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Basics Flashcards

1
Q

Clinical Features of Heart Disease

A

The following symptoms occur with heart disease:
• chest pain
• dyspnoea (breathlessness)
• palpitations
• syncope
• fatigue
• peripheral oedema.
The severity of cardiac symptoms or fatigue is classified accord- ing to the New York Heart Association (NYHA) grading of cardiac status (see Box 30.23).

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2
Q

Central Chest Pain Types: Angina

A
  1. Retrosternal Heavy or Gripping sensation
  2. w/ Radiation to the Left Arm or Neck
  3. Provoked by exertion
  4. Eased with Rest or Nitrates
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3
Q

Central Chest Pain Types: ACS

A

Similar pain AT REST

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4
Q

Central Chest Pain Types: Aortic Dissection

A
  1. Severe, Tearing chest pain
  2. Radiates through to the BACK
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5
Q

Central Chest Pain Types: Pericarditis

A
  1. Sharp, Central Chest Pain
  2. Worse with movement or respiration
  3. Relieved with sitting forward
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6
Q

Central Chest Pain Types: da Costa’s Syndrome

A
  1. Sharp, Stabbing Left Submammiry pain
  2. Associated with Anxiety
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7
Q

Dyspnoea

A

LVF causes dyspnoea due to Oedema of the Pulmonary Interstitium and Alveoli. → This makes the lungs stiff (less compliant) → This increases the Respiratory Effort required to Ventilate them

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8
Q

Dyspnoea: Tachypnoea

A
  1. Increased respiratory rate
  2. Present owing to stimulation of Pulmonary Stretch Receptors
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9
Q

Dyspnoea: Orthopnea

A
  1. Breathlessness on lying flat
  2. Blood is redistributed from the Legs to the Torso, leading to an increase in a Central and Pulmonary Blood Volume
  3. Patient uses an increasing number of pillows to sleep
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10
Q

Dyspnoea: PND

A
  1. Person woken from sleep fighting for breath
  2. Same mechanism as Orthopnoea
  3. However, as sensory awareness is reduced during sleep, the Pulmonary Oedema can become quite severe before the patient is awoken
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11
Q

Dyspnoea: CSAS: Cheyne Stokes Respiration

A
  1. Hyperventilation with alternating Episodes of Apnea
  2. Occurs in Severe HF
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12
Q

Dyspnoea: CSAS: Periodic Breathing

A
  1. Hypnopnea occurs rather than apnea
  2. but the two vibrations are known together as Central Sleep Apnea Syndrome
  3. This occurs due to malfunctioning of the Respiratory Centre in the Brain, caused by Poor Cardiac Output with concurrent Cerebrobascurlar Disease/ i.e. Poor CO w/ Cerebrovascular Disease → Malfunctioned Respiratory Centre → CSAS
  4. Sx of CSAS such as Daytime Somnolence and Fatigue, are similar to those of OSAS and there is considerable overlap with sx of HF
  5. CSAS is believed to lead to Myocardial Hypertrophy and Fibrosis, Deterioration in Cardiac Function and Complex Arryhtmias including Non-Sustained Ventricular Tachycardia, Hypertension and Stroke.
  6. Patients with CSAS have a worse prognosis than similar patients without CSAS
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13
Q

Palpitations

A
  1. Represent an increased awareness of the normal heart beat or the sensation of slow, rapid or irregular heart rhythms.
  2. The most common arrhythmias felt as palpitations are premature ectopic beats and paroxysmal tachycardias.
  3. A useful trick is to ask patients to tap out the rate and rhythm of their palpitations, as the different arrhythmias have different characteristics:
  4. Premature beats (ectopics) are felt by the patient as a pause followed by a forceful beat.
    1. This is because premature beats are usually followed by a pause before the next normal beat, as the heart resets itself.
    2. The next beat is more forceful, as the heart has had a longer diastolic period and therefore is filled with more blood before this beat.
  5. Paroxysmal tachycardias are felt as a Sudden, Racing heart beat.
  6. Bradycardias may be appreciated as Slow, Regular, Heavy or Forceful Beats. Most often, however, they are simply not sensed.
  7. All palpitations can be graded by the NYHA cardiac status (see Box 30.23).
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14
Q

Syncope

A
  1. Transient loss of Consciousness due to Inadequate Central Blood Flow. (see later for Cardiovascular Causes of Syncope)
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15
Q

Syncope: Vascular: Vasovagal Attack (NeuroCardiogenic)

A
  1. Simple Faint
  2. Most common cause of Syncope
  3. Mechanism begins with Peripheral Vasodilation and Venous Pooling of Blood
  4. → Reduction in amount of blood returned to heart
  5. → The near-empty hear responds by contracting vigoursly,
  6. → which in turn stimulates Mechanoreceptor in the Inferoposterior wall of the LV
  7. → These, in turn, trigger reflexes via the CNS, which act to reduce Ventricular Stretch (i.e. Further Vasodilation and sometimes Profound Bradycardia)
  8. → But this causes ad top in the BP and therefore Syncope
  9. Usually associated with Prodrome of Dizziness, Nausea, Sweating, Tinnitus, Yawning and a Sinking Feeling
  10. Recovery occurs within a free seconds, especially if the patient lies down .
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16
Q

Syncope: Vascular: Postural/Orthostatic Hypotension

A
  1. Drop in Systolic BP of 20mHg or more on standing from a sitting or Lying position
  2. Usually, Reflex Vasoconstriction prevents a drop in pressure, but if this is absent or the patient is Fluid-Depleted or on Vasodilating or Diruetic Drugs, Hypotension occurs
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17
Q

Syncope: Vascular: Postprandial Hypotension

A
  1. Drop in Systolic BP of 20mmHg or more
  2. OR the Systolic BP drops from over 100 mmHg to below 90mmHg within 2 hours of eating
  3. Mechanism is unknown, But may involve Pooling of Blood in Splanchnic Vessels
  4. In Normal People, this elicits a Homeostatic response via activation of Baroreceptors and the SNS, Peripheral Vasoconstriction, and an increase in CO
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18
Q

Syncope: Vascular: Micturition Syncope

A

Refers to loss of consciousness while passing urine

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19
Q

Syncope: Vascular: Carotid Sinus Syncope

A
  1. Occurs when there is an exaggerated Vagal Response to Carotid Sinus Stimulation
  2. Provoked by wearing a Tight Collar, Looking Upwards or Turning the head
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20
Q

Syncope: Obstructive

A
  1. All lead to syncope due to Restriction of Blood Flow from the Heart into the Rest of the Circulation
  2. OR Between the different chambers of the Heart
  3. Causes
    1. AS, HOCM, PS
    2. ToF
    3. Pulmonary Hypertension/Pulmonary Embolus
    4. Atrial Myxoma/Thrombus
    5. Defective Prosthetic Valve
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21
Q

Syncope: Arrhythmias

A
  1. Stokes Adams Attacks:
    1. Sudden LoC unrelated to Posture and caused by Intermittent:
    2. High Grade AV Block, Profound Bradycardia, or Ventricular Standstill
    3. Patient falls to the ground without Warning
    4. Is Pale and Deeply unconscious
    5. Pulse is usually very slow or absent
    6. After a few seconds, the patient Flushes Brightly and Recovers Consciousness as the Pulse Quickens.
    7. Often, there are no sequel but patients may injure themselves during falls
    8. Occasionally, a Generalized Convulsion may occur if the period of Cerebral Hypoxia is Prolonged, leading to a misdiagnosis of Epilepsy.
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22
Q

Fatigue

A
  1. Fatigue may be a symptom on Inadequate Systemic Perfusion in HF
  2. Other Contributing Factors may include:
    1. Poor Sleep
    2. Side effects of Medication, particularly BB
    3. Electrolyte Imbalance caused by Diuretic Therapy
    4. A Systemic Manifestation of Infection, such as Endocarditis
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23
Q

Peripheral Oedema

A
  1. Heart failure results in salt and water retention due to Renal Under Perfusion and consequent activation of the Renin–Angiotensin–Aldosterone system
  2. This leads to dependent pitting oedema.
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24
Q

Examination of the CVS: General

A
  1. General Fx of the patient’s wellbeing should be noted as well as the presence of Conjunctival Pallor, Obesity, Jaundice, and Cachexia
  2. Clubbing: Seen in Congenital Cyanotic Heart Disease, especially Fallot’s Tetralogy, and also in 10% of patients with Subacute Infective Endocarditis.
  3. Splinter Hemorrhages: Small, Subungual Linear Hemorrhages that are frequently due to Trauma but also seen in IE
  4. Cyanosis: Dusky blue discoloration fo the Skin (particularly the extremities) or of the Mucous Membranes when the Capillary Oxygen Saturation is below 85%.
    1. Central Cyanosis → Seen with Shunting of Deoxygenated Venous Blood into Systemic Circulation, as in the presence of a RtL Heart Shunt.
    2. Peripheral Cyanosis is seen in the Hands and Feet, which are Cold.
      1. It occurs in conditions a/w Peripheral Vasoconstriction and Stasis of Blood in the Extremities, leading to Increased Peripheral Oxygen Extraction
      2. Such conditions include: CHF, Circulatory Shock, Exposure to Cold Temps, and Abnormalities soft the Peripheral Circulation (such as Raynaud’s)
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25
Q

Examination of the CVS: Arterial Pulse

A

The first pulse to be examined is th Right Radial Pulse. a Delayed Femoral Pulsation occurs because of a Proximal Stenosis, Particularly of the Aorta (Coarcation)

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26
Q

Examination of the CVS; Arterial Pulse: RATE

A

The pulse rate should be between 60 and 80 beats per minute when an adult patient is lying quietly in bed.

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27
Q

Examination of the CVS: Arterial Pulse: RHYTHM

A
  1. The Rhythm is regular, except for a slight quickening in Early Inspiration and Slowing in Expiration (Sinus Arrhythmia)
  2. Premature Beats
    1. Occur as Occasional or Repeated Irregularities superimposed on a Regular Pulse Rhythm
    2. Similarly, Intermittent Heart Block is revealed by occasional beats DROPPED
  3. Atrial Fibrillation
    1. Produces an “Irregularly Irregular” Pulse
    2. This Irregular pattern persists when the Pulse quickens in response to Exercise, in contrast to Pulse Irregularity due to Ectopic Beats, which usually disappears on exercise.
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28
Q

Examination of the CVS: Character: Carotid Pulsations

A
  1. Not normally apparent on inspection of the neck
  2. But MAYBE visible (Corrigan’s Sign) in conditions associated with a Large-volume Pulse, including High-Output States (Thyrotoxicosis, Anemia, Fever, and in AR)
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29
Q

Examination of the CVS: Character: A “Collapsing” or “Waterhammer” Pulse

A
  1. Is a Large-Volume Pulse
  2. Characterized by a Short Duration with a Brisk Rise and Fall
  3. This is best appreciated by Palpating the Radial Artery with the Palmar aspect of Four fingers while Elevating the Patient’s arm above the level of the heart
  4. A collapsing Pulse is characteristic of AR, or a PDA
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30
Q

Examination of the CVS: Character: a Small-Volume Pulse

A
  1. Seen in Cardiac Failure, Shock, and Obstructive Valvular or Vascular Disease
  2. It may also be present during Tachyarrhythmias
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31
Q

Examination of the CVS: Character: A Plataeu Pulse

A
  1. Is Small in volume and Slow in Rising to a peak
  2. It is due to AS
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32
Q

Examination of the CVS: Character: An Alternating Pulse (Pulsus Alternans)

A
  1. Characterized by regular Alternate Beats that are Weak and Strong
  2. It is a fx of Severe Myocardial Failure and is due to the Prolonged Recovery time of Damaged Myocardium
  3. It indicates very POOR PROGNOSIS
  4. It is easily noticed when taking the BP b/c the Systolic Pressure may vary from beat to beat by as much as 50mmHg
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33
Q

Examination of the CVS: Character: A Bigeminal Pulse (Pulsus Bigeminus)

A
  1. Caused by a Premature Ectopic beat, following every sinus beat
  2. The Rhythm is not regular because every Weak Pulse is premature
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34
Q

Examination of the CVS: Character: Pulsus Bisferiens

A
  1. Found in HOCM and in Mixed Aortic Valve Disease (Regurgitation combined with Stenosis)
  2. The first Systolic Wave is the “Percussion Wave”, produced by Transmission of the LV pressure in Early Systole
  3. The Second Peak is the “Tidal Wave”, caused by Recoil of the Vascular Bed
  4. This normally happens in Diastole (The Dicrotic Wave), but when the LV empties slowly or is obstructed and cannot empty completely, the Tidal wave occurs in Late systole.
  5. The result is a Palpable Double Pulse
35
Q

Examination of the CVS: Character: A Dicrotic Pulse

A
  1. Results from an Accentuated Dicrotic Wave
  2. It occurs in Sepsis and Hypovolemic Shock and after AV Replacement
36
Q

Examination of the CVS: Character: Paradoxical Pulse

A
  1. Is a Misnomer, as it is actually an exaggeration of the Normal Pattern
  2. In normal subjects, the SP and PP (difference between the SP and BP) fall during inspiration.
  3. The normal fall of SP is less than 10 mmHg, and this can be measured using a Sphygmamometer
  4. It is due to Increased Pulmonary Intravascular Volume during Inspiration
  5. In Severe Airflow Limitation, especially SEVERE ASTHMA, there is an increased Negative Intrathoracic Pressure on Inspiration, which enhances the Normal Fall in BP.
  6. In patients with Cardiac Tamponade, the Fluid in the Pericardium increases the Intrapericardial Pressure, thereby impeding Diastolic Filling of the Heart. The normal Inspiratory increase in Venous Return to the RV is at the expense of th LV as both ventricles are confined by the accumulated Pericardial Fluid within the Pericardial Space
  7. Paradox can occur via a similar mechanism in Constrictive Pericarditis but is less common .

To truly understand the pathophysiology of pulsus paradoxus, we must explore the normal respirophasic effects of chest mechanics on blood pressure. In healthy individuals, there are normal phasic changes in cardiac output that occur with respiration. During inspiration, there is a small decrease in systemic arterial pressure of less than 10 mm Hg. As we inhale, intrapleural pressure drops; there is a decrease in intrathoracic pressure that promotes venous inflow into the chest increasing right heart filling. However, this does not equate to an increased filling of the left heart during inspiration. This is because, as one inhales, the lungs expand and pull radial traction on the pulmonary vasculature increasing its capacitance, momentarily sequestering blood in the chest, and dropping blood flow to the left heart, decreasing pre-load and consequently cardiac output. The opposite occurs during expiration, thus systolic pressure normally decreases during inspiration and increases during expiration. So why does the term pulsus paradoxus imply the drop in blood pressure during inspiration is paradoxical? The term pulsus paradoxus was coined by historic German physician Adolph Kussmaul who was referring to the palpated pulse of affected patients being of variable strength despite regular precordial activity.[8][9][10]

The pathophysiology of pulsus paradoxus is complex and varies depending on the etiology; there are several mechanisms involved. In cardiac tamponade resulting in pulsus paradoxus, the physiologic drop in cardiac output is exaggerated for several reasons; however, the most significant is enhanced ventricular chamber interaction, often referred to as ventricular interdependence. The increased pericardial pressure limits the ability of the right ventricular free wall to expand and accommodate the inflow of blood during inspiration. The result is increased bowing of the ventricular septum into the left ventricle as blood fills the right heart, resulting in a lower left ventricular end diastolic volume, a lower stroke volume and resulting lower systolic pressure. In more simple terms, in a non-compliant pericardial space, for the right heart to fill more in inspiration, the left heart must fill less. As pericardial pressure increases, the compliance of the ventricles decreases until, under extreme pressure, the effective compliance of all chambers meets that of the pericardial space. In advanced tamponade, intrapericardial pressure will be the key factor determining diastolic cardiac pressures. This is the reason that a clinician will see an equalization of chamber pressures during diastole in cardiac tamponade.

37
Q

Examination of the CVS: BP

A
  1. The Peak Systemic Arterial BP is produced by Transmission of LV Systolic Pressure
  2. Vascular Tone and an Intact AV maintain the Diastolic Pressure
38
Q

Examination of the CVS: JVP

A
  1. There ar enough valves between the IJV and the RA
  2. observation of the Column of Blood in the IJV system is therefore a good measure of RA pressure
  3. The EJV cannot be relied on because of it’s Valves and because it may be obstructed by the Fascial and Muscular Layers through which it passes; it can be used only if Typical Venous Pulsation is seen, indicating no Obstruction to flow.
39
Q

Examination of the CVS: JVP Measurement

A
  1. Elevation of the JVP occurs in HF
  2. An elevated JVP occurs also in:
  3. Constrictive Pericarditis and cardiac Tamponade (increases in Inspiration–Kussmaul’s Sign)
  4. Renal Disease with Salt and Water Retention
  5. Over-Transfusion or Excessive Infusion of Fluids
  6. Congestive Cardiac Failure
  7. SVC Obstruction
  8. A reduced JVP occurs in HYPOVOLEMIA
40
Q

Examination of CVS: JVP Wave

A
  1. This consists of Three Peaks and Two Troughs
  2. The peaks are described as a, c, v waves
  3. The troughs are known as x and y
  4. a wave → Is produced by Atrial Systole and is increased with RV Hypertrophy secondary to PH or PS. Giant Cannon waves occur in Complete HB and VT
  5. x descent → Occurs when Atrial Contraction finishes
  6. c wave → During the X descent and is due to transmission of RV Systolic Pressure before the Tricuspid Valve Closes
  7. v wave → Occurs with Venous Return filling the Right Atrium. Giant v Waves occur in Tricuspid Regurgitation
  8. y descent → Follows the v wave when the TV opens. A steep y descent is seen in Constrictive Pericarditis and Tricuspid Incompetence.
41
Q

Examination of the CVS: Precordium

A
  1. With the patient at 45 degrees, the Cardiac Apex is located in the 5th ICL, MCL
  2. Left Ventricular Dilation will displace the apex downwards and laterally
  3. it may be impalpable with Emphysema, Obesity, or Pericardial or Pleural Effusions
42
Q

Examination of the CVS: Precordium: Tapping Apex

A

Is a palpable First sound and occurs in Mitral Stenosis

43
Q

Examination of the CVS: Precordium: Vigorous Apex

A

May be present in diseases with Volume overload e.g. AR

44
Q

Examination of the CVS: Precordium: Heaving/Sustained Apex

A

May occur with LV Hypertrophy (AS, Systemic Hypertension, Hypertrophic Cardiomyopathy)

45
Q

Examination of the CVS: Precordium: Double Pulsation

A

May occur in Hypertrophic Cardiomyopathy

46
Q

Examination of the CVS: Precordium: Sustained LEFT Parasternal Heave

A

Occurs with RV Hypertrophy or LA Enlargement

47
Q

Examination of the CVS: Precordium: Palpable Thrill

A

May be felt overlying an abnormal Cardiac Valve e.g. Systolic Thrill with AS

48
Q

Examination of the CVS: Auscultation

A
  1. The Bell of the stethoscope is used for Low-Pitched sounds (heart sounds and mid-diastolic murmur in mitral stenosis).
  2. The Diaphragm is used for high-pitched sounds (Systolic Murmurs, Aortic Regurgitation, ejection clicks and opening snaps).
  3. Left-sided valve murmurs may be more prominent in expiration and right-sided in inspiration.
  4. Mitral murmurs may be more audible with the patient reclining to the left.
49
Q

Examination of the CVS: Ausculation: First Heart Sound

A
  1. This is due to Mitral and Tricuspid valve closure
  2. A loud S1 occurs in: Thin People, Hyperdynamic Circulation, Tachycardias, and Mild to Moderate MS
  3. A soft S1 occurs in: Obesity, Emphysema, Pericardial Effusion, Severe Calcific Mitral Stenosis, Mitral or Tricuspid Regurgitation, HF, Shock, Bradycardias and First Degree Block.
50
Q

Examination of the CVS: Auscultation: Second Heart Sound

A

This is due to A and P Valve Closure. Physiological Splitting of S2 occurs during Inspiration in Children and Young Adults.

51
Q

Examination of CVS: Auscultation: Third and Fourth HS

A
  1. These are pathological:
  2. A third heart sound (‘volume overload’) is due to rapid ven-
    tricular filling and is present in significant heart failure.
  3. A fourth heart sound (pressure overload) occurs in late di- astole and is associated with atrial contraction.
    1. Causes include Aortic Stenosis, Severe Systemic Hypertension and LV outflow obstruction, as in Hypertrophic Cardiomyopathy, i.e.
      causes of significant left ventricular hypertrophy.
    2. Singly or together, they will produce a gallop rhythm.
52
Q

Examination of CVS: Auscultation: Murmurs

A
  1. These are due to Turbulent Blood Flow and occur in Hyperdynamic States or with Abnormal Valves
  2. Innovent or Flow Murmurs are
    1. Soft
    2. Early Systolic
    3. Short and Not Radiating
    4. Symptomless
    5. Sounds S1 and S2 are normal
    6. Special Tests are normal (X-Ray, EKG)
    7. Sitting/Standing (Changes with position)
53
Q

Examination of CVS: Auscultation: Murmurs Grades

A
  • 1/6: Very faint, not heard in all positions
  • 2/6: Quiet, but not difficult to hear
  • 3/6: Moderately loud
  • 4/6: Loud with or without Thrills
  • 5/6: Very Loud with or without Thrills; heard with the stethoscope partly off the chest
  • 6/6L With or Without thrills, heard with the stethoscope completely off the chest.
54
Q

Cardiac Ix: Blood Tests

A
  1. Routine Hematology
  2. Serum Creatinine and Electrolytes
  3. Liver Biochemistry
  4. Cardiac Enzymes (Troponin; Creatine Kinase, Aspartate Aminotransferase (AST) and Lactate Dehydrogenase (LDH) may also be elevated.
  5. Thyroid Function
  6. B-Type Natriuretic Peptides (BNP)
55
Q

Cardiac Ix: CXR

A
  • Ideally this is taken in the Postero-anterior Direction at maximum inspiration with the Heart close to the Xray film to minimize Magnification with respect to the thorax
  • The AP view is often taken in emergency setting
56
Q

Cardiac Ix: CXR

Heart Size

A
  • Can be reliable assessed only from the PA chest film
  • The Maximum Transverse Diameter of the heart is compared with the Maximum Transverse Diameter of the Thorax measured from the inside of the ribs (the Cardiothoracic Ratio, CTR).
  • The CTR is usually less than 50%, except in Neonates. Infants, Athletes and Pateitns with skeletal Abnormalities such as Scoliosis and Funnel Chest.
  • Transverse Cardiac Diameter of more than 15/5 cm is abnormal
  • Pericardial Effusion or Cardiac Dilation causes an increase in the ratio.
57
Q

Cardiac Ix: CXR

Left Atrial Dilatation

A
  1. Certain patterns of specific chamber enlargement may be seen on the CXR
  2. LAD leads to
  3. Promminence of the Left Atrial Appendage
  4. Straightening or Convex bulging of the Upper Left Heart Border
  5. A double atrial Shadow to the Right of the Sternum
  6. and Splaying of the Carina because a Large Left Atrium elevates the Left Main Bronchus
  7. On a Lateral CXR, an enlarged LA bulges backwards, impinging on the Oesophagus
58
Q

Cardiac IX: CXR

Left Ventricular Enlargement

A
  1. Causes an increase in the CTR
  2. and Smooth Elongation and increased Convexity of the Left Heart Border
59
Q

Cardiac IX: CXR

Right Atrial Enlargement

A

Results in projection of the Right Border of the heart into the Right Lower Lung Field

60
Q

Cardiac Ix: CXR

Right Ventricular Enlargement

A
  1. Causes an increase in the CTR
  2. and Upward Displacement of the Apex of the Heart because the enlarging RV pushes the LV Leftwards, Upwards and eventually Backwards
  3. Differentiation of Left from Right Ventricular enlargement may be difficult using the shape of the Left Heart Border alone, but the
    1. Lateral view shows Enlargement ANTERIORLY for the RV
    2. and POSTERIORLY for the LV
61
Q

Cardiac Ix: CXR

Ascending Aortic Dilation or Enlargement

A
  1. Is seen as a Prominence of the Aortic Shadow to the RIGHT of the Mediastinum betweetn the RA and the SVC
62
Q

Cardiac IX: CXR

Dissection of the Ascending Aorta

A
  1. Is seen as a Widening of the Mediastinum on CXR but an US/MRI should be performed
63
Q

Cardiac Ix: CXR

Enlargement of the Pulmonary Artery

A
  1. Pulmonary Hypertension, Pulmonary Artery Stenosis, and LtoR Shunts
  2. Produces a prominent Bulge on the Left-Hand border of the Mediastinum below the Aortic Knuckle.
64
Q

Cardiac Ix: CXR

Calcification

A
  1. Calcification in the CVS occurs because of Tissue Degeneration
  2. Calcification is visible on a Lateral or a Penetrated PA film but is best studied with CT Scanning
65
Q

Cardiac Ix: CXR: Lung Fields

Pulmonary Plethora

A
  1. Results from LtoR shunts (e.g. Atrial or Ventricular Septal Defects)
  2. It is seen as a General Increase in the vascularity of the Lung fields
  3. and as an Increase in the Size of Hilar Vessels (e.g. in the Right Lower Lobe Artery), which normally should not exceed 16mm in diameter.
66
Q

Cardiac Ix: CXR: Lung Fields

Pulmonary Oligemia

A
  1. Occurs in situations where there is reduced Pulmonary Blood Flow, such as PE, Severe PS and ToF
  2. Paucity of Vascular Markings
  3. and a reduction in the Wide of the Arteries
67
Q

Cardiac Ix: CXR: Lung Fields

Pulmonary Hypertension

A
  1. May result from PE, Chronic Lung Disease, or Chronic Left Heart Disease, e.g LVF or Mitral Valve Disease such as Shunts due to VSD or Mitral Valve Stenosis.
  2. In addition tot eh Xray fx of these conditions
  3. The Pulmonary Arteries are PROMINENT CLOSE to the Hilt but are REDUCED in size (Pruned) in the PERIPHERAL lung fields.
  4. This pattern is usually symmetrical
  5. Normal Pulmonary Capillary Pressure is 5-14mmHg at rest.
  6. Mild Pulmonary Capillary Hypertension 15-20mmHg produces Isolated Dilatation of the upper Zone Vessels.
68
Q

Cardiac Ix: CXR: Lung Fields

Interstitial Oedema

A
  • Occurs when the pressure is between 21 and 30 mmHg
  • This manifests as Fluid Collections in the Interlobular Fissures, Interlobular Septa (Kerley B Lines) and Pleural Spaces
  • This gives rise to Indistinctness of the Hilar Regions and Haziness of the Lung Fluid.
69
Q

Cardiac Ix: CXR: Lung Fields

Alveolar Oedema

A
  1. Occurs when the pressure exceeds 30mmHg, appearing as
  2. Areas of Consolidation and Mottling of the Lung Fields and Pleural Effusions
  3. Patients with longstanding elevation of the Pulmonary capillary Pressure have Reactive Thickening of the Pulmonary Arteriolar Intima, which protects the Alveoli from Pulmonary Oedema.
  4. Thus, in these patients, the Pulmonary Venous pressure may increase to well above 30mmHg before frank Pulmonary Oedema develops.
70
Q

Cardiac Ix: Electrocardiography

AP

A
  1. The ECG is a recording of the Electrical Activity of the Heart
  2. It is the Vector Sum of the Depolarization and Repolarization potentials of all Myocardial Cells
  3. At the body surface, these generate potential differences of about 1mV, and fluctuations in these potentioals create the familiar PQRST pattern
  4. At rest, the Intracellular voltage of the Myocardium is polarized at -90mV compared with that of the Extracelllular Space
  5. This Diastolic Voltage difference occurs because of the High INTRACELLULAR Potassium concentration, which is pmaintained by the Sodium Potassium pump despite the FREe Membrane Permeability to Potassium.
  6. Depolarization of Cardiac Cells occurs when there is a sudden increase in the Permeability fo the Membrane to Sodium
  7. Sodium rushes into the Cell and the Negative Resting Voltage is lost (phase 0)
  8. The depolarization of a Myocardial Cell causes the Depolarization of adjacent cells and, in a healthy heart, the entire Myocardium is depolarized in a coordinated fashion
  9. During Repolarization, Cellular Electrolyte balance is slowly restored (Phases 1,2, and 3)
  10. Slow Diastolic depolarization )Phase 4) follows until the Threshold Potential Is reached. Another action potential then follows.
71
Q

Cardiac IX: Electrocardiography

Recording

A
  • The ECG is recorded from two or more simultaneous points of skin contact (electrodes).
  • When cardiac activation proceeds towards the positive contact, an upward deflection is produced on the ECG.
  • Correct representation of a three-dimensional spatial vector requires recordings from Three Mutually Perpendicular (Orthogonal) Axes.
  • The shape of the human torso does not make this easy, so the practical ECG records 12 projections of the vector, called ‘leads’ (Fig. 30.16).
  • Six of the leads are obtained by recording Voltages from the Limbs (I, II, III, aVR, aVL, and aVF)
  • The other six leads record potentials between points on the Chest Surface and an average of the Three Limbs: RA, LA, LL. These are designated V1-V6 and aim to select activity from the
    • RV (V1-V2)
    • Inter-ventricular Septum: V3-V4
    • and Left Ventricle: V5-V6
  • Note that
    • Leads AVR and V1 are oriented towards the cavity of the heart
    • Leads II, III and AVF face to the INFERIOR surface
    • and Leads I, AVL, and V6 face the LATERAL wall of the LV
    • a V4 is on the RIGHT side of the Chest (V4R is occasionally useful e.g. for the diagnosis of RV infarction)
  • Most ECG machines are simultaneous 3 channel recorders, with output given either as a continuous strip or with automatic channel switching.
  • Many ECG machines also analyze the recordings and print the analysis on the record. Usually, the machine interpretation is correct but many Arrhythmias still defy Automatic Analysis
  • Leads that face the lateral wall of the LV have predominantly positive deflections and leads looking into the Ventricular Cavity are usually negative. Detailed patterns depend on the Size, Shape and Rhythm of the Heart and the characteristics of the Torso
72
Q

Cardiac IX: Electrocardiography

P Wave

A
  1. The shape of the Normal ECG waveform has similarities, whatever the orientation
  2. P wave → The first deflection is caused by Atrial Depolarization. It is a Low-Amplitude, Slow Deflection called a P wave.
73
Q

Cardiac IX: ECG

QRS

A
  1. QRS Complex → Reflects Ventricular Activation or Depolarization, and is Sharper and Larger in amplitude than the P wave
    1. Q Wave → An initial downward Deflection is called the Q Wave
    2. R Wave → An initial Upward deflection is called an R wave
    3. S wave → Is the last part of Ventricular activation.
74
Q

Cardiac IX: ECG

T Wave

A
  1. T wave → Another Slow and Low Amplitude deflection that results from Ventricular Depolarization
75
Q

Cardiac IX: ECG

PR Interval

A
  1. PR Interval → The length of time from the START of the P wave, to the START of the QRS complex
    1. It is the time taken for activation to pass from the Sinus Node, through the Atrium, AV Node, and His-Purkinje System, to the Ventricle
76
Q

Cardiac IX: ECG

QT Interval

A
  1. QT Interval → Extends from the start of the QRS complex to the end of the T wave.
    1. This interval represents the time taken to Depolarize and Repolarize the Ventricular Myocardium.
    2. The QTInterval varies greatly with HR and is often represented sa a corrected QT interval (or QTc) for a given HR.
    3. There are a number of Formulae for derivation of QTc, but the most widely accepted are Bazett’s Formula and Fridericia’s Correction
    4. An abnormally prolonged QTc can predispose to a risk of dangerously Ventricular Arrhythmias.
    5. Prolongation of the QT interval may be Congenital or can occur in many acquired conditions
77
Q

Cardiac IX: ECG

ST Segment

A
  1. ST Segment → Period between the end of the QRS Complex and the start of the T wave.
    1. In the normal heart, all cells are depolarized by this phase of the ECG. That is, ST Segment represents Ventricular Depolarization
78
Q

Cardiac IX: ECG:

P wave duration

A

0.12 or 3 small boxes

79
Q

Cardiac IX: ECG:

PR Interval

A

0-12-0.20 seconds or 3-5 small boxes

80
Q

Cardiac IX: ECG:

QRS Duration

A

0.10 sec or 2.5 boxes

81
Q

Cardiac IX: ECG:

Corrected QT (QTc)

A
  1. 44 sec in males
  2. 46 sec in females
82
Q

Cardiac IX: ECG:

Corrected QT (QTc)

A
  1. 44 sec in males
  2. 46 sec in females
83
Q

Cardiac Ix: ECG

A

Cardiology (4 decks)

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