cardiology Flashcards
clinical signs on cardiovascular examination which will support the diagnosis of pulmonary hypertension
split loud P2 is the only direct sign - it is the sound of elevated PA pressur slamming the pulmonic valve shut at the end of systole
rest are all features of right heart failure.
- Parasternal heave is a sign of RV hypertrophy
- a prominent “a” wave is the wave of right atrial contraction, reflected from either a stenotic tricuspid valve or a stiff non-compliant right ventricle. This also suggests that the RV is hypertrophied.
- Features of tricuspid regurgitation suggest that the RV is also dilated, and possibly decompensating.
causes of mid diastolic murmur at apex
Mitral stenosis Aortic regurgitation Left to right shunts – VSD or a PDA Severe MR Acute rheumatic fever
Causes of pulsus bisferiens
a double peak with each cardiac cycle on palpation of the arterial pulse,
- AS + AR
- Severe AR
- HOCM
- IABP
Effects of norad
Improves preload (by venoconstriction)
Improves vasoplegia (by arterioconstriction)
Improves cardiac contractility (β-1receptor effect increases with increasing dose)
Improves diastolic filling of coronary arteries (by increasing diastolic pressure)
Improves diastolic filling of the ventricles (by producing a reflex bradycardia)
Consequences of HTN following CTS
Increased bleeding risk - particularly from the aortic cannulation site
Extension of an arterial dissection
Increased afterload and thus increased LV workload
Thus, increased risk of ischaemia
Increased risk of cardiac failure due to decompensated LV failure
Increased stress on grafted valves or repaired aortic root
Worsening of existing mitral regurgitation
Increased need for sedation
Bleeding from aortic cannulation site
Causes of HTN following CTS
Pain
Inadequate sedation in a partially paralysed patient
Pre-existing hypertension, and the perioperative cessation or regular medications
Artifactual hypertension (measurement error)
Unintelligent use of vasopressors
The sudden improvement of aortic flow following the repair of a stenotic aortic valve, which exposes the systemic circulation to being bullied by a massively hypertrophied left ventricle.
Mx of WPW in AF
vagal manoeuvres
AVOID ASV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
Procainamide, ibutilide or amiodarone are the only antiarrhytmics useful in WPW
DC synchronised cardioversion
Conditions associated with RAD
Right ventricular hypertrophy Left posterior hemi block Lateral myocardial infarction Acute right heart strain Drug toxicity (e.g. TCAs)
Complications of inferior STEMI
Bradycardia and heart block (2nd and 3rd degree)
Posterior infarction
Right ventricular infarction
Pericarditis
Inflammation of the pericardium (e.g. following viral infection) produces characteristic chest pain (retrosternal, pleuritic, worse on lying flat, relieved by sitting forward), tachycardia and dyspnoea.
ECG - Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).
Causes -
- infection (viral most common, but can be any)
- uraemia
- post Mi (Dresslers)
- post CTS
- paraneoplastic
- drugs - isoniazid
Myocarditis
Myocardial inflammation in the absence of ischaemia.
Often associated with pericarditis , termed myopericarditis.
Usually a benign disease without serious long-term complications.
In the acute setting can cause arrhythmias, cardiac failure, cardiogenic shock and death.
May result in delayed dilated cardiomyopathy.
Most common ECG changes - sinus tachycardia with non-specific ST segment and T wave changes.
Things that worsen Brugada syndrome
Ischameia
Hyperthermia or hypothermia
Hypokalemia
Cardioversion
Drugs:
Class 1 antiarrhythmics
Beta blockers and calcium channel blockers
Alpha-agonists
Nitrates
Cocaine and alcohol
Cholinergic agonists, eg. the “stigmine” drugs
Diagnosis of Brugada syndrome
Characteristic ECG changes
“Coved” ST elevation: the QRS complex finishes high, and the ST-segment slopes diagonally to form an inverted T-wave in V1 and V2
Inverted T waves
Also, one of the following:
documented polymorphic VT or VF
Family history of sudden cardiac death before the age of 45
Characteristic ECG changes in family members
Syncope
Induceable VT
Nocturnal agonal respiration
AR vs MS as cause of diastolic murmur
Aortic regurgitation
- Collapsing pulse / wide pulse pressure
- Decrescendo murmur heard over left 3rd intercostal space parasternally
- Murmur loudest sitting forward in expiration
- Signs associated with large pulse volume and peripheral vasodilation; eg Corrigans, De Musets. Quinckes, Duroziez.
- Evidence of associated conditions; Infective endocarditis, ankylosing spondylitis, other seronegative arthropathies, Marfans.
- Soft 2nd heart sound
- 3rd heart sound
- Displaced apex beat
- Signs of LV failure
Mitral stenosis
- Malar flush
- Atrial fibrillation
- Small pulse pressure
- Loud 1st heart sound
- Opening snap
- Low-pitched, rumbling diastolic murmur over apex loudest in left lateral position
- Pulmonary hypertension
classic clinical findings on praecordial examination in a patient with Tetralogy of Fallot.
- ESM or PSM
- Right ventricular heave
- A loud single second sound
causes of an irregularly irregular pulse.
AF
A flutter with variable block
multiple vent ectopics
multifocal atrial tachycardia
management of HOCM in cardiogenic shock
Ceasing positive inotropes Starting some negative inotropes Ensuring a slow rate Maintaining a sinus rhythm Increasing preload Inreasing afterload and diastolic pressure
classic cardiac auscultatory signs and typical findings on a right heart catheterization of atrial septal defect
Fixed split of second heart
sound
Mid diastolic flow murmur
over tricuspid area if significant shunt
Step up in oxygen
saturation at atrial level
classic cardiac auscultatory signs and typical findings on a right heart catheterization of ventricular septal defect
Harsh pansystolic murmur
confined to the left sternal edge
Mid diastolic flow murmur
over mitral area if significant shunt
Step up in oxygen
saturation at ventricular level
classic cardiac auscultatory signs and typical findings on a right heart catheterization of patent ductus arteriosus
A continuous murmur
heard over the pulmonary area
Mid diastolic flow murmur
over mitral area if significant shunt
Step up in oxygen
saturation at pulmonary artery level
signs indicating severe AS
Delayed carotid upstroke Diminished carotid pulse on palpation Apical impulse sustained (pressure loaded) Absent or decreased A2 S4 gallop Late peaking murmur Long murmur Murmur radiates to the neck
Characteristics of HOCM murmur
systolic ejection crescendo-decrescendo murmur
best heard between the apex and left sternal border, radiates to the suprasternal notch but not to the carotid arteries or neck
Increased preload (squatting, passive leg raise) or increased afterload ( eg handgrip) - quieter
Decreased pre load (valsalva) or decreased afterload (eg nitrates) -> louder
Effects of respiration on murmurs
Inspiration -> increase in right sided
Expiration -> increase in left sided
VSD - increase in expiration
HOCM - no change
ECG features of RVH
Right axis deviation
Dominant R wave in V1
Dominant S wave in V5-V6
Normal QRS duration (i.e. not a right bundle branch block)
Benefits of using troponin in critically ill
Cardiac specific (although is raised wth reasons other than ischaemia - CPR, Pulmonary embolism, Tachyarrhythmia, Post-defibrillation, Post-cardiotomy, Cardiac trauma, Myocarditis
Rapid rise allows earlier identification of ischaemia
Correlate well with risk stratification
Strongly associated with 30-day mortality
Pulsus paradoxus - what is it and what is physiology
an exaggeration (> 12 mmHg or 10%) of the normal inspiratory decrease in systemic blood pressure.
Decreased intrathoracic pressure with inspiration results in increased venous return to right heart and bulge of IVS to left. Because the ventricle can normally also expand outward, this septal shift is usually small, and the difference in the blood pressure is therefore small between inspiration and expiration (<10 mmHg). With tamponade, the left ventricle cannot expand outward, so the septal shift is exaggerated and the difference in BP is larger.
methods by which pulsus paradoxus may be elicited clinically
Palpation of pulse- disappears in deep inspiration
Sphygmomanometer- Korotkoffs sounds first heard in expiration only and then in inspiration with progressive deflation
Pulse Oximeter-particularly useful in paediatrics
Arterial pressure trace- exaggerated fall of systolic pressure in inspiration
clinical signs of acute pericardial tamponade
pulsus paradoxus
Hypotension
Elevated JVP (neck vein distension with inspiration- Kussmaul’s sign)
Muffled heart sounds
Tachypnoea
Exaggerated drop in diastolic CVP (Friedrich’s sign)
Absent y descent on CVP trace
Clinical signs of shock- decreased peripheral perfusion, slow capillary refill, oliguria, confusion.
electrocardiographic findings suggestive of pericarditis with cardiac tamponade
Tachycardia
Low QRS voltage trace
Electrical alternans
Global concave ST elevation
PR depression
echocardiographic features of cardiac tamponade
Visible pericardial effusion
Diastolic collapse of Right Atrium and Right Ventricle
Respiratory variation in left and right sided volumes. Atrial and ventricular septa move leftward during inspiration and rightward during expiration
Mitral and Tricuspid flow velocities are increased and out of phase. Mitral flow is increased on the first beat of inspiration and tricuspid flow is increased on expiration.
The IVC is distended and does not collapse on inspiration
Predictors of better outcome after cardiac arrest are:
Recovery of brainstem reflexes within 48 hours
Return of purposeful response within 24 hours
Hypothermia at the time of arrest
Young age
Effect of external factors on SSEPS
SSEP not influenced by sedatives, analgesics, paralysing agents or metabolic insults
Hypothermia affects SSEP test results: mainly delayed peaks (prolongation conduction times);no consistent effect on voltages (amplitudes)
- although Bilaterally absent N20 SSEP during hypothermia is a good predictor for absent N20 SSEP after rewarming, which means you can do SSEPs during the period of hypothermia
- SSEP not affected as much as EEG
Causes of VF:
Cardiac ischaemia Electrical myocardial injury Traumatic myocardial injury Irritating mechanical stimulus (eg. CVC guidewires, PA catheter) Myocarditis
Predisposition to VF:
Low potassium Low magnesium Hypoxia Arrhythmogenic drugs eg. theophylline, sympathomimetics Congential and idopathic predisposition Prior cardiac surgery Cardiac chamber hypertrophy
The roles of the team leader in a cardiac arrest include:
As per ARC -
- Directing and co-ordinating the resuscitation attempt
- The safety of the resuscitation team at the cardiopulmonary arrest
- Ending the resuscitation attempt when indicated, often in consultation with other resuscitation team members and medical staff otherwise in charge of the patient
- Documentation (including audit forms) and for communication with the relatives and other healthcare professionals involved in the patient’s management
- Organising resuscitation team debriefing.
To this, one might add the following responsibilities:
Assessing the rhythm and evaluating the need for defibrillation
Ensuring the correct application of ALS and BLS
Establishing a diagnosis for the cause of the arrest
Ordering the appropriate investigations
Ensuring minimal interruptions to CPR
Allocating roles to the rescuers, and coordinating their efforts.
Recruiting external resources (eg. cardiologists, ICU staff, cardiothoracic surgeons) into the resuascitation effort
Communicating with family and the primary admitting consultant
Fluid responsiveness
A functional assessment of response to fluid of cardiac output and arterial pressure
No fixed definition;
An increase in stroke volume of 10-15% following a 500ml fluid bolus over 15 mins
Use of CVP to assess fluid responsiveness
- a static measure
Rationale -
A hypovolemic patient is expected to have a low CVP
That patient’s CVP should increase in response to fluid challenge
If the patient remains relatively hypovolemic, the change in CVPwill be relatively small.
A patient who is “well filled” will have a large increase in their CVP.
Limitations -
CVP is unrelated to RA pressure, RV pressure, RV preload, or any of the other validated parameters of fluid responsiveness
Apart from RV preload and cardiac function, the CVP is influenced by numerous other physiological variables, including RV compliance, PEEP, tricuspid valve competence, wnd where in the CVP waveform the measurement is taken
ECG findings in hypokalaemia
ST depression T wave flattening and inversion U waves Long QT/QU interval (fusion of T and U waves) P wave amplitude increased (>2.5 mm in limb leads, >1.5 mm in chest leads) P wave width increased (>120 msec) PR interval prolonged (>200 msec) Supraventricular ectopics Ventricular ectopics Atrial fibrillation Atrial flutter Atrial tachycardia Torsade de pointes
Levosimendan effects
increased cardiac contractility
vasodilatation (coronary, systemic and pulmonary)
May also have anti-inflammatory, anti-oxidative and anti-apoptotic effects
Levosimendan uses
Heart failure - typically acute failure
- may be used after ACS
- in conjunction with LVAD to manage to RHF
- as a bridge to Tx (esp in patients with severe pulm HTN)
Indications for IABP
No choice but pump
- Failure to come off bypass
- Severe aortic stenosis, mitral regurgitation or ventricular septal defect with hemodynamic compromise, while waiting for repair
Probably harmless, but probably not useful
- High risk CABG patients (pre-op)
- High-risk PCI patients (pre-op)
- Cardiogenic shock while waiting for PCI
- Pulmonary oedema in spite of maximal medical management
Totally experimental
- Takotsubo cardiomyopathy
- Neurogenic stress cardiomyopathy of subarachnoid haemorrhage
Limitations to critical care echo
positioning
lung over distension with mechanical ventailtion
drains and dressings in the way
ongoing resus
Roles of critical care echo as per 2016 CICM statement
used for diagnosis, monitoring and management of critically ill
Estabilshed use in differentiation of causes of shock, Mx of difficult pt post CTS or arrest, guidence of urgent intervetniosn and assisting with placement of ECMO cannulas, drains etc
