Cardiology Flashcards
What is the relationship between aspirin and NSAIDS?
NSAIDS interferes with with asprin
Both NSAIDs and aspirin inhibit the activity of COX. However, NSAIDs primarily block COX-1 and COX-2 enzymes, which are involved in inflammation and pain. On the other hand, aspirin inhibits irreversibly COX-1, which plays a role in blood clotting. When NSAIDs and aspirin are taken together, NSAIDs might interfere with aspirin’s binding to COX-1, reducing its effectiveness in preventing blood clotting.
What forms the cardiac plexus
Sympathetic fibers from T1-T5
Parasympathetic fibers from vagus nerve
Visceral sensory fibers
What is the normal pulmonary artery pressure
24/10 mmHg/mmHg
What is angina
Chest pain
What is the normal pH of blood
7.35-7.45
What regulates vasodilation
RAAS NOT the parasympathetic ns
What does thrombopoetin do
Make more platelets
What is the effect of cAMP on platelet aggregation
Inhibits it
Explain the formation of prostacyclins and thromboxane A2 and link this to why asprin is inhibited by NSAIDS
Arachidonic acid is converted via cox1 and cox2 to prostaglandins. Then the prostaglandins either go to platelets and form TxA2 to promote coagulation OR go to the endothelium to form prostacyclin which is anticoagulant.
Asprin and NSAIDS both bind to cox1 (nsaids also bind to cox2) so they compete for that site > the action of asprin is reduced
Explain the functions of cAMP
Vasodilation
Increase HR
BRONCHODILATION
How do you treat sickle cell disease
Hydroxyurea > makes cells rounder and increases synthesis of foetal hb
what is now thought to cause sickle cell crisis
HbS causes endothelial damage which leads to platelet aggregation in capillaries in BONE and occlusion
CO formula
HRxSV
CO formula
HRxSV
BP formula
COxTPR
PP formula
pulse pressure
Systolic pressure - diastolic pressure
MAP formula
Diastolic pressure + 1/3PP
Define preload
The initial stretching of the heart before contraction
Define afterload
The pressure against which the heart has to contact to eject blood
explain different mechanisms for blood pressure control and secreted or circulating factors which influence blood pressure
1) myogenic autoregulation
Vasoconstrictors
- endothelin 1
- decreased BP
- angiotensin 2
- ADH
- adrenaline
Vasodilators
- low O2
- high CO2
- high adenosine from ATP breakdown
- increased K+
- increased H+
- increased metabolism (tissue breakdown products)
-NO
- prostacyclin
- ANP
- adrenaline vasodilates blood in muscles
baroreceptors and chemoreceptors in carotid sinus/carotid and aortic arch
medulla
sympathetic and parasympathetic system
RAAS
hypothalamus –> regulates skin BP in response to temperature
what are the layers of the heart?
pericardium
epicardium
myocardium
endocardium
how long is the delay at the AV node
0.1 s
where do you measure the central venous pressure?
in the right atrium
explain the heart sounds
S1 - closure of mitral and right av valves
S2 - closure of aortic and pulmonary valve
S3 - associated with the rapid filling of the ventricle during the early phase of diastole, usually caused by passive flow from the atria to the ventricles. It happens when the ventricles are overly compliant, allowing more blood to enter during the rapid filling phase.
When the atria contract to push additional blood into the ventricle during its filling phase (diastole), this added volume can create turbulent flow or vibrations, which can manifest as the S3 sound.
S4 - occurs just before the first heart sound (S1) and is associated with atrial contraction. It’s often heard when the atria contract forcefully to push blood into a stiff or non-compliant ventricle.
what is the normal arterial pressure
120/80 mmHg/mmHg
what is normal venous pressure
5-10 mmHg
what are the resting potential and threshold potential of cardiac myocytes?
-90 mV (resting)
-70 mV (threshold)
what does the phrenic nerve control
the diaphragm
what fibres form the phrenic nerve
C3-C5
what are the borders of the heart?
right to sternum - 3rd and 6th costal cartilages
left to sternum on midclavicular line - 2nd and 5th intercostal space
what chambers form the right and left borders of the heart in the chest x-ray
RA and LV
what were the % for right or left dominant circulations in the heart
70% have right dominant circulation, 20% left dominant and 10% both PDA and circumflex
what is foramen ovale and what does it turn to
foramen ovale shunts blood from RA to LA in the fetus to bypass the lungs and when the baby is born it turns into fossa ovalis
which valve in the heart is bicuspid
mitral
what are the muscles in the atria and ventricles in the heart
atria –> pectinate
ventricles –> papillary
between what 2 vessels is the thoracic duct
azygous and aorta
where does the lymphatic system join the venous system?
junction between left internal jugular vein and left subclavian vein
what were the splanchnic nerves
greater T5-T9
lesser T10-T11
least T12
lumbar L1-L2
what is Horner s syndrome and how does it present
condition characterised by interruption of sympathetic innervation to head (can be due to tumour on apex of lung which invades the sympathetic chain)
presents with:
miosis - small pupil
ptosis - droopy eyelid
anhidrosis - lack of sweating
what is miosis
small pupil
what is ptosis
droopy eyelid
what is anhidrosis
lack of sweating
explain why myocardial ischemia can manifest with pain in the chest and left arm
The heart is innervated by the cardiac plexus, composed of sympathetic and parasympathetic fibres.
The sympathetic fibres are from T1 -T5 via the cardiopulmonary splanchnic
nerves.
● The heart is also innervated by visceral sensory nerves, which convey sensory information from the heart back to the CNS - this sensation normally does not reach our conscious perception.
However, if the myocardium is ischaemic this sensation does reach our conscious perception and is interpreted as pain, tightness, crushing pressure or burning, which may be severe.
● Because the visceral sensory nerves travel back to the CNS alongside the
sympathetic fibres that innervate the heart, the visceral sensory information enters spinal cord segments T1 - T5.
● However, somatic sensory information from the skin of the chest wall, neck and arm also return to spinal cord segments T1 - T5.
● Therefore painful visceral sensory information from the heart and somatic sensory information from the chest wall both enter spinal cord segments T1 - T5.
what are 6 causes of thrombosis
atherosclerosis
inflammatory
infection
trauma
tumours
platelet driven
Why is Fondaparinux used instead of unfractionated heparin?
there is a much higher risk of bleeding in heparin
fondaparinux has a longer half life
what are medications and treatments used for coronary thrombosis/stroke?
Aspirin and other antiplatelets like P2Y12 inhibitors (and GPIIb/IIIa inhibitors)
Anticoagulants - LMWH or Fondaparinux or UFH
Thrombolytic therapy: streptokinase tissue plasminogen activator; TPA generates plasmin, degrades fibrin
Reperfusion – Catheter-directed treatments and stentsor CABG
what are treatments for thrombosis at other sites other than cerebral and coronary
Antiplatelets
Statins
Anticoagulants
Endovascular/Surgical intervention
what are the common sites of venous thrombosis
ileofemoral bifurcation
femoro-popliteal bifurcation
cerebral
visceral –>
Visceral thrombosis refers to the formation of blood clots in the veins or arteries of the abdomen, affecting organs such as the liver, spleen, intestines, or kidneys (usually due to slower blood flow)
what is the D dimer test
D-dimer is a blood test used to help diagnose or rule out conditions related to blood clotting. It measures a substance called D-dimer, a protein fragment produced when a blood clot dissolves in the body.
D-dimer is not highly specific. Elevated levels of D-dimer can indicate various conditions other than just blood clots. Several factors can cause D-dimer levels to rise, including:
DVT
PE
disseminated intravascular coagulation (DIC)
Inflammation
Surgery or Trauma
Pregnancy
what types of imaging can be used to diagnose DVT
ultrasounds
CT venogram
MRI venogram
what are the components of virchow’s triad
stasis
hypercoagulability
endothelial injury
what are medical conditions which predispose to thrombosis?
P - PT20210A mutation
L - lupus anticoagulant
A - antithrombin deficiency
S - S protein
C - C protein
O - oestrogen
M - malignancies
Factor V Leiden Mutation: the most common inherited clotting disorder. It involves a mutation in the gene responsible for producing Factor V –> increases the risk of blood clots
PT20210A Mutation: This is another genetic mutation that affects the prothrombin gene, resulting in higher levels of prothrombin -> increased tendency to form blood clots.
Antithrombin Deficiency: Antithrombin is a natural anticoagulant protein that helps regulate blood clotting. Deficiency in antithrombin increases the risk of clot formation
Protein C Deficiency: Protein C is another anticoagulant protein that helps regulate clotting. Deficiency in protein C leads to an impaired ability to control clot formation
Protein S Deficiency: Protein S is a cofactor for protein C in regulating clotting. Deficiency in protein S can result in an imbalance in the clotting process
Antiphospholipid Syndrome: This autoimmune disorder involves the production of antibodies that target phospholipids, which are essential components of cell membranes. These antibodies can interfere with the normal clotting process, increasing the risk of clot formation in veins and arteries.
Lupus Anticoagulant: This is an antibody seen in lupus and related autoimmune disorders. It increases the risk of blood clotting
Hyperhomocysteinemia: Elevated levels of homocysteine (an amino acid) in the blood are associated with an increased risk of blood clotting, although the exact mechanism is not fully understood.
Malignancy: Cancer can increase the risk of thrombosis
Estrogens: Hormonal factors like oral contraceptives or hormone replacement therapy can influence blood clotting factors
what is DOAC
Direct Oral Anticoagulant
A newer anticoagulant drug kind of like warfarin
Compared to traditional anticoagulants like warfarin, DOACs have several advantages, including a rapid onset of action, predictable anticoagulant effects (often not requiring frequent monitoring), fewer interactions with food or other medications, and fewer dietary restrictions.
how do you prevent thrombosis (prophylaxis) after surgery
Mechanical (compression stockings) thromboprophylaxis
antiplatelets
anticoagulants
Also early mobilisation after surgery and good hydration
what is APTT
The Activated Partial Thromboplastin Time (APTT) ratio is a laboratory test used to evaluate the clotting ability of the blood.
Thromboplastin is released from damaged tissues or cells when there’s injury or trauma to a blood vessel. This substance initiates the coagulation cascade.
Heparin
what class is it
how does it act
how do you administer it
how do you monitor it
heparin is a glycosaminoglycan
anticoagulant
enhances the activity of antithrombin, a natural inhibitor of thrombin
IV administration
Monitoring with APTT
Activate Partial Thromboplastin time
what is the difference between UMH and LMWH
LMWH is a smaller molecule, less variation in dose and renally excreted
Once daily, weight-adjusted dose given subcutaneously
Used for treatment and prophylaxsis
UMH is administered IV and needs monitoring
warfarin
how does it work
how do you administer it
how do you monitor
Orally active
Antagonist of vitamin K which helps with coagulant synthesis of factors 2, 7, 9, 10
Measure INR (international normalised ratio, derived from prothrombin time)
what is INR
INR standardizes the measurement of PT across labs
what are NOAC and DOAC
Orally active new anticoagulant therapies
No blood tests or monitoring needed
Used for extended thromboprophylaxis and treatment of AF and DVT/PE
Not used in pregnancy or metal heart valves
Why are DOAC/NOAC not used in metal heart valves?
Mechanical heart valves are more thrombogenic than natural valves or tissue valves. Patients with mechanical valves often need higher levels of anticoagulation to prevent clot formation on the valve surfaces. DOACs might not achieve the necessary level of anticoagulation in this scenario.
They are less effective in preventing thrombosis in patients with mechanical heart valves compared to traditional anticoagulants like warfarin.
Fondaparineux class and method of action
Pentasaccharide
Indirect Xa inhibitor
does a positive D-dimer test mean you have DVT
NO
normal excludes DVT but
positive does not confirm DVT
what is duplex ultrasonography?
Duplex ultrasonography is a non-invasive imaging technique that combines two types of ultrasound:
it includes Doppler Ultrasound which measures blood flow within the vessels by using the Doppler effect. It assesses the speed and direction of blood flow, detecting abnormalities such as blockages or turbulence.
DVT treatment
1st line DOAC apixaban or rivaroxaban
Long term LMWH, DOAC or warfarin, compression stockings, treat underlying cause
In pregnancy first line is LMWH
pulmonary embolism symptoms and signs
Symptoms:
breathlessness
pleuritic chest pain
symptoms of DVT
risk factors for DVT
Signs:
tachycardia
tachypnoea
pleural rub
Signs of DVT
Pulmonary Embolism investigations
Chest Xray
ECG
Blood gases: type 1 resp failure, decreased O2 and CO2
D-dimer: normal excludes diagnosis
CT pulmonary angiogram to visualise major segmental thrombi
Ventilation/ Perfusion scan: mismatch defects
treatment of pulmonary embolism
Supportive treatment: oxygen, pain relief, fluids, rest
LMW Heparin
Oral warfarin (INR 2-3)for 6 months
DOAC/NOAC
Treat underlying cause: identifying cause of clot formation
prevention of pulmonary embolisms
Anticoagulation
IVC filters
IVC (Inferior Vena Cava) filters are medical devices designed to prevent blood clots from travelling to the lungs (pulmonary embolism) in patients who are at high risk for blood clots but cannot tolerate or have failed anticoagulant therapy
what is the commonest cause of vascular disease
atherosclerosis
what are the steps of plaque formation
1) Endothelial Injury
2) Inflammation and Lipid Accumulation within the arterial wall. 3) Foam Cell Formation: Macrophages engulf the accumulated LDL particles and become foam cells
These foam cells contribute to the development of fatty streaks, the earliest visible signs of atherosclerosis.
4) Plaque Formation
Smooth muscle cells within the artery also proliferate and contribute to the growth of the plaque.
5) Plaque Rupture or Erosion: As the plaque enlarges, it can become unstable. Rupture or erosion of the plaque’s surface can occur, leading to the exposure of its contents –> contents react with clotting factors in the bloodstream
6) Thrombosis formation at the site of the plaque rupture –> thrombus can partially or completely block the artery, leading to reduced blood flow downstream. If this occurs in the coronary or cerebral arteries, it can result in heart attacks or strokes
what is the difference between embolic events and thrombosis
Embolic event does not involve endothelial damage it is because you have atrial fibrilation and you get blood stasis in the atria of the heart and one of the clots just gets pumped in the systemic circulation
Thrombosis is because of endothelial damage
what is chronic ischemia
Chronic ischemia is prolonged over time and progressive
ex.: atherosclerotic plaques are narrowing arteries and you get general symptoms like: I can walk fine but after a while, I have to stop cuz I can’t walk anymore -> has to stop when muscles require more flow
what is rest pain
Rest pain is end-stage chronic ischemia which is when the muscle isn’t getting enough blood to even survive anymore –> constant pain
what are the symptoms of chronic ischemia
Intermittent Claudication
Rest pain
Tissue loss
what happens if you get thrombosis in the SMA
You can get ischemic bowel –> very bad
what is the commonest location of an aneurysm
infra-renal aorta
What are the advantages of MRA over CTA?
MRA is magnetic resonance angiogram
CTA is CT angiogram
CT contrast is more toxic
no radiation in MRA
in CT heart needs to pump dye, if the patient has heart failure they can’t pump the dye
MRA can provide 3d images
what is claudication
Claudication refers to pain, cramping, or fatigue in the muscles of the legs, typically the calves, thighs, or buttocks, that occurs during physical activity and is relieved by rest. It’s a common symptom of Peripheral Artery Disease (PAD), a condition caused by atherosclerosis leading to reduced blood flow to the limbs.
what are invasive treatments for lower limb atherosclerosis
balloon angioplasty and stents
bypass surgery
balloon angioplasty and stents vs bypass surgery
higher morbidity and mortality in bypass
but bypass has a better patency and limb salvage rates
with angioplasty and stents, you need consistent monitoring after surgery for the rest of your life
treatment of AAA
Open Surgical Repair: A surgeon replaces the weakened portion of the aorta with a synthetic graft during open surgery. This procedure is often performed for larger aneurysms or in specific anatomical locations.
Endovascular Aneurysm Repair (EVAR): In this minimally invasive procedure, a stent graft is inserted into the aneurysm through small incisions in the groin or other access points. The graft reinforces the weakened aortic wall and diverts blood flow away from the aneurysm, reducing the risk of rupture. EVAR is suitable for some types of aneurysms and may have a shorter recovery time compared to open surgery.
how do you treat superficial venous disease
Lifestyle changes
Compression
Sclerotherapy
Endovenous Laser Ablation
Surgical stripping
NICE DOES NOT RECOMMEND OPEN SURGERY ANYMORE; IT RECOMMENDS SCLEROTHERAPY OR LASER TO KILL VEIN
what is the biggest risk factor for coronary artery disease
age
what is the difference between plaque rupture and plaque erosion
Plaque Rupture: when the fibrous cap covering an atherosclerotic plaque ruptures or breaks. When the cap ruptures, it exposes the plaque’s contents to the bloodstream and triggers thrombosis
Plaque Erosion: disruption or loss of the endothelial cell lining covering an atherosclerotic plaque without the rupture of the fibrous cap. This exposes the underlying plaque material directly to the bloodstream and triggers thrombosis
what medications would you use to treat atherosclerosis (include mechanism of action)
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel/Ticagrelor – inhibitors of the P2Y12 ADP receptor on platelets and other drugs with antiplatelet actions (you give to patient if aspirin intolerant)
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
PCSK9 inhibitors – monoclonal antibodies that inhibit PCSK9 protein in the liver which leads to improved clearance of cholesterol from the blood.
symptoms and diagnosis of unstable angina
cardiac chest pain at rest
chest pain with a crescendo pattern
new onset angina
diagnosis: history, ECG, troponin (no significant rise in unstable angina)
ST-elevation MI vs Non-ST-elevation MI
ST-elevation MI can usually be diagnosed on ECG at presentation
*Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available
what patients are at risk of silent myocardial infarction
diabetes patients
explain type1-4 MI
Type 1 MI: classic heart attack from an acute coronary event -> sudden rupture of a plaque leading to a blood clot that obstructs a coronary artery
Type 2 MI: occurs due to an imbalance between oxygen supply and demand
ex.: conditions such as severe anemia, rapid heart rate (tachycardia), very low blood pressure (hypotension), or any other situation where the heart’s demand for oxygen exceeds the available supply.
Type 3 MI: sudden cardiac death or cardiac arrest, and there’s evidence suggesting an ischemic event as the cause
cause of the cardiac arrest was related to acute ischemia or a heart attack, even if there wasn’t specific confirmation through testing.
Type 4 MI: This occurs as a complication of medical procedures intended to treat coronary artery disease, such as percutaneous coronary intervention (PCI), coronary stenting, or coronary artery bypass grafting (CABG).
acute ischemia vs chronic ischemia vs heart attack
acute - implies only ischemia of tissue, not necrosis. it is sudden and temporary.
chronic - it is progressive and over a longer period of time –> due to prolonged oxygen supply and demand mismatch
heart attack - involves NECROSIS of tissue
how many electrodes do you have in a normal ECG
12
what is a pathological Q wave a sign of
permanent myocardial damage
transmural MI
what is a STEMI due to LBBB
myocardial infarction due to left bundle branch blockage
when does the pathological Q wave usually develop
sometime after an acute infarction
which lead on an ECG shows an inverted wave compared to the others
aVR
non-Q wave MI vs Q wave MI
non-Q wave MI is basically NSTEMI; you have worse R wave progression and ST elevation
Q-wave MI is complete absence of the R wave and is associated with transmural MI
symptoms of MI
Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations
Chest pain
how do you manage an MI
Call 999
P - Perform an ECG - if ST elevation transfer for emergency coronary angiography
A – Aspirin 300mg +/- platelet P2Y12 inhibitor
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)
Consider beta-blocker
Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy
Oxygen if there is shortness of breath
what are the possible causes of type 2 MI
OXYGEN and PERFUSION mismatch
sepsis
acute lung pathology
pulmonary embolism
anaemia
haemorrhage hypotension/hypovolaemia
Drug abuse (amphetamines, cocaine)
Dissection of aorta/coronary artery
thyrotoxicosis
vasospasm –> will restrict the diameter of coronary arteries and further restrict blood flow (vasospasm can be caused by drugs, trauma)
what is Tako-Tsubo cardiomyopathy?
*Stress-induced cardiomyopathy
*Often precipitated by acute stress such as extreme emotional distress in susceptible individuals
*Causes transient left ventricular systolic dysfunction
what is the aspirin mode of action
irreversible cox 1 inhibitor
explain how P2Y12 inhibitors work
they inhibit P2Y12 which is on the platelet membrane and when activated is supposed to amplify the coag pathway
name 3 P2Y12 inhibitor medications and what their advantages and disadvantages are including adverse reactions
Ticagrelor
reversible
slightly increases the risk of bleeding
can cause dyspnoea and ventricular pauses
Clopidogrel
Prasugrel
it is better than clopidogrel because it can turn to an intermediate without CYP450 before becoming an active metabolite
ALL P2Y12 inhibitors can cause:
bleeding (GI bleeds, hematuria)
Rash
GI disturbances
what are GPIIb/IIIa antagonists
antiplatelet meds
they are very aggressive because the GPIIb/IIIa protein is meant to connect the platelets to one another to create a mesh
you can get very aggressive bleeding so used selectively
useful in STEMI patients undergoing primary PCI because P2Y12 given orally so takes longer to act
given IV
what is fondaparinux
anticoagulant
safer than heparins because it has a lower coagulation level
UFH vs LMHW
UFH is normal Heparin; requires constant monitoring and is strong
used in acute events like DVT and PE
LMHW is Lower Molecular Weight Heparin; has a longer half-life and does not need monitoring; used for prevention and prophylaxis of thrombosis
what test is used to monitor UFH
aPTT
active partial thromboplastin time
name an ACE inhibitor
ramipril
stable angina vs unstable angina
Stable Angina:
- Often triggered by physical exertion or emotional stress.
- lasts a short time a relieved by lifestyle changes, rest, and medication
-less immediately dangerous
Unstable Angina:
- Often unpredictable and can occur even at rest or with minimal physical exertion.
- It’s usually more severe and lasts longer than stable angina.
- associated more with STEMI. and NSTEMI
- high risk of heart attack
- Requires urgent medical attention
manifestation:
*Cardiac chest pain at rest
*Cardiac chest pain with crescendo pattern
*New onset angina
what are risk factors to ischemic heart disease
Age
Cigarette smoking
Family history
Diabetes mellitus
Hyperlipidemia
Hypertension
Kidney disease
Obesity
Physical inactivity
Stress
what are exacerbating factors of IHD
SUPPLY
Anemia
Hypoxemia
Polycythemia
Hypothermia
Hypovolaemia
Hypervolaemia
DEMAND
Hypertension
Tachyarrhythmia
Valvular heart disease
Hyperthyroidism
Hypertrophic cardiomyopathy
syncope vs pre-syncope
Syncope is a brief loss of consciousness due to decreased blood flow to the brain, often caused by a sudden drop in blood pressure or heart rate. Pre-syncope is a feeling of imminent fainting without complete loss of consciousness, presenting as lightheadedness or dizziness, signaling a potential impending fainting episode.
what do people with stable angina or who need secondary prevention from ACS carry with them at all times to use in case of an emergency? how does it work?
GTN spray
(glyceryl trinitrate) spray works by relaxing and dilating the blood vessels, primarily the veins, which reduces the workload on the heart and improves blood flow to the heart muscle.
give an example of a calcium channel blocker
amlodipine
can you give beta blockers to asthma patients?
No
beta blockers will block the activity of adrenaline and therefore block bronchodilation
how do nitrates work
dilates arteries and veins but stronger effect on veins
The dilation of veins reduces the amount of blood returning to the heart, which subsequently decreases the heart’s workload. This decrease in preload (the amount of blood entering the heart) reduces the heart’s oxygen demand and can help relieve symptoms of angina by improving blood flow to the heart muscle.
PCI vs CABG
PCI (Percutaneous Coronary Intervention) and CABG (Coronary Artery Bypass Grafting)
PCI
pro:
Less invasive
Convenient
Repeatable
Acceptable
con:
Risk stent thrombosis
Risk restenosis
Can’t deal with complex disease
Dual antiplatelet therapy
CABG
pro:
Good Prognosis
Deals with complex disease
cons:
Invasive
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay
Time for recovery
what is the standard calibration of the ECG
25 mm/s
0.1 mV/mm
where do you place the unipolar leads on the chest
V1 - right of sternum at 4th intercostal space
V2 - left of sternum at 4th intercostal space
V3 - left 4th intercostal space on midclavicular line
V4 - left 5th intercostal
V5 - left 5th anterior axillary line
V6 - 6th intercostal space midaxillary line
why is warfarin so crucial to monitor
Warfarin is crucial to monitor due to its narrow therapeutic window, meaning the effective dose for anticoagulation is relatively close to the dose that might cause bleeding. Therefore, monitoring the effect of warfarin is essential to ensure that the blood remains within the desired anticoagulation range while avoiding the risk of bleeding.
Warfarin interferes with the synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, and X) in the liver. The International Normalized Ratio (INR), derived from the prothrombin time (PT) test, is used to monitor and adjust warfarin doses to maintain the blood’s clotting ability within the target range for specific medical conditions.
Not all anticoagulants require the same level of close monitoring as warfarin.
describe the anatomy of the pericaridum
2 layers - visceral and parietal
visceral layer is adherent to pericardium
parietal layer is fibrous and thick
in between the layer you have pericardial serous fluid
visceral and parietal layer are continuous
do chronic and acute pericardial effusions always lead to cardiac tamponade?
NO
Acute yes
Chronic no
Cardiac tamponade is a serious condition where excessive fluid accumulation in the pericardial space puts pressure on the heart, compromising its ability to fill in diastole.
However, in chronic pericardial effusion, when fluid accumulates slowly over an extended period, the pericardium can adapt by stretching gradually. This slow adaptation and increased compliance of the pericardium mean that even a larger volume of fluid might not immediately lead to tamponade because the heart adapts to the slow increase in pressure over time.
However if fluid fills up the pericardium fast then the parietal fibrous layer will not be compliant and you enter cardiac tamponade
what is acute pericarditis
an inflammatory pericardial syndrome with or without pericardial effusion
how do you diagnose acute pericarditis
Clinical diagnosis made with 2 of 4 from:
Chest Pain (85-90%)
ECG changes (60%)
Pericardial effusion (up to 60% usually mild)
Friction rub (33%)
What are 2 viral causes of acute pericarditis
Enteroviruses –> Coxsackie B
Herpesviruses –> EBV
Adenoviruses
Parvovirus B19
explain cardiac muscle contraction
Calcium enters cell→ High intracellular Ca triggers release of more Ca from sarcoplasmic reticulum→ Released Ca attaches to troponin C→ tropomyosin moves→ actin-myosin cross bridges→ contraction
Cross bridges last as long as Ca occupies troponin
Removal of calcium induces relaxation – requires energy
what are 5 causes of sudden death?
Cardiac
CAD/IHD
Valve disease – AS, MR, IE,rheumatic valve disease
Myocardial disease – myocarditis, cardiomyopathies, amyloid, storage disorders, connective tissue disease
Grown-up congenital heart disease
Structural abnormalities of the conduction system
Drug toxicity – cocaine, amphetamines, ecstasy, cardiac drugs
Sudden arrhythmic death syndrome (no findings at pm) – channelopathies,metabolic disease, commotio cordis
Non-cardiac
PE
Pneumonia
Sepsis
Pancreatitis
Peptic ulceration and GI bleed
Aortic aneurysm dissection/rupture
Cerebral pathology – tumour, CVA, trauma
SUDEP - sudden unexpected death in epilepsy
Alcohol and drug toxicity
SADS - sudden arrhythmic death syndrome
name some inflammatory cytokines found in plaques
IL-1 - canakinumab
IL-6 – tocilizumab**
IL-8
IFN-y
TGF-b
MCP-1
(C reactive protein)
in what layer of the vessel wall does atherosclerosis form and what is the fatty streak made of
aggregations of foam cells and T lymphocytes within the intimal layer of the vessel wall
what are the layers of an arterial vessel?
endothelium
intima
media
adventitia
red thrombus vs white thrombus
Red thrombus = rbcs and fibrin; due to plaque rupture
white thrombus = platelets and fibrinogen; due to plaque erosion (discontinued endothelial layer)
what is Hypertrophic cardiomyopathy (HCM)
- unexplained cardiac hypertrophy (generally LV hypertrophy) due to sarcomeric protein gene mutations
- May cause angina, dyspnoea, palpitations, dizzy spells or syncope
what is Dilated cardiomyopathy (DCM)
Dilated cardiomyopathy (DCM) is a condition characterized by the enlargement (dilation) of the heart chambers, particularly the left ventricle (LV) and/or the right ventricle (RV). (4 chamber dilation and dysfunction)
it can be due to mutations in the cytoskeleton which leads to the dilation
usually presents with heart failure symptoms
what is Arrhythmia cardiomyopathy (ARVC/ALVC)
desmosome gene mutations lead to to structural change which predisposes heart to arrhythmias
muscle gets replaced with fatty tissue in myocardium
what is channelopathy
Inherited arrhythmia caused by ion channel protein gene mutations.
These usually relate to potassium, sodium or calcium channels.
But structurally you have a normal heart.
* Channelopathies include long QT, short QT
* May present with recurrent syncope
* Be aware of QT prolonging drugs – they can kill people with long QT syndrome
what is the most common reason of sudden death in a young person
Hypertrophic cardiomyopathy
what is familial hypercholsterolaemia
An inherited abnormality of cholesterol metabolism (abnormal LDL protein)
* Leads to serious premature coronary and other vascular disease
* Aortic aneurysm or dissection is often inherited
what is the main feature of Arrhythmia cardiomyopathy (ARVC/ALVC)
arrythmia
what pattern of inheritance do inherited cardiac conditions usually present
dominant
what is ARB
angiotensin receptor blocker
name 2 ACE inhibitors
ramipril
enalapril
perindopril
trandolapril
they all end in “pril”
what are the adverse effects of ACE inhibitors
- Related to reduced angiotensin II formationa. Hypotension
b. Acute renal failure
c. Hyperkalaemia –> indirect effect on aldosterone which affects potassium balance (aldosterone is supposed to absorb Na and excrete K)
d. Teratogenic effects in pregnancy - Related to increased kinins
a. Cough
b. Rash
c. Anaphylactoid reactions
In what diseases do you use Ca channel blockers and why
Hypertension –> decrease cardiac contractility
IHD –> the coronary vessels are narrowed so the Ca channel blockers cause vasodilation and reduced resistance
Arrythmia (tachycardia) –> decrease HR
name 3 Ca channel blockers with different effects
amlodipine - peripheral arterial vasodilator
verapamil - -ve chronotropic and inotropic effect on heart
diltiazem - heart and peripheral effects
what are adverse effects of Ca channel blockers
1) Due to peripheral vasodilatation (mainly dihydropyridines)
Flushing
Headache
Oedema
Palpitations
2) Due to negatively chronotropic effects (mainly verapamil/diltiazem)
Bradycardia
Atrioventricular block
3) Due to negatively inotropic effects (mainly verapamil) –> Worsening of cardiac failure
4) Verapamil causes constipation
give 2 examples of beta blockers
bisoprolol
atenolol
what are the adverse effects of beta-blockers
Fatigue
Headache
Sleep disturbance/nightmares
Bradycardia
Hypotension
Cold peripheries
Vivid dreams
Erectile dysfunction
Worsening of
- Asthma (may be severe) or COPD
- PVD – Claudication or Raynaud’s
- Heart failure – if given in a standard dose or acutely
explanation for worsening of PVD:
Beta-blockers reduce HR and CO, which may lead to reduced blood flow to the extremities, including the legs. In individuals with PAD, who already have compromised blood flow to the legs, further reduction in blood flow due to a decreased HR may worsen claudication symptoms.
Also decreasing HR and CO will decrease tolerance to exercise
what are the classes of diuretics
Thiazides and related drugs (distal tubule)
Loop diuretics (loop of Henle)
Potassium-sparing diuretics
give an example of a thiazide
bendroflumethiazide
give an example of a loop diuretic
furosemide
what are potassium-sparing diuretics and give an example
Potassium-sparing diuretics are a class of diuretic medications that help the body get rid of excess sodium and water while conserving potassium. Unlike other diuretics that may lead to potassium loss, potassium-sparing diuretics aim to retain potassium
spironolactone
what are adverse effects of diuretics
Hypovolaemia (mainly loop diuretics)
Hypotension (mainly loop diuretics)
Low serum potassium (hypokalaemia)
Low serum sodium (hyponatraemia)
Low serum magnesium (hypomagnesaemia)
Low serum calcium (hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Impaired glucose tolerance (mainly thiazides)
Erectile dysfunction (mainly thiazides)
do you give ACE inhibitors to Afro-Caribbean’s
no; ACE inhibitors don’t work as well in that ethnicity; you give beta blocker instead
what is heart failure
Heart failure = loss of efficiency of the heart pump caused by structural or functional abnormalities of the heart.
what is the most common cause of heart failure
coronary artery disease
what is the triple therapy of HFrEF
a combination of three classes of medications commonly used in the management of heart failure with reduced ejection fraction (HFrEF)
ACE inhibitors/ARB
Beta blockers
K sparing diuretics / Aldosterone receptor blockers
what is the first line of treatment for heart failure
ACE inhibitors and beta blocker therapy
Low dose and slow uptitration
give an example of an angiotensin 2 receptor blocker
valsatran
what is digoxin
class
mode of action
use
side effects
Digoxin
cardiac glycoside
inhibits cardiac Na+/K+ pump –> increase in intracellular sodium –> decrease sodium-calcium exchanger –> increase in intracellular calcium –> enhances force of myocardial contraction.
effect: increases the force of contraction and slows down the heart rate. (you have to uncouple more Ca from the troponin so requires more E and time)
treatment of heart failure (reduced ejection fraction) and certain types of arrhythmias
side effects:
nausea, vomiting, confusion, visual disturbances (such as seeing halos or yellow-green color changes), and arrhythmias, renal damage.
(narrow therapeutic window so it is quite toxic)
Digoxin is primarily eliminated through the kidneys.
amiodarone adverse effects
Anti-arrhythmic medication
QT prolongation
Polymorphic ventricular tachycardia
Interstitial pneumonitis - inflammation of the lung tissue
Abnormal liver function
Hyperthyroidism / Hypothyroidism
Sun sensitivity
Slate grey skin discolouration
Corneal microdeposits
Optic neuropathy
Multiple drug interactions
Very large volume of distribution - can affect tissues over a longer period of time (it can take 3 months to clear out all amiodarone from your system once you have stopped taking it)
what are the possible causes of pericarditis?
give examples
Viral Infections - EBV
Bacterial Infections - Mycobacterium tuberculosis
Autoimmune
Neoplastic - (second metastatic tumours) lung and breast cancers, lymphoma
Metabolic - uraemia (when the kidneys are unable to effectively filter waste products from the blood, leading to the accumulation of these waste products in the bloodstream.)
Trauma
Cardiac surgery/intervention
what are the symptoms of pericarditis
chest pain
sharp and pleuritic
radiates to arm, left anterior chest and epigastrium
relieved by sitting forward
exacerbated by lying down
dyspnoea
cough
hiccups (phrenic nerve irritation)
fever
signs of pericarditis
pericardial rub
sinus tachycardia
fever
signs of effusion
very audible heart sounds
Indication of pericarditis and cardiac tamponade
Beck’s triad:
1) Hypotension
2) Muffled Heart sounds due to fluid accumulation in the pericardial sac
3) Jugular Venous Distention (JVD): Elevated pressure in the venous system can lead to visible swelling of the jugular veins in the neck.
Pulsus paradoxes: exaggerated drop in systolic blood pressure during inspiration
(on inspiration RA normally fills more because of negative pressure which means that LV fills less and you get reduced CO and SV. When you have effusion from pericarditis the Right atrium and ventricle are even more compressed - REMEMBER THAT THEY ARE PREDOMINANTLY ON THE SIDE FACING THE PERICARDIAL SAC - so less RA filling will result in less blood to lungs and inherently less blood to LV which means decreased CO and SV –> decreased BP)
What are the features of a pericarditis ECG
saddle shape ST segment
PR depression
first-line investigations for pericarditis
Clinical examination with bell of stethoscope (pericardial rub)
ECG
FBC - full blood count
ESR
CRP
Troponin
CXR (Chest X-Ray)
Signs of tamponade
1) Pulsus Paradoxus: exaggerated drop in systolic blood pressure during inspiration
(on inspiration RA normally fills more because of negative pressure which means that LV fills less and you get reduced CO and SV. When you have effusion from pericarditis the Right atrium and ventricle are even more compressed - REMEMBER THAT THEY ARE PREDOMINANTLY ON THE SIDE FACING THE PERICARDIAL SAC - so less RA filling will result in less blood to lungs and inherently less blood to LV which means decreased CO and SV –> decreased BP)
2) Kussmaul’s Sign: abnormal increase in jugular venous pressure (JVP) during inspiration because RA compressed and can’t accommodate filling –> backup in jugular
3) Hypotension/Shock:
4) ECG Findings: tachycardia
5) Electrical Alternans: alternating amplitudes of QRS complexes on the ECG. It is a characteristic finding in cardiac tamponade and is caused by the swinging of the heart within the fluid-filled pericardial sac during cardiac cycles.
differential diagnosis of pericarditis
MI
Pleuritis: Inflammation of the pleura
Pneumonia:
GERD
Chostochondritis: Inflammation of the costosternal or costochondral junctions
Aortic Dissection
Dressler Syndrome
Connective Tissue Disorders: Autoimmune conditions like systemic lupus erythematosus (SLE) or rheumatoid arthritis may present with pericarditis.
Viral Infections
Tuberculosis
management of pericarditis
sedentary activity until resoultion of symptoms
NSAID
Colchicine
(colchicine is an antiinflammatory prescribed specifically for pericarditis)
what is a major complication of pericarditis
constrictive percarditis (calcification of the pericardium)
what is Dressler’s syndrome?
Dressler’s syndrome, also known as post-myocardial infarction syndrome, is a rare condition characterized by inflammation of the pericardium (the sac surrounding the heart), pleura (the membrane around the lungs), and, occasionally, the lungs themselves. It typically occurs several weeks to months after a myocardial infarction (heart attack) or cardiac surgery.
pneumonia-like symptoms
exact cause of this reaction is not known
what is the difference between amlodipine and verapamil?
amlodipine acts on blood vessel smooth muscle
verapamil acts only on the heart
what is first line of treatment for hypertension?
ACE inhibitors or if they aren’t suitable for the patient ARBs (angiotensin 2 receptor blockers)
ACE inhibitors can cause more kidney damage; not recommended in patients with nephropathies
Which conditions may contraindicate the prescription of a beta blocker and why?
- Asthma (blocking beta-2 adrenoceptors in the bronchi may cause broncho-constrictions and precipitate an asthma attack)
- Hypotension (a further drop in blood pressure due to vasodilation may result in symptoms of dizziness, blackouts and falls).
- Heart failure (Beta-blockers slow the heart and can depress the myocardium, meaning that cardiac output may reduce);
- Second- or third-degree heart block patients (may progress to complete heart block due to depression of the myocardium)
- frequent episodes of hypoglycaemia (beta-blockers can affect carbohydrate metabolism and the body’s autonomic response to hypoglycaemia, masking the symptoms and making it harder to spot)
what is heart block and what are the different types
Heart block occurs when there is a disruption or delay in the transmission of electrical signals between the atria and ventricles. There are three degrees of heart block:
First-degree: delayed transmission of electrical signals between the atria and ventricles.
doesn’t cause significant symptoms, and treatment may not be necessary.
Second-degree heart block: This is further divided into two types:
Type I (Mobitz I or Wenckebach): there is a progressive lengthening of the time it takes for the electrical signal to travel from the atria to the ventricles until a beat is skipped.
Type II (Mobitz II): occasional dropped beats occur without the progressive lengthening seen in Type I. It is considered more serious and may lead to complete heart block.
Third-degree heart block (complete heart block): complete block in the transmission of electrical signals between the atria and ventricles. As a result, the atria and ventricles beat independently, leading to a slower heart rate and potential symptoms such as dizziness, fatigue, and fainting.
