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.
what is the relevance of lipid-soluble/water-soluble beta blockers
Water-soluble beta-blockers are less likely to enter the brain, and may therefore cause less sleep disturbance and nightmares. Water-soluble beta-blockers are excreted by the kidneys and dosage reduction is often necessary in renal impairment
give an example of a water-soluble beta blocker
atenolol
what is the pill in the pocket method of prescribing
The “pill-in-the-pocket” approach is where a patient with paroxysmal (intermittent) atrial fibrillation takes their antiarrhythmic medication when they experience an episode of palpitations, rather than taking regular medication every day. The idea is to terminate the suspected episode of AF without having to present to a medical facility. The ‘prn’ method of use avoids side effects from taking tablets on days when they may not be necessary and is helpful for patients who are averse to taking regular medications.
when do aortic stenosis symptoms appear
when valve area is 1/4th of normal.
what are the types of aortic stenosis?
Supravalvular
Subvalvular
Valvular
what is a major risk factor for aortic stenosis
age
what are the congenital causes of aortic stenosis?
congenital aortic stenosis
congenital bicuspid valve
what are the acquired causes of aortic stenosis
Idiopathic age-related calcification
Rheumatic heart disease
what is the pathophysiology of aortic stenosis
A pressure gradient between the LV and the aorta leads to increased afterload
LV function is initially maintained by compensation with hypertrophy
When compensatory mechanisms are exhausted, LV function declines.
how do patients with aortic stenosis present
Syncope: (exertional) 15%
Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
Sudden death <2%
signs of aortic stenosis
1) Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)
2) Heart sounds- soft or absent second heart sound (due to stenosis of the aortic valve)
3) S4 gallop due to LVH.
4) Ejection systolic murmur- crescendo-decrescendo character.
“Loudness” does NOT tell you anything about severity
what investigations do you do for aortic valve stenosis? and why
Echocardiography
To measure:
1) Left ventricular size and function: LVH, Dilation, and EF
2) Doppler-derived gradient and valve area (AVA) - looks at the pressure differences between the LV and aorta and looks at the area of the aortic valve to determine the degree of stenosis (how narrow is the aortic valve)
how do you manage aortic stenosis?
General:
Fastidious dental hygiene/care
IE (infective endocarditis) prophylaxis in dental procedures
Can’t give medicine because it is a mechanical and structural problem
Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation
when do you perform interventions for aortic stenosis
Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF
Any patient undergoing CABG with moderate or severe AS
Asymptomatic patients with severe AS symptoms upon exercise testing
Chronic mitral regurgitation definition
Backflow of blood from the LV to the LA during systole
primary vs secondary mitral regurgitation
primary - disease of leaflets
secondary - normal valve architecture but impaired closure due to LV or LA structural change (ex.: dilated L atria/ L ventricle)
causes of mitral regurgitation
Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders –> abnormalities in collagen, elastin, fibrillin
Pathophysiology of Mitral regurgitation
Incomplete closure of the mitral valve results in the backflow of blood from the left ventricle to the left atrium during systole
Increased volume of blood in the left atrium results in atrial enlargement and pulmonary hypertension; over time this affects the right ventricle pumping blood towards the lungs as well
Initially, the left ventricle may undergo hypertrophy as a compensatory mechanism to maintain cardiac output.
Over time, the left ventricle, dealing with the continuous regurgitation, experiences progressive volume overload. It becomes dilated and loses its ability to effectively pump blood.
Signs of mitral regurgitation
Auscultation: pansystolic murmur at the apex radiating to the axilla
S3 (associated with symptoms of chronic heart failure and left atrium overload)
In chronic MR, the intensity of the murmur does correlate with the severity.
Displaced hyperdynamic apex beat - “hyperdynamic” refers to increased forcefulness or strength of the heartbeat at the apex and displaced means that the apex beat is not at the 5th intercostal space junction with the left midclavicular line, indicating a change in heart size or position
Exertion Dyspnoea: ( exercise intolerance)
Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation
Investigations for mitral regurgitation and what would you expect to see
ECG: May show LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
Transoesophageal echocardiography
Management of mitral regurgitation
Rate control for atrial fibrillation with beta-blockers, Ca channel blockers digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates
Diuretics
No indication for ‘prophylactic’ vasodilators such as ACEI, or hydralazine; prophylactic vasodilators given only if there is evidence of hypertension
Serial Echocardiography to monitor progression
IE prophylaxis for patients with prosthetic valves or a history of IE for dental procedures.
what are the indications for surgery in mitral regurgitation?
ANY Symptoms at rest or exercise (repair if feasible)
If the patient is Asymptomatic:
If Ejection Fraction <60%
Left Ventricular End-Systolic Diameter >40mm
If new onset atrial fibrillation/raised Pulmonary Artery Pressure >50 mmHg
what is the most common heart valve disease
aortic stenosis
define aortic regurgitation
Leakage of blood into LV during diastole due to ineffective closure of the aortic cusps
causes of aortic regurgitation
Bicuspid aortic valve
Rheumatic disease
Infective endocarditis
pathophysiology of aortic regurgitation
aortic valve can’t close properly so you get backflow of blood into the left ventricle
Combined pressure AND volume overload in the left ventricle leads to LV hypertrophy to try and maintain SV and CO
This also causes aortic root dilation
over time the LV can’t compensate anymore and it starts to dilate
signs of aortic regurgitation
Massive pulse pressure (systole - diastole)
Hyperdynamic and displaced apical impulse
Sounds:
Systolic ejection murmur: due to increased flow across the aortic valve
Diastolic blowing murmur (the decrescendo murmur) - heard at the left sternal border
Austin flint murmur (heard at the apex): mid-diastolic sound caused by blood flowing back into the ventricle which makes the mitral valve leaflet vibrate
S3 - the sound of very advanced aortic regurgitation; the ventricle has already dilated and you get turbulent flow during atrial systole
Investigations for aortic regurgitation and what you expect to see
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the aortic valve and aortic root with measurements of LV dimensions and function
Management of aortic regurgitation
General: consider IE prophylaxis depending of history
Medical: Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in congestive cardiac failure or hypertension
Serial Echocardiograms: to monitor progression.
Surgical Treatment
1) SAVR (Surgical Aortic Valve Replacement)
2) TAVI (Transcatheter Aortic Valve Implantation) in exceptional cases only if unsuitable for SAVR (Surgical Aortic Valve Replacement)
What are the indicators for surgery in aortic regurgitation?
ANY Symptoms at rest or exercise
Asymptomatic treatment if:
Ejection fraction drops below 50% or LV becomes dilated > 50mm at end-systole
mitral stenosis definition
Obstruction of LV inflow that prevents proper filling during diastole
cause of mitral stenosis
Rheumatic heart disease: 77-99% of all cases
Infective endocarditis: 3.3%
Mitral annular calcification: 2.7%
pathophysiology of mitral stenosis
LA dilation results in pulmonary congestion (reduced emptying)
this causes increased Transmitral Pressures and stenosis
LA dilation results in atrial fibrillation.
Pulmonary congestion leads to RV and RA backup of blood –> when RA contracts it sends blood towards RV but also towards jugular
Right heart failure symptoms: due to Pulmonary venous hypertension
signs of mitral stenosis
prominent “a” wave in jugular venous pulsations –> Pulmonary congestion leads to RV and RA backup of blood –> when RA contracts it sends blood towards RV but also towards the jugular. SO on jugular vein you would feel a pulse going up and one going down (“A”)
Signs of right-sided heart failure: in advanced disease
Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks
signs of right-sided heart failure
fatigue
increased peripheral venous pressure
oedema
ascites
enlarged liver and spleen
distended jugular veins
GI distress
signs of left-sided heart failure
fatigue
pulmonary oedema and congestion: wheezing, tachypnoea, crackles, coughs
Paroxysmal nocturnal dyspnea
confusion
exertional dysponea
orthopnea –> difficulty breathing when lying down
restlessness
tachycardia
Central cyanosis
Heart sounds of mitral valve stenosis
Decrescendo diastolic murmur:
Low-pitched diastolic rumble is most prominent at the apex.
Heard best with the patient lying on the left side in a held expiration
The intensity of the diastolic murmur does not correlate with the severity of the stenosis
Investigations for Mitral Valve stenosis
ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
transesophageal ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, pressure gradient and mitral valve area
Management of mitral valve stenosis
Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly
Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
beta-blockers, Calcium channel blockers, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Diuretics for fluid overload (oedema)
Identify patient early who might benefit from percutaneous mitral balloon valvotomy.
IE prophylaxis: Patients with prosthetic valves or a history of IE for dental procedures.
Indications for MV replacement
ANY SYMPTOMATIC Patient
Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV
when is high blood pressure an emergency
when there is evidence for immediate damage
papilloedema –> optic disc sweling
acute kidney injury
acute stroke
ACS
Aortic dissection
how much do you expect BP to drop from only 1 drug
blood pressure drop from one drug only won’t be more than 10 mmHg
systolic 8-10 mmHg
diastolic 4-6 mmHg
what lifestyle changes can reduce BP
weight loss
salt restriction
exercise
alcohol reduction
what are the main blood pressure-lowering drugs
calcium channel blockers
ACE inhibitors
Diuretics
B-blockers
can antidepressants cause high BP
yes
what medications can cause hypokalemia
diuretics
what part of the body do you examine when someone comes with high BP
eye for retinopathies –> you can see immediate blood vessle damage in eye
what are different ways to measure BP
measures in clinic
unattended automated office BP
home self-measurement: Patients use a home blood pressure monitor to measure their blood pressure at different times of the day, typically in the morning and evening
ambulatory blood pressure measurement: Ambulatory Blood Pressure Measurement involves continuous monitoring of blood pressure over a 24-hour period. This method provides a comprehensive assessment of blood pressure patterns, including daytime, nighttime, and average values.
Patients wear a portable blood pressure monitor
what conditions does hypertension cause
stroke
dementia
MI
heart failure
renal failure
PVD
at what BP do low and high CVD risk patients need treatment
low CVD risk - 160/100 mmHg
high CVD risk - 140/90 mmHG
do BP lowering drugs reduce symptoms
not really. only slight reduction in headache but patients will still complain that they have symptoms
what are BP targets for routine patients, previous stroke, heavy proteinuria and CKD, diabetes, older patients
Routine - <140/90 mmHg
Previous stroke - <130/80 mmHg
Heavy proteinurea - <130/80 mmHg
CKD and diabetes - <130/80 mmHg
Older patients <150/90 mmHg
what are drugs which increase BP
NSAIDs
SNRIs - Serotonin-Norepinephrine Reuptake Inhibitors (antidepressants)
Corticosteroids
Oestrogen oral contraceptives
Stimulants like Methylphenidate (ADHD medication)
Anti-anxiety drugs
Anti-TNFs
what is Marfan’s syndrome?
Marfan syndrome is a genetic disorder that affects the connective tissue, which provides support and structure to various parts of the body.
Marfan syndrome can impact the cardiovascular system, increasing the risk of aortic aneurysms and dissections.
Individuals with Marfan syndrome may also experience abnormalities in the heart valves, particularly the mitral valve.
in what circumstances do you withhold BP-lowering medications
if patients are going into surgery and will have general anaesthesia
what is tetralogy of fallot
what colour are the patients
a ventricular septal defect (whole between the 2 ventricles –> you get narrowing and stenosis of pulmonary artery which results in RV hypertrophy
also because R side is hypertrophic deoxygenated blood gets pushed through the septal whole towards the LV –> deoxygenated blood entering systemic circulation
The patients are BLUE
Physiology of Ventricular Septal defect
High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber
Therefore NOT blue
Increased blood flow through the lungs
what are adults with operated tetralogy of fallot susceptible to in their adult life
Often get pulmonary valve regurgitation in adult life and require redo surgery
also at risk of arrhythmias
which is the most common congenital heart defect
ventricular septal heart defect
what is eisenmengers syndrome
Eisenmenger’s syndrome is a condition that develops when a large, unrepaired ventricular septal defect (VSD) leads to significant changes in the blood flow within the heart, ultimately causing pulmonary hypertension and reversal of blood flow through the defect. Eisenmenger’s syndrome is a specific complication of certain congenital heart defects, including VSD.
High-pressure pulmonary blood flow damages the pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
The patient becomes BLUE - Cyanotic
signs of atrial septal defects
Pulmonary flow murmur
In a normal heart, the second heart sound (S2) is typically a combined sound produced by the closure of the aortic and pulmonary valves. In the presence of an ASD, there may be a persistent split S2 throughout the respiratory cycle. The split S2 is due to the delayed closure of the pulmonic valve, allowing the right ventricular ejection to extend into early diastole.
Big pulmonary arteries on CXR
Big heart on chest X ray
What are atrial septal defects
Abnormal connection between the two atria (primum, secundum, sinus venosus)
Common
Often present in adulthood
physiology of atrial septal defects
Slightly higher pressure in the LA than the RA
Shunt is left to right
Therefore NOT blue
Increased flow into right heart and lungs
if shunt is big Right side of heart dilatation and you get symptoms
if the shunt is small RA doesn’t dilate and you don’t have symptoms - no intervention needed
what is an atrio-ventricular septal defect
Basically a hole in the very centre of the heart
Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
Can be complete or partial
what neurological syndrome is associated with atrio-ventricular septal defects
Downs syndrome
what is coarctation of the aorta
Narrowing of the aorta at the site of insertion of the ductus arteriosus
what are the limitations of a bicuspid AV valve
Can be severely stenotic in infancy or childhood
Degenerate quicker than normal valves
Become regurgitant earlier than normal valves
Are associated with coarctation and dilatation of the ascending aorta
infective endocarditis definition
Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc).
How do you treat infective endocarditis
Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities
May require cardiac surgery to remove the infectious material and/or repair the damage
Treat complications: arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc
What are the different types of infective endocarditis
Native Valve Endocarditis (NVE) –> endocarditis due to infection of the actual native valve; usually due to bacterial infection
Prosthetic Valve Endocarditis (PVE) (post-op) - due to surgeries where prosthetic valves or devices like pacemakers were introduced
Intravenous Drug Abuse (IVDA) Endocarditis
what type of patient history would raise infectious endocarditis flags
Have an abnormal valve
regurgitant or prosthetic valves are most likely to get infected.
Introduce infectious material into the blood stream or directly onto the heart during surgery
IV drug user
Have had IE previously
causes of infectious endocarditis
increasing age
drug abuse
congenital heart disease
prosthetic heart valves
signs of infective endocarditis
new regurgitant heart murmur
embolic events of unknown origin
pulmonary embolus
kidney dysfunction
MI
sepsis of unknown origin
fever
new conduction disturbance
immunologic phenomena: roth spots, splinter haemorrhages, janeway lesions, osler’s nodes
peripheral abscess of unkown cause, petichiae
How do you diagnose endocarditis
2 Major Criteria
- Pathogen grown from blood cultures
- evidence of endocarditis on echo, or new valve leak
OR
5 Minor Criteria
- Predisposing factors
- Fever
- Vascular phenomena (ex.: stroke)
- Immune phenomena (roth spots, splinter haemorrhages, janeway lesions, osler’s nodes
- peripheral abscess of unkown cause
- petechiae
- Equivocal blood cultures
Definite IE
2 major
1 major+3 minor
5 minor
Possible IE
1 major
1 major+3 minor
5 minor
Imaging you can do for endocarditis investigation
Transoesophageal echocardiography (more invasive but much better pictures)
what are osler’s nodes
small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits
indicative of possible endocarditis
what are janeway lesions
erythematous, macular, nontender lesions on the fingers, palm, or sole
indicative of possible endocarditis
what are roth spots
retinal hemorrhages with a pale or white center
indicative of possible infectious endocarditis
what tests are used to diagnose infectious endocarditis
blood cultures –> 3 different blood cultures 6 hours apart
raised CRP
ECG
TTE (transthoracic echocardiogram) / TOE (transoesophageal echo)
when do you operate infectious endocarditis
the infection cannot be cured with antibiotics (ie reoccurs after treatment, or CRP doesn’t fall)
complications (aortic root abscess, severe valve damage)
to remove infected devices (always needed)
to replace valve after infection cured (may be weeks/months/years later)
To remove large vegetations before they embolise
what area of the nephron and channel does each type of diuretic act on
Thiazide - DCT
- inhibits NCCT (sodium chloride co-transporter)
Loop Diuretics - Thick ascending Loop of Henle
- inhibits NKCl2 (Na, K, and 2Cl co-transporter)
Potassium-sparing diuretics - Collecting ducts
There are 2 types:
1) ENaC inhibitors
2) aldosterone receptor antagonists
which type of diuretic increases Ca reabsorption
Thiazide diuretics
what type of diuretic is associated with the most Mg and Ca ion loss
Loop Diuretics
give an example of a potassium-sparing diuretic which is an aldosterone receptor antagonist
Amiloride
what do you want to routinely check in a patient who is taking diuretics?
uric acid levels - check for gout (inflammation around knuckles)
impaired glucose tolerance
what are the words for
1) a lower carotid pulse
2) a delayed carotid pulse
1) parvus
2) tardus
what is heart failure
An inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
causes of heart failure
IHD
Hypertension
alcohol excess
cardiomyopathy
valvular
endocardial
pericardial causes
what are the different types of right sided heart failure
HF with reduced ejection fraction (HFrEF)
HF with preserved ejection fraction (HFpEF)
who has a higher ejection fraction: men or women
women (65% vs 55%)
symptoms of heart failure
Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight
signs of heart failure
Tachycardia
Displaced apex beat
Raised JVP
Added heart sounds and murmurs
Hepatomegaly, especially if pulsatile and tender
Peripheral and sacral oedema
Ascites
what are the classes of heart failure and what do they mean
They are the New York Heart Association Classification
class 1: no symptom
class 2: slight symptoms with moderate exertion
class 3 : mild symptoms on exertion
class 4: inability to carry out any physical activity without discomfort –> severe heart failure
what is classed as HFrEF
EF<40%
what is classed as HFpEF
EF>50%
what is classed as HFmrEF
heart failure with mild reduced ejection fraction
41%-49%
what part of the cardiac cycle is affected in HFrEF
Systole
What part of the cardiac cycle is affected by HFpEF
Diastole
what are some diseases associated to HFrEF
MI
dilated cardiomyopathy
CAD
fibrosis of the myocardium
valve regurgitation
pericarditis with effusion; tamponade
aortic stenosis
what are some diseases associated to HFpEF
untreated hypertension
LV hypertrophy
what are risk factors for heart failure
Previous CVD
Age
Past Medical History of Heart Failure
Diabetes Mellitus
Medical History of IHD or cardiomyopathy
Excessive alcohol intake
Smoking
Arrythmias
Hypertension
CKD - CKD can lead to impaired sodium and water excretion by the kidneys, resulting in volume overload. This volume overload increases the preload on the heart, contributing to diastolic dysfunction
explain the pathophysiology of heart failure
Continued increases in preload leads to wear and tear of the heart → over time impaired contractility and decreased stroke volume
Fall in SV -> Fall in CO and BP → secretion of adrenaline, ADH and renin
Norepinephrine - prolonged high levels:
Alter beta receptor response to normal regulatory signals
Necrosis of myocardial tissue
Inflammation and oxidative damage of myocytes
Myocardial remodelling which leads to dysfunction
RAAS activation due to decreased BP and high adrenalin levels
Aldosterone - can lead to inflammation and fibrosis of myocardium
All of these lead to increased BP but also increased preload and afterload on the heart which the failing heart cannot cope with
what are 3 regulators of aldosterone secretion
angiotensin 2
CRH
increase in serum K+
adrenalin secretion
what are the investigations for heart failure
ECG
CXR
NT-proBNP levels
what is BNP and what are its effects
BNP is a hormone produced by the LV when it is stretched
Effects of BNP
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
Raised BNP levels could indicated other conditions other than heart failure as well; it just prompts further investigation
differential diagnosis of heart failure
Pneumonia
PE
Asthma
ILD - interstitial lung disease
ARDS - acute respiratory distress syndrome
how would you manage HFrEF
outline first-line, next-line and second-line treatments, interventions
first line
ACEi or ARB: Ramipril or Valsartan respectively
Beta-blockers: BISOPROLOL
next line
MRA (Aldosterone agonists/K sparring diuretic) –> SPIRONOLACTONE
SGLT-2 inhibitor (ex.: DAPAGLIFLOZIN)
Loop Diuretics (ex.: FUROSEMIDE)
second line
IVABRADINE
Sacubitril-valsartan –> Neprilysin inhibitor
Hydralazine + nitrate
Digoxin - cardiac glycoside
Interventions
Cardiac Resynchronisation Therapy and implantable devices
Revascularisation
Heart Transplant
at what ejection fraction do you decide to give a HFrEF patient Sacubitril-valsartan treatment
EF <35%
Do diuretics treat HF cause?
No, they only reduce symptoms
How do you treat HFpEF
Manage co-morbidities - eg HTN, DM
Address lifestyle factors - eg smoking, obesity
Patient education
Vaccinations -
Influenza - annually
Pneumococcal - usually a one off EXCEPT in adults w/ asplenia, splenic dysfunction or CKD who need a booster every 5 years
how do you treat Acute HF
100% oxygen
GTN spray
IV opiates - diamorphine
IV furosemide – to reduce fluid overload
Positive inotropic drugs like digoxin or dopamine
what type of drug is lidocaine, what does it do, and how does it work
antiarrhythmic
Following depolarization, sodium channels have an inactivation gate that closes, temporarily blocking the passage of additional sodium ions. This closure is essential for the repolarization phase of the action potential and prevents the continuous firing of the neuron.
Lidocaine is a sodium channel blocker, and it primarily prevents the inactivation gate from closing effectively. This means that lidocaine stabilizes the sodium channels in the inactivated position, making it more difficult for the channels to reset to their closed state. In this way lidocaine prolongs the refractory period.
why is digoxin a useful drug in treating supraventricular tachycardias
increases vagal tone (parasympathetic action) –> decreases the rate of action potentials by making the membrane more positive and prolonging the refractory period
amlodipine and verapamil are both calcium channel blockers/ what makes verapamil a better anti-arrhythmic than amlodipine
verapamil is selective for calcium channels in the heart –> it prolongs the action potential and also affects diastole, decreasing the heart rhythm
amlodipine only affects vascular smooth muscle
Which additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack?
they are beta blockers which have the additional property of sodium channel blocking. this means that besides decreasing HR they can also prolong the action potential –> help stabilize the cardiac cell membranes and suppress abnormal electrical impulses,
In the treatment of heart failure, which transport protein or ion channel is inhibited by the loop diuretic, furosemide
also, where is that channel in the nephron
Na/K/2Cl transporter
thick ascending loop of henle
ACE inhibitors reduce the circulating levels of which adrenal hormone ?
Aldosterone
NOT angiotensin 2 because the question is asking about an ADRENAL HORMONE!
Which drug exerts a direct inotropic effect (+ force of contraction) on heart muscle?
a) Ramipril
b) Furosemide
c) Losartan
d) Digoxin
e) Spironolactone
f) Glyceryl Trinitrate
Digoxin –> positive inotropic cuz reduces the heart rate but increases cardiac force of contraction
Inhibition of the sodium-potassium pump leads to an accumulation of intracellular sodium.
The increased intracellular sodium concentration indirectly affects the sodium-calcium exchanger (NCX) on the cell membrane. The sodium-calcium exchanger is a protein that normally transports one calcium ion into the cell in exchange for three sodium ions being pumped out.
This leads to increased Intracellular Calcium Levels
Elevated intracellular calcium levels enhance the contractility of cardiac myocytes, leading to a positive inotropic effect.
In chronic heart failure beta blockers are…..
a) Contra-indicated
b) Beneficial by slowing the heart rate
c) Beneficial by depressing the myocardium
d) Beneficial by increasing oxygen demand
e) Effective by blocking reflex sympathetic responses which stress the failing heart
e) Effective by blocking reflex sympathetic responses which stress the failing heart
For which CVS drug is BRONCHOSPASM a potential side effect?
Beta-blocker
For which CVS drug is COUGH a potential side effect?
ACE inhibitors
For which CVS drug is TOLERANCE a potential side effect?
nitrate
Which CVS drug is most likely to induce POSTURAL HYPOTENSION as a potential side effect?
1) Morphine
2) Beta blocker
3) Calcium antagonist
4) Aspirin
5) Nitrate
6) ACE inhibitor
3) Calcium antagonist –> causes vasodilation and affects the vaso-vagal effect –> when you stand up your vessels should contract but because of the calcium antagonist they don’t do it well
Doxazosin is an antagonist at which type of peripheral receptor?
a) Alpha-1 adrenoceptor
b) Purine receptor
c) Angiotensin II receptor
d) Vasopressin receptor
e) Beta-1 adrenoceptor
f) Dopamine receptor
Alpha-1 adrenoceptor
Atenolol is an antagonist at which type of peripheral receptor?
a) Alpha-1 adrenoceptor
b) Purine receptor
c) Angiotensin II receptor
d) Vasopressin receptor
e) Beta-1 adrenoceptor
f) Dopamine receptor
e) Beta-1 adrenoceptor
The antihypertensive action of lisinopril is due to inhibition of which peripheral enzyme?
a) Kininase II
b) Renin
c) Na/K ATP-ase
d) Angiotensin Converting Enzyme (ACE)
e) DOPA decarboxylase
d) Angiotensin Converting Enzyme (ACE)
Which of the following drug side effects is less likely to be seen when treating hypertension with an angiotensin receptor blocker (ARB) rather than an ACE inhibitor
a) Hyperkalaemia
b) Cough
c) Angioedema
d) Renal failure in the presence of bilateral renal stenosis
e) Cold hands/cold feet
b) Cough
How do beta-blockers work to relieve the pain from angina pectoris?
Reduce O2 demand by slowing the heart rate
Reduce O2 demand by reducing myocardial contractility
Improve O2 distribution by slowing the heart rate
What is the major mechanism by which glyceryl trinitrate can relieve the pain of angina pectoris?
a) Dilatation of veins to reduce the preload on the heart
b) Dilatation of arterioles to reduce the afterload on the heart
c) Dilatation of coronary arteries to increase cardiac perfusion
d) Opening of collateral blood vessels to improve cardiac perfusion
e) A positive inotropic effect
a) Dilatation of veins to reduce the preload on the heart
Which of the following drugs is likely to be more suitable for the treatment of variant angina due to coronary artery vasospasm?
a) Bumetanide
b) Losartan
c) Isosorbide
d) Amlodipine
e) Glyceryl trintrate
d) Amlodipine
Which of the following drugs might be used to reduce atheromatous disease, the underlying cause of angina pectoris
a) Atenolol
b) Amlodipine
c) Simvastatin
d) Glyceryl trinitrate
e) Enalapril
atheromatous disease = disease which builds atherosclerotic plaque
c) Simvastatin
what is ACS
Refers to three states of myocardial ischaemia: unstable angina (UA), non-ST elevation myocardial (NSTEMI) and ST elevation myocardial infarction (STEMI).
STEMI - ST segment elevation or new-onset left bundle branch block and raised troponins
NSTEMI - Non-specific signs of ischaemia or normal ECG, raised troponins
UA - Characteristic clinical features, non-specific signs of ischaemia or normal ECG, normal troponins
what are the risk factors for ACS
High cholesterol
Age
Hypertension
FHx
Smoking
Male sex
Diabetes
Premature menopause
Obesity
what causes ACS
Imbalance between the heart’s oxygen demand and supply
1) Atherosclerotic plaque formation → Impairment of blood flow by proximal arterial stenosis
2) Increased distal resistance → left ventricular hypertrophy
3) Reduced oxygen-carrying capacity of blood eg anaemia
ECG feature of NSTEMI
ST depression and T wave inversion
ECG feature STEMI
ST elevation
Q wave MI would indicate transmural infarct
T wave inversion can appear a few days/weeks after a STEMI
gold standard investigation for ACS
ECG + troponin levels
unstable angina vs NSTEMI vs STEMI diagnosis
unstable angina –> normal troponin and normal ECG but acute chest pain presentation
NSTEMI –> raised troponin and normal ECG or ST depression and T wave inversion
STEMI –> diagnosis based solely on acute presentation and ECG with ST elevation
differential diagnosis of ACS
Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Dissection of the aorta
Gastro-oesophageal (reflux, spasm, ulceration)
Musculo-skeletal chest pain
Psychological
Management of NSTEMI ACS
GTN spray → vasodilation of veins to reduce preload on heart
IV Morphine → reduce pain
Dual antiplatelet therapy → Aspirin 300 mg + P2Y12 inhibitor (Clopidogrel / Prasugrel / Ticagrelor 180mg)
Anticoagulation/antithrombin therapy → Fondaparinux
Consider intravenous glycoprotein IIb/IIIa antagonists for patients undergoing primary PCI
Background angina therapy: beta blocker + calcium blocker + long acting nitrate
!Don’t give beta blockers to asthma patients
Oxygen if there is shortness of breath
GRACE SCORE: decide on coronary angiography
PCI/CABG
what is the GRACE score
used to determine whether an NSTEMI patient needs urgent coronary angiography
management of STEMI ACS
GTN spray → vasodilation of veins to reduce preload on heart
IV Morphine → reduce pain
Dual antiplatelet therapy → Aspirin 300 mg + P2Y12 inhibitor (Clopidogrel / Prasugrel / Ticagrelor 180mg)
Anticoagulation/antithrombin therapy → Fondaparinux
Consider intravenous glycoprotein IIb/IIIa antagonists for patients undergoing primary PCI
Background angina therapy: beta blocker + calcium blocker + long acting nitrate
!Don’t give beta blockers to asthma patients
Oxygen if there is shortness of breath
after ECG shows ST elevation you refer for emergency coronary angiography
PCI if available within 2 hours of presenting
If not you do THROMBOLYSIS with TPA
what types of ACS can undergo CABG
only unstable angina and NSTEMI
what do you include in a pain history of ACS (details about the pain)
Mnemonic: OPQRS
Onset
Position (site)
Quality (nature/character)
Relationship (with exertion, posture, meals, breathing and with other symptoms)
Radiation
Relieving or aggravating factors
Severity
Timing
Treatment
What baseline investigations do you perform on a patient which presents with angina pectoris
Baseline bloods, including FBC, U&E, LFT, lipids and glucose
Chest x-ray to investigate for pulmonary oedema and other causes of chest pain
ECG once stable to assess the functional damage to the heart, specifically the left ventricular function
CT coronary angiogram
how do you monitor patient after ACS has been handled
ECG to assess the functional damage to the heart
Cardiac rehabilitation
Secondary prevention
- Aspirin 75mg once daily indefinitely
- Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
- Statins - Atorvastatin 80mg once daily
- ACE inhibitors (e.g. ramipril) titrated as high as tolerated
- Beta blocker - Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated DO NOT GIVE TO ASTHMA PATIENT
- Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Closely monitor the renal function in patients taking ACE inhibitors and aldosterone antagonists. Both can cause hyperkalaemia (raised potassium)
If PCI done repeat angiogram 3 months later to observe stent and coronary blood flow
how do you decide on wether to use ticagrelor or clopidogrel
ticagrelor for low bleeding risk patients
clopidogrel for high bleeding risk patients
complications of MI
Mnemonic: DREAD
D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
how can CKD cause heart failure
can lead to impaired sodium and water excretion by the kidneys, resulting in volume overload. This volume overload increases the preload on the heart, contributing to diastolic dysfunction
Continued increases in preload leads to wear and tear of the heart –> over time you get impaired contractility and decreased stroke volume
what is the gold standard investigation for heart failure
echocardiogram to get LVEF and chamber parameters
what ethnicity respond to enalapril treatment for HF
white. Black people don’t respond as well to ACEi
what is defined as hypertension
a BP of 140/90 mmHg on at least two readings on separate occasions
what BP is classed as stage 2 hypertension
160/100
what adrenal gland tumour can cause hypertension
pheochromocytoma –> too much release of adrenalin and noradrenalin
cause of hypertension
primary (95% of cases) - No clearly identifiable underlying cause ; silent killer cuz asymptomatic till acute
secondary (5% of cases)
1) endocrine –> too much aldosterone (primary aldosteronism),adrenalin (pheochromocytoma), cortisol (cushing’s), GH and IGF1 (acromegaly) secretion
2) renal disease (CKD)
3) drugs (glucocorticoids, oral contraceptives, SSRIs, NSAIDs, EPO)
4) congenital vascular defects –> coarctation of aorta
what are risk factors for hypertension?
FHx
Old age
Obesity
Salt-heavy diet
Sedentary lifestyle
Heavy alcohol consumption
Smoking
Race - Afro-carribean
name 4 drugs which increase BP
NSAIDs
SNRIs
Corticosteroids
Oestrogen oral contraceptives
Stimulants
Anti-anxiety drugs
Anti-TNFs
what is the difference between primary and secondary hypertension?
primary –> unknown cause
secondary –> due to renal, endocrine or congenital diseases, or due to medications
how does primary hypertension usually present
asymptomatic
investigations may reflect some end-organ damage
occasional headache
what is the gold standard investigation for hypertension?
ABPM - ambulatory blood pressure monitoring
only done if the office and home BP measurements are very discordant
what is the first line of investigation for hypertension?
Office BP or Out of office BP
what does ABPM entail
24-hour monitoring of BP during daily life and sleep
how do you diagnose hypertension?
combine office and out-of-office BP measurements to arrive to a conclusion
what BP is defined as malignant hypertension
180/120
after you diagnose someone with hypertension what are you concerned about that you need to check
end organ damage
any prescribed meds which could worsen BP
ECG
Nephropathies
Retinoapthies
what lifestyle changes can improve hypertension?
Smoking cessation
Drinking alcohol/caffeine in moderation
Healthy weight
Reducing dietary sodium
Staying physically active
Reduce stress
what do you do if a patient has to go under anesthesia but they are on ACEi or ARB? justify
u stop the ACEi and ARB cuz they have the risk of becoming hypotensive –> these meds have a vasodilatory effect
they also have the risk of being too sensitive to the anaesthetic agents (ACEi and ARBs affect the kidneys a lot)
how much do you expect the maximal dose of one medication for hypertension to decrease BP
systolic: 8-10 mmHg
diastolic: 4-5 mmHg
what is the blood pressure target in people who have had a previous stroke, heavy proteinuria or CKD and diabetes
130/80 mmHg
what is the blood pressure target in older patients with hypertension
150/90
how do you treat hypertension
Lifestyle changes
Step 1
in people below age 55 you give ACEi or ARB
if afro-carribean you give ARB
in people above 55 you give a calcium channel blocker
do not give ACE if patient has nephropathy
Step 2
you combine the ACEi/ARB with CCB (calcium channel blocker)
Step 3
add thiazide-like diuretic (indapamide) –> check patients on this med for gout
Step 4
Add spironolactone or doxazosin (alpha-blocker) or beta blocker (be careful with asthmatics)
how often do you check the BP of hypertension patients whilst adjusting their meds
every 2 to 4 weeks
what is the clinical test done to check for PAD
Buerger’s Test –> foot turns white when elevated, red when lowered
what is the most specific ECG finding of acute pericarditis
PR depression
gold standard investigation for pericarditis
echocardiogram
how do you treat a cardiac tamponade?
urgent pericardial paracentesis
does constrictive pericarditis present with pulsus paradoxus? explain
constrictive pericarditis→ thickening and fibrosis of the pericardium → rigid and non-compliant pericardial sac → limited variation in intrapericardial pressure during inspiration → no pulsus paradoxus
which is the most frequent valve affected by endocarditis
mitral
state the degrees in between which you find left axis deviation, RAD, and extreme axis deviation on an ECG
you can draw it out
LAD: -90 and -30
RAD: 90 and 180
Extreme axis deviation: -90 and 180
how do you estimate the deviation of an ECG
use leads 1 and aVF
look at whether the QRS is positive or negative (should be positive in both)
what are causes of right axis deviation
DISEASE CAUSES
right ventricle hypertrophy
anything that makes the RA and RV push harder (COPD, pulmonary embolism)
Lateral STEMI –> if LV isn’t really conducting then you will have a shift of the vector of depolarisation to the right)
Left posterior fascicular block
Hyperkalemia
Sodium channel block
WFW
HEALTHY PATIENT CAUSES; just different anatomy
dextrocardia –> congenital heart located on the wrong side of the chest
normal paediatric ECG (differences in heart size and position in child chest)
Tall and thin patient –> more vertically oriented heart
what are causes of left axis deviation
left ventricular hypertrophy
LBBB
inferior MI
WPW
Left anterior fascicular block
horizontally oriented heart –> short patients
what are causes of extreme axis deviation
hyperkalemia
ventricular tachycardia
ventricular ectopy
severe right ventricular hypertrophy
what is ventricular ectopy?
premature heartbeats originating in the ventricles of the heart –> appear before they should normally be in the cardiac cycle
what ECG change does WPW cause
short PR interval
what is the normal duration of the P wave
less than 0.12s (3 small squares)
what is the normal duration of the PR interval
0.12 - 0.20s
(3-5 little squares)
what is the normal duration of the QRS
0.11s (less than 3 little squares)
What is the normal duration of the QT interval
0.35-0.45s
what should be the pattern for R waves from V1 to V6
progressively higher amplitude cuz closer tp LV
what does a long PR interval suggest and how long should it normally be
first-degree heart block
0.12-0.2s (3-5 little squares or 1 large square)
what is the patter of S wave change in leads V1-V6
V1-V3: S wave growth (further from LV so bigger negative deflection)
V4-V6: S wave disappears
is it normal for ST to be slightly elevated in V1 and V2
yes
what are the 4 ECG features of a pathological T wave
symmetrical
tall
biphasic
inverted
where is the P wave best assessed
lead 2
in what lead can the P wave be biphasic without pathology
V1
what are P mitrale and P pulmonale
P mitrale –> P wave pathology due to left atrial enlargement. P wave has 2 notches
P pulmonale –> very high amplitude P wave due to right atrial enlargement
what is the normal amplitude of a P wave
not taller thamn 2.5mm
what causes the 2 R waves in RBBB
delayed activation of the right ventricle
what causes the W shape in LBBB
delayed activation of the LV
what are the ECG features of a LBBB
W shape in V1
Long QT interval
explain the different types of heart blocks
Type 1 –> PR interval longer than 0.2s (1 large square)
Type 2 Morbitz type 1: progressively longer PR interval which results in 1 skipped beat
Type 2 Morbitz type 2: there is a fixed ratio of atrial beats to ventricular beats
Type 3: complete heart block; no pattern in SAN and AV conduction
what is sinus tachycardia?
what causes it
tachycardia in which the PQRST complex looks fine
it is not caused by cardiac problems, it is due to other underlying conditions which increase sympathetic nervous system stimulation (thyroid disorders, anaemia, anxiety, caffeine, fever, drugs, dehydration, pheochromocytoma, heart failure etc.)
what is the difference between atrial fibrillation and atrial flutter?
atrial fibrillation is very chaotic and disorganised beats whereas atrial flutter has clear patterns; the ECG looks much more organised
what are F waves and what rate are they usually at
F waves are the extar small waves from atrial flutter
rate 300 bpm
what leads do you assess atrial flutter in
2, 3, aVF (all of the inferior looking leads) + V1 (lead which looks at septum)
what do you call it when a patient has a tachyarrhythmia which resolves spontaneously?
Paroxysmal atrial fibrillation
why are CCBs contra-indicated for HFrEF
because they not only slow down the action potential, but they also decrease heart contractility
what is supraventricular tachycardia?
tachycardia which originates from the atria but it si not due to AFib or atrial flutter
ex.: can be due to WPW or digoxin toxicity or anatomic abnormalities
what is the physiology of supraventricular tachycardia?
electrical signal renters atria from ventricles through another pathway
what is ventricular tachycardia? and what is it most often caused by
most dangerous type of tachycardia
ventricles are beating chaotically; you get a very with QRS, can’t see P or T waves
may see AV dissociation
most commonly due to scarring from previous MI
what are the 4 classes of antiarrhythmics?
1 –> sodium channel blockers
1a) moderate blockers - quinidine
1b) weak blockers - lidocaine
1c) strong blockers - flecanide
2 –> beta blockers
3 –> Potassium channel blockers
4 –> calcium channel blockers
what are big amplitude Q waves suggestive of on an ECG
previous MI
what is the beat in atrial fibrillation described as
irregularly irregular
what antiarrhythmic class is lidocaine
1b
which coagulation pathway does warfarin affect and what test is it monitored with
extrinsic pathway
PT/INR
which coagulation pathway does heparin affect and what test is it monitored with
intrinsic pathway
aPTT
what is shock
Medical emergency when the body isn’t getting enough blood flow to carry out aerobic cellular respiration → Generalised hypoxia
what is defined as a low systolic BP
systolic <90 mmHg
what are the causes of shock and explain their physiology
Cardiogenic: heart pump failure
Hypovolemic: blood loss or fluid loss causes a reduction on preload
Septic : damage to endothelial cells by endotoxins –> release of NO + activation of complement pathway –> vasodilation + systemic inflammatory response –> leaky capillaries
Anaphylaxis: general immune inflammatory response –> leaky capillaries and sudden droop in BP
Neurogenic: damage to CNS, loss of SNS causing vasodilation and low BP
what are different causes of hypovolemic shock
Haemorrhagic causes
Trauma
GI bleeding
Ruptured aortic aneurysms
Non-haemorrhagic (fluid loss)
Burns – heat increases permeability of capillaries so more plasma leaks
Severe diarrhoea and vomiting → dehydration
Intestinal obstruction (fluid accumulates in intestines)
Pancreatitis → inflammation causes systemic inflammatory response which results in vasodilation. Initially, you get peripancreatic edema, then you get ascites, and finally, you get shock
what are the key presentations of shock
Rapid and weak pulse
Pale
Cold
Sweaty
Low BP → arterial BP NOT a good indicator of shock since it will be maintained until a very large amount of blood loss
Reduced urine output
Confusion
Capillary refill time takes more than 3 seconds to turn pink after 5 seconds of compression
what investigations do you do for shock
FBC, Blood glucose, arterial blood gases, Blood lactate
You want to check heart:
D-dimers → for pulmonary embolism
Echocardiogram
You want to check for kidney damage:
Serum creatinine
Electrolytes
Urine
You want to check for liver damage or coagulopathies from shock:
Coagulation → Shock itself, regardless of the underlying cause, can induce changes in coagulation parameters. You can get DIC (bad cuz leads to consumption of all clotting factors)
Liver biochemistry
how do you manage cardiogenic shock
ABCDE, resuscitation
how do you manage hypovolemic shock
ABCDE, 100% oxygen, IV fluids, vasodilator
how do you manage septic shock
ABCDE, broad spectrum antibiotics (vancomycin)
how do you manage anaphylactic shock
ABCDE, IV adrenaline
how do you manage neurogenic shock
Neurogenic shock: damage to CNS, loss of SNS causing vasodilation and low BP
ABCDE, IV atropine → antimuscarinic; blocks actions of ACh
what is the most common causes of mitral valve stenosis
rheumatic fever
what is the x descent in JVP
decrease in JVP due to ventricular systole which makes more space in the pericardium and hence allows atrial filling
how can you temporarily increase JVP for the examination?
by pressing on the liver
which are the 2 most common indications for valve replacement (in order)
1) aortic stenosis
2) mitral regurgitation
what is hydralazine
a vasodilator
what is AVNRT
AV node reentry tachycardia
Tachycardia due to the presence of two functionally and anatomically distinct conduction pathways in the AV node
in what situation do you get cyanosis in atrial septal defect
Eisenmengers syndrome
what developmental condition is Atrio-Ventricular Septal Defect associated with
Down’s syndrome
what is Torsades de Pointes
Polymorphic ventricular tachycardia in which the QRS amplitude varies and the QRS complexes appear to twist around the baseline. It is associated with prolonged QT interval. It will either terminate spontaneously and revert back to sinus rhythm or progress into ventricular tachycardia.
what are the types of aortic dissection and where is the most common location for an aortic dissection
Type A - before brachiocephalic artery
Type B - after left subclavian artery
most common location - sinotubular junction where aortic roots becomes tubular aorta
pathophysio of aortic dissection
Tear in the intima causes blood to pass through the media creating a false lumen. As the dissection spreads, flow through the false lumen can occlude flow through branches of the aorta including coronary, brachiocephalic, carotid, intercostal, renal and visceral > ischemia of supplied regions.
key presentation in aortic dissection
Sudden and severe ripping/tearing pain in chest
Asymmetrical blood pressure in arms (>20mmHg), hypotension, radial pulse deficit (radial pulse in one arm is decreased/absent and doesn’t match apex beat), diastolic murmur, focal neurological deficit (e.g., muscle weakness/paralysis – carotid and spinal arteries), interscapular and lower pain
gold standard investigation for aortic dissection and management
CT angiogram or transoesophageal echocardiogram
management
1st line – immediate surgery. Type A (open surgery to replace aortic defect with stent), Type B (TEVAR thoracic endovascular aortic repair). Maintain haemodynamic stability (fluids, adrenaline, transfusion)
what is the tetralogy of Fallot?
A congenital condition where there are 4 existing pathologies:
1. Ventricular septal defect.
2. Overriding aorta.
3. Pulmonary valve stenosis (RV outflow obstruction).
4. Right ventricular hypertrophy
What is the most common side effect of amlodipine?
Swelling in ankles or legs
What hypertension medications are teratogenic - don t give to pregnant women
ACEi and ARB
What bacteria causes rheumatic fever
Strep pyogenes
What is a common side effect of statins
Muscle pain
What is the fontaine classification
The 4 stages of chronic limb ischemia in PAD
Stage 1 - asymptomatic
Stage 2 - intermittent claudication
Stage 3 - rest pain/nocturnal pain
Stage 4 - necrosis/gangrene
DVT 1st line and gold standard investigations
1st line
Well’s score —> determines risk of DVT
Score under 2 is unlikely DVT so u order a D-dimer
If D-dimer raised order doppler USS
Score over 2 order immediate doppler USS
Gold standard: doppler USS
What are the 1st line and gold standard treatments for PAD
1st line
Ankle brachial pressure index
Gold standard
CT angiogram —> shows occlusions
What is first line treatment of DVT in pregnancy
LMWH
DVT key presentations
Calf swelling
Warmth
Tenderness
Pitting oedema
Dilated superficial veins
Colour change to leg
Erythema
What are the 6Ps or peripheral artery disease
Pain
Pale
Pulseless
Perishing cold
Paresthesia
Paralysis
Treatment of PAD
Modifiable risk factor management
Statins
Anti platelet - clopidogrel
Very severe - Re vascularisation surgery
What is the most severe complication of DVT
Pulmonary embolism
What scores calculate risk of stroke and bleeding from anticoagulants
For what kind of patients would you use them
CHA2DS2-VASC - stroke
ORBIT - bleeding
Used for afib and atrial flutter patients
Differential diagnosis of narrow QRS
Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter
What is WPW syndrome
Atrioventricular REENTRY TACHYCARDIA
there is an accessory pathway
What is the name of the accessory pathway in WPW
Bundle of Kent
WPW ECG changes
Short PR
Wide QRS
Slurred upstroke of QRS - delta wave
Management of haemodynamically stable and haemodynamically unstable SVT
Stable
1st line - vagal manoeuvres like valsalva and carotid massage
2nd line - IV adenosine
3 - CCB (verapamil)
4 - DV CARDIOVERSIN
unstable
Jump to 3 and 4
What is the most common cause of supraventricular tachycardia
AVNRT
ECG changes in AVNRT
P waves are within QRS
narrow QRS
Atrial fibrillation vs atrial flutter management
Haemodynamically unstable: DC cardioversion
Haemodynamically stable: You need to do rate control (beta blockers or CCB) and rhythm control (amlodipine or flecaininde)
Long term: catheter ablation
Atrial flutter is pretty much the same except that in haemo stable you do
1st line rate control with beta blocker + anticoagulant
2nd electrical cardioversion
3rd flecainide - pharmacological cardioversion
Long term - catheter ablation
What is the biggest concern with untreated atrial fibrilation
Stroke
