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CICM > cardiology > Flashcards

cardiology Flashcards

1
Q

clinical signs on cardiovascular examination which will support the diagnosis of pulmonary hypertension

A

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.
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2
Q

causes of mid diastolic murmur at apex

A 
Mitral stenosis
Aortic regurgitation
Left to right shunts – VSD or a PDA 
Severe MR
Acute rheumatic fever
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3
Q

Causes of pulsus bisferiens

A

a double peak with each cardiac cycle on palpation of the arterial pulse,

  • AS + AR
  • Severe AR
  • HOCM
  • IABP
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4
Q

Effects of norad

A

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)

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5
Q

Consequences of HTN following CTS

A

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

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6
Q

Causes of HTN following CTS

A

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.

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7
Q

Mx of WPW in AF

A

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

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8
Q

Conditions associated with RAD

A 
Right ventricular hypertrophy
Left posterior hemi block
Lateral myocardial infarction
Acute right heart strain
Drug toxicity (e.g. TCAs)
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9
Q

Complications of inferior STEMI

A

Bradycardia and heart block (2nd and 3rd degree)
Posterior infarction
Right ventricular infarction

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10
Q

Pericarditis

A

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
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11
Q

Myocarditis

A

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.

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12
Q

Things that worsen Brugada syndrome

A

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

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13
Q

Diagnosis of Brugada syndrome

A

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

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14
Q

AR vs MS as cause of diastolic murmur

A

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
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15
Q

classic clinical findings on praecordial examination in a patient with Tetralogy of Fallot.

A
  • ESM or PSM
  • Right ventricular heave
  • A loud single second sound
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16
Q

causes of an irregularly irregular pulse.

A

AF
A flutter with variable block
multiple vent ectopics
multifocal atrial tachycardia

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17
Q

management of HOCM in cardiogenic shock

A 
Ceasing positive inotropes
Starting some negative inotropes
Ensuring a slow rate
Maintaining a sinus rhythm
Increasing preload
Inreasing afterload and diastolic pressure
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18
Q

classic cardiac auscultatory signs and typical findings on a right heart catheterization of atrial septal defect

A

Fixed split of second heart
sound

Mid diastolic flow murmur
over tricuspid area if significant shunt

Step up in oxygen
saturation at atrial level

19
Q

classic cardiac auscultatory signs and typical findings on a right heart catheterization of ventricular septal defect

A

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

20
Q

classic cardiac auscultatory signs and typical findings on a right heart catheterization of patent ductus arteriosus

A

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

21
Q

signs indicating severe AS

A 
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
22
Q

Characteristics of HOCM murmur

A

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

23
Q

Effects of respiration on murmurs

A

Inspiration -> increase in right sided

Expiration -> increase in left sided

VSD - increase in expiration
HOCM - no change

24
Q

ECG features of RVH

A

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)

25
Q

Benefits of using troponin in critically ill

A

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

26
Q

Pulsus paradoxus - what is it and what is physiology

A

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.

27
Q

methods by which pulsus paradoxus may be elicited clinically

A

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

28
Q

clinical signs of acute pericardial tamponade

A

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.

29
Q

electrocardiographic findings suggestive of pericarditis with cardiac tamponade

A

Tachycardia

Low QRS voltage trace

Electrical alternans

Global concave ST elevation

PR depression

30
Q

echocardiographic features of cardiac tamponade

A

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

31
Q

Predictors of better outcome after cardiac arrest are:

A

Recovery of brainstem reflexes within 48 hours
Return of purposeful response within 24 hours
Hypothermia at the time of arrest
Young age

32
Q

Effect of external factors on SSEPS

A

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
33
Q

Causes of VF:

A 
Cardiac ischaemia
Electrical myocardial injury
Traumatic myocardial injury
Irritating mechanical stimulus (eg. CVC guidewires, PA catheter)
Myocarditis
34
Q

Predisposition to VF:

A 
Low potassium
Low magnesium
Hypoxia
Arrhythmogenic drugs eg. theophylline, sympathomimetics
Congential and idopathic predisposition
Prior cardiac surgery
Cardiac chamber hypertrophy
35
Q

The roles of the team leader in a cardiac arrest include:

A

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

36
Q

Fluid responsiveness

A

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

37
Q

Use of CVP to assess fluid responsiveness

- a static measure

A

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

38
Q

ECG findings in hypokalaemia

A 
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
39
Q

Levosimendan effects

A

increased cardiac contractility
vasodilatation (coronary, systemic and pulmonary)

May also have anti-inflammatory, anti-oxidative and anti-apoptotic effects

40
Q

Levosimendan uses

A

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)
41
Q

Indications for IABP

A

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
42
Q

Limitations to critical care echo

A

positioning
lung over distension with mechanical ventailtion
drains and dressings in the way
ongoing resus

43
Q

Roles of critical care echo as per 2016 CICM statement

A

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

CICM (20 decks)

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