CVS Flashcards
Hypertension management- what is the 1st drug go to offer if <55 or T2DM
ACE inhibitor or angiotensin 2 receptor blocker
Hypertension management- what is the 2nd step to offer if <55 or T2DM
ACEI or ARB + calcium channel blocker
Or
ACEi or ARB + thiazide like diuretic
Hypertension management- what is the 3rd step to offer if <55 or T2DM
ACEi or ARB + Calcium channel blocker + thiazide like diuretic
Hypertension management- what is the 4th step to offer if <55 or T2DM
Look at K
If < 4.5 add spironolactone
If > 4.5 add alpha or beta blocker
Hypertension management changes in > 55 and no T2DM or black ethnicity
Start on calcium channel blockers
What is the 2nd stage of hypertension management for black patient
Already on calcium channel blocker therefore add ARB not ACEi
what is acute limb ischaemia and how is it caused
sudden decrease in limb perfusion which threatens viability of limb = surgical emergency
caused by embolism (thrombus which breaks off), thrombus in situ (atheromatous plaque rupture), trauma (compartment syndrome)
what is the clinical presentation of acute limb ischaemia
6 Ps
painful pallor perishingly cold pulseless paraesthesiae paralysis
what happens in acute limb ischaemia
occlusion of blood vessel → ischaemia and infarction → death of limb
investigations for acute limb ischaemia
- bedside - vitals, ECG
- bloods
- lactate - anaerobic respiration
- thrombophilia screen (if <50)
- group and save - transfusion
- imaging - Doppler US (reduced blood flow through limb), contrast angiography (visualisations of blood vessels - occlusion and narrowing)
management of acute limb ischaemia
- SURGICAL EMERGENCY
- revascularisation required within 4-6 hours
- embloectomy - removal of clot
- angioplasty - balloon catheter and stent
- by pass surgery
- heparin infusion after surgery
what conditions does chronic limb ischaemia include
peripheral artery disease
critical limb ischaemia
intermittent cluadication
what is peripheral artery disease, critical limb ischaemia and intermittent claudication
Peripheral Arterial Disease results in symptomatic reduced blood supply to the limbs. This often occurs as a result of atherosclerosis causing narrowing of the arteries supplying the limbs and periphery.
Critical Limb Ischaemia is the end stage of peripheral arterial disease where there is an inadequate supply of blood to a limb and it cannot function normally at rest.
Intermittent Claudication is the symptom of having ischemia in a limb during exertion that is relieved by rest. This pain is typically a crampy, achy pain in the clad muscles associated with muscle fatigue when walking beyond a certain intensity.
risk factors for acute limb ischaemia and peripheral vascular disease
acute - smoking, diabetes, AF
PVD - smoking, coronary or cerebral artery disease, diabetes, hypertension, hyperlipidaemia
what is the cause of peripheral artery disease
atherosclerosis which narrows the arteries -> reduced blood flow to downstream organs -> ischaemia
how would someone present with peripheral vascular disease
claudication
night pain
ulcers and gangrene skin changes weak pulses pallor coldness increased CR peripheral bruits
what is vascular claudication
intermittent crampy pain in the limb during exertion
relieved by rest
occurs after walking in the heart and thigh or buttock
what beside tests can we measure in someone with chronic limb ischaemia
ankle brachial index
ECG
bloods - FBC, U&Es, lipids, blood glucose
what is the ABPI and what is the severity classification
ankle brachial pressure index - compares BP of upper and lower limb
<0.9 = peripheral vascular disease
> 0.9 normal
0.8-0.9 mild
0.5-0.8 moderate
<0.5 severe
what imaging techniques can be used for chronic limb ischaemia
doppler US
angiography
what is the management for asymptomatic and intermittent claudication in chronic limb ischaemia
conservative management
- lifestyle advice
- statin therapy
- anti-platelets (clopidogrel)
- diabetes and BP control
- encourage exercise
what is the surgical management for chronic limb ischaemia
- angioplasty - with or without stenting (opens up narrowed vessels
- bypass grafting - younger patients
- amputations - if gangrene → sepsis (attempt to preserve knee)
what drug should be prescribed to patients with PVD?
clopidogrel and atorvastatin
what is shock?
reduction of effective blood flow and inadequate tissue perfusion with decreased delivery of oxygen to the capillary exchange bed
what are the 2 causes of shock
reduction in CO (cardiogenic, hypovolaemic)
loss in systemic vascular resistance (septic, anaphylactic, neurogenic)
what are the different types of shock
cardiogenic
hypovolaemic
neurogenic
distributive - septic, anaphylactic
signs of cardiogenic shock
low BP increased systemic vascular resistance increased HR decreased CO cold and clammy
signs of hypovolaemic shock
increased systemic vascular resistance increased HR decreased BP decreased CO cold and clammy
signs of septic shock
reduced systemic vascular resistance increased HR normal/increased CO decreased BP warm and well perfused
signs of neurogenic shock
damage to spinal cord (unopposed parasympathetic innervation) reduced BO reduced systemic vascular resistance low BP warm (then goes cool)
what is the significance of tachypnoea in shock?
increased lactate - metabolic problem
bedside investigations for shock
ECG
bloods - troponin, cardiac enzymes, U&Es, ABG
management of hypovolaemic shock
raise legs
fluids
management of cardiogenic shock
- O2
- analgesia - diamorphine
- investigations - CVP, BP, ABG, ECG, urine
- fluid status - plasma expanders of inotropic support
- reverse causes - MI, PE
what is cardioresp arrest
patient who is unresponsive and not breathing properly is in cardiorespiratory arrest and requires CPR
causes of cardioresp arrest
Reversible causes for Cardiorespiratory Arrest are (4H’s, 4T’s):
4H’s:
Hypoxia
Hypovolemia
Hyper/Hypokalaemia
Hypothermia
4T’s:
Thrombosis
Tension Pneumothorax
Tamponade
Toxins
basic life support management for cardioresp arrest
- call arrest team and bring fibrillator
- ABC approach
- airway - chin lift
- breathing -Look, listen and feel for breathing for no more than 10 seconds
- circulation and chest compressions
- heel of one hand on the centre of the chest
- second hand on top and interlock fingers
- ratio of 30 compressions to 2 rescue breaths until a defibrillator becomes available
advanced life support for cardioresp arrest
- Chest compressions should be stopped for less than 5 seconds to assess the rhythm and determine if it is shockable or non-shockable
- shockable = VF [irregular] or pulseless VT [regular] (wide QRS complex tachy)
- non-shockable - asystole
- shockable rhythm
- defibrillate then continue CPR
- repeat defibrillation
- give adrenaline and amiodarone after 3 shocks
- non-shockable
- continue CPR
- obtain IV access and secure airway
- give adrenaline
what is an arterial aneurysm?
localized dilatation of an artery, involving all three layers of the blood vessel, by at least 50% of its original size
what is a triple A?
abdominal aortic aneurysm - dilatation of abdominal aorta by more than 50% of its original size
where is the most common site for a triple A?
between the renal arteries (L1) and the bifurcation of aorta (L4)
because abdo aorta lacks vasa vasorum so it is weaker
what is an unruptured AAA classed as?
abdo aorta larger than 3cm across
risk factors for AAA
Smoking Age Atherosclerosis Gender (Male) Ethnicity Connective Tissue Disorders - Marfan's Syndrome or Ehlers-Danlos
differentials for AAA
Kidney Stones
Back/Muscle Strain
Thoracic Aortic Aneurysm
Myocardial Infarction
Perforated Bowel
which gender is a AAA more common in?
3 times more common in men
what are the different types of aneurysms?
true - all 3 layers of blood vessels are involved in the aneurysm
pseudoaneurysm - hole in artery allowing blood to spill out and pool around the artery
fusiform - symmetrical bulging of the aneurysm
saccular/berry - asymmetrical bulging of aneurysm (one side of blood vessel dilates, resulting in turbulent flow or weakness)
what law increases the risk of aneurysm rupture
Laplace
what are the clinical features of an unruptured AAA
asymptomatic
can present with abdo/back pain
pulsatile and expansile abdo mass (in time with heartbeat)
what are the clinical features of a ruptured AAA
severe and acute onset abdo pain - radiates to back
hypotension
pulsatile and expansile abdo mass
signs of shock from ruptured AAA
pale, cold, clammy, mottled skin
tachycardia
hypovolaemia
oliguria (decreased urine output)
decreased GCS
tachypnoea
what does a ruptured AAA present as in an elderly patient
renal colic - kidney stones
suspect this in the elderly
what are the 3 layers of a blood vessel
tunica intima - in direct contact with flowing blood, endothelial cells
tunica media - smooth muscle cells, maintain vascular tone
tunica adventitia - fibroblasts, collagen, macrophages involved in cell trafficking, signalling and repairing injured vessels = contains vasa vasorum
what is the pathophys of an arterial aneurysm
Trigger - genetic predisposition, local haemodynamic stress
Cellular migration - macrophages, neutrophils, T and B cells
Inflammatory infiltrate - increased chemokines, free radicals, increased MMP activity
Collagen degradation - weakening of tunica media, aneurysmal dilatation, degradation of the collagen through small damages to the vessel wall. Aorta is weakened dilatates over time
Once aneurysm is formed there is progressive enlargement
bedside investigations for arterial aneurysm
vital signs - tachycardic, tachypnoeic, hypotensive
what blood tests would be organised for an arterial aneurysm
FBC - anaemia
U&Es - renal function
what imaging can be ordered for arterial aneurysm?
US or CT (if suspected rupture)
what is the national screening programme for unruptured AAA?
for all men aged 65+ offered US scan
negative test <3cm
positive test >3cm
if positive result on screening for AAA - when will the scan be repeated?
small AAA (3-4.4cm) - repeat in 1 year
medium AAA (4.5-5.4cm) - repeat in 3 months
> 5.5cm - urgent referral to vascular surgeons for elective surgery
what is the management of a ruptured AAA?
ABC
supplemental O2
large bore IV access
urinary catheter
bloods - cross match
patient needs URGENT surgery
what are the 2 methods of repair for ruptured AAA?
endovascular anuerysm repair (EVAR)
open surgical repair - midine laparotomy
what is an EVAR and which patient group is it used on
enter through iliac artery - insert stent guided by X-ray
has long term complications - require life long surveillance (ensure functioning)
preferred in patients with co-morbidities (physiologically deranged) - not young and healthy patients
what is an open surgical repair for a ruptured AAA - which patient group is it used in
midline laparotomy
move duodenum and small bowel out of the way
clamp above and below aneurysm (open aneurysm and stitch in graft)
sow in tube or trouser stent
associated with high mortality - clamping -> end organ ischaemia also large blood loss
for young and healthy patients
which type pf AAA rupture has the best prognosis
retroperitoneal rupture (tamponade -> limit blood loss)
anterior rupture = high mortality
what are the complications of a AA?
rupture - haemorrhage
thrombosis and embolism - occlusion of downstream blood vessels -> limb ischaemia
fistula formation
pressing on other structures
haemorrhagic stroke - if rupture in cerebral circulation
what is an aortic dissection
tearing in wall of aorta
tunica intima splits from tunica media and externa/adventitia
media splits which creates a new channel for blood flow = false lumen
what are the layers of the blood vessel wall
LIMA
lumen
intima
media
adventitia/externa
how would someone with aortic dissection present
tearing pain between shoulder blades
hypertension
asymmetrical pulses (different in each arm)
risk factors for aortic dissection
hypertension
connective tissue disorder - marfans
pregnancy
bicuspid aortic valve
what are the 5 killer chest pains
aortic dissection MI oesophageal rupture tension pneumothorax PE
what are the 2 ways aortic dissection creates pathology?
reduces blood flow through true lumen = reduces blood flow to other tissues -> ischaemia and infarction
external rupture of aortic dissection leading to cardiac tamponade (compression of great vessels) -> reduced preload and decreased CO
bedside tests for aortic dissection
vital signs - symmetrical radial pulses, asymmetrical brachial BP
imaging for aortic dissection
CT - see false lumen
X-ray - see wide mediastinum
what are the 2 classes of aortic dissection
type A - involves ascending aorta = most serious requires surgical repair
type B - does not involve ascending aorta = less serious, medical management strict BP control
what are the complications of a type A aortic dissection
compromise blood flow:
carotid dissection -> stroke
coronary dissection -> MI
rupture into pericardium -> tamponade
stretching of aortic valve -> aortic regurgitation
external rupture into thoracic cavity -> exsanguination
what are the complications of type B aortic dissection
occlusion of coeliac or mesenteric a = gut ischaemia
occlusion of renal arteries = renal failure
extension to iliac arteries = lower limb ischaemia
what is haemostasis
physiological response that involves the formation of a solid plug due to damage at a blood vessel
prevents loss of blood from circulation
what is inflammation
body’s response to any form of cellular injury (infection, heat, trauma, hypoxia, radiation)
what is the aim of inflammation
to remove injurious agents, clear away any dead tissue and trigger healing of damaged tissue
what are the harmful effects of inappropriate activation of inflammation
anaphylactic shock
autoimmune disease
what are the effects of inappropriately activated haemostasis
thrombosis
what are the 2 types of inflammation
acute inflammation - transient (involves vascular changes and neutrophil accumulation)
chronic inflammation - persistent (on-going tissue destruction and repair)
what are the cardinal signs of acute inflammation
redness heat pain swelling loss of function
what is the inflammatory cell of acute inflammation
what are the 2 major events of acute inflammation
neutrophils
vascular changes = blood vessels dilate to increase blood flow to injury site
endothelial cell activation =increased permeability of capillaries so fluid and small proteins (fibrinogen) leak into the area of damage
coagulation cascade is activated (thrombin produced to convert fibrinogen to fibrin)
neutrophil leukocytsis and accumulation in area of damage
BM increases neutrophil production
endothelial cells are activated which leads to up-regulation of adhesion molecules on endothelial cells (CAM) = neutrophils migrate here
overall both stages lead to formation of acute inflammatory exudate in area of damage
what accounts for the warmth and redness in acute inflammation
cells damage and die -> activation of endothelial cells
endothelial cells become separated -> capillary bed becomes leaky
therefore fluids and protein leak out into the tissue space -> swelling
what are the 2 types of leak
transudate (watery) = oedema
exudate (protein + water) = get this in acute inflammation which contains fluid, fibrin and neutrophils
what are the 3 parts to acute inflammation
cell injury (triggering factor) neutrophils vascular changes
what role does fibrin have in acute inflammation
acts as a solid scaffold which neutrophils can use to move around areas of inflammation
neutrophils phagocytose and kill microorganisms and release enzymes to break down damaged tissue - necrotic material can be cleared away
if there is severe injury, what systemic effects occur in response to inflammatory mediators (IL-1, IL-6, TNF-a)
fever
CRP secreted by liver
hormone production (ADH, cortisol, adrenaline) = malaise, weakness, appetite loss
what does bacteria induce macrophages to produce
IL-6 which acts on hepatocytes (liver) to induce synthesis of acute phase protein (CRP)
CRP activates complement cascade and is an opsonin
therefore, CRP facilitates phagocytosis of bacteria
CRP is not specific to bacterial infections - can be high in other inflammatory conditions
what are the 3 outcomes of acute inflammation
1 - regeneration with resolution
2 - repair with scarring
3 - chronic inflammation - ongoing injury and tissue response
what happens in split thickness skin graft
zimmer powered dermatome is used to harvest skin
graft contains all epidermis and variable amount of dermis
what cells are unable to regenerate
permanent - post mitotic cells
brain, cardiomyocytes
what does tissue repair result in and what are the 2 steps of reapir
fibrous scar formation
organisation and scar formation
what happens in the organisation process of fibrous scar formation
acute inflammatory exudate is replaced by granulation tissue (healing tissue) = red colour
what does granulation tissue consist of
fragile complex of proliferating interconnecting capillaries, fibroblasts and macrophages
what happens during scar formation
granulation tissue is replaced by scar tissue - laid down by fibroblasts
fibrous tissue contains collagen fibres hence white colour
what is the disadvantage of scar tissue
lacks specialised function of original tissue but it is mechanically strong
what is an abscess and what infection initiates it
localised collection of pus within a newly formed cavity on a tissue
staph aureus - inflammatory response causes emigration of neutrophils which after phagocytosis release lysosomal enzymes -> damage to tissues and cavity
what are the zones of an abscess
cavity containing pus (necrotic tissue with dead neutrophils, fibrin, oedema)
periphery = layer of living neutrophils and fibrin
wall/membrane has 2 zones (repair process by body)
- inner layer of granulation tissue
- outer layer of fibroblastic tissue (scar tissue)
what is the difference between empyema and abscess
empyemas are accumulations of pus in pre-existing cavity
whereas abscess is a newly formed cavity
what are the advantages and disadvantages of abscess wall/membrane
advantage = prevents further spread of infection
disadvantage = prevents release of abscess contents - healing cannot occur therefore requires incision and drainage
what is chronic inflammation and list some examples
inflammation persists for weeks-months
due to persistent injury
there is an ongoing attempt to heal by fibrosis
persistent infection = H.pylori, TB, hep C
autoimmune disease
non living material = asbestosis, pneumonoconiosis
what are the 3 inflammatory cells of chronic inflammation
lymphocytes
macrophages
plasma cells (B cells make ab)
what 3 processes occur during a chronic gastric ulcer
persistent tissue injury and destruction at surface
ongoing inflammatory response to limit damage
fibrosis at base of ulcer
consequences of chronic inflammation
scarring - obstruction
tissue destruction - perforation or haemorrhage
development of cancer h.pylori, gastric carcinoma)
diversion of nutrients
amyloidosis
what type of inflammation is granulomatous
chronic
what is a granuloma
aggregate of activated/epitheloid macrophages
common causes of granulomatous inflammation
TB
sarcoidosis
crohns disease
what type of granuloma is seen in mycobacterium infection
caseous necrosis - surrounded by activated macrophages
protective
what is the purpose of granulomatous structure in TB
contains the mycobacterium to stop progression of infection
can be reactivated if immune system suppressed
where does atherosclerosis occur
in arteries
which layer of the arterial wall does atherosclerosis affect
intima
what are the modifiable risk factors for atherosclerosis
smoking
hypertension
DM
dyslipidaemia
what is the bodys response to cell injury in the arteries
smoking, hypertension = increases arterial pressure
leads to endothelial dysfunction and inflammatory response = increased permeability, adhesion of macrophages and T lymphocytes to endothelium
leads to migration of inflammatory cells to the intima
macrophages are activated -> production of free radicals which drives LDL oxidation
growth factors are produced and stimulate migration of smooth muscle cells from media
oxidised LDL accumulates within macrophages beneath endothelial cells = foam cells
smooth muscle cells proliferate and produce collagen and other ECM proteins = forms a cap which stabilises the cap
what happens when the endothelium is damaged (atherosclerosis)?
- damaged endothelial cells become dysfunctional - increased permeability
- endothelial cells produce adhesion molecules and cytokines which attract inflammatory cells
- VCAM1 binds to monocytes of T cells
this leads to recruitment of inflammatory cells to site of injury
-monocytes and T cells adhere to endothelium and migrate into the intima = monocytes become macrophages
what is the role of macrophages once inside the initima?
- produce free radicals to drive LDL oxidation = oxidised LDL = atherogenic
- engulf oxidised LDL and cholesterol crystals = foam cells
- foam cells produce GFs to stimulate migration of smooth muscle cells from media to intima
what happens after oxidised LDL accumulates under endothelial cells
lipid laden macrophages sit in the intima layer can progress to atherosclerotic plaque
as the foam cells die, their lipid cytoplasm is released
smooth muscle cells secrete collagen and other ECM proteins -> formation of fibrous cap (scarring)
