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Flashcards in Heart Physiology Deck (73):

Frank-Starling Relationship -when is it valid? -physiological basis for this?

-stroke volume increases with LV end-diastolic volume (the more you fill the heart, the better it contracts) -It is only valid for a given afterload, and if you increase the afterload you decrease the slope of the curve -stretched myocytes contract harder and faster (like an elastic band) -when streched too far the myosin and actin don't overlap, so it can't contract very well when overstretched


Define preload

- the stretch of the myocytes before the heart contracts -synonymous with LVEDV


Define afterload

- the wall stress in the ventricle during contraction (how much tension is being generated in the muscle cells during contraction)


Define wall stress in words

The tension generated in any one myocyte during contraction


What does wall stress depend on?

-radius- the more stretched a myocyte is the more tension it can generate -pressure: you need pressure to open aortic valve. If you have HTN you need even more. If you have stenosis you need more. -wall thickness decreases the wall stress


Does high afterload mean high blood pressure?

No! It could be stenosis....


What does the heart do if it has a chronically high afterload?

- the ventricles concentrically hypertrophy to decrease the wall stress (myocytes gain more myofibrils in parallel). -A hypertrophied ventricle is less compliant, so the overall work is more, but the work of each myocyte is lessened


What is the Law of Laplace ?

AKA Wall stress or tension is proportional to: (P*r)/thickness


Why does contraction happen more slowly with a heavier load?

- at high afterload myocytes develop more tension so there are fewer free myocytes available to contract so it takes longer to get the blood out of your heart.


Ejection fraction equation -common measurement technique

stroke volume/EDV -ofter measured with echo by dividing the smallest width by the largest width during a contraction


What is the origin of S1, S2, S3 and S4 heart sounds?

S1: mitral + triscuspid close S2: aortic and pulmonic valves close S3: rapid filling and expansion of the ventricle (e.g. CHF) S4: atrial contraction into a ventricle that cannot expand further (e.g. ventricular hypertrophy)


What can cause murmurs (and examples of each class)?

-flow across a partial obstruction (aortic valve stenosis) -Increased/disturbed flow through normal structures -Ejection into a dilated vessel/chamber (aortic aneurysm) -Regurgitant flow across an incompetent valve (e.g. mitral regurg) -Abnormal shunting from high to low pressure (e.g. ventricular septal defect)


What is a gallop murmur?

S1+S2 and either S3 or S4


What is physiological splitting of S2? -what is the reason?

On inspiration S2 can be heard as (A2, P2), whereas on expiration S2 is heard as a single sound. -on inspiration, negative intrathoracic pressure draws venous return to the RA. This extra volume causes delayed closure of the pulmonary valve.


Where to best hear S1

The apex of heart (5th interspace, midclavicular line)


Where to best hear S2

The aortic and pulmonic areas (right and left 2nd interspaces)


When does a heart valve close?

When the pressure upstream exceeds the pressure downstream


Does opening of valves produce a sound?

No- not physiologically


Define heart failure - characterized by?

- 3 main etiologies of HF

The inability of the heart to adequately pump blood/oxygen to perfuse peripheral tissues, or when it does so at abnormally high filling pressures. Characterized by decreased CO +/- volume overload *** this is a diagnosis. It doesn't say anything about etiology***

3 main etiologies:

-impaired contractility

-high afterload

-impaired ventricular filling


Define cardiomyopathy

A disease of the heart muscle that can be due to a number of causes- clinically manifested by HF


Define systolic heart failure (+ 2 main causes for it)

Poor systolic performance resulting in increased venous pressures and decreased cardiac output. IMPAIRED CONTRACTION. LVEF < 40%

- impaired contractility (e.g infarction, ischemia, volume overload (regurg, VSD)

-increased afterload (stenosis, HTN)


Define diastolic HF (+ 2 main causes for it)

Poor performance in diastole resulting in increased venous pressures and decreased CO. IMPAIRED RELAXATION LVEF high or low

-impaired ventricular filling (mitral stenosis, tamponade)

-impaired ventricular relaxation (hypertrophy, ischemia, restrictve cardiomyopathy)


Can you have both diastolic and systolic HF? -commonality in both?

Yes, they frequently coexist. Both have high ventricular filling pressures.


Most common cause of hospitalization is people over 65? Most expensive single disease? Survival rates after one hospitalization for HF?

CHF CHF 1 billion per year Not very good- prognosis is similar to those of some aggressive cancers


Too much preload results in... Too much afterload results in....

Chronic volume overload Chronic pressure overload


How does the heart respond to chronically high preload?

The chamber dilates (remodels eccentrically) to compensate . SV is maintained, but over time the increase in diameter leads to less efficiency and lower stroke volume.


How does the heart respond to chronic pressure overload?

The chamber wall becomes thicker to preserve stroke volume, but over time thicker walls don't relax as well, so filling pressure increases causing dilatation (remodeling), and a further decrease in stroke volume


Do ischemic cells result in diastolic or systolic dysfunction? Do infarcts result in diastolic or systolic dysfunction?

Diastolic- oxygen is required for relaxation Systolic- cells are dead and cannot contract


What are the components of stroke volume? -what affects the "efffective SV"?

-preload -afterload -contractility -back flow affects the effective SV


Some common causes of heart failure

hypertension valvular disease ischemic heart disease cardiomyopathy


Things that could cause low LV preload

mitral stenosis, LV hypertrophy, pericardial constriction


Things that could cause high afterload

hypertension, aortic stenosis


Things that could cause backflow

shunts, aortic regurgitation, mitral regurgitation


Contrast concentric and eccentric remodelling

Concentric- the outer diameter stays the same, the lumen decreases. The relative wall thickness increases. Sarcomeres are added in parallel.

Eccentric- the outer diameter and the lumen may change. The relative wall thickness decreases. Sarcomeres are added in series. 


How to characterize murmurs

-intensity (grade 1-6) -timing (sys, dia, continuous or early, mid, late sys or dia) -Sound character (shape, pitch, quality) -Location (maximal intensity) -Radiation - Response to maneuvres


Examples of types of lesions causing aortic stenosis

- Calcific degenerative -Congenital bicuspid - Rheumatic Ao stenosis


How does the pressure differential between LV-Ao change in stenosis?

-Usually LVP~AoP in systole -With stenosis LVP> AoP in order to drive blood through a narrowed +/- stiffened valve


Define pulsus parvus et tardus

a weak ("parvus") and late ("tardus") pulse. Seen in aortic stenosis


Chest radiograph changes in aortic stenosis

- Normal LV size -Dilated ascending aorta -May see calcification of the aortic valve in the lateral view


One big difference between aortic/pulmonary valves and atrioventricular valves

-aorti/pulmonary are semilunar and completely passive -atrioventricular valves are attached to papillary muscles via chordae tendinae that hold them in place during contraction


Options for valve replacement

Open heart surgery with a St. Jude bileaflet valve or a Carpentier-Edwards porcine valve. Percutaneous catheter for Edwards transcatheter heart valve


When you will hear AV valve and aortic/pulmonary valve regurgitation?

Mitral/Tricuspid: systole Aortic/Pulmonic: diastole


What are the commonest valve lesions?

-Aortic or mitral stenosis -Aortic or mitral regurg **right-side valvular lesions not as common


Frank-Starling curve for normal and impaired hearts


What happens to preload, afterload and wall stress with stenosis? What kind of remodelling occurs?

Afterload: increases in the chamber upstream of the stenosis

Preload: increases because more volume is required to maintain normal stroke volume, and the ventricle is less compliant after hypertrophy

Wall stress: increases because of the increased pressure. After hypertrophy, a smaller radius and thicker wall would decrease wall stress somewhat. 

Remodelling would be concentric hypertrophy because the ventricle needs more force to push the blood out. 


What happens to preload, afterload, and wall stress with regurgitation?


What kind of remodelling occurs?

Preload: increases because regurgitant fluid is added to normal fluid return. This helps maintain SV.

Afterload: decreases overall because the blood can take two paths out of the ventricle. But the increased EDV would act to increase preload because it is stretching the ventricle

Wall Stress: decreases for the reasons mentioned above

Remodelling would be eccentric because the ventricle needs more volume to keep the SV normal, and the afterload is not increased. The ventricle would dilate.


What are lines A-B, B-C, C-D and A-D?


AB- ventricular filling (diastole)

BC- isovolumetric contraction

CD- ventricle emptying into the ventricle

DA- isovolumetric contraction


What is stroke volume, afterload, preload, contractility?

Stroke volume= Volume of B- volume of A

Afterload: Point C

Preload: Point B

Contractility: a tangent drawn to point D. Lower slope is lower contractility


What would happen to a PV loop of a heart with higher preload, but the same contractility and afterload?

Stroke volume increases, ESV stays the same


What would happen to a PV loop of a heart with higher contractility but the same preload and afterload?

Stroke volume increases, ESV decreases


What would happen to the PV loop of a heart with higher afterload, if preload and contractility remain the same?

SV decreases and ESV increases


Key features in history, physical and imaging for aortic stenosis


  • usual gradual onset
  • presents with angina, syncope, SOB or combination


  • crescendo-decrescendo mid-systolic mumur, radiates to carotids
  • pulsus parvus et tardive
  • S4 


  • Increased ejection velocity
  • No hypertrophy on radiograph until v. late in disease course


Key features in history, physical and imaging for aortic regurgitation


  • usually gradual onset
  • most likely to present with dyspnea. Angina and syncope uncommon.



  • wide pulse pressure (--> water hammer pulse, nailbed capillary pulsations)
  • decresendo early-diastolic murmur
  • S3
  • displaced PMI


  • backwards flow from Ao to LV on echo
  • chest radiograph shows enlarged LV and Ao


Key features in history, physical and imaging for mitral stenosis


  • dyspnea usually 1st symptom
  • sometimes presents with pregnancy
  • progresses more quickly than aortic stenosis, so younger people get it


  • opening snap
  • mid-diastolic mumur (obstructed filling)
  • pre-systolic crescendo murmur (obstructed atrial contraction) 


  • High transmitral flow on echo
  • Large LA on readiograph, large LV, pulmonary congestion



Key features in history, physical and imaging for mitral regurgitation


  • gradual onset, dypnea and fatigue
  • usually murmur is first thing to come to attention


  • blowing pansystolic murmur
  • S3


  • backflow in echo
  • LV and LA enlargement on CXR


Conservative, pharmacological and invasive management of valvular stenosis and regurgitation

Eventually the valve has to be replaced

No conservative treatment

Pharmacological treatment for heart failure (reduce preload, increase inotropy) and arrhythmias that develop



How to treat a patient with low blood pressure?

1st: increase preload by IV fluids

2nd: increase inotropy +/-  vasoconstrict


Neurohumoral changes associated with heart failure

-what do they ultimately do?

Heart failure is the inability to adequately perfuse all the tissues, so:

  • RAS is activated to bring up blood pressure (= more fluid, more preload, more filling pressure, more afterload (vasoconstriction), myocardial fibrosis)
  • SNS is activated to bring up blood pressure (= increased work (risk of ischemia), fibrosis/remodelling/hypertrophy, vasoconstriction (inc. afterload), cardiotoxicity)

Within the heart pressures are high, so:

  • ANP and BNP are released from the atria and ventricles respectively


***the compensatory mechanisms (except ANP/BNP) make the HF worse ***


Signs of heart failure

Signs of low CO

  • cool +/- mottled extremities
  • hypotension + tachycardia (can be hypertensive too...)

Signs of volume overload

  • Elevated JVP
  • Rales
  • S3 or S4
  • Peripheral edema or ascites
  • Use of accesory muscles to breath


Symptoms of heart failure

Symptoms of low CO:

  • confusion
  • fatigue
  • angina

Symptoms of volume overload

  • SOB (orthopnea, PND)
  • Nocturnal cough
  • leg swelling/ abdominal bloating



Important findings in history of a HF patient

  • Possible causes of cardiomyopathy
  • Functional status (NYHA classification)
  • Thorough ROS to identify cardiomyopathy from other sources (e.g. receiving breast cancer drugs..)


Characteristics of right vs. left sided HF (+ most common cause of right-sided HF)

Right sided results in systemic edema- most common cause is left-sided HF

Left sided results in pulmonary edema (will hear rales in lungs)


Contrast compensated and decompensated HF (+ acute vs. chronic)

Compensated HF has minimal symptoms because the compensatory mechanisms of the heart are working

Decompensated HF is symptomatic and the compensatory mechanisms of the heart are overwhelmed.

Acute means the symptoms are happening right now

Chronic means that the symptoms/diagnosis have been around and stable for a while


Possible complications of pathologic hypertrophy


-increased infarct size if there is an MI

-sudden death (e.g. arrhythmias)

-heart failure


What else changes, besides the structure of the heart, in pathologic hypertrophy?

  • Signalling within the cell, receptor expression, ANP/BNP expression, fuel utilisation....LOTS
  • It's post-ischemic recovery is poorer than a non-hypertrophied heart


What tells a cardiac myocyte to hypertrophy?

- stretch receptors

-hormones (ang II, NE/Epi)

-growth factors


***multiple responsible pathways***


Contrast physiologic and pathologic hypertrophy

  • Physiological utilizes more FA, whereas path. uses glucose :(
  • Pathologic has more fibrosis
  • Physiologic recovers much better from ischemia


Steps in the initial stabilization of an acute HF patient

- Airway (oxygenate, may need CPAP or intubation)


-IV access

-Seated posture

-diuresis (Lasix) and vasodilation (if BP good)

**inotropes and vasopressors used only for severe +/- refractory symptoms


Goals of acute HF treatment

-decrease preload

-decrease pulmonary edema

-decrease wall stress

-increase CO

-support BP as necessary


Device therapies for HF

ICD: implantable cardioverter-defibrillator

Resynchronization therapy (biventricular pacemaker)

LVADs;: left ventricular assist device, usually as a bridge to transplant


Be able to draw a WIgger's diagram:

-LV pressure, Ao Pressure, LA pressure

-EKG that goes along with it and the volumes


What are the a,c and v waves in LA pressure on the WIgger's diagram?

a= atrial contraction increases pressure

c= ventricl contracts and pushes valve back into the atrium, increases pressure

v= atrium filling while the mitral valve is closed. 


What are the hemodynamic consequences of tachycardia and bradycardia?

Tachycardia: as heart rate increases, stroke volume decreases (decreased filling time and preload) and eventually cardiac output drops, blood pressure drops, syncope and confusion can ensue. Myocardial demand increases (extra work) and supply is reduced (reduced diastolic time) so coronary flow is reduced

Bradycardia: slow heart reduces cardiac output and therefore blood pressure. preload is probably unchanged, possibly increased, and coronary flow is probably unaffected due to increased diastolic time. But this depends on how slow the heart is going and if it's CO is so low as to decrease the Aortic root-LVP gradient.