cardiology cards Flashcards

1
Q

Define Shock

A

life-threatening generalised form of acute circulatory failure with inadequate oxygen delivery to , and consequently oxygen utilisation by the cells.

often defined by low bp (mean arterial pressure <65mmHg), evidence of tissue hypoperfusion, raised serum lactate.

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2
Q

Investigations for shock

A

Assess using ABCDE

capillary refill time: takes more than 3 seconds to turn pink after 5 second of compression: earliest and most accurate sign of shock

additional ix based on suspected underlying cause: ecg, troponin, cxr

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3
Q

clinical manifestations of anaphylactic shock

A

-warm and flushed skin
- itching
-sweating
-may be breathlessness and wheeze
-cyanosis
-low bp
-tachycardia
-pulmonary oedema

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4
Q

clinical manifestations of septic shock

A
  • warm and flushed skin
    -pyrexia and rigors
  • nausea and vomiting
  • bounding pulse
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5
Q

clinical manifestations of cardiogenic shock

A
  • signs of heart failure eg : raised jvp, pulmonary oedema
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6
Q

clinical manifestations of hypovolaemic shock

A
  • cold and clammy skin
    -confusion and drowsiness
  • increased sympathetic tone
    -tachycardia or bradycardia: depending on stage
  • initially narrow pulse pressure and weak pulse until there is compensation, and then again when there is failure of compensation
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7
Q

General signs and symptoms of shock

A
  • tachycardia
    -tachypnoea
    -pulse is weak: pulse pressure reduced - mean arterial pressure (MAP) may be maintained until a very large amount of blood has been lost!
  • skin is warm and flushed - in warm shock
    skin is cold and clammy: in cold shock
  • reduced urine output
    -weakness
    -confusion
    -collapse
    -coma
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8
Q

pathophysiology/ aetiology of shock

A

bp is key determinant of tissue perfusion:
bp = co * resistance to blood flow

co= sv *hr

shock is basically ischaemia on global scale - circulatory failure of whole body.

blood flow to tissues is dangerously low, leading to cellular injury, damage of multiple organs and even lead to multiple organ failure if not treated immediately.

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9
Q

pathophysiology of hypovolaemic shock

A

induced by a low fluid volume of blood. loss of around 20% of total blood volume can be enough to induce hypovolaemic shock. can be haemorrhagic or non-haemorrhagic :

non - loss of fluid volume isnt from bleeding eg dehydration, burns
haemoragic - loss of blood volume through ruptured blood vessels (loss of blood volume from bleeding ) - eg gi bleeding, trauma, peri/post-operative

results in total volume filling of heart going down which causes stroke volume to go down. causes decreased cardiac output and thend ecreased blood pressure.

when cardiac output goes down, catecholamines eg : epinephrine and norepinephrine, adh, and angiotensin 2 are released. cause vasoconstriction of blood vessels, increases vascular resistance and heart rate, in turn increases cardiac output. combined effects increase bp.

an indicator that tissues arent getting enough oxygen due to hypovolemia is a decreased mixed venous oxygen saturation (MVO2). this is the amount of oxygen bound to haemoglobin in the blood coming to the right side of the heart from the tissues. if blood volume is down, then oxygen is down, and so MVO2 will be donw.

as blood flow also give sheart to tissues, when its down, skin feels cool and clammy.

COlD SHOCK.

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10
Q

pathophysiology of cardiogenic shock

A

shock related to pathology of the heart, prevents it from pumping enough blood to tissues.

most common cause: acute MI. when cardiac myocytes die, it cant contract as hard, sv and co is reduced.

another cause is due to obstruction which doesnt allow the heart to fill properly with blood : eg pericardial effusion/cardiac tamponade physically constricts the ventricles and prevents the heart from expanding and contracting normally, reducing the sv and co..

other causes: arrhythmias, pulmonary embolus, tension pneumothorax, myocarditis, valvular disease, aortic dissection.

body releases vasoconstrictors to increase vascular resistance and help maintain bp. MVO2 will also be down since theres less oxygen being pumped out. - reduction in cardiac o utput leads to lowered blood flow, so skin gets cool and clammy: COLD SHOCK.

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11
Q

pathophysiology of neurogenic shock

A

the nervous system gets damaged and cant control the bodys bp
eg : spinal cord injury, epidural or spinal anaesthesia

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12
Q

pathophysiology of anaemic shock

A

not enough oxygen being carried in blood

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13
Q

pathophysiology of cytotoxic shock

A

cells are poisoned

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14
Q

pathophysiology of anaphylactic shock

A

an allergic reaction that causes dangerously low bp. massive release of histamine and other vasoactive mediators causes haemodynamic collapse.

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15
Q

distributive shock types

A

septic, anaphylactic , neurogenic

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16
Q

what is distributive shock

A

typically leakiness of blood vessels and excessive amount of arteriole vasodilation.

if arteriole dilate, vascular resistance to blood flow goes down, bp goes down, less perfusion, distribution of blood to organs and tissues.

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17
Q

pathophysiology of septic shock

A

endotoxins found on pathogens (usually gram negative) in the blood cause a cascade of events leading to lowered perfusion. they directly damage endothelial cells and cause release of vasodilators. they then activate the complement pathway, which stimulates mast cell release and activates other immune cells producing inflammatory cytokines. these help to destory the pathogen but also results in release of further inflammatory molecules eg platelet activating factor and ROS. these damage the endothelial cells and increase vascular permeability making the vessels leaky.

endothelial cells also express a procogaulant called tissue factors. these combined with decrease in anti-coagulants create net increase in coagulation and clotting in microvasculature. clotting creates further blockages and adds to decreased perfusion.

in this case, MVO2 may be normal or increased as blood doesnt have a chance to unload its oxygen to tisses.

also an increase in flow in the peripheral blood vessels, so skin becomes warm and flushed , therefore distributive shock is WARM shock.

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18
Q

management of shock

A

depends on cause

abc:
airways - intubation if needed
breathing: give o2
circulation: establish iv access, raise legs if hypovolemic, fluid resus and blood transufsion if necessary, ensure haemostasis

medications that increase heart contractility, cause vasoconstriction and retain fluid can nbe administered

manage underlying causes eg:

septic shock may require abx

anaphylactic shock: remove causative agent _+ adrenaline, chlorphenamine and hydrocortisone

cardiogenic shock: may require revascularisation

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19
Q

complications of shock

A

organ failure due to prolonged hypotension

kidneys - acute tubular necrosis
lung - acute respiratory distress syndrome (ARDs)
heart - Myocardial ischaemia and infarction
brain - confusion - irritability and coma

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20
Q

what is acute respiratory distress syndrome

A

life-threatening condition wher elungs cant provide the bodys vital organs with enough oxygen.

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21
Q

clinical presentation of acute respiratory distress syndrome

A

-cyanosis
-tachypnoea
-tachycardia
-peripheral vasodilation

22
Q

pathophysiology of acute respiratory distress syndrome

A
  • alveolar capillary membrane injury results in leakage of fluid into alveolar spaces
  • resulting neutrophil invasion attracting more neutrophils = exudative phase
    eventually fibroblasts come in and initiate healing= proliferative phase

and make scare tissue = fibrotic phase

results in severely stiff lungs and thus severe difficulty in ventilation and o2 blood perfusion.

23
Q

aetiologies of acute respiratory distress syndrome

A

extrapulmonary :
shock of any cause
head injury
drug reaction
sepsis

pulmonary:
pneumonia
chemical pneumonitis
smoke inhalation
near drowning

24
Q

Define rheumatic fever

A

autoimmune condition triggered by streptococcus bacteria.

25
Q

what is the peak age of rheumatic fever and where is it most common?

A

5-17 yrs

common in developing world

26
Q

aetiology of rheumatic fever

A

group a beta-haemolytic streptococcus pyogenes infection (rheumatic fever usually follows strep throat)

27
Q

risk factors of rheumatic fever

A

malnutrition
hla class II
overcrowding
fhx of rheumatic fever
developing world: disease of poverty, lower rates in devleoped world due to imrpvoement in abx use and hygiene
childhood and adolescene: peak 5-17 yrs old.

28
Q

pathophysiology of rheumatic fever

A

it develops 2-4 weeks after pharyngeal infection with group a beta-haemolytic streptococcus pyogenes, in susceptible population.

some strep bacteria have an m protein on their cell wall. immune system recognises it as a foreign molecule and mounts an immune response which produces antibodies against these proteins.
these antibodies also crossreact with proteins on someo f the bodys own cells eg cells in the myocardium and heart valves, the joints, the skin adn the brain. this is known as molecular mimicry and is a type 2 hypersensitivity reaction.

once bound to cardiac tissue, antibodies activate nearby immune cells , which causes a cytokine-mediated inflammatory response and tissue destruction.

most pts experience joint effects and pan-carditis (inflammation affecting all layers of the heart - endocarditis, myocarditis, pericarditis) - histologically, ASCHOFF BODIES (NODULES) are found in hearts of people with rehumatic heart disease due to inflammation.

if repeatedly exposed to group a beta-hemolytic streptococcus, body continues to launch immune attacks against the various tissues leading to chronic rheumatic heart disease.
here, the valves (typically mitral valve) develop scare tissue from repeated inflammation. leaflets of valves become thicker and can fuse together. the chordae tendinae which are attached to the valves can become thickened aswell.
these changes can cause complications with the valves, most commonly regurgitation. this can progress to stenosis and might even increase the risk of infective endocarditis due to microbial attachment.

29
Q

signs of rheumatic fever

A

heart murmur: strongly associated with mitral stenosis (chronic) and regurgitation (acute) and aortic regurgitation

  • tachycardia or bradycardia
    -pericardial rub on auscultation
  • palpitations
  • tender joints: usually not swollen
  • erythema marginatum - punk or red macules (flat) or papules (Raised) with a clear centre on the trunk or limbs

subcutaneous nodules: firm lumps under the skin made up of collagen, on extensor surfaces

30
Q

symptoms of rheumatic fever

A

recent sore throat or scarlet fever (occurs 2-4 weeks before chest pain)

chest pain : plerutici

sob

fever and rigors
non-pruritic rash

joint pain: oligo- or poly-arthritis - severe pain, often involves lower limbs, migratory : different joints become inflamed and improve at different times

Sydenham’s chorea : rapid, uncoordinated jerking movements of the face, hands feet.
due to autoimmune reaction against the basal ganglia of the brain. occurs up to 6 months after initial infection (late symptom)

31
Q

investigations for rheumatic fever

A

throat swab
anti-streptococcal antibodies (ASO) titres
chest xray - cardiomegaly and/or evidence of congestive heart failure
echocardiogram: mitral and aortic valvular pathology, and presence of pericarditis or pericardial effusion

blood cultures: if patient is pyrexial

raised wcc
raised esr and crp

32
Q

what is the jones criteria?

A

used to diagnose rheumatic fever and is dependent on evidence of recent streptococcoal infection in addition to 2 major criteria, or 1 major and 2 minor

recent evidence of strep infection:
- rapid group a strtococcal antigen test: positive
throat culture: positive
streptococclar antibodies (DNase B, or anti-streptolysin O) : elevated or rising

  • recent scarlet fever

major criteria:
j - joint arthritis
o - organ inflammation eg carditis
n - nodules
e - eryhtema marginatum rash
s - sydenham chorea

minor criteria:
fever
ecg changes (prolonged pr interval) without carditis
arthralgia without arthritis
raised inflammatory markers (CRP and ESR)

33
Q

what is the prognosis for rheumatic fever?

A

if left untreated it resolvers within 12 weeks but with treatment it can resolve within a few weeks. 30-50% of pts develop chronic rheumatic heart disease.

34
Q

complications of rheumatic fever

A

rheumatic heart disease - commonly affects mitral valve, followed by aortic valve.

heart failure: may occur in chronic or recurrent casses

infective endocarditis: previous rheumatic heart disease increases the risk of infective endocarditis

atrial fibrillation

35
Q

what is the management of rheumatic fever?

A

initial mx:
conservative: bed rest, analgesia, immobilise joints in severe arthritis.
antibiotic therapy: benzylpenicillin IV STAT, followed by oral phenoxymethylpenicillin for 10 days.

aspirin and steroids: used to treat carditis

haloperidol or diazepam: if severe Sydenham’s chorea is present

proxylaxuis:
all pts put on longterm, regular antibiotics to lower chance of develop chronic rheumatic heart disease

antibiotics: IM benzylpenicillin. duration depends on pt factors (could be upto 10 yrs)

36
Q

Define Hypertension

A

persistent elevation of arterial bp.
bp reading of >140/90 mmHg (abpm >135/85mmHg) - categorised into primary or secondary htn, depends on whether cause can be identified

normal bp = 120/80 mmHg

37
Q

risk factors for htn

A

nonmodifiable rf: increase age, african heritage, fhx

modifiable rf: obesity, sedentary lifestyle, alcohol excess, smoking, high sodium intake (>1.5g/day), stress

38
Q

stages and subtypes of htn

A

stage 1 - clinic reading of over 140/90 and ambulatory/home of over 135/85

stage 2 - over 160/100 or over 150/95

stage 3 - over 180/120

39
Q

explain the white coat effect

A

a discrepancy of over 20/10 mmHg between the clinic reading and average daytime ABPM reading suggests “white-coat” htn

40
Q

explain malignant (accelerated htn)

A

severe increase in bp over 180/120 mmHg with signs of retinal haemorrhage and/or pappilloedema, associated with target organ damage. EMERGENCY

41
Q

signs of htn

A

malginant (accelerated htn over 180/120):
- htn retinopathy
-visual distrubance
- cardiac symptoms eg chest pain
- oliguria or polyuria

secondary htn: signs of underlying cause : eg hyperthyroidism causes weight loss, sweating and palpitations

42
Q

symptoms of htn

A

asymptomatic : most common presentation
headaches: classically occipital and worse in the morning

43
Q

how should u monitor for htn?

A

every 5 yrs to screen for htn. measure more often in pts that are on borderline for diagnosis (140/90) and every yr in t2dm pts.

44
Q

complications of htn

A

hypertensive retinopathy

chronic kidney disease: increased levels of bp are associated with development of renal disease

congestive heart failure: hypertensive patients are 3 times more likely to develop congestive ehart failure

cerebrovascular accident: linear association ebtween increased bp and risk of developing a cerebrovascular accident

coronary artery disease: for every 20/10 mmHg increase in Bp, there is a doubling of mortality related to IHD.

45
Q

Mx for htn

A

Step 1 : if you have t2dm or you under 55 and arent from black african or african-caribbean family - give ACEI or ARB

if over 55 or black african/african carribean of any age give CCB

Step 2: if t2dm or under 55 and not black african give acei or arb and ccb or thiazide like diuretic
step 3: acei or arb+ccb_ thiazide like diuretic

step 2 for over 55 or blackafrican: ccb + acei or arb or thiazide like diuretic
step 3: same

step 4 :
confirm resistant hypertension: confirm elevated bp with ABPM or HBPM, check for postural hypotension and discuss adherence .

consider seeking expert advice or adding:
- low-dose spironolactone - if blood potassium level is <4.5 mmol/L
alpha blocker or beta blocker if blood potassium level is over 4.5 mmol/l

seek expert advice if BP is uncontrolled on optimal tolerated doses of 4 drugs.

46
Q

investigations for htn

A

blood pressure reading - both arms - if BP in clinic is over 140/90 take second reading. record lower of 2 measurements . if different in BP between arms is over 20 repeat. if reading remain over 20 , then subsequent measurement should be from arm with higher reading.
ambulatory bpm - offer to all pts with clinic bp between 140/90 and 180/120 to confirm diagnosis. measured over 24 hr period, with at least 2 measurements per hr during waking hours. overall at least 14 measurements needed.
hbpm - if abpm isnt appropriate: check manually throughout day. pt seated 2 consecutive measurement are required at least 1 minute apart. bp should be measured twice daily, usually in the morning and evening, ideally recorded for days but at least 4 days. 1st day ignore, remaining days average.

47
Q

investigations for htn

A

blood pressure reading - both arms - if BP in clinic is over 140/90 take second reading. record lower of 2 measurements . if different in BP between arms is over 20 repeat. if reading remain over 20 , then subsequent measurement should be from arm with higher reading.
ambulatory bpm - offer to all pts with clinic bp between 140/90 and 180/120 to confirm diagnosis. measured over 24 hr period, with at least 2 measurements per hr during waking hours. overall at least 14 measurements needed.
hbpm - if abpm isnt appropriate: check manually throughout day. pt seated 2 consecutive measurement are required at least 1 minute apart. bp should be measured twice daily, usually in the morning and evening, ideally recorded for days but at least 4 days. 1st day ignore, remaining days average.

48
Q

name some other ix for htn

A

fundoscopy - assess for hypertensive retinopathy

12-lead ecg - assess for ischaemic changes and evidence of lv hypertrophy

albumin: creatinine ratio (acr) and urinalysis : assess for renal dysfunction , as evidenced by elevated acr and proteinuria or haematuria on urinalysis.

bloods: hba1c, u&es , total cholestrol and hdl cholestrol

use 1 risk to discuss prognosis and healthcare options

49
Q

what is the diagnosis criteria for htn?

A

clinic bp of 140/90 or higher and abpm daytime average of hbpm average of 135/85 or higher.

50
Q

pathophysiology/ aetiology of htn

A

any changes in bp and consequently the development of htn occur due to alterations in cardiac output and peripheral resistance.

primary (essential htn) - no underlying cause. responsible for 90-95% of cases of htn. some contributing factors:
genetic susceptibility, excessive sns activity, abnormalities of na+/k+ membrane transport , high salt intake, abnormalities in renin-angiotensin -aldosterone system

secondary htn : indicates known underlying causes: examples include:

renal disease - glomerulonephritis, polycystic kidney disease, renal artery stenosis, chronic kidney disease
pregnancy - preeclampsia
medication - glucocorticoids, ciclosporin, atypical antipsychotics, combined oral contraceptive pill
endocrine disorders - primary hyperaldosteronism , phaeochromocytoma, cushings, hyperthryroidism, acromegaly