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CVS > Acute Coronary Syndromes and Heart Failure > Flashcards

Acute Coronary Syndromes and Heart Failure Flashcards

1
Q

What are the differential causes of chest pain?

A
  • respiratory (pneumonia, pulmonary embolism)
  • cardiac (ischaemia, pericarditis)
  • Musculoskeletal (costrochondiritis or fractures)
  • GI conditions (reflux, peptic ulcers)
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2
Q

What is the difference between pain due to pleural or pericardial sac and pain due to lung or heart tissue disorders?

A
  • tissue disorders create a dull, poorly localised pain that is generally worse on exertion (visceral pain)
  • pleural/ pericardial disorders cause sharp, well localised pain that is worse on coughing/ movement
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3
Q

Describe the chest pain and secondary symptoms caused by pneumonia

A
  • sharp, well localised pain that is usually off to one side, that is worse on movement and coughing
  • comes with cough, fever and breathlessness
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4
Q

Describe the pain caused by a pulmonary embolism

A
  • sharp pain off to one side that is worse on breathing in or coughing
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5
Q

Describe the pain caused by ischaemia of the heart muscle

A
  • dull pain, often described as crushing or burning
  • retrosternal (central check behind sternum)
  • not well localised
  • radiates down neck, jaw, shoulders, left arm
  • worse on exertion
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6
Q

Describe the pain caused by pericarditis, how else can it be differentiated from an MI?

A
  • retrosternal
  • sharp and localised
  • worse on inspiration, coughing and lying flat
  • eased by sitting up and leaning forward
  • pericardial rub (harsh coarse sound) heard under stethoscope
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7
Q

What is pericarditis and what can cause it?

A
  • inflammation of pericardium
  • secondary to viruses (adenovirus, herpres, EBV), TB, autoimmune conditions, radiotherapy, kidney failure, thypothyroidism, cancer, heart attacks ect
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8
Q

describe the pain caused costochondritis or rib fractures

A
  • sharp and well localised
  • more painful on palpation
  • coughing and inspiration/ movement also make it worse
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9
Q

Describe the pain caused by reflux

A
  • burning pin running up chest or centrally
  • worse when lying flat or after meals
  • can be similar to MI
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10
Q

List the modifiable and non- modifiable risk factors for acute coronary syndromes

A

modifiable: smoking, hypertension, high cholesterol, diabetes, obesity, sedentiary life
non modifiable: age, familly history, male

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11
Q

What is the difference between stable and unstable angina?

A

In stable angina, plaque is occluding artery but not ruptured and so the pain is only felt on exertion

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12
Q

What will an ecg of someone with stable angina look like at rest and on exertion?

A

at rest- normal

exertion- ST depression in effected arreas (ischaemia occuring)

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13
Q

Will a GTN spray releive symptoms of someone with unstable angina?

A

no- it will only work with stable angina

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14
Q

What investigations are needed for someone with stable angina?

A
  • FBC- check non aneamic, cholesterol, thyroid function and renal function for other causes
  • ECG- abnormal Q wave suggest previous MI
  • CXR- other causes of pain
  • troponin- check no necrosis
  • angiogram/ CT to check which coronary artery is occluded
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15
Q

How is stable angina managed?

A
  • low cholesterol diet (no butter, cheese, sausage, more rabbit food)
  • statins
  • aspririn to lower clot risk
  • beta blockers to lower cardiac demand
  • ACE inhibitors to lower demand and BP
  • oral nitrate (like GTN spray but lasts longer)
  • calcium channel blockers if cant take beta blockers
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16
Q

What will be the ECG and troponin results of someone with unstable angina?

A
  • ST depression and/ or T wave flattening or inversion

- troponin normal as myocytes ischaemic but not yet dead

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17
Q

What is the difference between and NSTEMI and a STEMI?

A

In NSTEMI there is no ST elevation (there will be depression and/ or T wave inversion or flattening) because lumen or coronary artery is severely blocked. Troponin is raised in both

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18
Q

how do you differentiate between unstable angina and NSTEMI?

A

In UA troponin is normal in NSTEMI troponin is raised. Also pain tends to be worse in NSTEMI

19
Q

What is the difference in presentation of someone with NSTEMI and STEMI?

A
  • STEMI often looses consciousness

STEMI often presents with cardiac arrest

20
Q

What investigations needed for someone with acute coronary syndrome?

A
  • ECG- STEMI/ NSTEMI/ angina?
  • troponin- STEMI/ NSTEMI?
  • bloods- anaemia, systemic effects/ other causes?
  • CXR- any other causes?
  • Angiogram - which vessel occluded
  • blood glucose - if high on admission, low survival rate
21
Q

What surgeries are there to correct an acute coronary syndrome?

A
  1. PCI- put wire down coronary artery and ballon to widen space or use wire to put stent in place over narrowing
  2. CABG- bypass the occluded section using internal mammary artery or saphenous vein
    - only really done in STEMI and younger pts with high risk of recurrance
22
Q

How can are acute coronary syndromes managed?

A
  • ressus
  • pain relief
  • aspirin
  • O2
  • anticoagulants like streptokinase/ heparine in NSTEMI
  • nitrates may releive pain
  • B blcokers, ACE inhibitors, calcium channel blockers
23
Q

What is the presentation of someone with an acute coronary syndrome?

A
  • dull, crushing restorsternal chest pain radiating to neck, jaw, left arm at rest with nothing that will relieve it
  • look very unwell
  • pale, sweaty, nausious due to increase autonomic output
  • may have acute heart failure, heart murmers
24
Q

define heart failure

A

heart fails to maintain adequate ciculation for the needs of the body. This provokes a neural and hormonal response which effects the kidneys in particular.

25
Q

Give some causes of heart failure

A
  • ischaemic heart disease (most common in uk)
  • hypertension
  • dilated cardiomyopathy
  • congenital
  • pericardial disease
  • arrhythmias
  • high- output failure (demand for body increases an heart cant keep up)
26
Q

Describe the progression from class 1- 4 heart failure.

A
  1. no symptomatic limitations of physical activity
  2. slight limitation of physical activity but none at rest
  3. marked limitations of physical activity but still no symptoms at rest
  4. inability to carry out any physical activity without symptoms, may have symptoms at rest
27
Q

What is left ventricular heart failure (reduced ejection fraction) and give examples of when it can occur

A
  • impaired contractability (from LV dilation, MI, ischaemia, mitral or aeortic regurgitation) or increased afterload (aeortic stenosis, severe hypertension) on heart leads to
  • ejection fraction decrease to less than 50%
  • cardiac output therefor decreases
28
Q

What is heart failure with preserved ejection fraction (HDpEF)/ diastolic heart failure and when can it occur?

A

reduced compliance of the LV meaning less filling- such as in LV hypertrophy, tamponade, myocardial fibrosis (all chronic) or transient ischaemia (acute)

29
Q

What complications occur due to left systolic dysfunction?

A
  • fibrosis leads to electrical changes such as bundle branch blocks and arrhythmias
  • can get mitral valve incompetence as it gets stretched
30
Q

What is the name for when you get left and right sided heart failure?

A

congestive heart failure

31
Q

What is the effect of sympathetic nervous system activation as a result of heart failure?

A
  • Initially it improves CO, HR, contractability and vasdilation
  • but in long term makes it worse:
  • B receptors down regulated
  • myocytes hypertrophy and myocyte apoptosis
  • increased myocyte oxygen demand (more myocyte death)
  • RAAS system also activated means hypertension leading to wall stress and distension or hypertophy
32
Q

What is the result of RAAS system activation in heart failure?

A

increases blood pressure leading to more strain on heart

33
Q

When are the natriuetic peptides released and what is their effect?

A
  • ANP and BNP release due to myocyte distension
  • they decrease RAAS by vasodilation renal arterioles
  • this is helpful to help reduce hypertension
34
Q

What systemic effects of systolic failure are there?

A
  • skeletal muscle mass loss due to reduced blood flow- leads to fatigue and exersice intolerance
  • kidney gets smaller as less perfusion
  • anaemia develops as kidneys are a source of EPO and they atrophying, also due to expanded plasma volume, ACE inhibitors and iron malabsorbtion
35
Q

What are the signs and symptoms of left sided heart failure?

A
  • fatigure
  • dyspnoea (from pulmonary venous congestion)
  • orthopnoea
  • paroxysmal noctural dyspnoea
  • tachycardia
  • displaces apex beat due to enlarged LV
  • 3rd or 4th heart sounds
  • mitral regurg
  • pulmonary crackles from pulmonary oedema
  • peripheral pitting oedema from fluid retention
  • pin throthy mucus
  • cough
36
Q

Describe the signs and symptoms of right sided heart failure

A
  • more obvious pitting oedema
  • enlarged internal jugular vein with pulse
  • fatigue
  • orthodyspnoea
  • anoerxia and nausia (due to build up of oedema in GI)
  • tender and smooth liver enlargement (oedema)
  • ascites
  • if left sided heart failure is cause- symptoms of this also
37
Q

What can cause right sided heart failure?

A
  • most common is LV systolic heart failure
  • chronic lung diseases
  • pulmonary embolisms
  • left to right shunts
  • pulmonary/ tricuspid diseases
  • –> anything that increases afterload, the RV is very compliant so doesn’t mind increased preload
38
Q

What investigations are done in heart failure?

A
  • BNP high (not conclusive)
  • Echogardiogram to see thickness of ventircles
  • ECG to see conductance
  • is internal jugular vein enlarged (right sided heart failure)
  • are valves ok- asculation
  • HR - usually high
  • FBC- often anaemic
  • kidneys ok? - U&E
39
Q

How is heart failure treated?

A
  • ACE inhibitors- reduce RAAS and pressure so filling is optimal for contraction (see starlings law)
  • betablockers- reduce BP and HR
  • diruetics help symptoms of oedema but don’t help long term prognosis
  • MRA in systolic failure
  • treat cause (may need valve replacement ect)
  • eliminate precipitating factors (infections, hyperthyroidism, excessive Na intake, renal failure, hypertension, PE, MI ect)
40
Q

what are the main detrimental effects of angiotensin 2 release from RAAS activation in heart failure?

A
  • stroke from atherslcerosis, vasoconstriction ect
  • hypertension
  • MI (LV hypertrophy, fibrosis, remodelling, apotosis)
  • Renal failure
41
Q

when will LV hypertrophy occur and when will LV dilitation occur?

A

Dilation is due to volume overload for example in chronic mitral or aeortic regurgitation.
Hypertrophy is due to chronic pressure overload eg in hypertension or aeortic stenosis

42
Q

What is the difference between concentric and eccentric remodelling of the heart muscle?

A

concentric is sarcomeres adding in parellel leading to hypertrophy after chronic pressure overload
eccentic is sarcomeres adding in series leading to distension/ diliatation due to volume overload

43
Q

How is an acute pulmonary oedema be treated?

A
  • O2
  • sit them up
  • morphine reduces anxiety and venodilator
  • fast acting diuretic reduces blood vol and preload
  • iniotrophic drug to increase CO and move reduce pulmonary blood pressure

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