Cardiovascular Flashcards
What is Cardiac Failure?
The failure of the heart to maintain the cardiac output required to meet the body’s demands
LHF + RHF = Congestive Heart Failure
What does it mean by ‘Output States’ in relation to Cardiac Failure?
Low Output State = heart fails to pump in response to normal exertion
High Output State = cardiac output is normal but there are higher metabolic needs such as pregnancy, anaemia, hyperthyroidism
What are the ways in which Cardiac Failure can be classified?
- By EF
- By time
- By LHF or RHF
What are the parameters for classifying Cardiac Failure by EF?
- Patients with reduced LVEF (< 35-40%) have HF-rEF
This is due to systolic dysfunction (impaired myocardial contraction) - Patients with normal (preserved) LVEF have HF-pEF
This is due to diastolic dysfunction (impaired filling during diastole)
LVEF measured using echocardiography
Causes of Systolic and Diastolic dysfunction for Heart Failure
SD
- Ischaemic Heart Disease
- Dilated CMO
- Myocarditis
- Arrhythmias
DD
- Hypertrophic Obstructive CMO
- Restrictive CMO
- Cardiac Tamponade
- Constrictive Pericarditis
What are the parameters for classifying Cardiac Failure by time?
Acute or Chronic
- Acute typically refers to an acute exacerbation of chronic
- Most urgent symptoms are often due to LV failure resulting in pulmonary oedema
What are the parameters for classifying Cardiac Failure by LHF and RHF?
HF-rEF and HF-pEF typically develop left-sided heart failure. This may be due to increased left ventricular afterload (e.g. arterial hypertension or aortic stenosis) or increased left ventricular preload (e.g. aortic regurgitation resulting in backflow to the left ventricle).
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).
History and Examination for LHF
Respiratory symptoms
- Increased heart and respiratory rate
- Arrhythmia
- Dyspnoea
- Nocturnal cough (may have pink frothy sputum)
- Fatigue
History and Examination of RHF
Swelling symptoms
- Swelling
- Fatigue
- Raised JVP
- Reduced exercise tolerance
- Anorexia
- Nausea
- Nocturia
- Ascites
Clinical Diagnosis for Cardiac Failure by Framingham Criteria
2+ majors or 1 major and 2 minors from:
Investigations for Cardiac Failure
CHRONIC
-NT-proBNP (nice)
- 2000ng/litre, urgent referral for transthoracic echo in 2/52
- 400-2000ng/litre, same as above but in 6/52
ACUTE
- BNP > 100ng/litre
- NT-proBNP > 300ng/litre
- Perform transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities
- ECG
- Bloods - FBCs, U&Es, LFTs, TFTs, BNP
- Chest X-Ray
- Transthoracic Echocardiography
- Coupled with Doppler
- Can calculate EF (normal 50-70%)
Findings for Cardiac Failure on X-Ray
- Alveolar Oedema
- Cardiomegaly
- B-lines (Kerley)
- Dilated upper lobe vessels and upper lobe
- Effusion
Management of Cardiac Failure if Acute
ABCDE approach
- Sit patient upright
- Give oxygen (target 94-98%)
- GTN infusion if concomitant myocardial ischaemia, severe hypertension or left-sided regurgitation
- Can cause hypotension
- IV furosemide for pulmonary oedema
- CPAP if not responding to treatment and in respiratory failure.
- Inotropic agents such as dobutamine should be considered with severe left ventricular dysfunction and cardiogenic shock (hypotensive).
- Stop beta-blockers if HR < 50, second or third degree heart block, or shock
Management of Cardiac Failure if Chronic
- Treat underlying cause
- Treat exacerbating factors
- Lifestyle modifications
- Drugs
- ACE inhibitor - give to all patients with LV dysfunction (reduced EF) and beta-blocker - reduce O2 demand on heart
- Aldosterone agonist
- Spironolactone, eplerenone
- Monitor potassium to avoid hyperkalaemia
- SGLT-2 inhibitors for reduced ejection fraction
- Ivabradine if sinus rhythm > 75/min and EF < 35%
- Sacubitril-valsartan if EF < 35% and symptomatic on ACEi’s or ARBs (initiate after wash-out period)
- Digoxin if coexistent atrial fibrillation
- Consider hydralazine and nitrates in Afro-Caribbean patients
- Cardiac resynchronisation therapy if widened QRS
- Annual influenza vaccine
- One-off pneumococcal vaccine
What are complications of Cardiac Failure?
- Respiratory complications
- Renal failure
- Acute exacerbations
What is Deep Vein Thrombosis?
Deep vein thrombosis (DVT) is a significant medical condition characterised by the formation of a thrombus within the deep venous system, typically in the lower extremities.
What do patients with DVT usually present with?
- Pain + tenderness + swelling in affected leg
- Warmth + redness in affected leg
- Shortness of breath and chest pain (suggestive of PE)
What scoring system is carried out for suspected DVT?
Well’s Score
Investigations for DVT
If scores from Well’s Score:
- Is >2 : Ultrasound of affected leg, D-dimer if negative
- Is <2 OR US can’t be carried out in 4 hours : D-dimer, give DOAC in meantime
- If +ve D-dimer, stop DOAC and do US in a week
Management for DVT
The management of DVT involves the following steps:
- Apixaban or rivaroxaban
- If unsuitable, severe renal impairment or antiphospholipid syndrome then low molecular weight heparin followed by vitamin K antagonist (warfarin)
- 3 months for provoked VTE
- 6 months for unprovoked VTE
- Compression stockings: These help to prevent swelling and improve blood flow in the affected leg.
- Elevation of the affected leg: This helps to reduce swelling and improve blood flow.
- Thrombectomy: This is a surgical procedure to remove the blood clot in the affected vein
What are risk factors for DVT?
- Age
- Smoking
- Alcohol
- Recent surgery
- Medication
- Trauma
- Malignancy
- Obesity
- Being inactive
- Diabetes
What is the NICE definition of Hypertension?
- A clinic reading persistently above 140/90 mmHg
- A 24 hour BP average reading of 135/85 mmHg
What are the two types of Hypertension?
Primary - no single disease causing the rise in BP, complex series of physiological changes
Secondary - precipitates from a particular disease
Renal causes of Hypertension
- Glomerulonephritis
- Chronic pyelonephritis
- Adult polycystic kidney disease
- Renal artery stenosis
Endocrine causes of Hypertension
- Primary hyperaldosteronism
- Phaeochromocytoma
- Cushing’s
- Liddle’s
- CAH
- Acromegaly
- Thyroid problems
H&E of Hypertension
Usually asymptomatic unless very high BP
Patients may experience
- Headaches
- Visual disturbance
- Seizures
Ensure there is no end-organ damage
What is very important to assess when a patient has newly diagnosed hypertension?
End organ damage
- Fundoscopy to check for hypertensive retinopathy
- Urine dipstick to check for renal disease (cause or consequence
- ECG to check for LV hypertrophy or IHD
Investigations for hypertension
24 hour BP monitoring
ABPM or HBPM
U&E - renal disease
HbA1c - DM
Lipids - Hyperlipidaemia
ECG
Urine dipstick
Management of hypertension
STEP 1
<55 or T2DM = ACEi or ARBs
>55 / Afro-caribbean + No T2DM = CCBs
STEP 2
A+C or A+D
STEP 3
A+C+D
STEP 4
If K+ < 4.5 add low-dose spirinolactone
If K+ > 4.5 add alpha or beta blocker
If still not controlled have specialist review
What is Unstable Angina?
Chest pain, considered to be present in patients with ischaemic symptoms suggestive of ACS + no elevation in troponins, +/- ECG changes indicative of ishcaemia
Troponins may elevate some hours later, treated same as NSTEMI until Troponin result known
H&E of Unstable Angina
- Chest pain
- May radiate to jaw or left arm
- Often described as ‘heavy’ or ‘crushing’
- Not relieved by rest
- Certain patients e.g. diabetics or elderly may not experience pain
Other symptoms of ACS:
- Dyspnoea
- Sweating
- N+V
Investigations for Unstable Angina
- ECG
- Cardiac markers e.g. troponin
Simplified management of NSTEMI/Unstable Angina
- Aspirin 300mg, Fondaparinux if no immediate PCI planned
- Estimate 6 month mortality with GRACE
- Low risk - Conservative - Ticagrelor
OR
Intermediate or high risk - PCI - offer immediately if unstable otherwise in 72hrs
Give prasugrel or ticagrelor, give unfractionated heparin, drug-eluting stents used in preference
Further treatment of NSTEMI/Unstable Angina
MONA
- morphine for severe pain
- oxygen if <94%
- nitrates
- aspirin 300mg
Antithrombin treatment for patients at high risk of bleeding
GRACE Risk Assessment
Takes into account:
- age
-HR, BP
- Cardiac (Killip class) and renal function (serum Cr)
- Cardiac arrest on presentation
- ECG
- Troponin levels
What is Pulmonary Embolism?
Life-threatening condition resulting from dislodged thrombi occluding the pulmonary vasculature; RHF and cardiac arrest may ensue if not aggressively treated
RF for PE?
- Age
- DVT
- Recent surgery
- Long bed rest
- Previous thromboembolic event
- Malignancy
- Trauma
- COCP
H&E of PE
- Pleuritic chest pain
- Dyspnoea
- Haemoptysis
- Collapse if severe
- Tachycardia
- Tachypnoea
- Fever
PE rule-out criteria (PERC)
Used to exclude PE in patients known to have a low pre-test probability (<15%)
Age >= 50
HR >= 100
O2 Sats <= 94%
Previous DVT or PE
Recent surgery or trauma in last 4 weeks
Haemoptysis
Unilateral leg swelling
Oestrogen use (e.g. HRT, contraceptives)
2-Level PE Wells score
Clinical signs and symptoms of DVT - 3
Alternative diagnosis less like than PE - 3
HR > 100 - 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks - 1.5
Previous DVT/PE - 1.5
Haemoptysis - 1
Malignancy - 1
PE LIKELY - MORE THAN 4 POINTS
PE UNLIKELY - 0-4 POINTS
Investigations for PE
If PE likely:
- CTPA : if +, PE diagnosed / if -, consider proximal leg vein ultrasound
- Interim therapeutic anticoagulation - DOAC
If PE unlikely:
- D-dimer test : if + = CTPA, if - = stop anticoagulation
- V/Q scan instead of CTPA if renal impairment
- Arterial blood gas
- ECG sinus tachycardia, may also see RBBB, right axis deviation, S1Q3T3
- CXR - Westermark’s sign : wedge shaped opacification
Management of PE is haemodynamically unstable (SBP<90)
- Thrombolysis (alteplase)
- Respiratory support
- Unfractionated heparin
- Then switch to DOAC
Management of PE if haemodynamically stable
- DOAC
- if severe renal impairment or antiphospholipid syndrome, give LMWH and warfarin
Give treatment for 3 months if VTE was provoked, 6 months if unprovoked
If repeat PE despite treatment consider inferior vena cava filters
VTE prevention for PE
Everyone must be VTE risk assessed within 24 hours of hospital admission
- Compression stockings
- Low molecular weight heparin (tinzaparin)
What is Pericardial Disease?
Refers to any condition that affects the pericardium, the sac-like membrane that surrounds the heart.
Can cause inflammation, fluid accumulation or constriction of the pericardium.
Acute is lasting for less than 4-6 weeks
Aetiology of Pericardial Disease
- Viral infections (Coxsackie)
- TB
- Uraemia
- Post-MI
- early (1-3 days) : fibrinous pericarditis
- late (weeks to months) : autoimmune (Dressler’s syndrome)
- Radiotherapy
- Connective tissue disease
- SLE
- RA
- Hypothyroidism
- Malignancy (lung/breast)
- Trauma
H&E of Pericardial Disease
History :
- Pleuritic chest pain
- Relieved by sitting forwards
- SOB
- Non-productive cough
- Fever
- Fatigue
- Palpitations
Exam :
- Muffled Heart sounds
- Pericardial rub
H&E of Constrictive Pericarditis
- RHF symptoms
- Elevated JVP
- Ascites
- Oedema
- Hepatomegaly
- Pericardial knock : Loud S3
- Positive Kussmaul’s sign : paradoxical rise in JVP on inspiration
Investigations for Pericardial Disease
- First-line is ECG
- PR depression
- Saddle-shaped ST elevation
- All patients with suspected acute pericarditis should have a transthoracic echo
- Bloods : CRP and ESR
- Raised troponin indicates myopericarditis
- CXR for constrictive pericarditis
- Pericardial calcification
Management of Pericardial Disease
- Combination of NSAIDs and Colchicine for patients with acute idiopathic or viral
- Until symptom resolution and normalisation of inflammatory markers, taper doses
- High-risk features e.g. fever and raised troponin, treated as inpatient
- Treat any underlying cause
- Avoid strenuous physical activity
- If pericardial effusion is causing significant symptoms of haemodynamic compromise, pericardiocentesis may be necessary
- If cases of chronic or constrictive pericarditis, surgical interventions such as pericardiectomy or pericardial window may be required
What is Haemochromatosis?
- Autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation
- Caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*
- Often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia
H&E of Haemochromatosis
Early symptoms include fatigue, ED and arthralgia (often hands)
Reversible symptoms:
- ‘bronze’ skin pigmentation
- cardiac failure secondary to dilated CMO
Irreversible symptoms:
- DM
- Liver : stigmata of CLD, hepatomegaly, cirrhosis, hepatocellular deposition
- Hypogonadism (2nd to cirrhosis and pituitary dysfunction)
- Arthritis
Screening of Haemochromatosis
Screening:
Gen. Pop.
- Transferrin saturation is considered the most useful marker
- Ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
Family members:
- Genetic testing for HFE mutation
Investigations for Haemochromatosis
Typical iron study profile in patient with haemochromatosis
- Transferrin saturation > 55% in men or >50% in women
- Ferritin raised and iron
- Low TIBC
Also:
- LFTs
- Molecular genetic testing for C282Y and H63D mutations
- MRI to quantify liver and cardiac iron
- Liver biopsy if suspected cirrhosis
Management of Haemochromatosis
- Venesection
- Transferrin saturation should be kept below 50% and serum Ferritin concentration below 50 ug/L
- Desferrioxamine may be used second line
