What is the average VO₂ and VCO₂ for humans?

(What is the ¨v¨?)

V (with a dot above it) means minute production or consumption of a gas.

Humans normally consume 200mL O2/min and produce 180mL CO2/min.

R=VCO2/VO2

(CO2 exhaled by lungs)/(O2 taken up by lungs)

R=RQ

What is this and what is the normal value?

Steady state = nml is 0.8

Respiratory Exchange ratio=respiratory quotient

amount of O2 bound to hemoglobin + the amount of O2 dissolved in plasma.

=1.36(Hb)(%Sat*) + (0.003)(PaO2**)

*%Sat=put in decimals.  More saturation=redder blood.

**PaO2=partial pressure in artery

Hypoventilation - PACO2 inversely porportional to aveolar CO2 ¨blow off¨...the slower you breath, the greater CO2 you have in  your bld

V/Q mismatch:

a) low V, high Q regions add large amounts of poorly ventilated, high CO2 blood

b) high v, low Q add small amounts of well ventilated, low CO2 blood.

=0.863(VCO2)/V_A*

* V_A is aveolar ventilation that blows off CO2.

What determines P_AO2?

= P_IO2 - (*P_ACO2/R)

Partial pressure of inspired O2 - (amount of O2 exchanged for CO2 divided by Respiratory exchange ratio)

*P_ACO2 from radial arterial sample.

What is the term for the difference between aveolar and arterial O2 concentrations? 

What is normal on room air?

A-a gradient

5-10mmHg on room air.

A-a gradient = PA_O2 − Pa_O2

• PA_O2 = alveolar PO₂ (calculated from the alveolar gas equation)

• Pa_O2 = arterial PO₂ (measured in arterial blood A-a gradient)

The A-a gradient is useful in determining the source of hypoxemia. The measurement helps isolate the location of the problem as either intrapulmonary (within the lungs) or extrapulmonary (somewhere else in the body).

A normal A-a gradient is less than 10 mmHg, but can range from 5–20 mmHg. Normally, the A-a gradient increases with age. For every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg. An abnormally increased A-a gradient suggests a defect in diffusion, V/Q (ventilation/perfusion ratio) defect, or right-to-left shunt

1) hypoventilation: respiratory drive impairment, neural pathway damage, neuromuscular disease, respiratory muscle disease.

2) V/Q mismatch

3) Shunt: bld bypasses lung and gets no O2

4) diffusion impairment: disease of lung

5) decreased PIO2: could be due to altidude

respiratory drive impairment*, neural pathway damage, neuromuscular disease, respiratory muscle disease can all cause...

*Name 4 causes of respiratory drive impairment.

hypoventilation=hypoxemia

Respiratory drive impairment:

1) CNS (tumor, stroke, hemorrhage)

2) CNS depressants (barbituates, opiates, benzdiazepines

3) Obesity-hypoventilation syndrom

4) Mechanical (kyphoscoliosis, diaphragm paralysis post-CABG)

1) CNS (tumor, stroke, hemorrhage)

2) CNS depressants (barbituates, opiates, benzdiazepines

3) Obesity-hypoventilation syndrome

4) Mechanical (kyphoscoliosis, diaphragm paralysis post-CABG)

all of these can cause...

Neurological diseases that affect ventilation...lead to hypoventilation then hypoxemia.

Amyotrophic lateral sclerosis

Dx of Hypoventilation:

Hypoxia is always associated with corresponding incr or decr in PCO2?

How is A-a gradient affected?

Hypoxia is always associated with corresponding incr  in PCO2?

A-a gradient is normal b/c underlying lung is normal.

High V/low Q supplies small/large amounts of well/poorly oxygenated blood.

Low V/high Q supplies small/large amounts of well/poorly oxygenated blood.

The result causes....

What are 4 diseases associated with V/Q mismatch.

High V/low Q supplies small amounts of well oxygenated blood.

Low V/high Q supplies large amounts of poorly oxygenated blood.

...hypoxia..

1) COPD (bronchitis, emphysema, CF)

2) Asthma

3) PE

4) Pneumonia

V/Q mismatch:

State the levels/effects of the following

1) PCO2

2) A-a gradient

3) O2 mask on pt

1) PCO2 elevated

2) A-a gradient ALWAYS elevated

3) O2 mask on pt corrects hypoxia.

Right to left circulation that does not participate in gas exchange.

What is this?  Name 3.

Right to Left Shunts:

1) Intracardiac Shunt (patent foramen ovale, septal defects)

2) Pulm arteriovenous malformation

3) Diseases filling the aveolus with fluid (CHF, pneumonia, ARDS).

A pt has an elevated A-a gradient. 

Hypoxia is not corrected with O2 mask. 

You see bubbles in ECG study

What is your Dx?

Emphysema,

Pulm Fibrosis (thickened membrane),

Lung Resection (partial removal of part of lung)

Pulmonary Fibrosis

Edema Fluid

You ask pt to inhale known conc of CO, hold breath for 10 sec, and exhale.

What are you testing for?

If the test is positive, what should be the A-a gradient?

Testing diffusion capacity for CO (DL_CO) to make a diagnosis of diffusion impairment. DL_CO is porportional to the diff btwn inspired and expired CO

A-a gradient will be high in diffusion impairment.

check ABG

measure A-a gradient.

volume where the inward elastic recoil of forces of the lung equal the outward forces of the chest wall

What is this called (2 names: formal and informal)?

What occurs here?

Buffers...

Prevents...

functional residual capacity

¨resting¨position of lung and chest wall

gas exchange occurs here.

buffers changes in PCO2 and PO2 that occur with aveolar ventilation.

prevents wide pH swings.

external intercostals

AND

accessory muscles during resp distress

normal tidal breathing

1) Inspiration: FRC, pleural pressure, aveolar pressure

2) Expiration: how does it happen?: FRC, uses of expir muscles.

1) inspiratory muscles incr thoracic volume above FRC, pleural pressure and aveolar pressure becomes negative.

2) expirations happens passively from the relaxation of inspiratory muscles to return lung/chest wall system to FRC.  Used for cough, exercise, and resp distress.

Lung Compliance = (formula and definition)

At what volumes is the lung more and less compliant?

(change in V) / (change in Pressure)

the ability of the lungs to stretch during a change in volume relative to an applied change in pressure

More compliance=lower lung volumes (easy to inflate)

Less compliance=higher lung volumes (harder to inflate)

**FYI

• fibrosis is associated with a decrease in pulmonary compliance.
• emphysema/COPD may be associated with an increase in pulmonary compliance due to the loss of alveolar and elastic tissue.

1) surface tension

2) elastic and colagen fibers of the lung

High compliance, easy inflation, low elastic recoil, and low flow during expiration are a result of...

Give an example of a disease.

Destruction of elastic and collagen fibers.

Emphysema=Obstructive lung disease.

(Paper bag model).

Obstruction vs Restriction...state whether the following are high, normal or low.

a) compliance

b) elastic recoil

c) airway resistance

d) expiratory flow rate

What would you use to make a medical diagnosis

of the cause of dyspnea,

determine obstructive vs restrictive lung disease,

rule out pulmonary cause of dyspnea,

measure effect of disease on pulm function,

follow the course of disease process/tx???

Spirometry can measure all lung volumes and capacities except what 2 volumes...

What is the formula to calculate each of these volumes?

FRC = RV +ERV

&

RV =TLC -VC = (FRC + IC ) - VC

**FYI**

*Functional Residual Capacity (FRC) is the volume of air present in the lungs at the end of passive expiration. At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles.

*Residual Volume (RV) The amount of air left in the lungs after a maximal exhalation. The amount of air that is always in the lungs and can never be expired (i.e.: the amount of air that stays in the lungs after maximum expiration).

The volume inspired with each breath.

What is normal?

Tidal Volume (TV)

Nml: 5mL/kg IBW

Expiratory Reserve Volume (ERV)

**FYI**

*Functional Residual Capacity (FRC) is the volume of air present in the lungs at the end of passive expiration. At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles.

max volume of gas than can be exhaled after max inspiration

(Name and formula)

State the 4 types of this.

Vital Capacity (VC)=IRV+VT+ERV

1) Slow VC: VC measured with slow expiratory maneuver

2) Forced VC (FVC): VC measures with maximal forced exhalation

3) Combined VC: calculation = IC+ERV

4) Inspired vital capacity: VC calculated by measureing complete inhalation from RV

max volume of gas the lungs can contain.

How do you obtain this (procedure and 2 formulas)

Total Lung Capacity (TLC)

TLC= VC+RV

TLC=FRC+IC

Use body box

4 TYPES of VITAL CAPACITIES:

1) VC measured with slow expiratory maneuver

2) VC measures with maximal forced exhalation

3) calculation = IC+ERV

4)VC calculated by measuring complete inhalation from RV

1) Slow VC: VC measured with slow expiratory maneuver

2) Forced VC (FVC): VC measures with maximal forced exhalation

3) Combined VC: calculation = IC+ERV

4) Inspired vital capacity: VC calculated by measureing complete inhalation from RV

Average rate of flow furing the middle half of the volume expired during FVC maneuver

Max flow obtained during FVC manuever.

Tangent of volume-time curve at start of flow.

Effort dependent.

Obstructive Lung Disease:

1) FVC is nml/reduced/elev?

2) FEV-1 is nml/reduced/elev?  Give %.

3) FEV-1% is nml/reduced/elev? Give %.

Obstructive Lung Disease:

(Asthma, Emphesyma, Chronic Bronchitis, COPD

1) FVC is nml/reduced

2) FEV-1 is reduced. <80% predicted

3) FEV-1% is reduced. <75%.

**FYI**Wikipedia's list of Obstructive Lung Diseases:**

Restrictive Lung Disease:

1) FVC is nml/reduced/elev?

2) FEV-1 is nml/reduced/elev?

3) FEV-1% is nml/reduced/elev?

Is spirometry diagnositc of restriction?

Restrictive Lung Disease:

1) FVC is reduced

2) FEV-1 reduced

3) FEV-1% is nml/elev

Is spirometry diagnositc of restriction?

**FYI on Restrictive Lung Diseases from Wikipedia**

Restrictive lung diseases may be due to specific causes which can be intrinsic to the parenchyma of the lung, or extrinsic to it.

Intrinsic

• Asbestosis caused by long-term exposure to asbestos dust.
• Radiation fibrosis, usually from the radiation given for cancer treatment.
• Certain drugs such as amiodarone, bleomycin and methotrexate.
• As a consequence of another disease such as rheumatoid arthritis.
• Hypersensitivity pneumonitis due to an allergic reaction to inhaled particles.
• Acute respiratory distress syndrome (ARDS), a severe lung condition occurring in response to a critical illness or injury.
• Infant respiratory distress syndrome due to a deficiency of surfactant in the lungs of a baby born prematurely.

Many cases of restrictive lung disease are idiopathic (have no known cause). Examples are:

• Idiopathic pulmonary fibrosis
• Idiopathic interstitial pneumonia, of which there are several types
• Sarcoidosis
• Eosinophilic pneumonia
• Lymphangioleiomyomatosis
• Pulmonary Langerhan’s cell histiocytosis
• Pulmonary alveolar proteinosis

Conditions specifically affecting the interstitium are called interstitial lung diseases.

12% FEV-1 & >200cc improvement in peak flow

OR

12% FVC & >200cc improvement in peak flow

OR

30% improvement in FEF 25-75%

methacholin, histamine, and carbachol are three agents that are used for...

how are they used/dosed/ and what is the response that rules out asthma as a diagnosis and @ what dose?

nonspecific bronchoprovocation testing

Begin with low dose (.03mg/ml), double concentration until >16mg/ml or until FEV-1 decreases.

NOT Asthma: <20% decr in FEV-1 @ 16mg/ml.

P₁V₁=P₂V₂

What is this and what is it used for?

Boyle's Law.

Pressure times volume is constant if temperature is constnat.  Use this for body box method.

P₁V₁=P₂V₂ + (change in volume).

P1 and P2 are measured.  Change in V calculated.

A low FEV-1% defines...(give %)

A low TLC defines...(give %)

A low FEV-1% defines obstructive disease (<75%)

A low TLC defines restrictive lung disease (<80%)

UPPER AIRWAY

Name 4 extrathoracic obstructions.

Name 3 variable intrathoracic obstructions.

EXTRATHORACIC

-vocal cord paralysis

-thyromegaly

-tracheomalacia*

-neoplasm

INTRATHORACIC

-Airway collapse furing expiraltion

-Neoplasm
-Tracheomalacia*

**FYI**

Tracheomalacia =flaccidity of the tracheal support cartilage which leads to tracheal collapse especially when increased airflow is demanded.

The trachea normally dilates slightly during inspiration and narrows slightly durig expiration.

These processes are exaggerated in tracheomalacia, leading to airway collapse on expiration.

The usual symptom of tracheomalacia is expiratory stridor or laryngeal crow. and narrows slightly during

flow volume loops

[image]

1) What is the outer covering of heart? What is attached to it?

2) Majority of heart wall thickness.

1) dense connective tissue around heart.  valves attached to connective tissue with reinforced rings.

2) Myocardium (cardiac muscles cells)

Endocardium:

1) type of cell

2) extends into...

1) simple squamous epithelium,

2) extends into all the BVs (blood always separated from tissues)

Cardiac Tamponade: pericardial cavity filled with excess fluid.

**FYI**

Cardiac tamponade, also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death.

SVC+IVC>RA>tricuspid>RV>pulm valve>lungs>LA>mital valve>LV>aortic valve

Landmarks on outside of body:

¨Artists Paint The Murals¨

[image][image]

Diastole

Systole

Diastole=ventricles relax and are filling

Systole=ventricles contract and pump out blood.

These cells represent 1-2% of myocardial cells.  They are not capable of contracting.  They generate their own rhythmic action potential and have no stable resting membrane.

What are they, where are they located?

Cardiorhythmic/Pacemaker cells.

SA node at RA & SVC junction.

AV node next to tricuspid valve. 

AV bundle goes through interventricular septum & divides in bundles of his and then purkinje fibers.

State the Action Potentials/Minute

1) SA node

2) AV node

3) Bundle of His and Purkinje Fibers

What sets the rhythm of the heart?

Why do atria and ventricles contract at slightly different times?

1) SA node 70-80

2) AV node 40-60

3) Bundle of His and Purkinje Fibers 20-40

The fastest node sets the rhythm of the heart.  Nml HR 60-100, ideally 75.

1/10th of a second delay for impulse to get over entire heart and this creates and atrial to ventricular delay.

Inside cardiac muscles cells there are large numbers of ______________ which make ATP by ______________.

In the absense of O2, myocardial cells use __________to make ATP which is 20x less efficient.

Inside cardiac muscles cells there are large numbers of mitochondria which make ATP by oxidative phosphorylation.

In the absense of O2, myocardial cells use glycolysis to make ATP which is 20x less efficient.

What protein appears in the blood after recent death of a cardiac cell, possibly after an MI?

How does this protein cause muscle contraction?

Troponin C

Troponin lies within the groove between actin filaments in muscle tissue.  When the muscle cell is stimulated to contract by an action potential, calcium channels open and release calcium into the sarcoplasm. Some of this calcium attaches to troponin, causing a conformational change produce muscle contraction.

*FYI*

Troponin is a complex of three regulatory proteins that is integral to muscle contraction in skeletal and cardiac muscle, but not smooth muscle.

Duration of cardiac cell action potential (AP) is how many times longer than peripheral neurons?

What is unique to cardiac cells that creates this long action potential?

250x

Unique to cardiac cells: Voltage gated Ca channels throughout membrane allow Ca++ to leak in slowly, creating an action potential plateau.

[image]

Na rushes into cell very fast, Na pumps close, Ca begins leaking in slowly (voltage gated Ca channels)….while Ca channels open, K channels stay shut.

*P=permeability.

ECG deflection polarization and time intervals:

1) P wave polarization

2) PR interval time

3) QRS wave polarization and time

4) ST segment polarization

5) T wave polarization

1) P wave polarization = atrial depol

2) PR interval time = 0.12-0.20 sec

3) QRS wave polarization and time= ventricular depol (atrial repol), <0.10sec

4) ST segment polarization = no polarization, its @ baseline

5) T wave polarization= ventricular repolarization

[image]

elevated ST segment (nml is @ baseline).

120mmHg= LV pressure when aortic valve just opens (beginning of systole)

80mmHg= LV pressure just as aortic valve closes (beginning of diastole)

Cardiac OUtput (CO)=?

(*give units)

What are the effects of the sympathetic and parasympathetic nervous systems on CO?

CO (mL/min)= stroke volume (mL/beat) x HR (beat/min)

Sympathetic = cardiac accelerator=increase CO

-incr rate of spontaneous depolarization in SA node (incr HR)

-incr contractility of atra and ventricles (incr stroke volume)

Parasympathetic(vagus CN X)=slows shit down= decr CO

-decr spontaneous depol in SA node (decr HR)

ratio of max cardiac output to resting cardiac output

(max CO)/(resting CO)

what is the range for healthy pts, cardiac pts, and trained athletes?

cardiac reserve

healthy pt= 4-5

cardiac pt= 1-2

 trained athlete=7-8

**more athletic = greater max CO**

sympathetic = sympathetic ganglionic chain (stimulate, incr HR)

&

parasympathetic = vagus nerve CNX (Parar en español = slows shit down, decr HR)

stroke volume (SV)=volume of blood pumped from one ventricle of the heart with each beat.

It is calculated by subtracting the volume of blood in the ventricle at the end of a beat from the volume of blood just prior to the beat. 

LV and RV stroke volumes are generally equal, both approximately 70 ml in a healthy 70-kg man.

SV=

[end-diastolic volume (120mL)] - [end-systolic volume (50mL)]

= 70mL

IV infusion...incr RA pressure...atrial receptor stimulation...bainbridge reflex...incr HR

*Wiki: The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions.

IV infusion...incr CO...incr arterial BP...baroreceptor reflex...decr HR

*Wiki: The baroreflex/baroreceptor reflex is one of the body's homeostatic mechanisms for maintaining blood pressure. It provides a negative feedback loop in which an elevated blood pressure reflexively causes heart rate and thus blood pressure to decrease

Arteries vs. Veins

1) thickness & layers

2) pressure

3) unique physiologic features

4) what system controls vasoconstriction?

Arteries and veins have the same layers (from outside to inside):

-connetive tissue (thickest layer in vein)

-smooth muscle layer (thickest layer in artery

-elastic membrane

-simple squamous epithelial endothelium/endocardium extension

Arterial layers are thicker, have more elastic tissue and more muscle.

Arterial Pressure 93mmHg, Venous pressure=20mmHg 

veins have valves to keep blood flowing to heart.

sympathetic system=vasocontriction.

Capillaries

1) state flow from RV to LA

2) walls: layers?, which molecules get through in passive diffusion?

3) thickness and relation to diffusion capacity

1) RV...pulm art...lungs...

arteries...arterioles...capillaries...venules...veins...

pulm vein...LA

2) wall is a 1-layer simple squamous endothelium with basement membrane that allows gas and lipophilic molecules to pass through without the need for special transport mechanisms. This transport mechanism allows bidirectional diffusion depending on osmotic gradients

3) 1 RBC thick...max exposure for max diffusion

Blood flow is directly porportional to ________ and inversely porportional to __________. 

Give formula.

Blood flow is porportional to pressure and inversly porportional to resistance. 

Cardiac Output=ΔP/R= change in pressure/resistance

Vascular Resistance is determined by what 3 factors?

**state the relationship of obesity to BP and resistance.

1) Vessel Radius (resistance porportional to 1/r⁴).  VERY SMALL CHANGES IN RADIUS = BIG INCR IN RESISTANCE.

2) Viscosity: largely determined by hematocrit, which is content of RBCs.  More hematocrit=thicker bld=harder to pump.

3) Total Vessel length**

**We don´t grow more BVs during adulthood EXCEPT in adipose tissue.  An incr in adipose tissue=incr BV=incr total vessel length=incr resistance....THIS IS WHY OBESITY IS ASSOCIATED WITH HTN

BARORECEPTOR REFLEX (BAROREFLEX):

1) function

2) 2 most sensitive baroreceptor locations and innervations.

3) Responses to high/low BP

1) homeostatic control of BP

2) carotid sinus (glossopharyngeal n. CN IX)

& aortic arch (vagus n. CN X)

¨cag & ava¨

3) High BP? a negative feedback loop causes HR and BP to decrease.

Low BP? depresses the baroreflex, causing HR and BP to rise.

CHEMORECEPTOR REFLEX & BP CONTROL:

1) where are the chemoreceptors and what do they monitor?

2) Impulses from these chemoreceptor go to...via what nerves?...

3) chemoreceptors in the medulla oblongata monitor...

4)effects of decr blood O2, incr CO2, decr pH on ANS, HR, Stroke volume (SV), BP.

WATCH THIS VIDEO:

http://highered.mcgraw-hill.com/sites/0072943696/student_view0/chapter13/animation__chemoreceptor_reflex_control_of_blood_pressure.html

1) Chemoreceptors in carotid and aortic bodies monitor blood O2, CO2, and pH

2) impulses go to control centers for heart and BVs via glossopharyngeal (carotid) and vagus (aortic) nerves.  ¨cag & ava¨

3) CO2 & pH

4) decr blood O2, incr CO2, decr pH:

-decr parasym stim of heart (vagus)= incr HR

-incr sympathetic stim of heart (symp chain)=incr HR, SV, vasoconstriction (incr BP).

Renin-angiotensin-aldosterone system (RAAS):

1) definition

2) when blood volume is low, how does RAAS increase BP? (this is the combination of 2 effects)?

3) how does the RAAS system contribute to HTN?

1) hormone system that regulates BP and H2O balance (blood volume).

2) Low blood volume (or drop in BP...hemorrhage): kidneys secrete renin...renin stimulates angiotensin I production:

-angiotensin I causes vasoconstriction (incr BP).

-ACE converts Ang I to Ang II

-angiotensin II stimulates aldosterone secretion from adrenal cortex...aldosterone causes kidney tubules to incr reabsorption of Na & H₂O...incr body fluids...incr BP.

3) HTN= overactive RAAS system.

[image]

This protein causes vasocontriction and incr in BP.  It is the major target for HTN drugs.  It stimulates release of aldosterone (to promote Na retention=incr BP). 

There are 4 types (ANGIOTENSIN I-IV):

a) which is formed by the action of renin?

b) which is target for inactivation by ACE inhibitor drugs, which decrease the rate of production.

ANGIOTENSIN (I-IV)

 Ang I) formed by the action of renin

Ang II) target for inactivation by ACE inhibitor drugs, which decrease its rate of production.

disease causing dilation of superficial veins of legs. 

What is this and 2 risk factors?

When arterial internal pressure greatly exceeds external pressure.

What is this?

Dangers?

Name 4 types of this condition.

Aneurysm: bulging of arterial wall (often in lg vessels like aorta and femoral a.) causes wall to become thin. 

Danger=rupture potential.

[image]

**FYI: You can get a ventricular aneurysm (eg post-MI)

Thrombus formation

1) associated with...(3)

2) valvular thrombi associated with....(2 diseases)

3) danger of...

1. Associated with atherosclerosis, vascular trauma, pooling of blood
2. Valvular thrombi associated with endocarditis and rheumatic heart disease
3. Danger of vessel occlusion and of dislodging (thromboembolism)

Name 6 different types of embolisms:

¨AAFF BaTh¨

1. Thromboembolism - usually from DVT in leg
   
2. Air Embolism – bubbles in bld
3. Amniotic Fluid Embolism – during childbirth
4. Bacterial Embolism – assoc with endocarditis.  Chunks of growing bact mass break free
5. Fat Embolism – fractures of limbs can cause bone marrow in circulation
6. Foreign Matter

HTN:

1) Primary (essential): cause?  % of Hypertensives?

2) secondary: most common causes (4), % of hypertensives.

3) Malignant HTN: progression?

1) primary HTN: idiosyncratic.  90-95% of pts

2) secondary HTN: kidney disease, pheochromocytoma (tumor of adrenal gland), DM, coarc of aorta.  5-8% of pts.

3) Malignant HTN: rapidly progressing, life-threatening.  can cause encephalopathy, papilledema, cardiac failure, uremia, retinopathy, cerebrovascular accidents.

1) incr HR

#s 2 - 4 lead to narrowing of vessels/vasospasm:

2) incr insulin resistance...endothelial dysfunction

3) vascular remodeling

4) procoagulant effects

a decrease in arterial blood pressure on standing with failure of normal compensatory mechanisms=dizziness, vision blurring, syncope, falls.

what is it?

BP drops by how much?

gender/age predominance?

% of adult pop affected?

Orthostatic (Postural) Hypotension

The decrease is typically greater than 20/10 mm Hg

more Men

40-70yrs

18% adults

condition in which an artery wall thickens as the result of a build-up of fatty materials. It is a chronic inflammatory response in the walls of arteries, largly due to the accumulation of macrophage WBCs and promoted by LDL-oxidation without adequate removal of fats and cholesterol from the macrophages by functional HDLs.  Multiple fibrous  plaques within the arteries with collagen cap forms.

what is this?  where does it form, usually?  what is the risk?

atherosclerosis

usually forms near arterial branching areas: thought to be in response to injury from turbulent blood flow.

Risk of rupture of collagen cap to release lipid core which can completely occlude vessel.

the most frequent sites of this disease are:

abdom/thoracic aorta, illiac, femorals, popliteals

proximal coronary arteries**...(what disease is this, specifically?)

internal carotids

vertebral, basilar, and cerebral arteries

atherosclerosis

CAD= atherosclerotic heart disease= accumulation of atheromatous plaques within the walls of the coronary arteries

severe chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries

What is this and what is the #1 cause?

Angina pectoris

#1 cause= CAD (atherosclerosis of coronary arteries)

chest pain that changes or worsens.

It has at least one of these three features:

1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

*if this chest pain occurs unpredictably at rest, it may be a serious indicator of ....

UNSTABLE ANGINA

**if this UA occurs unpredictably at rest, it may be a serious indicator of ....an impending heart attack

the pathophysiology of the atherosclerosis:

1) stable angina, the developing atheroma is protected with a fibrous cap.

2) This cap (atherosclerotic plaque has large lipid core and thin cap) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.

ischemic attack < 20min

MI > 20min

SITES of MI - STATE VESSEL INVOLVEMENT:

1) A posterior (inferior) MI involves the occlusion of....

2) massive anterolateral MI...

3) anteroseptal MI...

4) lateral MI...

1) A posterior (inferior) MI = RCA (R coronary a.) occlusion

2) massive anterolateral MI= LCA (L coronary a.) occlusion

3) anteroseptal MI=LAD (L ant desc a.) occlusion

4) lateral MI=LCX (L circumflec coronary a.) occlusion

[image]

A little review of the heart sounds (*from wikipedia):

S1

S2

S3

S4

S3+S4

S₁ :

-closure of the AV valves, (mitral and tricuspid)

-beginning of systole.

S₂ :

-closure of  semilunar valves (aortic valve closure heard)

-Inspiration, A₂ and P₂ split

-at the beginning of ventricular diastole

S₃: ventricular gallop

-the "Kentucky"  (S1=ken; S2=tuc; S3=ky).

- beginning of diastole after S2

-lower in pitch than S1 or S2

-not of valvular origin. 

-benign in youth and some trained athletes

- later in life= signal cardiac problems (LV failure in dilated CHF)

- oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria.

S₄: 

-rare, sometimes audible in healthy children and again in trained athletes

-in an adult= presystolic gallop or atrial gallop, pathologic LV failure or restrictive cardiomyopathy.

-produced by the sound of blood being forced into a stiff/hypertrophic ventricle.

- just after atrial contraction ("atrial kick") at the end of diastole and immediately before S1

- "Tennessee" gallop (S4 = the "tenn-" ).

-heard at the cardiac apex,  left lateral decubitus position,held breath.

S₃ + S₄= quadruple gallop.

-At rapid heart rates, S3 and S4 may merge to produce a summation gallop.

Blood flow inside a vessel = (change in P)/(R)

1) What is P?  How does the liver and kidney effect P?

2) What is R?  What 3 factors effect R?

1) Pressure: protein + osmotic pressure pull water into blood system:  Liver failure (no prot synthesis) & renal failure (proteinuria: no reabsorption of prot) cause low protein in bld = diminished oncotic pressure = edema

2) Resistance:

• Length of vessel
• Blood Viscosity: chronic smokers, COPD=hypoxia=stimulates incr of RBC production to survive low O2= thicker blood (incr coagulation)
• Radius of vessel: Resistance porportional to 1/r⁴.  Small decrease in vessel radius= great incr in resistance.

What is especially important in chronic adaptation for Cardiac Output maintaince?

1) Renin-angiotensin-aldosterone system (RAAS): autonomic hormone system that regulates BP and fluid balance.

2) Arginine vasopressin (AVP) aka antidiuretic hormone (ADH):

• #1: regulate water retention (anti-diuretic enzyme)
• #2 moderate peripheral vasoconstriction (incr BP)
• released from posterior pituitary as a response to dehydration/hypovolemic shock (hemorrhage)

3) Atrial natriuretic peptide (ANP) & Brain natriuretic peptide (BNP):

• net effect of BNP and ANP is a decrease in blood volume and a decrease in cardiac output.
• ANP= powerful vasodilator secreted by STRETCHED atrial myocardial cells
• incr BNP = dx of acute CHF & incr chance of heart failure

RAAS

1) function

2) what type of system?

3) 3 factors stimulating of Renin (where is it secreted from, what does it do?)

4) angiotensin production and effects

5) aldosterone effects

renin-angiotensin-aldosterone system (RAAS)

1. regulates BP and water balance
2. autonomic hormone system
3. Decr arterial BP (baroreceptors), decr NaCl levels, beta-1 adrenergic receptors.
   • stimulates renin enzyme to be secreted from kidney juxtaglomerular apparatus.  
   • renin stimulates production of angiotensin I
4. Angiotensin I converted by ACE (angiotensin converting enzyme) to angiotensin II
   • angiotensin II incr BP by vasoconstriction
   • *ACE inhibitor drugs for HTN
   • angiotensin II stimulates production of aldosterone from adrenal cortex
5. Aldosterone causes kidney tubules to incr reabsorption of Na and H₂O.
   • incr body fluid volume (incr BP)

AVP/ADH System:

1) function

2) stimulated by and released from where?

Arginine vasopressin (AVP) aka antidiuretic hormone (ADH)

1)#1: regulate water retention (anti-diuretic enzyme), #2 moderate peripheral vasoconstriction (incr BP).

2) released from posterior pituitary with dehydration/hypovolemic shock (hemorrhage)

ANP/BNP systems

1) net effect

2) ANP secretion and effect

3) incr BNP signifies...

Atrial natriuretic peptide (ANP) & Brain natriuretic peptide (BNP):

1. net effect of BNP and ANP is a decrease in blood volume and a decrease in cardiac output.
2. ANP= powerful vasodilator secreted by STRETCHED atrial myocardial cells. Reduces the H₂O, Na, and adipose loads on the circulatory system, thereby reducing blood pressure.
3. incr BNP = dx of acute CHF & incr chance of heart failure

volume of blood remaining in ventricle at end of diastole and beginning of systole (when it begins ejecting blood into system).

preload (best described as end-diastolic volume, EDV).

pressure against which the contraction of the ventricle has to fight in order to inject blood into circulation, largely dependent on aortic pressure.

afterload (assoc with end-systolic volume, ESV)

*FYI*

Diseases that increase afterload

LV: HTN, aortic stenosis, aortic insufficiency

RV: pulm HTN

Diseases that decrease afterload

LV: mitral regurg

Pressure-Volume Loop of the Heart

1)displays pressure and volume of....

2) when does isovolumic pressure change occur?

3) the width of the loop represents...

4) labeling of x & y axises

1) LV

2) Isovolumetric pressure changes:

• from preload (EDV) and beginning of systole (Aortic valve opens)

AND

• from closure of aortic valve (ESV) to beginning of diastole (opening of mitral valve, ventricular filling).

3) width= stroke volume

4) x= volume (mL), y=pressure (mmHg)

[image]

 let's say your very unlucky pt has a hemorrhage OR is severely dehydrated, what are the effects on blood volume, ventriculr loads, stroke volume, & cardiac output?

 hemorrhage/dehydration=decr blood volume=

decr preload=smaller stroke volume =

low Cardiac Output

You have an older pt with rigid arteries. What are the effects on BP, ventricular loads, stroke volume, & cardiac output?

Rigid arteries=HTN=

incr afterload=

decr stroke volume=

decr CO

What can you conclude about the relationship of preload/afterload and stroke volume/CO?

PRELOAD IS  DIRECTLY RELATED TO STROKE VOLUME.

(Incr preload, incr SC and CO)

AFTERLOAD IS  INDIRECTLY RELATED TO STROKE VOLUME.

(Incr afterload, decr SV and CO)

CARDIAC FUNCTION PARAMETERS

***KNOW THIS ALL...IT IS ON THE TEST (possibly written, not multiple choice)!!!!!

1) Cardiac Output (CO)=

*nml=

2) Cardiac Index=

*a fat person's index would be high or low?

3) Stroke Volume (SV)=

*nml=

4) Ejection Fraction =

*nml=

*at what values should you be VERY concerned about pt?*

5) Pulse Pressure=

*healthy=

1) CO = SV x HR

*nml= 5L/min

2) Cardiac Index= CO/(body surface area)

*a fat person's index would be small*

3) SV=EDV - ESV

*nml=50mL

*EDV=preload, ESV=afterload

4) Ejection Fraction= SV/EDV

*nml=65%

*DANGER <30%

5) Pulse Pressure= systolic P - diastolic P

*120mmHg-80mmHg= 40mmHg

1) Preload (EDV as volume concept)

2) Afterload (ESV as pressure concept)

3) Contractility (inotropy): incr with Sympathetic stimulation; direct effect on afterload

as EDV (preload) increases, so does systolic inotropy=incr SV up to critical point, after which SV decreases.

translation: the more we stretch the ventrical, the more it will contract when given the opportunity...THINK ABOUT A RUBBER BAND.

the  ability of cardiac muscle to reach above normal requirements

Heart Failure Compensatoy Mechanisms:

1) impaired contractility + pressure overload =

2) impaired contractility + volume overload =

3) system that increases HR, inotropy, and peripheral vasocontriction

4) system that increases blood voume and vasocontriction

5) system that increases blood volume

impaired contractility + pressure overload =ventricular hypertrophy (thickened muscular walls, *not always associated with cardiomegaly)

impaired contractility + volume overload = ventricular dilation (thin walls)

3)Sympathetic Nervous System stimulation: increases HR, inotropy, and peripheral vasocontriction

4)RAAS: increases blood voume and vasocontriction

5) AVP/ADH: increases blood volume

**exhausted compensatory mechanisms = source of HF**

Cardiac output not adequate to meet metabolic needs (initially w/ exercise and later at rest).

what is this?

what are 2 hemodynamic consequences?

Heart Failure

=poor tissue perfusion/performance & incr venous pressure (edema)

Failure= lower cardiac output

Congestion= higher EDV (preload)

TYPES OF HEART FAILURE:

1) exogenous (CO?, 3)

2) endogenous (CO?, 2 most common causes)

3) Acute (2)

4) Chronic (3)

5) temporal (what is most common type of HF?)

6) physical

1) exogenous: high cardiac output (low vascular resistance): anemia, septicemia, hyperthyroidism

2) endogenous: low cardiac output (high vasc resistance): LHF from HTN, CAD

3) Acute: MI, arrhythmias

4) Chronic: HTN, CAD, valvular disease

5) temporal: systolic HF (impaired ejection, *most common) vs. diastolic HF (impaired filling)

6) physical: LHF vs. RHF

What is the most common type of heart failure?

2 mechanisms

top 3 etiologies

3 pathophysiologies

Systolic HF

decreased inotropy & decr Ej fraction (...this causes V dilation characterized by cardiomegaly and thin/overstreched myocardial wall)

causes: #1 CAD, #2 chronic HTN, #3 dilated cardiomyopathy

Pathophysiologies: compromised muscle performance, Volume overload, Pressure overload.

¡¡¡This will be on written portion of exam!!!

5 Clinical Clues of systolic left sided HF

• Hx of MI
• Cardiomegaly on PE & CXR
• Pulsus alternans
• Mitral Regurg (pansystolic, high pitched murmur)
• S3 gallop (early diastole, LLD position, @ apex)

This heart failure is characterized by insufficient ventricular filling because of a small chamber size, reduced compliance, and restricted filling.

What type of HF is it?  Etiology?

Diastolic HF as seen in

HTN,

Aortic Stenosis,

HOCM (hypertrophic obstructive cardiomyopathy),

DM (small vessel diseases)

...all lead to ventricular hypertrophy.

This heart failure impairs cardiac output and pulmonary circulation by ¨back up¨ leading to activity intolerance and decr tissue perfusion.

What is it and what are 4 causes? 

Left HF

causes: MI, cardiomyopathy, HTN, Aortic Valve Disorders

Right Sided Heart Failure:

1) etiology (4) leading to....

2)  what happens to the R ventrical?

3) what is a characteristic sx and PE finding?

1) Causes: #1 LHF, pulm HTN, PE, COPD

...leads to cor pulmonale*

2) RV dilation

3) peripheral, dependent edema & engorged liver

*FYI:

Cor pulmonale (Latin cor, heart + New Latin pulmōnāle, of the lungs) or pulmonary heart diseaseright ventricle of the heart as a response to resistance or high blood pressure in the lungs. is damage to the

Chronic cor pulmonale usually results in right ventricular hypertrophy (RVH), whereas acute cor pulmonale usually results in dilation.

Hypertrophy is an adaptive response to a long-term increase in pressure. Individual muscle cells grow larger and change to drive the increased contractile force required to move the blood against greater resistance.

Dilation is a stretching of the ventricle in response to acute increased pressure.

To be classified as cor pulmonale, the cause must originate in the pulmonary circulation system. Two major causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury, chemical agents, etc.), and chronic hypoxic pulmonary vasoconstriction. RVH due to a systemic defect is not classified as cor pulmonale.

When untreated, cor pulmonale can lead to right-heart failure and death.

Tx of HF:

1) reduction of preload (2)

2) reduction of LV afterload (2)

3) increase inotropy (1)...contraindicated in...?

4) improve ventricular relaxation (1)....used in what type of HF?

1) diuretics, ACE inhibitors=reduction of preload

2) vasodilators, ACEi=reduction of LV afterload

3) Digoxin increases inotropy ...contraindicated in diastolic HF where there is Ventricular Hypertrophy (the muscle is already thick and powerful, don't want to make it contract more, which would make it hypertrophy ever more).

4) CCBs (Ca channel blockers) improve ventricular relaxation in diastolic HF.

intrinsic myocardium disorders not secondary to other cardiovascular diseases.  Causes could include infectious disease, toxins, nutritional deficiencies, and rheumatic diseases.

What is this and name 3 classifications.

cardiomyopathies

1) dilated: enlarged ventricles

2) hypertrophic: thickened ventricle walls

3) restrictive: ventricle walls become stiff

Dilated cardiomyopathy

1) impairs which heart function?

2) #1 & #2 causes....

3) Tx & reasoning: (3)

1) impaired systolic function

2) 50% idiopathic, #2 alcohol (toxin/vitamin def)

*others: infections, chemo, recurrent MIs

3) digoxin, diuretics, anticoagulants (blood sits in the ventricle, risk of clotting)

Upon heart exam, hypertrophic cardiomyopathy (HCM) sounds exactly like....

How do you tell the difference between this and the other sound that is the answer to the question above?

Aortic Stenosis (AS):

Upon auscultation, the HCM murmur will sound similar to the murmur of aortic stenosis. However, a murmur due to HCM will increase in intensity with any maneuver that decreases the volume of blood in the left ventricle (such as standing or the strain phase of a Valsalva maneuver). Classically, the murmur is also loudest at the left parasternal edge, 4th intercostal space, rather than in the aortic area.

Hypertrophic Cardiomyopathy

...develops into diastolic HF.

Sx are a result of decr SV and CO.

diastolic dysfunction because of rigidity of muscular wall.  Causes include infiltrative disorders: amyloidosis, hemochromatosis, glycogen storage disorder.

What is this and what does it resemble in signs and sx?