CardioResp Flashcards
Preload measurement
End diastolic volume
End diastolic pressure
Right atrial pressure
Afterload measurement
Diastolic bp
Heart sounds
S1: closure of mitral valve
S2: closure of aortic valve
S3(just after S2): congestive HF
S4(just before S1): hypertension etc
Alveolar cells
Type 1(95%): thin, gas exchange Type 2(5%): secrete antiprotease and surfactant, replicate to replace type 1
Function of nasal conchae
Warm and humidify air
Filter large particles
Lung capacities
Tidal volume Inspiratory capacity Functional residual capacity Vital capacity Total lung capacity
Positive and negative pressure breathing
Negative is normal
Positive is CPAP or mechanical ventilation
Shifts in HbO2 sat and PO2 graph
Right shift: high temp, CO2, 2,3DPG, acidosis
Left shift: low temp, CO2, 2,3DPG, alkalosis, HbF
Down shift: anaemia
Up shift: polycythaemia
Down and left: HbCO
Severe left shift: myoglobin
Endogenous regulation of heart
SA node controls pulse
Phase 0: upstroke from Ca influx
Phase 3: repolarisation from K efflux
Phase 4: pre potential from Na influx
Cardiac muscle action potential
Phase 0: Na influx(depolarisation) Phase 1: K efflux(early repolarisation) Phase 2: Ca influx(plateau) Phase 3: K efflux(repolarisation) Phase 4: RMP
Exogenous regulation of heart(brain)
Vasomotor centre(VMC) in medulla
Sympathetic/paraympathetic on SA node
M2 receptor(ACh)
Beta-1 receptor(NA)
Exogenous regulation of heart(kidney)
BP detected by baroreceptors
Sympathetic->renin->AT2-> vasoconstriction and raise bp
AT2->aldosterone->Na reabsorption-> blood volume rise
Exogenous regulation of heart(blood vessels)
Low filling/pressure->low baroreceptor firing->sympathetic activity
Vasoconstrictors: thromboxane A2, adrenaline
Vasodilators: NO, ANP
Control of lung function
4 nuclei in medulla
Dorsal respiratory group: inspiration
Ventral respiratory group: expiration and inhibits apneustic centre
Apneustic centre: stimulates DRG
Pneumotaxic centre: regulates depth and frequency, inspiratory off switch
Afferent lung receptors
Irritant: induces cough
Stretch: excessive inflation->DRG & VRG
J: detects oedema->breathing frequency
Type of vessel with highest resistance
Arteriole
Variation of perfusion and ventilation in lung
Highest at base, lowest at apex
Arteriole vasodilation
Active hyperaemia e.g. skeletal muscle
Arteriole vasoconstriction
Myogenic autoregulation e.g. GI arterioles
What is heart failure(causes, symptoms, tests, treatment)
Preserved(<50%) or reduced(<40%) ejection fraction
Causes: hypertension, cardiac damage, valve disease
Symptoms: exertional dyspnoea
Tests: elevated BNP and cardiomegaly
Treat with drugs that reduce heart exertion
Atrial arrhythmias
AF: disorganised electrical activity WPW: tachycardia and abnormal electrical conductance Symptoms: palpitations and chest pain ECG: Absent p wave and irregular rhythm(AF) QRS delta wave(WPW)
Conduction block
1: prolonged P-R interval
2: Mobitz 1(increasing) and 2, missing QRS
3: no relationship between P and QRS
Treatment: discontinue AV blocking drugs and implant pacemaker if severe
Acute coronary syndrome types, cause, symptoms, biomarker and treatment
Angina, NSTEMI, STEMI
Caused by atherosclerosis
Angina: chest pain on exertion
NSTEMI: chest pain, sweating, nausea
STEMI: radiating chest pain, sweating, nausea
High troponin in NSTEMI & STEMI
Treat with vasodilators, coronary stent, CABG, anti platelets, pain relief
COPD comprises of
Emphysema: alveolar destruction
Chronic bronchitis: mucus hypersecretion
Small airway disease: small airway fibrosis
COPD cells and mediators
Neutrophils secrete proteases (neutrophil elastase and MMP) Macrophages T lymphocytes TNF alpha IL8
Tetralogy of Fallot
Pulmonary stenosis
Right ventricle hypertrophy
Interventricular septal defect
Widening of aorta
Aortic stenosis causes
Rheumatic heart disease
Calcium build up
Aortic stenosis pathogenesis
Endocardial injury
Inflammation
Leaflet fibrosis and calcium deposition on valve
Low aortic leaflet mobility
High afterload->left ventricle hypertrophy
Aortic stenosis presentation
Ejection systolic murmur
High LDL
Chest pain
Exertional dyspnoea
Aortic stenosis management
Aortic valve replacement
Balloon aortic valvuloplasty
Antihypertensive
Statins
Aortic regurgitation causes
Acute: infective endocarditis, trauma
Chronic: rheumatic fever
Aortic regurgitation pathogenesis
Acute:
Infective endocarditis->rupture of leaflets
Chronic:
Rheumatic fever->fibrotic changes-> thickening and retraction of leaflets
Aortic regurgitation presentation
Acute:
Tachycardia
Cyanosis
Pulmonary oedema
Chronic:
Wide pulse pressure
Aortic regurgitation management
Treat underlying cause first
Acute: vasodilators and valve replacement/repair
Chronic asymptomatic: drugs if LV function normal
Chronic symptomatic: valve replacement and adjunct vasodilator therapy
Mitral stenosis causes
Rheumatic fever
SLE
Carcinoid syndrome
Mitral stenosis pathogenesis
Acute cause Formation of multiple foci Infiltrate endo and myocardium Valve thickens, calcifies and contracts High left atrial pressure Pulmonary oedema&hypertension Low left ventricle filling Low cardiac output
Mitral stenosis presentation
Dyspnoea
Orthopnoea
Diastolic murmur
Hepatojugular reflux
Mitral stenosis management
Progressive asymptomatic: no therapy
Severe asymptomatic: adjuvant balloon valvotomy
Severe symptomatic: diuretic, valve repair/replacement, beta blockers
Mitral regurgitation causes
Acute: Infective endocarditis Chronic: Rheumatic heart disease SLE
Mitral regurgitation pathogenesis
Infective endocarditis Abscess formation Rupture of chordae tendinae Leaflet perforation Eccentric hypertrophy
Mitral regurgitation presentation
Dyspnoea Pan systolic murmur Fatigue Orthopnoea Chest pain Atrial fibrillation
Mitral regurgitation management
Acute:
Emergency surgery, diuretics, intra aortic balloon counterpulsation
Chronic asymptomatic: ACEi, beta blockers, surgery if EF<60%
Chronic symotomatic: surgery, intra aortic balloon counterpulsation if EF<30%
Dilated cardiomyopathy type of dysfunction
Systolic
Most common valve disease
Mitral regurgitation
Dilated cardiomyopathy presentation
Dyspnoea Displaced apex beat Systolic murmur Pulmonary congestion Low cardiac output High natriuretic peptides
Dilated cardiomyopathy management
Fluid and Na restrict
Treat underlying cause
Antihypertensive
Hypertrohpic cardiomyopathy type of dysfunction
Thick left ventricular wall
Diastolic
Hypertrophic cardiomyopathy presentation
S3 gallop Syncope Dizziness Palpitations Double carotid artery impulse
Hypertrophic cardiomyopathy management
Check Hb, BNP, troponin levels
Beta blockers
Calcium channel blocker
Pacemaker
Disopyramide
Restrictive cardiomyopathy type of dysfunction
Normal wall thickness but stiff muscle
Diastolic
Restrictive cardiomyopathy presentation
Ventricular pressure rises quickly but ventricular volume rises slowly
Low filling
Low cardiac output
Hepatomegaly with pain
Peripheral oedema
Hepatojugular reflux
Restrictive cardiomyopathy management
Amyloidosis check
Antihypertensive Antiarrhythmic Immunosuppression Pacemaker Cardiac transplant
Broad QRS complex
LBBB or RBBB
High take off on ST segment
Benign early repolarisation
Tall T wave
Hyperkalaemia
Inverted T wave
V1-3: RBBB
V4-6: LBBB
V5-6: left ventricular hypertrophy
Widespread: HCM
Biphasic T wave
Hypokalaemia
Asthma cells and mediators
Eosinophils
Mast cells
Type 2 lymphocytes
IL4,5,13
Asthma allergic sensitisation test
Skin test: wheel and flare reaction
Blood test: specific IgE
Asthma diagnosis
Spirometry FEV1/FVC<0.7
Bronchodilator reversibility >12%
Exhaled nitric oxide(FeNO)>35ppb(child) or 40ppb(adult)
Asthma management
Inhaled corticosteroids Leukotriene receptor antagonist Beta 2 agonist Anticholinergic therapy Anti IgE antibody (mepolizumab) Anti IL-5 Anti IL-5 receptor
Most common and most deadly resp infections and most commonly infected age group
Common: rhinovirus
Deadly: tuberculosis
Age: 0-10
Pneumonia grading
CURB65
Confusion Urea >7mmol/L Resp rate >30 breaths/min BP <90systolic or <60diastolic Age >65
Bacterial pneumonia management
Supportive: oxygen, fluids, analgesia
Penicillin (amoxicillin)
Macrolides (clarithromycin)
Viral bronchiolitis management
Supportive: fluids, oxygen, analgesia
Antiinflammatory: steroids, anti IL6, anti IL6R
Vaccine
Antivirals: remdesivir, paxlovid, casirivimab
Types of resp failure
Type 1: hypoxaemic
Type 2: hypercapnic
Type 3: perioperative
Type 4: intubated and ventilated during shock
ARDS symptoms
Dyspnoea
Tachypnoea
Cyanosis
ARDS pathophysiology
Fluid accumulation in lungs not from heart failure
Alveolar injury and surfactant dysfunction
Inflammation: TNF, DAMPs, cytokines
Compliance is reduced
ARDS diagnosis
Acute onset
Bilateral opacities on imaging
Respiratory failure not caused by heart failure
Decreased PaO2/FiO2 ratio
ARDS treatment
Mechanical ventilation
Prone position
Fluid management(diuresis)
ECMO
Lung cancer epidemiology
Age >75
M>F
Smoking history
Genetics
Types of lung cancer
Squamous cell carcinoma: bronchial
Adenocarcinoma(common): peripheral
Large cell lung cancer
Small cell lung cancer: highly malignant
Lung cancer oncogenes
BRAF
ALK
ROS1
EGFR
Tyrosine kinase inhibitor for systemic treatment
Lung cancer symptoms
Weight loss Haemoptysis Cough Breathlessness Chest pain
Lung cancer biopsies
Bronchoscopy for central airway
Endobronchial ultrasound and transbronchial needle aspiration of lymph nodes: stage mediastinum
CT guided biopsy: peripheral tumours
Lung cancer management
Surgery: lobectomy and lymphadenectomy
Radical radiotherapy: SABR
Oncogene systemic
Immunotherapy systemic: block PDL1 but PDL1 must be >50%
Cytotoxic chemotherapy: platinum based regime, good with pembrolizumab(immuno)
Palliative and supportive care
Primary haemostasis failure causes
Thrombocytopenia(leukaemia, B12 deficiency, ITP, DIC)
Impaired platelet function(aspirin, clopidogrel, NSAIDs)
Von willebrand factor disease(hereditary)
Vessel wall(ageing, vasculitis, scurvy)
Primary haemostasis failure symptoms
Prolonged bleeding
Petechiae(blanches with pressure):thrombocytopenia
Purpura(doesnt blanch):platelet/vascular disorders
Easy bruising
Primary haemostasis failure treatment
Replace missing factor/platelets
Stop drugs
Immunosuppression if autoimmune(ITP)
Splenectomy for ITP
Secondary haemostasis failure causes
Low factor production(haemophilia A/B, drugs, liver disease)
Dilution(blood transfusion)
High consumption(DIC)
Secondary haemostasis failure features
Haemarthrosis(haemophilia)
Superficial cuts dont bleed
Bleeding into deep tissue, muscle, joints
Raised PT, normal APTT
Factor VII
Normal PT, raised APTT
Factors VIII, IX, XI, XII
Raised PT and APTT
Liver disease, anticoagulants, DIC, transfusion dilution
Secondary haemostasis failure treatment
FFP: contains all factors
Cryoprecipitate: mainly fibrinogen
Factor concentrates: except factor V
Haemophilia treatment
Gene therapy
Bispecific antibodies(A):mimics factor VIII
RNA silencing: targets antithrombin
Desmopressin: raises VWF and factor VIII
Tranexamic acid: antifibrinolytic
Virchow’s triad thrombosis
Blood(venous) Vessel wall(arterial) Blood flow(mixed)
Thrombophilia presentations
Thrombosis at young age
Spontaneous thrombosis
Thrombosis while on anticoagulants
Thrombophilia causes
Low antithrombin, protein C, protein S
High factor VIII, II
Factor V Leiden
Myeloproliferative disorders
Vessel wall and blood flow thrombosis
Vessel wall: inflammation
Blood flow: reduced flow increases risk(long haul flight)
Heparin
Enhances antithrombin: inactivates IIa and Xa
Unfractionated: IV, short half life, greater effect
Low molecular weight: subcutaneous
Warfarin
Blocks recycling of vit K
Many drug interactions
Side effects: bleeding, skin necrosis, purple toe syndrome, embryopathy
Warfarin montoring using INR
DOAC
Rapid onset No food effect Few drug interactions No monitoring Some renal dependence Reversible with antidotes
Layers of vascular endothelium
Tunica adventitia
Tunica media
Tunica intima
Atherosclerosis risk factors and causes
Hypercholesterolaemia Diabetes mellitus Smoking Obesity Hypertension Sex hormone imbalance Ageing Oxidative stress Infectious agents Haemodynamic forces
Nitric oxide in different types of flow
Laminar: high NO production
Turbulent: low NO production
Nitric oxide functions in vessel wall
Reduce LDL oxidation Vasodilation Reduce platelet activation Inhibit monocyte adhesion Reduce superoxide release
Where is LDL deposited in atherosclerosis
Subintimal space
Binds to matrix proteoglycans
Role of macrophages in atherosclerosis
Inflammation from LDL deposition
LDL oxidised by free radicals
Macrophage phagocytosis
Foam cell formation, apoptosis after
Receptors on macrophage(atherosclerosis)
LDL receptors undergo -ve feeback when LDL in cell is high
Scavenger receptors have no feedback so high influx of OxLDL
Atherosclerosis enzymes invloved
NADPH oxidase(O2-)
Myeloperoxidase(bleach)
Metalloproteinase(MMP): degrades collagen, causing bleeding
Atherosclerosis cytokines and chemokines, chemoattractant and growth factor
IL-1
Monocyte chemotactic protein(MCP-1)
Platelet derived growth factor(PDGF)
TGF beta
Transcription factor in atherosclerosis activated by __ and activates __
Nuclear factor kappa B gets activated by scavenger receptors and IL-1
Activates MMP and IL-1 secretion
Macrocytic anemia causes
B12 deficiency: diet, gastrectomy, pernicious anaemia, Crohn’s
Folate deficiency: diet, proximal jejunum(coeliac disease), high demand
Drugs that inhibit DNA synthesis
Liver disease/ethanol toxicity
Haemolytic anaemia causes
Membrane integrity: hereditary spherocytosis, autoimmune haemolytic anaemia
Structure and function: sickle cell anaemia
Cellular metabolism: G6PD deficiency
Blood test for autoimmune haemolytic anaemia
Direct antiglobulin test (DAT)
Causes of microcytic anaemia and which chain is affected
Iron deficiency(haem)
ACD(haem)
Thalassaemia(globin)
Iron deficiency causes
Blood loss: menorrhagia, GI
Insufficient intake: vegetarian, coeliac, H. Pylori gastritis
Increased requirement: pregnancy
Iron deficiency blood test results
Low ferritin
High transferrin
Normal ESR
ACD blood test results
High ferritin
Low transferrin
High ESR
ACD pathology
Rheumatoid arthritis, autoimmune disorder, malignancy or TB/HIV
IL-1, TNFa, IL-6
Low erythropoietin, high hepcidin
Hb electrophoresis thalassaemia
HbA2 is raised: beta thalassaemia
MI treatment
Anticoagulants
Primary percutaneous coronary intervention
Alternative: thrombolysis or CABG
Mild VWD treatment
Desmopressin: increases VWF and FVIII
Murray score ARDS
PaO2/FiO2(on 100% O2)
CXR
PEEP(positive end expiratory pressure)
Compliance(ml/cmH2O)
3 or more->ECMO
