of contraction of the heart.
Why may the preload compensatory mechanism for heart failure be ineffective?
In patients with heart failure the failing myocardium isn’t able to contract that much more in response to increased preload - cardiac output cannot be maintained and may decrease.
Outflow resistance is made up of which three things?
Pulmonary and systemic resistance.
Physical characteristics of the vessel walls.
The volume of blood that is ejected.
Why may the outflow resistance compensatory mechanism for heart failure be ineffective?
Increase in afterload increases end-diastolic volume (cardiac output decreases). Increase in end-diastolic volume means ventricle must work harder - exacerbating the problem.
Outflow resistance is made up of which three things?
Pulmonary and systemic resistance.
Physical characteristics of the vessel walls.
The volume of blood that is ejected.
Why may the renin-angiotensin compensatory mechanism for heart failure be ineffective?
RAA system asks the heart to beat more forcefully to increase cardiac output. This causes a mismatch between supply (inadequate oxygen due to IHD) and demand (increased respiration for contraction). Ultimately the cardiac myocytes die and cardiac output decreases.
Describe how activation of the sympathetic system is a compensatory mechanism for heart failure.
During heart failure, arterial pressure decreases and venous pressure increases. These changes are detected by baroreceptors, which send out sympathetic stimulation to beta-1-adrenoceptors to increase the force of contraction and the heart rate with the aim of increasing cardiac output.
Why may the renin-angiotensin compensatory mechanism for heart failure be ineffective?
RAA system asks the heart to beat more forcefully to increase cardiac output. This causes a mismatch between supply (inadequate oxygen due to IHD) and demand (increased respiration for contraction). Ultimately the cardiac myocytes die and cardiac output decreases.
Describe how activation of the sympathetic system is a compensatory mechanism for heart failure.
During heart failure, arterial pressure decreases and venous pressure increases. These changes are detected by baroreceptors, which send out sympathetic stimulation to beta-1-adrenoceptors to increase the force of contraction and the heart rate with the aim of increasing cardiac output.
Where are baroreceptors located?
In the arterial wall of the aorta and carotid. In the walls of the heart and in the major veins.
Why may activation of the sympathetic system as compensatory mechanism for heart failure be ineffective?
Chronic sympathetic stimulation causes down regulation of the beta-1-adrenoceptors (fewer receptors), reducing the sympathetic activation of the heart and reducing cardiac output.
Name the four main types of heart failure.
Systolic.
Diastolic.
Acute.
Chronic.
Name four other types of heart failure.
Left-sided.
Right-sided.
Low-output.
High-output.
Describe systolic heart failure.
The inability of the ventricles to contract normally.
Give two characteristics of systolic heart failure.
Cardiac output decreases.
Ejection fraction < 40%.
Give three causes of systolic heart failure.
IHD, MI, cardiomyopathy.
Describe diastolic heart failure.
The inability of the ventricles to relax and fill fully.
Give two characteristics of diastolic heart failure.
Cardiac output decreases.
Ejection fraction > 50%.
What is tamponade?
When the pericardial fluid builds up and constricts the heart.
Other than hypertrophy, name three other causes of diastolic heart failure.
Aortic stenosis.
Constrictive pericarditis.
Tamponade.
What is tamponade?
When the pericardial fluid builds up and constricts the heart.
Describe acute heart failure.
Almost exclusively new onset or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension.
Describe chronic heart failure.
Develops slowly. Venous congestion is common but arterial pressure is well maintained until very late.
What is venous congestion?
When arterial flow is greater than venous flow.
A diagnosis of heart failure is made using which criteria?
Framingham criteria.
Name nine major criteria for heart failure.
Paroxysmal nocturnal dyspnoea. Crepitations. S3 gallop. Cardiomegaly. Increased central venous pressure. Weight loss. Neck vein distension. Acute pulmonary oedema. Hepatojugular reflux.
What is paroxysmal nocturnal dyspnoea?
Attacks of severe shortness of breath or coughing, typically at night.
What are crepitations?
Crackles of the lung.
What is S3 gallop caused by?
Rapid ventricular filling. Occurs in early diastole.
Describe the hepatojugular reflux.
Distension of the neck veins occur when pressure is applied to the liver.
Name seven minor criteria for heart failure.
Bilateral ankle oedema. Dyspnoea on ordinary exertion. Tachycardia. Decrease in vital capacity. Nocturnal cough. Hepatomegaly. Pleural effusion.
How is a diagnosis of heart failure made using the Framingham criteria?
Diagnosis of heart failure can be made if (two major criteria) or (one major and two minor) criteria are met.
Give seven other signs of heart failure.
Cyanosis. Cold peripheries. Hypotension. Narrow pulse pressure. Ascites. Murmurs. Displaced apex beat.
Give four examples examples of tests which may be performed to diagnose heart failure.
Blood tests.
Chest X-ray.
ECG.
Echocardiography.
Which blood tests may be performed to diagnose heart failure?
BNP.
FBC.
U&E.
Liver biochem.
Describe how BNP may be a marker for heart failure.
Brain natriuretic peptide is secreted from the ventricles in response to myocardial wall stress. Therefore BNP levels will be increased in patients with heart failure.
What may a chest X-ray of a person with heart failure show?
Alveolar oedema.
Cardiomegaly.
Dilated upper lobe vessels of lung.
Effusion (pleural).
What may an ECG show for a person with heart failure?
The underlying causes of the heart failure, including ischameia and left ventricular hypertrophy.
When is an echocardiogram performed on a patient with suspected heart failure?
If BNP and ECG are abnormal.
