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Med Sci Yr 2 > Module 2.01 > Flashcards

Module 2.01 Flashcards

1
Q

Define cardiac output

A

Amount of blood ejected by each ventricle in one minute

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2
Q

Define stroke volume

A

Volume of blood pumped by each ventricle with each beat ( ml/ beat)

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3
Q

What is the formula for cardiac output?

A

Stroke volume x Heart rate

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4
Q

what are the 4 determenants of cardiac output?

A

1) heart rate
2) preload
3) after load
4) contractility

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5
Q

what factors inflence your heart rate?

A

positive chronotropes (increase heart rate):
- sympathetic stimulation
-drugs e.g. atrupine
negative chronotropes (decrease heart rate):
-parasympathetic stimulation
- drugs e.g. adenosine

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6
Q

what is preload?

A

how end diastolic volume causes pressure on the ventricle walls, the amount of blood that enters the ventricles during diatole

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7
Q

what influences preload?

A
  • venous return
  • fluid volume
  • artrial contraction
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8
Q

what is afterload?

A

the resistance ventricles must overcome to circulate the blood

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9
Q

what factors increase after load?

A

-hypertension
- athlerosclerosis
- vasoconsriction

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10
Q

what factors influence contractility?

A

positive ionotropes (increases contractility):
- sympathetic stimulation
- drugs e.g. dobutamine
negative ionotropes (decreases contractility):
- parasympathetic stimulation
- drugs e.g. beta- blockers and calcium channel blockers

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11
Q

what is starlings law?

A

the theory states that a higher end diastolic volume = higher preload = more forceful contraction = higher stroke volume
- meaning the more the muscle is stretched the stronger the contraction

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12
Q

how does chronic heart failure present?

A
  • breathlessness worsened with exertion
  • cough. may produce white/pink sputum
  • orthopnoea (shortness of breath on lying flat)-> ask how many pillows they use when sleeping
  • Paroxysmal Nocturnal Dyspnoea
  • Peripheral oedema
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13
Q

what are the 2 causes of heart failure?

A
  • impaired left ventricular contraction, systolic heart failure
  • impaired left ventricular relaxation, diastolic heart failure
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14
Q

what happens when someone has heart failure (impaired left ventricular contraction or relaxation)?

A

the heart is unable to pump blood into the aorta, this means blood collects in the ventricle and begin to flow back into the atrium and then into the lungs.

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15
Q

what is Paroxysmal Nocturnal Dyspnoea?

A
  • suddenly waking up with severe attack of acute shortness of breathe and cough
  • patients may try relive it by sitting on the end of the bed or walking around or opening a window for fresh air
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16
Q

what is the mechanism of Paroxysmal Nocturnal Dyspnoea? (3)

A
  • lying flat allows fluid settle across a large surface area of the lungs, standing up means fluid moves to the bottom of the lungs and upper lung becomes more clear to use
  • when sleeping respiratory centre becomes less responsive so the respiratory rate and respiratory effort decreases and does not respond to hypoxia
  • during the night adrenaline decreases meaning the myocardium can become even more relaxed, further worsening cardiac function and making their heart failure worse at night
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17
Q

what is the clinical assesment involved in diagnosing heart failure?

A
  • take a history
  • examination: listen for bibasal crepitation (crackles), look for peripheral odema
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18
Q

how is heart failure diagnosed (apart from clinical assesment)?

A
  • BNP blood test-> N-terminal pro-B-type natriuretic peptide (NT- proBNP)
  • echocardiogram
  • ECG
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19
Q

what can lead to heart failure?

A
  • Ischaemic heart disease
  • valvular heart disease - e.g. aortic stenosis
  • hypertension
  • arythmias e.g. AF
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20
Q

how would a doctor manage a patient with heart failure?

A
  • check BNP, if BNP>200 urgent referral to specialist, if BNP<200 routine referral to specialist
  • medical managment
  • surgical treatments: aortic stenosis, mitral regurgitation
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21
Q

describe the medical management of heart failure (types of drugs used)

A

-ACE INHIBITOR (e.g. ramipril)
-> ARB can be used instead of ace inhibitor
-> ace inhibtor should be avoided in valvular heart disease
-BETA BLOCKER (e.g. bisoprolol)
-ALDOSTERONE ANTAGONIST (e.g. spironolactone, epleronone)
->don’t start straight away, when there is a reduced ejection fraction and symptoms are not controlled with an ACEi and beta blocker
-LOOP DIURETICS (e.g. furosemide, bumetanide)

kidneys should be monitored as ace inhibitors, beta blockers and loop diuretics can cause electrolyte disturbances

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22
Q

what is meant by tachycardia and bradycardia?

A

tachycardia- rate is increased
bradycardia- rate is decreased

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23
Q

what are the 4 stages of the cardiac cycle?

A

1) atrial systole
2) atrial diastole
3) ventricular systole
4) ventricular diastole

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24
Q

what happens when you hear S1 (first heart sound)?

A

-“lub”
-you hear the atrioventricular valves closing
- this happens at the start of ventricular systole

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25
Q

what happens when you heart S2 (second heart sound)?

A
  • “dub”
  • semilunar valves shut
  • after ventricular systole is complete
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26
Q

what is happening when you hear S3 (third heart sound)?

A
  • subtle, and roughly 0.1s after S2
  • rapid ventricular filling
  • the chordae tendinae making a sound (like a guitar strong)
  • normal in young patients
  • in older patients can indicate heart failure (chordae tendinae are stiff and weak and reach limit sooner)
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27
Q

what is happening if S4 is heard ( a fourth heart sound)?

A
  • heard just before S1 ,”le” before the lub
  • always abnormal
  • relativley rare
  • caused by a stiff/hypertrophic ventricle
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28
Q

when should the bell or diaphragm of the stethoscope be used during auscultation?

A

-bell for low pitched sounds
-diaphragm for high pitched sounds

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29
Q

where are the 4 areas you listen to the heart (for murmurs)?

A
  • aortic area- 2nd intercostal space to the right of sternum
  • pulmonary area - 2nd intercostal space to the left of sternum
  • tricuspid area - 5th intercostal space to the left of sternum
  • mitral area- 5th intercostal space in midclavicular line (apex area)
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30
Q

where is the best place to listen for the heart sounds?

A

ERBs point- 3rd intercostal space on left sternal border

31
Q

what is the mechanism of beta blockers?

A
  • beta blockers reduce blood pressure and do this by blocking the action of adrenaline
  • Beta blockers cause the heart to beat more slowly and with less force, which lowers blood pressure. Beta blockers also help widen veins and arteries to improve blood flow
32
Q

what are side effects of beta blockers?

A
  • cold hands or feet, weight gain, fatigue
  • less common: depression, shortness of breath and trouble sleeping
  • In people who have diabetes, beta blockers may block signs of low blood sugar, such as rapid heartbeat
  • They can cause a slight rise in triglycerides, and a modest decrease in good cholesterol, or high-density lipoprotein (HDL) cholesterol. These changes often are temporary.
  • stopping to take beta blockers abruptly could increase risk of a heart attack
33
Q

what is the mechanism of ACE inhibitors?

A
  • stop the formation of angiotensin II, which is a vasoconstricter
  • this will lower blood pressure
  • the heart has less work to do to
33
Q

what is the mechanism of ACE inhibitors?

A
  • stop the formation of angiotensin II, which is a vasoconstricter
  • this will lower blood pressure
  • the heart has less work to do to overcome the resistance to circulate the blood (afterload)
34
Q

what is the mechanism of an aldosterone antagonist?

A

They work by blocking the receptor for the hormone aldosterone, which your body makes. Aldosterone makes your kidneys hold on to salt and water, which raises your blood pressure. Aldosterone is one of the ways your body adjusts blood pressure naturally in your blood vessels.

When you take an aldosterone blocker, your kidneys are able to release excess water and salt from your blood. The extra water and salt come out in your pee

35
Q

what is the mechanism of loop diuretics?

A

Loop diuretics reduce sodium chloride reabsorption in the thick ascending limb of the loop of Henle. This is achieved by inhibiting the Na-K-2Cl carrier in the luminal membrane in this segment, thereby minimizing the entry of luminal sodium and chloride into the cell. The loop diuretics are highly protein bound and therefore enter the tubule primarily by secretion in the proximal tubule, rather than by glomerular filtration

36
Q

define coronary heart disease (CHD)?

A

Coronary heart disease is the term that describes what happens when your heart’s blood supply is blocked or interrupted by a build-up of fatty substances in the coronary arteries.
- aka ischaemic heart disease or coronary artery disease

37
Q

define acute coronary syndrome

A

Acute coronary syndrome is a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart. One such condition is a heart attack (myocardial infarction) — when cell death results in damaged or destroyed heart tissue.

38
Q

define myocardial infarction

A

A heart attack is a serious condition where the supply of blood to the heart is suddenly blocked. It needs to be treated as quickly as possible.

39
Q

describe the pathophysiology of acute coronary syndrome?

A

Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

40
Q

what are the 3 types of ACS?

A

-Unstable Angina
-ST Elevation Myocardial Infarction (STEMI)
-Non-ST Elevation Myocardial Infarction (NSTEMI)

41
Q

what is the first investigations when a patient presents with ACS?

A
  • an ECG
  • If there is ST elevation or new left bundle branch block the diagnosis is STEMI.
  • If there is no ST elevation then perform troponin blood tests
42
Q

How is a troponin blood test used to diagnose ACS (after a STEMI has been ruled out with an ECG) ?

A

-If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
- If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain

43
Q

what are the symptoms associated with MI?

A
  • central, constricting chest pain
  • Nausea and vomiting
    -Sweating and clamminess
    -Feeling of impending doom
    -Shortness of breath
    -Palpitations
    -Pain radiating to jaw or arms
44
Q

If a patient has symptoms of an MI which settle with rest after 20 mins what should be considered?

A
  • angina
45
Q

what is a ‘silent MI’?

A
  • Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”
46
Q

what ECG changes are seen to diagnose a STEMI?

A
  • ST segment elevation in leads consistent with an area of ischaemia
  • New Left Bundle Branch Block also diagnoses a “STEMI”
47
Q

how do ECG changes diagnose an NSTEMI?

A

-ST segment depression in a region
-Deep T Wave Inversion
-Pathological Q Waves (suggesting a deep infarct – a late sign)

48
Q

why can raised troponins indicate an ACS?

A
  • troponins are proteins found in cardiac muscle
  • diagnosis of ACS usually requires serial troponins (6 or 12 hours after onset)
  • A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle
  • They are non-specific, meaning that a raised troponin does not automatically mean ACS.
49
Q

what investigations are carries out for ACS?

A

-Physical Examination (heart sounds, signs of heart failure, BMI)
-ECG
-FBC (check for anaemia)
-U&Es (prior to ACEi and other meds)
-LFTs (prior to statins)
-Lipid profile
-Thyroid function tests (check for hypo / hyper thyroid)
-HbA1C and fasting glucose (for diabetes)

50
Q

what are further treatments for a patient presenting with a STEMI?

A

-Primary PCI (if available within 2 hours of presentation)
-Thrombolysis (if PCI not available within 2 hours)

51
Q

what is a PCI (Percutaneous Coronary Intervention)?

A
  • involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance
  • contrast is then injected to idnetify area of blockage
  • This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage
  • Usually a stent is put in to keep the artery open
52
Q

what is thrombolysis?

A
  • involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots.
  • There is a significant risk of bleeding which can make it dangerous.
    -Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase
53
Q

what drugs are used to treated NSTEMI? (BATMAN)

A

B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm

54
Q

how is the GRACE score used to asess for need of PCI in NSTEMI?

A

This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
- <5% Low Risk
- 5-10% Medium Risk
- >10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

55
Q

what are the complications of an MI? (DREAD)

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

56
Q

what is dresslers syndrome?

A

This is also called post-myocardial infarction syndrome.
- It usually occurs around 2-3 weeks after an MI.
- It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart).
-It is less common as the management of ACS becomes more advanced

57
Q

what are alternative causes of raised troponins?

A
  • Chronic renal failure
    -Sepsis
    -Myocarditis
    -Aortic dissection
    -Pulmonary embolism
58
Q

how does dresslers syndrome present and how can a diagnosis be made?

A
  • presentation: pleuritic chest pain, low grade fever, pericardial rub on auscilltation
  • diagnosis: ECG, echocardiogram and raised inflammatory markers
59
Q

what lifestyle changes can prevent ACS?

A

-Stop smoking
-Reduce alcohol consumption
-Mediterranean diet
-Cardiac rehabilitation (a specific exercise regime for patients post MI)
-Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

60
Q

how is atherosclerosis caused?

A
  • inflamation and activation of immune system in artery wall (thickening)
  • deposits of lipids
  • followed by development fibrous, atheromatous plaques
61
Q

what do atheromatous plaques cause?

A
  • stiffening of artery wall, leading to hypertension
  • stenosis, reduces blood flow
  • plaque rupture, can break off and cause a thrombus, causing ischaemia and is the most common cause of ACS
62
Q

what are the risk factors of cardiovascular disease?

A

non- modifiable: old age, family history, male
modifiable: alcohol, smoking, poor diet, low exercise, obesity, poor sleep, stress

63
Q

what medical co-morbidities increase risk of atherosclerosis formation?

A
  • diabetes, type 1 and 2
  • hypertension
  • chronic kidney disease
  • inflammatory condition (e.g. rheumatoid arthiritis)
  • atypical antipsychotics (that may be used in schizophrenia)
64
Q

what is the Q-risk score?

A
  • percentage chance that a patient will have a stroke or an MI in the next 10 year
  • if score is above 10% NICE reccomends you should start a statin (e.g. atorvostatin 20mg)
  • NICE reccomends to check lipids 3 months after starting a statin, increase dose and aim for a 40% decrease in Non- HDL cholestrol
65
Q

what is the secondary prevention to CVD? (four As)

A

A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months)
A – Atorvastatin 80mg
A – Atenolol (or other beta-blocker – commonly bisoprolol) titrated to maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose

66
Q

define angina

A

narrowing of coronary arteries, during times of high demand the blood is unable to supply the myocardium. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms.

67
Q

what is the difference between stable and unstable angina?

A

Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome

68
Q

what is a CT Coronary Angiography and when is it used?

A
  • investigation for angina
  • This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing
69
Q

what baseline investigations are carried out for angina?

A
  • Physical Examination (heart sounds, signs of heart failure, BMI)
  • ECG
    -FBC (check for anaemia)
    -U&Es (prior to ACEi and other meds)
    -LFTs (prior to statins)
    -Lipid profile
    -Thyroid function tests (check for hypo / hyper thyroid)
    -HbA1C and fasting glucose (for diabetes)
70
Q

what are the four principles of managment of angina? (RAMP)

A

R – Refer to cardiology (urgently if unstable)
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions

71
Q

how is immediate symptomatic relief given for angina?

A

-Their GTN spray is used when required. It causes vasodilation and helps relieves the symptoms.
-Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.

72
Q

what drugs are used for long term symptomatic relief with angina?

A
  • Beta blocker (e.g. bisoprolol 5mg once daily) or;
  • Calcium channel blocker (e.g. amlodipine 5mg once daily)
  • other options: long active nitrates, Ivabradine, Nicorandil, Ranolazine
73
Q

what is the secondary prevention for angina?

A

Aspirin (i.e. 75mg once daily)
Atorvastatin 80mg once daily
ACE inhibitor
Already on a beta-blocker for symptomatic relief

Med Sci Yr 2 (2 decks)

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