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PFizz S2015 > CVS L5: Hypertension & Shock > Flashcards

CVS L5: Hypertension & Shock Flashcards

1
Q

Patient 01: DDx

A 55-year-old male smoker with a history of high blood cholesterol visits his family physician for a health checkup.

His Blood Pressure records 180/120 mmHg. Blood test: a high plasma renin activity.

Special test: Renal angiogram reveals a significant asymmetric renal artery stenosis at the upstream junction of the left renal artery and abdominal aorta that reduces the entrance to the renal artery by 75%.

A

Most likely diagnosis in patient 01: Systemic Hypertension due to renal artery stenosis

Other differential:

  • Primary hyperaldosteronism
  • Cushing’s syndrome
  • Reninoma
  • Pheochromocytoma
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2
Q

Mechanisms causing hypertension:

A
  • Increased peripheral vascular resistance
  • Increased blood viscosity
  • Prolonged increase in cardiac output
  • Increased blood volume
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3
Q

COMMON CAUSES OF HYPERTENSION

A
  • Essential hypertension
  • Coarctation of aorta
  • Salt sensitivity
  • Renal abnormalities
  • Abnormalities of the RAAS
  • Disorders of adrenal gland
  • Neurological disorders
  • Nitric oxide deficiency
  • Insulin resistance
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4
Q

Coarctation of the Aorta:

A
  • Congenital narrowing of the aorta distal to the origin of the left subclavian artery
  • Blood pressure is elevated in the arms, head, and chest but lowered in the legs
  • Because of low renal blood flow, plasma renin level is increased
  • Stimulation of Renin-angiotensin-aldosterone system in a positive feedback manner
  • Elimination of the constriction by resecting the narrowed segment of the aorta usually cures the condition
  • The pressure tracings from the thoracic and abdominal aorta obtained from a 4-month-old infant who exhibited dyspnea, difficulty feeding, and poor weight gain
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5
Q

Renal causes for hypertension:

A
  • Constriction of one or both renal arteries, Ex. fibromuscular dysplasia, arteriosclerotic change
  • Tumors of the renin-secreting juxtaglomerular cells
  • Ureteral obstruction: Increase in renal interstitial pressure and stimulation of renin secretion
  • Acute and chronic glomerulonephritis: a) Activation of RAAS and/or b) ECF volume expansion due to abnormal salt and water handling by the kidneys.
  • Liddle’s syndrome: a condition in which there is abnormal Na+ retention due to over-activation of the epithelial sodium channels (ENaC)
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6
Q

Liddle’s syndrome

A
  • Young patient presenting with high BP
  • H/O family members with early onset severe hypertension
  • Autosomal dominant transmission
  • Suppressed renin
  • Suppressed aldosterone
  • Abnormality of epithelial sodium channels (ENaC) in distal nephron
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7
Q
A
  • The vascular function curve
  • An inverse relationship exists between RAP and VR in the range 0 to 7 mm Hg of RAP
  • No further increase in VR occurs when RAP < 0 mm Hg as veins collapse at negative pressures
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8
Q

Combining cardiac function curve and vascular function curve

A

Combining the two curves helps to predict the changes in CO/VR under various conditions

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9
Q

Factors that change the cardiac and vascular function curves

A

C for C; V for V

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10
Q

Effect of increasing myocardial contractility on combined curves:

A

Positive inotropic agents Eg:Sympathetic nerves, digitalis

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11
Q

Effect of increasing total blood volume on combined curves:

A

Increased blood volume: Eg:Infusion of IV fluids

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12
Q

Progressive course of the Heart

A

Immediate effect of reduced contractility: (Point B) There is a reduction in CO; This soon changes due to the compensatory changes in the heart

Compensated failure: (Point C)

Blood volume expansion has partially restored the
CO by Starling’s mechanism; This gradually progresses to massive volume expansion

Decompensated failure: (Point D)
As failure progresses, there is severe reduction in contractility despite extreme increase in preload due to overstretching of ventricle.
At this point, increase in preload is harmful to heart!

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13
Q

causes and types of shock:

A

A. Hypovolemic shock:

Inadequate volume of blood to fill the vascular system
B. Distributive shock (also called vasogenic or low-resistance shock):

Increased size of the vascular system produced by vasodilation in the presence of a normal blood volume
C. Cardiogenic shock:

Inadequate output of the heart as a result of myocardial abnormalities
D. Obstructive shock:

Inadequate cardiac output as a result of obstruction

of blood flow in the lungs or heart

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14
Q

Physical findings in Hypovolemic Shock:

A
  • Hypotension (systolic pressure <90)
  • A rapid, low volume, thready pulse
  • Cold, pale, clammy skin
  • Intense thirst
  • Rapid respiration
  • Restlessness or Low activity
  • Markedly decreased urine output
  • Altered mental status

Do not rely on systolic BP as the main indicator of shock. Compensatory mechanisms prevent a significant decrease in systolic BP until the patient has lost 30% of the blood volume.

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15
Q

Compensatory reactions activated by Hypovolemic Shock:

A
  • Vasoconstriction & consequences
  • Tachycardia
  • Venoconstriction
  • Tachypnea – cause and benefit
  • Increased movement of interstitial fluid into capillaries
  • Increased secretion of ADH
  • Increased secretion of glucocorticoids
  • Stimulation of renin-angiotensin-aldosterone
  • Increased secretion of erythropoietin
  • Increased synthesis of plasma proteins
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16
Q

Refractory Shock:

A
  • The shock persists for hours and eventually reaches a state in which there is no longer any response to vasopressor drugs
  • Even if the blood volume is returned to normal, cardiac output remains depressed
  • Factors that make shock refractory are:
  • Precapillary sphincters are constricted for several hours but then relax while postcapillary venules remain constricted. Therefore, blood flows into the capillaries and remains there.
  • Cerebral ischemia depresses vasomotor and cardiac discharge, causing blood pressure to fall and making the shock worse.
  • Reduced myocardial blood flow.
17
Q

Traumatic Hypovolemic Shock:

A
  • Traumatic shock involves severe damage to muscle and bone - as seen in battle casualties and automobile accident victims
  • Significant bleeding into the injured areas
  • Breakdown of skeletal muscle is a serious additional problem when shock is accompanied by extensive crushing of muscle (crush syndrome)
  • Free radicals generated at the sites cause further tissue destruction (reperfusion-induced injury) •Increased Ca2+ in damaged cells can reach toxic levels
  • Large amounts of K+ enter the circulation
  • Myoglobinuria worsens renal failure
18
Q

Distributive shock:

A

Conditions:
• Anaphylaxis
• Sepsis
• Fainting (neurogenic)

  • In distributive shock, most of the symptoms and signs described under hypovolemic shock are present
  • Vasodilation causes the skin to be warm rather than cold and clammy
19
Q

Septic shock: a form of distributive shock

A
  • Most common cause of death in ICUs in USA
  • Initiated by release of bacterial toxins
  • A complex condition that includes:
    • -Hypoperfusion resulting from loss of plasma into the tissues (“third spacing”)
    • -Reduced cardiac function resulting from toxins that depress the myocardium
    • -Excess production of Nitric oxide and vasodilation
    • -Capillary endothelial damage and depletion of intravascular volume
    • -Cellular hypoxia, lactic acidosis & multiorgan failure
20
Q

How to assess the type of shock?

A

Pulmonary artery catheterization (Swan- Ganz catheter) and measurements of pressures

21
Q

Cardiogenic shock: Conditions:

A
  • Myocardial infarction
  • Congestive Heart Failure
  • Arrhythmias
22
Q

Cardiogenic Shock: Pathophysiology

A
  • Extensive infarction of LV (>30%)
  • Impaired pumping of blood to myocardium
  • Inadequate resting metabolic needs
  • Positive feedback vicious cycle
  • Congestion of the lungs and viscera resulting from failure of the LV to put out all the venous blood (“congested shock“)

The symptoms are:

  • Those of hypovolemic shock plus congestion of lungs and viscera
  • The incidence of shock in patients with myocardial infarction is about 10%, and the mortality rate is 60–90%
23
Q

Obstructive shock: Conditions:

A
  • Pulmonary embolism (massive)
  • Tension pneumothorax
  • Cardiac tamponade
  • Cardiac tumor
24
Q

Patient 04: DDx

A 54 year old man develops sudden onset of dyspnea and hypotension in the coronary care unit. He was admitted five days back following an acute MI. He was on thrombolytic agents.
PE: tachycardia; weak, thready pulse; tachypnea; low BP; Pallor; cool, moist skin; mild cyanosis of lips and fingers; He has significant pulsus paradoxus (fall in arterial pulse is 16 mm Hg with inspiration); Elevated JVP with absence of “y” descent Auscultation of heart: Heat sounds are muffled Auscultation of lungs: not significant
ECG: Low voltage waves

Imaging: Diastolic compression of the right ventricle;

pericardial effusion

A

The most likely diagnosis in patient 04 is: Cardiac tamponade

Other differentials:

  • Myocardial infarction
  • Pulmonary embolism
  • Tension pneumothorax
  • Constrictive pericarditis
25
Q

Cardiac tamponade (an example of obstructive shock):

A

Sudden filling of the pericardial space with fluid

Diagnosis:

  • Sudden onset of shortness of breath
  • Physical examination findings:
  • Three classic signs of Cardiac tamponade (Beck’s triad):
    • Hypotension
    • Elevated jugular venous pressure, and
    • Muffled heart sounds
  • Additional finding: Paradoxic pulse (pulsus paradoxus)
26
Q

Hemodynamics of Cardiac tamponade:

A
  • [Normal: The pericardium is filled with 30–50 mL of fluid; Intrapericardial pressure is about the same as the intrapleural pressure]
  • Sudden addition of fluid → Increase in intrapericardial pressure to the level of the RA and RV pressures → RV collapses, preventing filling of the heart from systemic veins
  • Equilibration of ventricular and pulmonary artery diastolic pressures with RA and LA pressures, all at approximately intrapericardial pressure.
27
Q

Jugular Venous Pulse in Cardiac tamponade:

A
  • JVP is elevated due to fluid in the cavity
  • JVPulse tracing shows:
  • -Normal “x” descent since RA can fill during ventricular contraction (systole)
  • -Absent “y” descent: Filling of RA during ventricular diastole is prevented by the pericardial fluid surrounding that chamber (RA).
  • Loss of the “y” descent associated with an elevated JVP is diagnostic of Cardiac tamponade
28
Q

Comparison of JVP tracings in Normal and abnormal conditions

A
29
Q

Pulsus Paradoxus in Cardiac tamponade:

A

Marked inspiratory drop in systolic blood pressure (>10 mm Hg) is an important physical finding in the diagnosis of cardiac tamponade

30
Q

The ECG findings in tamponade:

A
  • Low voltage (amplitude) of the QRS complexes
  • Electrical alternans (cyclic beat-to-beat shift in the QRS axis)

Other causes of low voltage ECG:

  • -chronic obstructive pulmonary disease
  • -pleural effusion
  • -pneumothorax
  • -cardiomyopathy
  • -obesity

PFizz S2015 (35 decks)

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