Breathlessness - Cardiac Flashcards
LO: explain the pathophysiology of breathlessness as a mismatch between instructions for ventilation sent by the brainstem and the sensory feedback from the thorax
Revise: Neural mechanisms that control breathing
What areas of the brain are involved?
What is this group collectively known as?
- Control of breathing relies on a no of brain centres including respiratory centre - in pons and medulla.
- The pons modulates respiratory output
- the medulla generates the central pattern of breathing - sends signals via cranial and spinal nerves to motor neurones that innervate the respiratory muscles
- In the medulla: there are two respiratory groups:
- 1) The dorsal respiratory group (DRG) - primarily sensory and coordinates input from peripheral chemoreceptors/ pulmonary stretch receptors. Contains inspiratory neurones that synapse with motor neurones to respiratory muscles. Generates normal pattern and active in quiet breathing.
- 2) The ventral respiratory group (VRG)- primarily motor - contains both inspiratory and expiratory neurones. Has regions that drive expiration and synapse with motor neurones that innervate the accessory muscles of expiration (forced expiration). Also regions that drive forced inspiration - muscles of pharynx and larynx.
LO: explain the pathophysiology of breathlessness as a mismatch between instructions for ventilation sent by the brainstem and the sensory feedback from the thorax
Revise: Sensory inputs to respiratory centres
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Peripheral chemoreceptors in carotid and aortic bodies - primarily detect changes in pO2 - can also respond to pCO2 and pH which enhances sensitivity to hypoxia.
- aortic bodies under arch of aorta
- carotid bodies located at bifurcation of common carotid
- Formed by glomus cells - detect arterial blood gas and receive very high blood flow
- most important are the carotid bodies - signal via glosspharyngeal nerve to DRG of medulla.
- Aortic bodies signal via vagus nerve.
- Afferent signals synapse with DRG to increase RR and depth of inspiration therefore restore pO2 back to normal.
- rapid response within 1-3 hypoxia being detected.
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central chemoreceptors - primarily detects pCO2 by change of pH of CSF.
- Located on ventral medulla inside BBB.
- Major source of feedback for tonic drive of breathing
- CSF secreted by choroid plexus, pH of CSF determined by HCO3- secretion from choroid P cells and by [H+] from diffusion of CO2 from arterial blood across BBB into CSF
- H+/HCO3- unable to cross BBB but CO2 freely diffusible –> therefore CSF pH determined by pCO2 in arterial blood
- when high, pH of CSF becomes more acidic, causes signalling from central chemoreceptors to DRG to increase ventilation rate and excrete more CO2.
- pulmonary stretch receptors in the lung - terminate inspiration and prevent inspiration via Hering breuer reflex - pulmonary stretch receptors signal via vagal afferents to the DRG - modulates output to respiratory muscles by inhibition of phrenic output.
- higher brain centres- modulate breathing pattern for speaking/swallowing etc.
LO: explain the pathophysiology of breathlessness as a mismatch between instructions for ventilation sent by the brainstem and the sensory feedback from the thorax
- Dysponea = an uncomfortable awareness of ones own breathing - considered abnormal when it occurs at a level of physical activity that is not expected to cause a problem
- Occurs when there is a mismatch between pulmonary ventilation and the drive to breathe - due to mismatch between afferent receptors and central respiratory motor activity.
- Multiple interactions between sensory receptors and CNS respiratory centres
- Respiratory centre of brain –> dorsal and ventral respiratory groups and pontine grouping
- pontine grouping further split into pneumotaxic and apneustic centres
- dorsal medulla - inhalation
- ventral - exhalation
- pontine - intensity and frequency of medullary signals - pneumotaxic group limits inhalation, apneustic centre prolongs and encourages inhalation.
- mechanoreceptors in airways/trachea/ lung/ pulm vessels –> slow adapting stretch spindles that convey volume information vs rapid adapting receptors that convey chemical irritation and volumes. Signal via CNX to brain to increase rate and volume of breathing or stimulate coughing reflex.
- peripheral chemoreceptors - carotid and aortic bodies - monitor paO2, pH and PCO2 increase sensitivity. Hypoxia detected –> signal via CNIX to Nucleus tractus solarius –> stimulates excitatory neyrones increase ventilation
- central chemoreceptors - majority of control over respiratory drive - pH changes in CSF detected via diffusion of PaCO2 over BBB to ventral medulla. Acidic –> hyperventilation, basic –> hypoventilation
- Resp centres in medulla and pons receive all this sensory information and modify the baseline respiratory rhythm.
- signal sent via phrenic nerve to muscles of respiratory, diaphragm, external intercostals, scalene muscles.
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What are the differentials related to cardiac breathlessness?
Acute causes vs chronic causes
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Acute:
- Acute cardiogenic pulmonary oedema (excess fluid within the pulmonary interstitium due to primary cardiac or circulatory cause)
- acute coronary syndrome (unstable angina, NSTEMI, STEMI)
- cardiac tamponade
- arryhthmia (see palpitations)
- acute valvular heart disease (see heart murmurs)
-
Chronic:
- __Chronic heart failure
- coronary artery disease (See chronic chest pain)
- valvular heart disease (see heart murmurs)
- constrictive pericarditis
- pericardial effusion
Chronic cause of cardiac breathlessness: Heart Failure
What are the 4 main functions of the heart?
Define heart failure
What is congestive heart failure
- 4 main functions of the heart:
- Delivery of deoxygenated blood to the lungs for oxygenation
- delivery of oxygenated blood to the body
- delivery of nutrients
- removal of waste
- Heart failure = Condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure
- Congestive heart failure term - reserved for patients with breathlessness, and abnormal sodium and water retention resulting in oedema.
Causes of cardiac breathlessness: Heart failure
what are the different types of heart failure?
-
Systolic heart failure = or heart failure with reduced EF ventricle unable to contract normally –> leading to reduced CO with EF < 40%
- often IH/MI or cardiomyopathy as cause
-
Diastolic heart failure = or heart failure with preserved ejection fraction ventricle cannot relax normally, therefore passive filling of ventricles is not as effective but with increased filling pressures, with EF> 50%
- often constrictive pericarditis, tamponade, restrictive cardiomyopathy and hypertension
- (Remember ejection fraction of 50-75% indicates normal pumping ability, below 50% abnormal, below 40% severe).
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Left sided HF
- Backlog of blood into the pulmonary veins causing predominant symptoms of: 1) dysponea, 2) fatigue 3) orthopnea 4) paroxysmal nocturnal dysponea 5) nocturnal cough (+/- pink frothy sputum)
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Right sided HF
- R ventricle too weak to pump enough blood to the lungs, leads to venous congestion in the body causing predominant symptoms of: 1) nausea 2) anorexia 3) reduced mobility 4) peripheral oedema
- HF can affect the Left and right ventricles individually or together = Biventricular heart failure
- If LVF is untreated it leads to RVF to due resulting high right pressure load (RV has to contract against increase pressure within pulmonary circulation = COR PULMONALE)
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High output cardiac failure: (pregnancy/ hyperthyroidism/ anaemia)
- Caused by higher demand on the heart - e.g. anaemia where a lack of oxygen means the heart has to work harder to deliver O2 to the tissues).
- Low output cardiac failure - low CO that fails to increase with any exertion - cause by excessive preload (e.g. fluid overload, pump failure, chronic excessive afterload as in aortic stenosis or HTN)
Causes of cardiac breathlessness:
Heart failure causes?
Common?
Other causes?
- Common causes of heart failure:
- Coronary artery disease - post mI and chronic ischaemia
- hypertension - heart struggles against high afterload
- valvular disease - regurgitation of vavle leads to congestion, stenosis of valve requires extra force to pump through
- myocarditis (mnemonic = my very chronic heart )
- Other causes:
- High output: thyrotoxicosis, pregnancy, anaemia
- congenital heart disease
- pericardial disease
- toxin - heroin/alcohol/cocaine/amphetamines
- chemotherapy
- infection (bacterial/fungal/ viral (HIV), parasitic (chagas disease) )
- cardiomyopathies (disease of myocardium - restrictive (heart wall stiff), hypertrophic(heart wall thickened) or dilated (heart wall stretched))
- arrythmias
- endocrine - diabetes, thyroid, adrenal disease
- nutritional - thiamine deficiency or obesity
- infiltrative - sarcoidosis (development of abnormal collections of inflammatory cells - granulomas, can develop in heart) or amyloidosis (abnormal amyloid deposition in heart).
History of heart failure:
Common symptoms of left sided
Common symptoms of right sided
Left sided:
- Dysponea
- fatigue
- orthopnea
- paroxysmal nocturnal dysponea
- nocturnal cough (w or w/out pink frothy sputum)
Right sided:
- Dysponea
- fatigue
- peripheral oedema
- anorexia
- nausea
- ascites
History of heart failure: Risk factors?
Risk factors:
- Old age
- Male
- Family hx of heart failure
- PMH: MI, diabetes mellitus, hypertension, left ventricular dysfunction or hypertrophy, renal insuffiency, valvular heart disease, sleep apnoea, rheumatic fever
- Cocaine abuse or exposure to cardiotoxic agents (chemotherapy)
- smoking/ tobacco/ alcohol –> risk factors for CV disease
Key signs on exam for heart failure?
- End of bed - GTN spray/ accessory muscle use/ cyanosis
- Dysponea - on exertion (NYHA stages 2-3) or at rest (NYHA stage 4)
- Orthopnea - sudden increase venous return - increased preload
- Hands –> cap refill, sweaty or clammy/ cyanosis/ janeway lesions or oslers nodels, clubbing, tar staining
- Pulse –> tachycardia, irregular pulse - think atrial flutter or fibrillation. Character - thready vs bounding vs weak?
- tachypnoea
- Blood pressure –> HTN?
- Eyes and mouth –> xanthelasmata, conjunctival pallor, mouth- central cyanosis. dehydration?
- Inspect –> scars or pacemaker placement?
- Palpation –> Cardiomegaly - displaced apex beat = hypertrophy, heaves and thrills ( valvular disease)
- Auscultation –> s3 gallop - prognosis of heart failure and lung fields (rales/ crackles - pulmonary oedema)
- Hepatojugular reflex - elevated and JVP raised - neck vein distention
- hepatomegaly or splenomegaly
- ascites
- ankle oedema - pitting oedema
Key investigations for heart failure?
-
Bedside:
- Observations
- ABG
- BM - blood glucose - diabetes
- ECG
- Left ventricular hypertrophy –> large R wave and largest S wave = > 45 mm in chest leads
- Left axis deviation –> Lead 1 positive and lead III will be negative
- Normal axis –> Lead 1 and lead 3 both positive
- right axis deviation –> lead 1 negative and lead III positive
- strain –> ischaemia (ST depression, T wave inversion)
-
Lab tests:
-
Bloods
- FBC- anaemia and infection
- U &E’s - renal failure can cause HF, check urea and creatinine for renal disease, medication baseline renal function
- BNP - measuring ventricular function - protein released by ventricular myocardium when stressed
- normal < 100 pcg/ml
- raised 100-400 pcg/ml
- high > 400 pcg/ ml
- Troponin - rule out ACS
- D dimer - PE
- TFTs - rule out thyrotoxicosis
- LFT - heart failure can cause liver failure
-
Bloods
-
Imaging:
- CXR
-
Special tests:
- Echocardiogram –> ejection fraction, wall size and motion and valvular disease
- cardiac magnetic resonance imaging —> ventricular function, wall size and motion
Key signs of heart failure on a chest xray?
ABCDE
Alveolar oedema - patchy opacification on both sides often in a batwing distribution
B - Kerley B lines - curved lines that run across from the pleura
C cardiomegaly - takes over 50% of the thorax
D - upper lobe diversion (vasculature and vessels are diverted and more prominent
E Effusion - pleural effusion - large difference in the size of the lung fields, meniscus line where water level meets the lung
What does this X ray show?
Upper lobe diversion - where the vasculature and vessels are diverted to upper lobes and more prominent (due to hypoxaemic pulmonary vasoconstriction).
sign of heart failure
CXR interpretation:
revise methodology
Confirm patient details - name/DOB/patient no/ date and time film taken/ previous imaging for comparison
RIPE
Rotation - medial aspect of clavicle equidistant from spinour processes? Spinous processes vertically orientated against vertebral bodies
Insipiration - the 5-6 anterior ribs, lung apices and both costophrenic angles and lateral rib edges should be visible
Projection - film AP or PA? Pa = standard, AP cannot assess cardiomegaly. (If scapula not crossing over lung borders then its PA).
Exposure- left hemidiaphragm should be visible to spine and vertebra visible behind the heart
ABCDE
Airway - trachea (deviation?), carina (NG tube should bisect, R main bronchus wider & shorter, more vertical than L) , bronchi, hilum (hilar usually same size, asymmetry suspect pathology - e.g. lymph nodes or mass)
Breathing - lungs (lung markings) and pleura (inspect borders of each lung, any fluid in pleural space?)
Cardiac - heart size (cardiothoracic ratio < 0.5 only in PA xray) and borders (should be well defined)
Diaphragm - R hemidiaphragm often higher than Left due to liver, stomach often underlies L - gastric bubble. Diaphragm should be indistinguishable from underlying liver, if air there - urgent review. Costophrenic angles - should be visible and acute angle. Loss of angle - fluid or consolidation in this area or hyperinflation
Everything else - mediastinal contours (aortic knuckle, , bones (fractures or lytic lesions) , soft tissues (hamaetoma), tubes (NG/ central lines, ECG), valves (artifical heart valves = ring shaped structures), pacemakers (radioopaque disc or oval in infraclavicular region connected to pacemaker wires positioned within the heart).
Congestive heart failure:
Management of Acute decompensated HF?
Acute management of HD - acute but stable - A-E assessment:
OMFG (Oh my f-ing G od) Oxygen, morphine, furosemide and GTN
Correct hypoxaemia - O2 - if really struggling CPAP (NIV)
IV furosemide
Diamorphine
GTN - under cardiology advice if BP normal
Fluid restriction
Daily weights and U&E’s
Strict input and output monitoring
Management of chronic heart failure?
Conservative management:
- Smoking cessation
- Fluid intake restriction
- Alcohol reduction
- Salt restriction
- Cardiac rehabilitation (exercise)
- Regular weighing (monitoring)
Medical management:
- ACE inhibitors (or sacubitril + valsartan if not tolerant)
- B blockers (Carvedilol, metoprolol, bisprolol)
- Diuretics (furosemide, bumetanide, thiazides or K+sparing)
- Can add nitrates and hydralazine (vasodilator) for symptomatic HF
- Can add digoxin for patients with reduced LVEF (can reduce sx and control rhythm)
- Can add ivabradine (severe HF rEF < 35%, slows HR for more efficient pumping)
- Can add vasopressin antagonist - for patients with persistent congestion
- Treat underlying cause (HTN/ arrhythmia etc)
Surgical Management:
- Cardiac resynchronisation (pacemaker)
- Treat underlying cause (e.g. valvular disease or IHD)
What are the diagnostic criteria for Heart Failure?
Framingham Diagnostic Criteria Or NYHA classification
Framingham criteria split into major and minor criteria.
NYHA classification split into 4 classes, beginning at 1 = asymptomatic, Class II mild sx with moderate exertion, Class III sx with minimal activity, class IV sx at rest
Framingham diagnostic criteria for HF:
What are the criteria?
Major Criteria:
- Acute pulmonary oedema
- cardiomegaly
- Hepatojugular reflex
- Neck vein distention
- Paroxysmal nocturnal dysponea or orthopnea
- Rales
- Third heart sound gallop
Minor criteria:
- Ankle oedema
- dysponea on exertion
- hepatomegaly
- nocturnal cough
- pleural effusion
- tachycardia (> 120 bpm)
What is the normal myocardial response to exertion or stress?
What happens in HF?
Normal myocardial response:
- Exertion or stress –> leads to 1) vasodilation in muscles which reduces SVR , 2) increased adrenergic stimulation of myocardium leading to —> tachycardia and increase myocardial contractility + increased CO with little increase in systemic BP
In Heart failure:
- Exertion or stress –> cardiac reserve does not permit an increase in contractility –> more energy consumption, tachycardia and only a small increase in CO
Why do congestive HF patients get oedema and fluid overload?
- Simply put: salt and water retention
- RAAS is activated in CCF due to reduced renal perfusion which causes stimulation of Renin production
- Renin –> Angiotensin 1 (from angiotensinogen) –> angiotensin II produced (by ACE in pulmonary vasculature) –> Causes an increase in NA and Aldosterone release –> sodium retention in distal convulted tubule –> water retention –> increased intravascular volume
Pathophysiology of atherosclerotic process?
Atherosclerosis:
- Damage to tunica intima endothelial cells:
- Hyperlipidaemia, ↑ cholesterol / LDL
- Hyperglycaemia
- Hypertension ( turbulent blood flow)
- Bacterial/ viral toxins
- Toxins from smoking
- Damaged endothelium become dysfunctional endothelium that release inflammatory cytokines and express adhesion molecules for monocytes and T lymphocytes.
- Endothelial dysfunction allows LDL to enter tunica intima
- Dysfunctional endothelium also releases ROS
- Oxidises LDL which induces monocytes to infiltrate and become macrophages
- Macrophages ingest oxLDL becoming Foam cell.
- Foam cells and T lymphocytes form inital fatty streak.
- Foam cells release GF’s which stimulate SMC’s in media to infilitrate intima and divide.
- SMC’s migrate over fatty core forming a fibrous cap. - Stable Plaque.
- Plaque rupture- balance of collagen production vs protease release from foam cells. Proteases degrade the ECM of the fibrous cap
- Loss integrity of endothelium and fibrous cap exposes blood to highly thrombogenic subendothelium:
- Collagen/ vWF/ TF.
- Platelet activation and adhesion- primary haemostatic plug
- TF- coagulation cascade- formation of secondary haemostatic plug with crosslinked fibrin.
ECG interpretation: Unstable angina
Unstable angina - ECG may often be normal or have transient ST segment depression (> 0.05mv) or T wave inversion (> 0.2 mV)
ST segment depression - in at least two anatomically contiguous leads
T wave inversion - in at least two anatomically contiguous leads
If ongoing ischaemia susptect and recurrent sx –> 12 lead ECG, take serial repeats (15-30 min intervals during 1st hour).
ECG interpretation: NSTEMI
-
ST segment depression
- may be present in variable no of leads and varibale morphology
- ST depression due to subendocardial ischaemi usually widespread
- typically in leads 1, 2, and V4-6)
- ST depression cannot localise an MI - if localised to particular territory more likely to represent reciprocal change due to STEMI.
-
T wave inversion (in example shown in lead 1 and lead 2, v4-v6)
- for MI needs to be at least 1mm deep
- present in 2 contiguous leads with dominant R waves (upright QRS complexes)
- Note wellens syndrome - pattern of inverted or biphasic T waves in V2-V4 - highly specific for critical stenosis of LAD
ECG interpretation: STEMI
- STEMI diagnosis requires ST elevation in 2 or more contiguous leads or new LBBB
- First change in ECG during STEMI = hyeracute T waves –> peaked and related to localised hyperkalaemia
- ST segment elevation localises to affected myocardium
- 1mm ST elevation in 2 contiguous leads
- EXCEPT: anterior STEMI requires > 2mm elevation in V2 + V3
- posterior STEMI - may be ST depression in V1-V3 as vectors reversed
- Note to diagnose a STEMI need 1 consistent clinical hx, ECG w ST elevation or new LBBB, raised cardiac markers.
ECG territories and location of the infarct?
Which vessel is occluded?
- Leads II, III, aVF = inferior infarct (RCA or circumflex artery if non dominant RCA)
- Leads V1-V3 - anteroseptal infarct = LAD
- Leads 1, aVL, V4-V6 - anterolateral (circumflex artery or dominant RCA)
- isolated posterior infarcts are rarer, extension of inferior or lateral infarct into posterior myocardium indicates greater myocardial damage. Not directly visualised by standard 12 lead ECG, reciprocal changes of STEMI sought in anteroseptal leads V1-V3 (horizontal ST depression).
Management STEMI
Initial approach:
- Cardiac monitoring + bed rest 12-24 hours
- O2 (if sats < 90%)
- Aspirin 300 mg immediately - do not wait for troponin! Then 75 mg OD after + antiplatelet (ticagrelor/prasugrel/clopidogrel) - loading dose then OD after
- morphine - relieve pain and decreased SNS activity (which fruther increase myocardial o2 demand)
- Nitrates - GTN immediately consider IV nitrates if no effect
Haemodynamically unstable –> emergency revascularisation within 48 hrs, if PCI fails urgent CABG
- Antiplatelet and anticoagulant therapy:
- Aspirin + ticagrelor or prasugrel (P2Y12 inhibitors)
- Unfractionated heparin
- Analgesia –> morphine
- O2
- Glycaemic control (insulin if needed)
Electrically unstable (Cardiac arrest but been resucitated now haemodynamically stable) –> Emergency revascularisation
Haemodynamically stable –> PCI with stenting (bare metal or drug eluting). Failed PCI go to CABG.
If no PCI available and no contraindications to thrombolytic therapy –> thrombolysis. PCI tx of choice, more effective and higher re-patency rates. Should have adjunctive antiplatelet therapy + anticoagulant therapy
Ongoing: Secondary prevention
- Dual Antiplatelet therapy (DAPT) - aspirin and clopidogrel
- Anticoagulant - unfractionated heparin or NOAC
- BB
- Ace I /ARB
- Statin (aim LDL <1.8)
- Lifestyle changes - exercise smoking cessation, healthy diet, lowered alcohol, stress
Causes of acute cardiac breathlessness:
Cardiac tamponade
Anatomy refresh: pericardium
Anatomy:
- Fibrous pericardium on the outside - continuous with central tendon of diaphragm, made of tough connective tissue and relatively non-distensible. Prevents overfilling of the heart but can cause cardiac tamponade
- Serous pericardium - enclosed within fibrous pericardium - divided into two layers (outer parietal layer and internal visceral layer that forms the outer layer of the heart - epicardium). Each layer made up of mesothelium.
- Inbetween the outer and inner serous layer = pericardial cavity –> contains small volume lubricating serous fluid –> minimises friction as the heart contracts.
History of cardiac tamponade?
What is Beck’s triad?
Signs on examination?
Becks triad:
- Hypotension
- Distant heart sounds
- Elevated JVP
Patients often complain of chest pain and SOB/dysponea.
PMH: malignancy, recent invasive cardiac procedure, aortic dissection, pericarditis, TB.
Exam:
- Tachycardic to maintain CO
- Pulsus paradoxus - abnormally large decrease in stroke volume during inspiration, abnormal large decrease in SBP and pulse wave amplitude during inspiration.
- In cardiac tamponade - pulsus paradoxus due to two ventricles competing for space in pericardial sac. Any increase in right ventricular volume (which normally occurs during inspiration which leads to increased venous return) leads to interatrial / ventricular septum bulging into the left.
- Hypotension
- Distant heart sounds
- may have fever or pericardial rub
Investigations and interpretation in cardiac tamponade?
Bedside: ECG
-
ECG: Electrical alternans (lead II in pic)
- alternately tall R wave in one QRS complex, then short, then tall, then short etc.. –> heart swings around in pericardial fluid towards and away from the ECG electrodes, hence alternans
- Electrical alternans v common in cardiac tamponade and pericardial effusion.
- Very low voltage QRS complexes
Bloods:
- FBC –> aneamia/ infection
- ESR –> indicate chronic inflammation
- Cardiac enzymes –> if suspecting MI
Imaging:
- CXR – > enlarged cardiac silhouette, cardiomegalu but no other evidence of heart failure (e.g. no alveolar oedema, kerley B lines, effusion).
- Transthoracic echocardiogram –> fluid > 20mm in pericardial space, chamber collapse and variation of ventricular filling with respiration
