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ICP > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Symptoms in Systemic Enquiry

A
  • CHEST DISCOMFORT/ PAIN
  • BREATHLESSNESS
  • Ankle swelling
  • Dizziness (faintness, SYNCOPE)
  • Fatigue
  • Claudication
  • PALPITATION
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2
Q

Describe factors within chest discomfort

A
  • Site and radiation
  • Severity and character
  • Duration and periodicity
  • Aggravating and relieving factors
  • Location
  • Associated symptoms
  • Relation to exercise/ meals/ posture/ movement/ emotion
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3
Q

Describe breathlessness

A
  • On exertion
  • Orthopnoea
  • Paroxysmal nocturnal; dyspnoea
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4
Q

What do we look for in a general examination?

A
  • Build, demeanour
  • Face: central cyanosis, xanthelasma, corneal arcus
  • Hands: tobacco staining, clubbing, pallor, signs of endocarditis
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5
Q

Describe pulses

A 
-Radial pulse
=Rate and rhythm
=Volume
-Both radial synchronous
-Radial and femoral synchronous
-Blood pressure
-Jugular venous pulse (JVP)
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6
Q

What would you inspect?

A 
-•	inspection praecordium: scars, pulsations
•	heart
apex site (character)
heaves/thrills
heart sounds
heart murmurs (presence or absence, radiation)
carotid bruit
•	lung bases
•	oedema (ankle, tibial, sacral)
•	aortic aneurysm
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7
Q

Describe the peripheral circulation information

A
  • inspection for ulcers/ hair loss /varicosities /scars /colour
  • temperature
  • perfusion & capillary return, colour
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8
Q

Where are the pulses?

A
  • Radial
  • Brachial
  • Carotid
  • Femoral
  • Popliteal
  • Dorsalis pedis
  • Posterior tibial
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9
Q

What is disability?

A

Reduced effort tolerance

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10
Q

What is handicap?

A

Unable to work, look after relatives

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11
Q

What are causes of chest discomfort?

A
  • Ischaemic (angina)
  • Pleuritic (pneumonia/ PE)
  • Musculoskeletal
  • GI (oesophagitis)
  • Anxiety
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12
Q

What is breathlessness a distinguishing of?

A
  • Heart failure= typical age, associated symptoms, postural nature, relevant PMH
  • Asthma= typical age, diurnal pattern, precipitants, wheeze, PMH
  • Low cardiac output (valve disease, congenital defects)
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13
Q

What are the four main mechanisms of blackouts?

A
  • Cardiac syncope
  • Neurocardiogenic syncope
  • Postural hypotension
  • Seizures
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14
Q

Describe Cardiac syncope

A 
-Pattern:
=Little/ no warning
=Sudden LOC, usually for seconds only
=Rapid recovery
-Causes:
=Extreme bradycardia or tachycardia
=Mechanical obstruction (aortic stenosis)
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15
Q

Describe neurocardiogenic syncope

A

-Pattern:
=Seconds to minutes warning, light headed, warm, flushed
=Sometimes gradual or incomplete LOC, 2-3 minutes
=5-10 minutes recovery, sweating, dizzy
-Causes
=Vasovagal syncope
=Hypersensitive carotid sinus syndrome

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16
Q

Describe postural hypotension

A 
-Pattern:
=Episodes triggered by sudden change in posture
=Sometimes incomplete LOC, seconds only
=Rapid recovery on sitting/ lying, dizzy
=Not confused
-Causes
=Increasing age, diabetes, Parkinson's disease
=Vasoactive drugs, diuretics
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17
Q

Describe Seizures

A

-Pattern
=Prodromal aura/ altered consciousness
=Classically rigidity followed by clonic seizure but not all seizures follow this pattern
=Tongue biting and incontinence may occur
=Slow recovery, confusion, transient neurological symptoms
-Causes
=Primary epilepsy
=Mass lesions, stroke

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18
Q

What to inspect in the head and the neck?

A
  • Eyes= jaundice, high cholesterol
  • Mouth= central cyanosis
  • Conjunctivae= clinical anaemia
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19
Q

What is examined in the abdomen/ lower limbs?

A
  • Hepatomegaly, abdominal distension (ascites)
  • Venous system= varicose veins, venous pigmentation, ulcers
  • Arterial system= lower limb pulses, lower limb perfusion, ischaemic toes
  • Oedema= pitting and non-pitting, check sacral pad
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20
Q

Describe coronary heart disease

A
  • Acute myocardial infarction is caused by necrosis of myocardial tissue due to ischaemia,
    usually due to blockage of a coronary artery by a thrombus
    -The new criteria for diagnosing myocardial infarction are detection of rise and/or fall of cardiac
    biomarkers (preferably troponin) with at least one of 5 criteria including symptoms of ischaemia
    and ST changes
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21
Q

What are the modifiable risk factors for atherosclerosis?

A

-Smoking
-Diabetes mellitus (and impaired
glucose tolerance)
-Metabolic syndrome
-Hypertension
-Hyperlipidaemia
-Obesity
-Physical
inactivity

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22
Q

What are the symptoms and signs of myocardial infarction?

A
  • Characteristic central or epigastric chest pain radiating to arms, shoulders, neck or jaw
  • Substernal pressure, squeezing, aching, burning, sharp pain
  • Sweating, nausea, vomiting, dyspnoea, fatigue, palpitations
  • Low-grade fever, pale and cool, clammy skin
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23
Q

What are the investigations for myocardial infarction?

A
  • Bloods= FBC, UEs, CRP, lipids, troponin
  • ECGs (serial and continuous)
  • CXR= assess heart size, heart failure and pulmonary oedema
  • Pulse oximetry and blood gases for oxygen saturation
  • Cardiac catheterisation and angiography
  • Echocardiography= extent of infarction, ventricular function, acute mitral regurgitation, left ventricular rupture, pericardial effusion
  • Myocardial perfusion scintigraphy
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24
Q

What is the pre-hospital treatment for MI?

A

-Pain relief with GTN sublingual/spray and/or an intravenous opioid 2.5-5 mg diamorphine or 5-
10 mg morphine intravenously with an antiemetic
• Aspirin 300 mg orally
• IV access/ pre hospital thrombolysis more common in more rural setting

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25
Q

What is the in hospital treatment for MI?

A

-Patency of the occluded artery can be restored by percutaneous coronary intervention (PCI) or by
giving a thrombolytic drug. PCI is the preferred method.
• Long-term low-dose aspirin reduces overall mortality, non-fatal re-infarction, non-fatal stroke and
vascular death.
•Clopidogrel, in combination with low-dose aspirin, is recommended for AMI with ST-segment
elevation.
•Beta-blockers:When started within hours of infarction, beta-blockers reduce mortality, non-fatal
cardiac arrest and non-fatal re-infarction
•Angiotensin-converting enzyme (ACE) inhibitors:These reduce mortality whether or not patients have
clinical heart failure or left ventricular dysfunction. They also reduce the risk of non-fatal heart failure.
•Cholesterol-lowering agents: Ideally, initiate therapy with a statin as soon as possible for all patients
with evidence of cardiovascular disease (CVD) unless contra-indicated

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26
Q

What needs to be considered post MI?

A
  • Driving
  • Employment
  • Depression
  • Cardiac Rehab
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27
Q

What is heart failure?

A

Heart failure is a clinical syndrome resulting in a reduced cardiac output and/or elevated intracardiac
pressures
The left ventricular ejection fraction (LVEF) is the percentage of the blood in the left ventricle
which is pumped out with each heartbeat

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28
Q

What are the signs and symptoms of heart failure?

A

-Tachycardia at rest, low systolic blood pressure (BP), a displaced apex (LV dilatation) or RV heave
(pulmonary hypertension), a narrow pulse pressure or pulsus alternans (alternating large and small
pulse pressures) and a raised JVP.
•There may be a gallop rhythm due to presence of or murmurs of mitral or aortic valve disease.
•Bilateral basal end-inspiratory crackles ± wheeze (‘cardiac asthma’).
•Tachypnoea.
•Pleural effusions.
•Tender hepatomegaly with ascites.
•Often extensive peripheral oedema. There may be swollen ankles, sacral oedema or ascites

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29
Q

What investigations are used in heart failure?

A 
NT-proBNP
•ECG
•Echo
•Bloods
•CXR
•Consider staging: NYHA I-IV
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30
Q

How do we manage heart failure?

A

•Prognosis is poor on the whole, with approximately 50% of people with heart failure dying
within five years of diagnosis
•Community-based heart failure nurses provide an important adjunct to self-care, as well as a
bridge to secondary care.
•Smoking, diet, fluid intake, alcohol, exercise
•Drugs: diuretics, ACE-I, b-blocker, morphine (end stage)
•Palliative care

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31
Q

What are the signs and symptoms of lower extremity arterial disease (peripheral vascular disease)?

A

The most common symptom is muscle pain in the lower limbs on exercise (intermittent
claudication)
•Walking impairment - eg, fatigue, aching, cramping or pain in the buttock, thigh, calf or foot,
particularly when symptoms are quickly relieved at rest. Pain comes on more rapidly when
walking uphill than on the flat
•Ischaemic rest pain
•The Edinburgh Claudication Questionnaire has been shown to be a specific and sensitive
diagnostic tool

32
Q

What are the risk factors of peripheral vascular disease?

A 
Smoking
Diabetes mellitus
Hypertension Hyperlipidaemia
Physical inactivity
Obesity
33
Q

Describe the examination/ baseline investigation for peripheral vascular disease

A

-Examination of the lower limbs should include auscultation of the femoral arteries at the groin
level.
•The affected leg may be pale and cold, with a loss of hair and with skin changes.
•Inspection of the feet, noting the colour, temperature and integrity of the skin, and the presence
of ulcerations. There may be poorly healing wounds of the extremities. Patients with severe PAD
or critical lower-limb ischaemia may have ulceration or gangrene.
•Palpation of the femoral, popliteal, dorsalis pedis and posterior tibial pulses. Examination usually
reveals weak or absent pulses
•The main method to confirm the diagnosis is Doppler ultrasonography (ABPI)
•Bloods

34
Q

How is peripheral vascular disease managed?

A

-Most patients’ symptoms improve with optimal medical treatment and invasive intervention is
often not required. Approximately 20% will deteriorate and develop critical limb ischaemia.
•STOP SMOKING
•A supervised exercise programme has been shown to be a very important part of management
and should be offered to all patients with intermittent claudication
•Medication: statins and antiplatelet drugs
•Surgery: NICE states that angioplasty should be offered when risk factor modification has been
discussed, supervised exercise has failed to improve symptoms and imaging shows angioplasty is
suitable for the patient

35
Q

General symptoms common to all medicine

A
  • Check that appetite and weight are stable
  • Ask about sleep and sleep patterns, snoring and daytime sleepiness (OSA)
  • Ask about alcohol, smoking and use of drugs and herbal remedies
  • Ask about possible inherited or family illnesses
36
Q

What is syncope?

A

Transient loss of consciousness/ loss of consciousness and muscle strength characterised by a fast onset, short duration, and spontaneous complete recovery.

  • Vasovagal syncope (fainting)
  • Stokes Adams attacks
37
Q

What causes syncope?

A

It is caused by a decrease in blood flow to the brain, typically from low blood pressure

38
Q

What do you feel before syncope?

A

There is frequently a prodrome which may include feeling warm, lightheaded, blurred vision, nausea and an unpleasant gastric sensation accompanied occasionally by borborygmi and eructation

39
Q

What is presyncope?

A

Vasovagal Syncope may also be associated with a short episode of muscle twitching. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope

40
Q

What questions should be asked around vasovagal syncope?

A
  • Precipitating factors (emotion, sight of blood, pain)
  • Prodromal symptoms (nausea, blurred vision)
  • Colour change (pallor, grey, and sweatiness)
  • Recovery (spontaneous, sudden, complete)
  • There should be an absence of confusion or drowsiness
  • Pallor and sweating indicate release of catecholamines to overcome hypotension
  • Vasovagal syncope may run in families

Collateral history from a witness is very valuable and should be sought in every case

41
Q

Describe Stoke-Adams attacks

A

-Typically an attack occurs without warning, leading to sudden loss of consciousness.
-During an attack, a patient may be pale with hypoperfusion.
-Abnormal movements may be present, typically consisting of twitching after 15–20 seconds of unconsciousness.
=These movements, which are not seizures, occur because of brainstem hypoxia and not due to cortical discharge as is the case for epileptiform seizures
-Breathing typically continues normally throughout the attack, and, upon recovery, the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into the systemic circulation, which has become dilated due to hypoxia.
-As with any syncopal episode that results from a cardiac dysrhythmia, the fainting does not depend on the patient’s position.
-If it occurs during sleep, the presenting symptom may simply be feeling hot and flushed on waking.

42
Q

Why is asking about prodrome important?

A
  • A prodrome may precede Vasovagal Syncope
  • A prodrome is absent in Stokes-Adams attacks
  • Pallor by a flush as consciousness returns is typical
  • A cold sweat is less of a feature of Stokes-Adams attacks
  • Recovery is sudden and complete without sequelae

-May occur with tachycardia as well as bradycardia

43
Q

What are the causes of syncope during exercise?

A
  • Cardiac failure and cardiomyopathy
  • Outflow tract obstruction (aortic stenosis and HCM)
  • Aberrant origin of the RCA
  • Occasionally VVS after severe exertion (benign)

Suggests structural heart disease/ causes often reversible

44
Q

What is a palpitation?

A

An abnormal awareness of heartbeat

45
Q

Causes of palpitations

A
  • Simple ectopic beats
  • Normal cardiac rhythms (sinus tachycardia)
  • Cardiac arrhythmia
46
Q

What are palpitation ectopic beats?

A
  • Ectopic beats are common. Many people without any cardiac disease experience ectopic beats. Many asymptomatic people will have ectopic beats on routine ambulatory ECG monitoring.
  • In some people they are very intrusive and cause symptoms.
  • They are often described as “missed beats” when in fact they are premature additional beats. Because they are premature cardiac filling is incomplete and so the beat may be impalpable at the wrist, hence the “missed beat” sensation.
  • They commonly occur at rest, for example lying in bed, sitting and after meals. They may occur in runs and last for a variable amount of time. They frequently superess with activity.
  • They are more frequent with any intercurrent illness, stress, fatigue and anxiety.
47
Q

What is palpitation sinus tachycardia?

A
  • Sinus tachycardia is common
  • Catecholamine hormones (adrenaline and noradrenaline will make the heart beat harder and faster
  • Increased circulating concentrations of these hormones occur with anxiety, stress, panic disorder
  • Sinus tachycardia may occur with thyrotoxicosis (increased sensitivity to catecholamines) and anaemia
  • While the onset of tachycardia may be sudden the sensation of palpitation eases off gradually
48
Q

Symptoms of palpitation sinus tachycardia

A 
Gradual onset
Gradual termination
Associated symptoms
Thyrotoxicosis
Anaemia
Panic
Stress and Anxiety

Cardiac Failure
Volume depletion

49
Q

Describe cardiac arrhythmia

A
  • A cardiac arrhythmia occurs independent to external influences
  • They occur secondary to an intra-cardiac circuit or due to an automatic focus discharging
  • They are sudden in onset
  • They terminate abruptly
  • They usually have a rapid rate (which is constant apart from AF)
  • They may be regular (SVT or VT) or irregular (AF)
  • There may be associated symptoms
  • There may be precipitating and relieving factors (Valsalva Maneuver)
  • They may be followed by polyuria
50
Q

What are the types of tachycardia?

A
  • Paroxysmal tachycardia= sudden onset and termination. Rate relatively constant during period of tachycardia. Look at rate changes with activities compared to rate during tachycardia.
  • Narrow complex tachycardia= sudden or abrupt within one or two beats
  • Ventricular tachycardia= relatively constant rate
51
Q

How does the age of the patient affect which cardiac arrhythmia they may have?

A
  • Younger patients consider sinus tachycardia or SVT
  • Older patients suspect paroxysmal atrial fibrillation if irregularity of rhythm is described during tachycardia
  • Patients with heart disease (particularly previous myocardial infarction or cardiomyopathy) especially if there is a history of syncope or pre-syncope following the onset of tachycardia consider ventricular tachycardia

Remember to ask for family history of Sudden Cardiac Death

52
Q

Describe atrial fibrillation

A

Atrial fibrillation is the commonest cardiac arrhythmia. It may be permanent, persistent or paroxysmal. It may occur in the young or the older patient. The key feature of the history is that the cardiac rhythm is irregular.

53
Q

What is AF related to in younger patients?

A

Training
Alcohol
Thyrotoxicosis

54
Q

What is AF related to in older patients?

A

Obesity
Sinoatrial disease (common)
Hypertension
Sleep apnoea syndrome

55
Q

What causes AF?

A

While mitral stenosis due to rheumatic fever remains the classic cardiac disease to cause atrial fibrillation any cardiac disease that increases left atrial pressure may be associated with atrial fibrillation. Cardiac failure, myocardial infarction, cardiomyopathy and valve disease

56
Q

What are the major complications of AF?

A

One of the major complications off atrial fibrillation is embolic stroke and systemic embolism. This can be prevented by anticoagulation treatment. There is a score that can be calculated from the history.

57
Q

What is the CHADS score?

A 
C Cardiac failure (1)               
H hypertension  (1)                
A age > 75 years  (1)             
D diabetes  (1)                      
S systemic embolism (2)

CHADS Score > 1 anti-coagulate with warfarin or DOAC

58
Q

What structures in the chest cause chest pain?

A
  • Chest wall pain (muscles, ribs, sinews, cartilage)
  • Pain radiating from the spine and nerves
  • The lungs and pleura (pleuritic pain)
  • The oesophagus
  • The heart
  • The aorta
59
Q

How might chest pain present?

A

-Point pain
-L.infra-mammary pain
-Rib pain and costochondritis
-Neuralgic pain (Herpes -Zoster or shingles)
-Gastro-oesophageal reflux
Pleurisy
-Pericardial pain
-Angina

60
Q

What is CAD?

A

-Coronary artery disease (CAD) is common and
heart disease due to CAD remains an important
cause of Hospital Discharges
-CAD is increasingly commonly detected (increasing use of CT) and many individuals will have coronary disease and have no symptoms

61
Q

Describe Angina

A

-Angina is a very specific clinical syndrome
-It may be caused by coronary artery disease
-It may be due to cardiomyopathy
It may be due to aortic stenosis
-The accurate translation of angina is “choking”
-It is precipitated by effort and relieved promptly by rest
-Prompt relief by using the GTN is characteristic
-It may present in the chest, and radiate to arms, jaw and teeth
-Breathlessness and chest tightness are not always angina

62
Q

What causes angina?

A

Angina is believed to be due to myocardial ischaemia. This occurs when myocardial oxygen demand exceeds myocardial oxygen delivery. Exercise or effort increases oxygen demand.
=It may be caused by CAD, cardiomyopathy and aortic stenosis. Non-cardiac causes remain thyrotoxicosis and anaemia.

63
Q

What does Myocardial ischaemia present as on an ECG?

A

Myocardial ischaemia can be demonstrated on the ECG recording as ST segment depression. Myocardial ischaemia will increase with continuing exercise and resolve promptly with rest

64
Q

What is the link between angina and exercise?

A
  • Exercise increases heart rate and blood pressure (increases myocardial work and myocardial oxygen demand) and rest reduces heart rate and blood pressure.
  • GTN causes immediate vasodilatation and will lower blood pressure.
  • True angina resolves very quickly within a minute or two.
  • Chest tightness that resolves over the course of many minutes is unlikely angina
65
Q

What is the link between angina and eating a meal?

A

-Angina is more easily precipitated after a meal. This is because eating increases myocardial work. There is an increase blood flow (cardiac output) to the gut.
=Heart rate increases just as it would with exercise. Blood pressure falls due to splanchnic vessel dilatation. Peripheral blood vessels (systemic) constrict and this also contributes to the increasing in myocardial work.

66
Q

What is the link between angina and the weather?

A

-Angina is more troublesome or more easily precipitated in cold weather. This is because exposure to cold increases peripheral resistance due to vasoconstriction and blood pressure.
=This means that angina develops with less effort in cold weather because the person is starting with increased cutaneous vasoconstriction. This is why your hands go white in the cold.

67
Q

What are the risk factors for angina?

A
  • Irreversible= family

- Reversible= smoking, diet, diabetes, hypertension, cholesterol

68
Q

What is dyspnoea?

A
  • Breathlessness due to the heart is thought to be related to an increase the left atrial pressure.
  • This increasing in left atrial pressure is transmitted back to the pulmonary capillaries.
  • This changes the trans-capillary pressure gradient and fluid exudes into the alveoli causing pulmonary oedema.
  • The reduction in capacity for gas exchange due to the oedema causes breathlessness.
69
Q

What is Starling’s Law of the Heart?

A
  • The most important determinant of the left atrial pressure is Starling’s Law of the heart.
  • This states that the heart will contract more, the more it is stretched. The more cardiac filling the more blood it will eject.
  • This will occur until the filling pressure reaches the critical point that affects the trans-pulmonary capillary pressure gradient.
  • In a diseased myocardium the curve is much flatter.
70
Q

What causes breathlessness?

A
  • Breathlessness (dyspnoea) is an important symptom that may indicate cardiac disease
  • It is also an important symptom for respiratory disease
  • Breathlessness may occur with anaemia
  • Breathlessness may occur with obesity
  • Breathlessness may occur with hyperventilation
71
Q

Describe cardiac dyspnoea

A
  • Cardiac dyspnoea occurs in any situation where there is an increase in left atrial pressure
  • Exercise, lying flat, sleep and transfusion of blood and fluids will all increase filling pressures
  • Typically cardiac dyspnoea occurs with effort (muscle contraction increases venous return)
72
Q

What is orthopnoea?

A

Typically cardiac dyspnoea occurs when lying flat due to increased venous return

73
Q

What is paroxysmal nocturnal dyspnoea?

A

Typically cardiac dyspnoea causes the patient to wake suddenly from sleep and sit up

74
Q

Cardiac dyspnoea vs asthma

A
  • Cardiac dyspnoea= consistent (exertion), associated with orthopnoea an paroxysmal nocturnal dyspnoea, peripheral oedema
  • Asthma= wheeze and nocturnal cough, diurnal variation in symptoms
75
Q

How to take a history of ankle swelling/ oedema

A
  • The ankle swelling should pit
  • Pitting (one finger, one minute, bony prominence)
  • Cardiac oedema gets worse during the day
  • Cardiac oedema improves overnight
  • Should be distinguished from subcutaneous fat
  • Should be distinguished from non-pitting oedema

ICP (7 decks)

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