PV loops

Where on an EKG is S1?

S1 is when the mitral and tricuspid valve closes, it is seen at the QRS complex

Where on the EKG is the S2 sound?

This is from the aortic and pulmonary value closing in diastole and it occurs around the end of the T-wave

Why can splitting be heard sometimes in S2?

The pulmonic sound can be delayed from inspiration

What case cause the pulmonic valve to close before the aortic?

Left bundle branch block

Why does an S3 sound occur and what can cause it?

Its from an unusual rate of flow into ventricles

Ventricle based problem:Dilated hypertrophy ( cardiomyopathy)

Flow based problem (extra flow): pregnancy, heart failure, mitral regurgitation

The S4 sound is associated with?

Stiff ventricles

Muscle thickened hypertrophy: hypertension, aortic stenosis, or hypertrophic cardiomyopathy

Muscle infiltration can be restrictive cardiomyopathy

What is EDV??

Volume after atrial contraction → The amount of blood in the right/left ventricle after diastole

Normally around 120 mL

What is ESV??

The amount of blood remaining in the ventricles at the end of contraction ( systole)

Normally 50ml

How is cardiac output calculated?

HR x SV =CO

What can effect stroke volume?

1. Preload

2. After load

3. Inotropy

More blood to eject is what?

Increased preload

Preload

Is the volume of blood filling at ventricles at end of diastole. Greater filling (↑ pre-load) increases how much the muscles stretch increasing muscle contractility to allow more pressure.

↓ preload vs ↑ preload

Lower fluid or volume will have less pressure or ejection

High fluid to start with ( higher EDV) more pressure or ejection

Afterload

The resistance / pressure ventricles must overcome to push out blood

Decreased afterload means decreased resistance

Positive inotropy Will

Increase contractility

This is the sympathetic portion ( adgenergic )

What can cause an increase? Digoxin, digital

Negative inotropy

Decreased contractility

Parasympathetic (cholenergic)

What Can cause a decrease? CAD, myocarditis, calcium channel blockers

How is inotropy determined

Intercellular calcium concentration

Ejection fraction can be an index for

Inotropic state of the heart

↑ Inotropy = ↑ ejection fraction

What do cardiac glycosides do in the heart?

Inhibit na+/k ATPase to increase output force by allowing for more intercellular calcium.

Examples of high afterload

HTN and aortic stenosis

What is ventricular wall stress

This is the tension w/n the myocardial walls during systole

Laplaces law to find wall stress

Wall stress (T) = pressure x radius/ 2x wall thickness

↑Pressure =↑ wall stress

↑Radius= ↑ wall stress

↑ wall thickness =↓ wall stress

A dilated eccentric heart is likely to fail at what phase and why?

At systole and this is because the ventricles lack contractility, less ejection fraction

A hypertrophic concentric heart fails in what phase and why?

Diastole and the ventricles are too rigid to properly fill.

Treatment for inotropy/ chronotropy

Beta blockers: blocks epinephrine/ norepinephrine on the heart decreasing heart rate and contractility

Treatment for reducing afterload

ACEI ARBs diuretics

Treatment for reducing preload

Vasodilators

What is the most common cardiomyopathy

Dilated cardiomyopathy

What is dilated hypertrophy associated with?

Decreased contractility meaning volume overload and over filling the ventricle

How does a dilated cardiomyopathy heart function

It is less strong in systole (when it should contract → which is why it has to dilate) and has loud filling making S3 sound

Pathophysiology of dilated cardiomyopathy

↓ Contractility to ↓ cardiac output to ↑ systemic vascular resistance leads to î preload finally leading to ↑ dilation

Common causes of 2° dilated cardiomyopathy

A- alcohol

B-beri beri: in severe thiamine deficiency

C- chagas disease: parasite that resides in the heart ( South America)

C- cocaine

C- Coxsackie virus type B

D- Doxorubicin toxicity

Peripartom

What is the second most common cardiomyopathy?

Hypertrophic cardiomyopathy, a concentric type which is due to pressure overload

Hypertrophy most prominent at interventricular septum

How does the heart function in hypertrophic cardiomyopathy

Maintains strength in systole, but due to LV strength it fills poorly ( diastolic HF)

Makes the S4 sound

Pathophysiology of HOCM

↑ in septal hypertrophy leads to 2 issues. First the LV outflow obstruction second is ↓ diastolic LV filling. Both lead to HF preserved ejection fraction ( greater than 40)

Causes of HOCM

Familial → a mutation in 1 of the nine sarcomere genes ( Heavy Chain Myosin - HCM - is most common)

Frederic's ataxia and fabry disease

2 ° cause is tacrolimus

What cardiomyopathy does not have hypertrophy?

Restrictive caralomyopathy

Tissue may enlarge, but this not due to muscle mass but here immune infiltration or microscopic fibrosis

Pathophysiology of restrictive CM

↑ myocardial infiltration → stiffer ventricles and ↓ diastolic LV filling → HFpEF

There is still normal contractivity

Etiology of restrictive CM

Amylodosis, hemochromatosis, sarcoidosis

How dilated cardiomyopathy causes heart failure ( left side)

Left side HF finding

↓ CO on left →↑ ESV → ↑ LA pressure →increases pulmonary valve pressure → ↑ pulmonary cap wedge pressure

Consequence: Pulm. Edema

Symptoms of dilated CM

Orthopnea, paroxysmal nocturnal dysprea, SOB especially on exertion

Diagnostic: CXR

DCM right side

↓ CO on right → ↑ ESV → ↑ RA pressure →↑ Central venous pressure this futhers:

• SVC - JVD ( kussmaul sign- inspiration makes JVD more pronounced)

• IVC - ↑ hepatic congestion→hepatomegaly / cirrhosis and portal HTN → ascites, esophageal varices, and Caput medusae

• IVC - pitting edema

HOCM pathophysiology for signs

↑CO on left →↑ ESV → ↑ LA pressure →increases pulmonary valve pressure → ↑ pulmonary cap wedge pressure

Leads to pulmonary edema and this to dysprea

Signs symptoms of HOCM

From ↓ CO it can effect the brain and heart therefore it's SAD: syncope, angina, and dyspnea

What are the most extreme events of someone w / HOCM over exerting themselves

Ventricular tachycardia, Vfib, and sudden cardiac death

When does the murmur for HOCM get louder?

When blood flow to the heart is further reduced - can see this in valsalva or standing position

• Can Be from low pre-load ( less EDV - less that the ventricles fill)

• Low afterload because that means there is less resistance→ less S resistance = easier to eject and more blood is ejected out

Why does inspiration decrease the murmur sound of HOCM

This is because inspiration ↑ venous return to heart ↑ preload

What med should not be used for hypertrophic C.M.

Diuretics because it can ↓ preload