This document discusses various symptoms related to cardiovascular and respiratory systems. It defines palpitations as a sensation of irregular heartbeat and lists potential cardiac, psychiatric and miscellaneous causes. Dyspnea is defined as subjective breathing discomfort that can vary in intensity. Cough is described as an essential protective function, with excessive coughing having potential complications. The mechanism of cough and types based on duration are outlined. Hypoxia and its effects on cells, cardiovascular system and central nervous system are summarized. Various causes of hypoxia including respiratory, anemic, carbon monoxide poisoning and more are listed with brief descriptions.

1. CVS & RS SYMPTOMS
- MOTE
SRIKANTH

2. PALPITATIONS

3. DEFINITION
 Intermittent “thumping,” “pounding,” or “fluttering”
sensation in the chest
intermittent/
sustained
regular/
irregular
 Also described as unusual awareness of the
heartbeat

4. CAUSES:
 Cardiac (43%)
 Psychiatric (31%)
 Miscellaneous (10%)
 Unknown (16%)
In general, hyperdynamic CV
states caused by
catecholaminergic stimulation
from exercise, stress can lead
to palpitations
Palpitations are
common among
athletes

5. CARDIAC CAUSES:
CONDITION PALPATIONS
Premature atrial &
ventricular contractions
Intermittent
Supraventricular &
ventricular arrhythmias
Regular, sustained
Atrial fibrillation Irregular, sustained
Mitral valve prolapse
Aortic insufficiency
Atrial myxoma Positional
Pulmonary embolism

6. PSYCHIATRIC CAUSES:
 Panic attacks or disorders
 Anxiety states
 Somatization
MISCELLANEOUS:
 Thyrotoxicosis
 Drugs (atropine, thyroxine, cocaine, caffeine,
amphetamines)
 Ethanol
 Spontaneous skeletal muscle contractions of the
chest wall
 Pheochromocytoma
 Systemic mastocytosis
Report a longer
duration of sensation
(>15 min)

7. DYSPNEA

8. The American Thoracic Society defines dyspnea as
a “subjective experience of breathing discomfort
that consists of qualitatively distinct sensations that
vary in intensity”

9. COUGH
Often a clue to the
presence of
respiratory disease

10. IMPORTANCE OF COUGH ??
Cough performs an essential protective function for
human airways & lungs

11. WHAT IF COUGH REFLEX IS ABSENT ?
Risk for retained airway secretions & aspirated
material predisposing to infection, atelectasis &
respiratory compromise.

12. SO IS EXCESSIVE COUGHING GOOD ?
 Nope, excessive coughing can be exhausting
 Can be complicated by emesis, syncope, muscular
pain, or rib fractures
 Can aggravate abdominal or inguinal hernias &
urinary incontinence

13. COUGH MECHANISM:
 Normally, afferent nerve endings richly innervate
the pharynx, larynx, & airways to the level of the
terminal bronchioles & extend into the lung
parenchyma.
 Spontaneous cough is triggered by stimulation of
these sensory nerve endings (that are thought to be
primarily rapidly adapting receptors & C fibers)
 Stimuli: chemical (capsaicin) & mechanical
(particulates in air pollution)
TYPE 1 VANILLOID
RECEPTOR – found on
rapidly adapting receptors
& C fibers – receptor for
capsaicin
Expression
increased in
patients with
chronic cough

14.  Sensory signals travel via the vagus & superior
laryngeal nerves to a region of the brain stem in the
Nucleus Tractus Solitarius (NTS) – “Cough center”
CHANGES OCCURING:
 Vocal cords adduct, leading to transient upper
airway occlusion
 Expiratory muscles contract, generating positive
intra-thoracic pressures as high as 300 mmHg.
 With sudden release of laryngeal contraction, rapid
expiratory flows are generated, exceeding the
normal envelope of maximal expiratory flow
 Bronchial smooth muscle contraction together with
dynamic compression of airways narrows airway
lumen & maximizes the velocity of exhalation

15. IMPAIRED COUGH:
 Weak or ineffective cough
 Compromises the ability to clear lower respiratory
tract infections
 Predisposing to more serious infections & their
sequelae
MC CAUSE: Weakness,
paralysis or pain of the
expiratory (abdominal &
intercostal) muscles

16. CLASSIFICATION BASED ON
DURATION:
Duration of cough
is a clue to its
etiology
TYPES CAUSES
ACUTE COUGH (< 3 weeks) • Respiratory tract
infection
• Aspiration
• Inhalation of noxious
chemicals or smoke
SUB-ACUTE (3-8 weeks) Common residuum of
tracheobronchitis, as in
pertussis or “post-viral
tussive syndrome”
CHRONIC ( >8 weeks) • Cardio-pulmonary
diseases
(inflammatory,
infectious,
neovascular)
Regardless of cause,
cough often worsens
upon first lying down at
night, with talking, or with
the hyperpnoea of
exercise; and frequently
improves with sleep

17. SYSTEMIC DISEASES WHERE COUGH IS ONE
OF THE CLINICAL MANIFESTATIONS ?
 Sarcoidosis
 Vasculitis

18. HOW DO YOU EVALUATE A PATIENT WITH
CHRONIC COUGH ??
 Chest radiograph
 Examination of expectorated sputum (in case of
chronic productive cough)

19. MOST COMMON CAUSES OF CHRONIC COUGH WITH
A NORMAL OR NON-CONTRIBUTORY CHEST
RADIOGRAPH?
 Cough-variant asthma
 GERD
 Postnasal drainage
 Medications (ACE inhibitors)
 Chronic eosinophilic bronchitis
Cough due to asthma
in the absence of
wheezing, shortness
of breath, and chest
tightness
Reflux of gastric contents
into the lower esophagus
 trigger cough via reflex
pathways initiated in the
esophageal mucosa
Retrosternal burning after
meals or on recumbency,
frequent eructation,
hoarseness and throat
pain  indicative of
GERD
Postnasal drainage of any
etiology  cough as a response
to stimulation of sensory
receptors of the cough-reflex
pathway in the hypopharynx or
aspiration of draining secretions
into trachea
ACE inhibitors 
accumulation of
bradykinin 
sensitization of
sensory nerve endings
Normally ACE
metabolizes
bradykinin & other
tachykinins, such as
substance P
SAFE
ALTERNATIVE:
ARBs – do not
cause cough

20. HOW DO YOU TREAT A PATIENT WITH CHRONIC
COUGH ??
 GERD – Antacids, H2 receptor antagonists, PPIs
- Dietary changes, elevation of the head,
torso during sleep & other medications
 COUGH-VARIANT ASTHMA – responds well to
inhaled glucocorticoids & intermittent use of inhaled
beta agonist bronchodilators
To neutralize or
decrease the
production of
gastric acidTo improve
gastric
emptying

21. COUGH HYPERSENSITIVITY
SYNDROME:
 Also called chronic idiopathic cough
 Often experienced as a tickle or sensitivity in the
throat
 More common in women
 Typically “dry” or at most productive of scant
amounts of mucoid sputum
HOW DO YOU APPROACH ?
 First exclude any underlying cardiopulmonary
pathology
 Then attempt at cough suppression

22. WHAT DO YOU DO FOR COUGH SUPPRESSION ?
 MOST EFFECTIVE: Narcotic cough suppressants –
codeine/ hydrocodone
 DEXTROMETHORPHAN
 BENZONATATE
MOA: Act in the
“cough center” in
the brainstem
ADVERSE EFFECTS:
• Drowsiness
• Constipation
• Potential for
addictive
dependence
Over-the-counter centrally
acting cough suppressant
with fewer side effects&
less efficacy than the
narcotic cough
suppressants
Inhibits neural activity of
sensory nerves in the
cough-reflex pathway. It is
generally free of side
effects

23. HEMOPTYSIS

24. WHAT IS HEMOPTYSIS ?
 Expectoration of blood from the respiratory tract
Can arise at any
location from the
alveoli to the glottis
To be distinguished from
epistaxis (bleeding from
the nasopharynx) &
hematemesis (bleeding
from upper GIT)

25. RANGE ??
Can range from the expectoration of blood-tinged
sputum to that of life-threatening large volumes of
bright red blood

26. MOST COMMON ETIOLOGY ?
 Infection of medium-sized airways
MOST
COMMONLY with
Mycobacterium
tuberculosis

27. OTHER ETIOLOGY:
 From alveoli: Diffuse alveolar hemorrhage
 Inflammatory – small vessel vasculitis
 Systemic autoimmune diseases – SLE
 Abs to alveolar BM – Goodpasture’s disease
 Direct inhalational injury – inhalation of toxic chemicals, illicit
substances (cocaine), thermal injury from fires
 From small- to medium- sized airways:
Bronchovascular bundle
Based on
potential sites of
bleeding
Proximity of bronchial
artery & vein to the
airway, with these
vessels & the bronchus
running together
Gives rise to more
significant
hemoptysis
While alveolar hemorrhage
arises from capillaries that are
part of the low-pressure
pulmonary circulation, bronchial
bleeding generally originates
from bronchial arteries, which
are under systemic pressure &
thus are predisposed to larger-
volume bleeding
Many causes of DAH
can be part of
pulmonary-renal
syndrome
Hence specific
enquiry into a H/o
renal insufficiency
is important

28.  Any infection of the airways
 Acute bronchitis
 Exacerbation of chronic bronchitis
 Pneumonias
 Tuberculous infection (which can lead to bronchiectasis
or cavitary pneumonia) – MC
 Lung abscess
 Chronic inflammation
 Bronchiectasis (a permanent dilation of airways with
loss of mucosal integrity)
Why ??
Coz chronic inflammation &
anatomic abnormalities bring
the bronchial arteries closer
to the mucosal surface
One common presentation of
patients with advanced cystic
fibrosis – the prototypical
bronchiectatic lung disease –
is hemoptysis which can be
life threatening

29.  Rasmussen’s aneurysm – source of massive, life-
threatening hemoptysis in the developing world
 Bronchogenic Lung cancer – MOST FEARED
cause of hemoptysis
Dilation of a
pulmonary artery in
a cavity formed by
previous tuberculous
infection) -
Although
hemoptysis is a
presenting
symptom in only
10% of patients
Patients to be asked for cigarette
smoking history as it predisposes to
chronic bronchitis & increases the
likelihood of bronchogenic
carcinoma

30.  Airway irritation:
 Inhalation of toxic chemicals
 Thermal injury
 Direct trauma from suctioning of airways (particularly in
intubated patients)
 Disease of pulmonary vasculature
 Pulmonary AV malformations
 Pulmonary embolism
 Pulmonary paragonimiasis
CONGESTIVE
HEART FAILURE
Elevation of LA
pressure
Transmission to
pulmonary veins
Rupture of small
alveolar
capillaries

31. DIAGNOSTIC EVALUATION:
 Chest X-ray
 CT of chest (if source of bleeding not identified on
plain x-ray)
 Lab studies
 CBC (to assess hematocrit, platelet count & coagulation
studies)
 Renal Function test
 Urinalysis
 Bronchoscopy (if all the above studies are
unrevealing)

32. CATAMENIAL HEMOPTYSIS:
 Monthly hemoptysis in a woman
 CAUSE: Pulmonary endometriosis

33. MASSIVE HEMOPTYSIS:
 > 200-600 mL/24 hrs

34. HYPOXIA

35. FUNDAMENTAL PURPOSE OF
CARDIORESPIRATORY SYSTEM ??
 To deliver oxygen & nutrients to cells and to remove
carbon-di-oxide & other metabolic products from
them
Proper maintenance of this
function depends not only on
intact CV & Respiratory
systems, but also on an
adequate number of RBCs &
Hb and a supply of inspired gas
containing adequate oxygen

36. RESPONSES TO HYPOXIA ??
Decreased oxygen availability to cells
Inhibition of oxidative phosphorylation
Increased anaerobic glycolysis
(Switch from aerobic to anaerobic metabolism)
Maintains some, though reduced ATP production

37. In severe hypoxia,
ATP production inadequate to meet the energy
requirements
Cell membrane depolarization
Uncontrolled Ca influx
Activation of Ca dependent phospholipases & proteases
Cell swelling, activation of apoptotic pathways
CELL DEATH

38. SO HOW DOES OUR BODY ADAPT TO HYPOXIA
??
Up-regulation of
 Genes encoding a variety of proteins, including
glycolytic enzymes, such as phosphoglycerate
kinase & phosphofructokinase
 Glucose transporters Glut-1 & Glut-2
 Growth factors (VEGF)
 Erythropoietin
ENHANCE RBC PRODUCTION
The hypoxia induced
increase in expression of
these key proteins is
governed by the hypoxia-
sensitive transcription
factor, hypoxia-inducible
factor 1 (HIF-1)

39. CHANGES THAT OCCUR DURING HYPOXIA ?
HYPOXIA
Reduction in ATP concentration
Opening of K ATP channels
in vascular smooth muscle
cells
Systemic arterioles dilate
Inhibition of K channels in
pulmonary vascular smooth
muscle cells
Depolarization
Activation of voltage-gated
Ca channels
Raising cytosolic Ca

40. Pulmonary arterial constriction
• Shunts blood away from poorly
ventilated portions toward better
ventilated portions of the lung
• Increases pulmonary vascular
resistance & right ventricular
afterload

41. EFFECTS OF HYPOXIA ON CNS ??
 Impaired judgment
 Motor incoordination
 Clinical picture resembling acute alcohol
intoxication
Pulmonary arterial
constriction  capillary
leakage  high-altitude
pulmonary edema (HAPE)
HAPE intensifies
hypoxia, further
promoting
vasoconstriction
As hypoxia becomes more
severe, the regulatory centers
of the brainstem are affected,
& death usually results from
RESPIRATORY FAILURE

42. EFFECTS ON CVS ??
 Stimulates the chemoreceptor reflex arc – to induce
venoconstriction & systemic arterial vasodilation
 Accompanied by transiently increased myocardial
contractility, followed by depressed myocardial
contractility with prolonged hypoxia

43. CAUSES OF HYPOXIA:
1. Respiratory hypoxia
2. Hypoxia secondary to high altitude
3. Hypoxia secondary to right-to-left extra-pulmonary
shunting
4. Anemic hypoxia
5. CO intoxication
6. Circulatory hypoxia
7. Specific organ hypoxia
8. Increased oxygen requirements (eg: exercise)
9. Improper oxygen utilization (HISTOTOXIC
HYPOXIA) – eg: cyanide poisoning

44. RESPIRATORY HYPOXIA:
Respiratory failure
PaO2 declines
ARTERIAL HYPOXEMIA (reduction of oxygen
saturation of arterial blood) CYANOSIS
When respiratory failure is persistent,
Hb-O2 dissociation curve is displaced to right
Greater quantities of oxygen released at any level of tissue PO2

45. CAUSES:
 Ventilation-perfusion mismatch (resulting from
perfusion of poorly ventilated alveoli) – MC
 Hypoventilation (assoc. with an elevation of
PaCO2)
 Shunting of blood across the lung from the
pulmonary arterial to venous bed (intrapulmonary
right-to-left shunting) by perfusion of non-ventilated
portions of the lung (eg: pulmonary atelectasis,
pulmonary AV connections)
Rx (for 1 & 2):
Inspiring 100% O2 for
several minutes

46. HYPOXIA SECONDARY TO HIGH ALTITUDE:
High altitude (3000 m/ 10,000 feet)
Reduction of O2 content of inspired air
Decrease in alveolar PO2 to approx. 60 mmHg
HIGH-ALTITUDE ILLNESS
At higher altitudes,
arterial saturation
declines rapidly &
symptoms become
more serious
At 5000 m, unacclimated
individuals usually cease
to be able to function
normally owing to the
changes in CNS function

47. HYPOXIA SECONDARY TO RIGHT-TO-LEFT
EXTRA-PULMONARY SHUNTING:
CAUSES:
Congenital cardiac malformations
 Tetralogy of Fallot
 Transposition of great arteries
 Eisenmenger’s syndrome

48. ANEMIC HYPOXIA:
 Reduction in Hb concentration of the blood
accompanied by a corresponding decline in the
oxygen carrying capacity of the blood
 PaO2 – normal

49. CO INTOXICATION:
 Hb that binds with CO – unavailable for O2
transport
 In addition, presence of COHb shifts the HbO2
dissociation curve to the left – so that O2 is
unloaded only at lower tensions  further
contributing to tissue hypoxia

50. CIRCULATORY HYPOXIA:
 PaO2 – normal (like anemic hypoxia)
But venous & tissue PaO2 values are reduced as a
consequence of reduced tissue perfusion & greater
tissue O2 extraction
Increased arterial-mixed venous O2 difference or
gradient
Generalized C.H
occurs in HEART
FAILURE most
forms of SHOCK

51. SPECIFIC ORGAN HYPOXIA:
Localized circulatory hypoxia may occur as a result of
 Decreased perfusion secondary to arterial
obstruction (eg: localized atherosclerosis in any
vascular bed)
 Vasoconstriction (eg: Raynaud’s phenomenon)
 Venous obstruction  resultant expansion of
interstitial fluid  arteriolar compression 
reduction of arterial inflow
 Edema (by increasing the distance through which
O2 must diffuse before it reaches cells)
In an attempt to maintain adequate
perfusion to more vital organs in
patients with reduced cardiac output
secondary to heart failure or
hypovolemic shock, vasoconstriction
may reduce perfusion in the limbs &
skin  hypoxia of these regions

52. ADAPTATIONS TO HYPOXIA:
1. Hypoxia
Stimulation of special chemosensitive cells in carotid
& aortic bodies + in respiratory center in brainstem
Increases ventilation with a loss of CO2
RESPIRATORY ALKALOSIS
When combined with the
metabolic acidosis
resulting from the
production of lactic acid,
the S.HCO3 levels
decline

53. 2. With reduction of PaO2
Cerebrovascular resistance decreases
Cerebral blood flow increases (in an attempt to
maintain O2 delivery to brain)
However when reduction of PaO2
is accompanied by hyperventilation
& a reduction of PaCO2,
cerebrovascular resistance rises 
cerebral blood flow falls & tissue
hypoxia intensifies

54. 3. Diffuse systemic vasodilation
Increases cardiac output
4. Increase in Hb conc. & in number of RBCs in the
circulating blood (i.e., development of
polycythemia secondary to erythropoietin
production) – ONE OF THE IMPORTANT
COMPENSTAORY MECHANISMS FOR
CHRONIC HYPOXIA
But in patients with underlying
heart disease, the
requirements of peripheral
tissues for an increase of
cardiac output with hypoxia
precipitates CHF

55. CHRONIC MOUNTAIN SICKNESS:
 Develops in persons with chronic hypoxemia
secondary to prolonged residence at a high altitude
(>13,000 feet, 4200 m)
 Characterized by blunted respiratory drive, reduced
ventilation, erythrocytosis, cyanosis, weakness,
RVH secondary to pulmonary HT

56. CYANOSIS

57.  Bluish color of skin & mucous membranes resulting
from an increased quantity of reduced Hb (i.e.,
deoxygenated Hb) or of Hb derivatives (meth Hb,
sulf Hb) in the small blood vessels of those tissues.
 Cyanosis becomes apparent when the
concentration of reduced Hb in capillary blood
exceeds 4 g/dL
 Most marked in the lips, nail beds, ears, & malar
eminences

58. MECHANISM:
 Increase in the quantity of venous blood (coz of
dilation of venules) /
 Reduction in the SaO2 in the capillary blood
Increase in quantity of reduced Hb
CYANOSIS
It is absolute, rather than
the relative, quantity of
reduced Hb that is
important in producing
cyanosis

59. TYPES:
CENTRAL PERIPHERAL
SaO2 is reduced or an abnormal
Hb is present (decreased SaO2
results from a marked reduction in
the PaO2)
Due to slowing of blood flow &
abnormally great extraction of O2
from normally saturated arterial
blood
Mucous membranes & skin- both
are affected
Mucous membranes of the oral
cavity or those beneath the tongue
may be spared
MC cause – seriously impaired
pulmonary function, through
perfusion of unventilated or poorly
ventilated areas of the lung or
alveolar hypoventilation
MC cause – normal
vasoconstriction resulting from
exposure to cold air or water
Occurs
• Acutely in – extensive
pneumonia, pulmonary edema
• Chronically in – chronic
pulmonary diseases
(emphysema)
When cardiac output is reduced,
cutaneous vasoconstriction
occurs as a compensatory
mechanism so that blood is
diverted from skin to more vital
areas such as CNS & heart, and
cyanosis of the extremities may
result even though the arterial
blood is normally saturated

60. In conditions such as
cardiogenic shock with
pulmonary edema 
mixture of both types

61. POINTS TO REMEMBER:
 Cyanosis present since birth or infancy is usually
due to CHD
 Massage or gentle warming of a cyanotic extremity
will increase peripheral blood flow & abolish
peripheral but not central cyanosis
 Combination of cyanosis & clubbing is frequent in
patients with CHD and right-to-left shunting
 In contrast, peripheral cyanosis or acutely
developing central cyanosis is not associated with
clubbed digits

62. CLUBBING
Refer my old PPs

63. CONDITION WHERE CLUBBING IS REVERSIBLE
?
 Following lung transplantation for cystic fibrosis